9HawisAbdul_General Romanian Neurosurgery (2015) XXIX (XXII) 1: 77 - 84 77 For residents General considerations in lumbar spinal stenosis Hawis Abdul Salam Abdul Rahman1, Gabriel Iacob2 1Syria, 2Neurosurgery Clinic Bucharest Romania “The secret of being a bore is to tell everything” Voltaire - Sept Discours en Vers sur l'Homme, 1738 Definition Lumbar spinal stenosis (LSS) is a common and often disabling, well-recognized spinal disorder that generally occurs in the sixth or seventh decade of life, although it can uncommonly occur in younger individuals, congenital or acquired, focal or diffuse (multilevel), defining a osteo-ligamentous narrowing (congenital) or shrink (secondary – acquired) of the lumbar spinal canal, a conflict between the lumbar spinal canal with vertebral body osteophytes, hypertrophy of the ligamentum flavum, zygapophyseal joint, lumbar disc hernia or a combination of these and the content represented by the cauda quina roots, lumbar spinal roots and ganglia, generating a complex set of symptoms of which the hallmark is neurogenic claudication, physical findings and radiological abnormalities. Lumbar spinal stenosis or “loss of epidural reserve” could affect the central lumbar spinal canal ± lateral recess ± the neuroforamen or any combination of these, causing nervous impingement and vascular structures compression (1-4). It can coexist with cervical stenosis too. It’s important to underline that diagnosis of LSS should be defined by symptoms and clinical findings that must be supported by neuro- imagistic evidences. Computed tomography and magnetic resonance imaging are often non- specific and there may be discrepancies between clinical symptoms and imaging findings in cases of LSS. Example: for central stenosis according to the sagittal diameter of the lumbar spinal canal there are absolute lumbar spinal stenosis <10 mm and relative lumbar spinal stenosis 10 to 14 mm (5-7). Spinal stenosis was first described only sixty five years ago by Verbiest (8): “It is characterized by narrowing of the spinal canal, the nerve root canals or the neural foramina and can produce a debilitating condition in older adults” History (1-3) (9-18) 1803 – the first medical report of spinal stenosis: Portal in France postulated that back and leg pain could be caused by bone impingement on the nerves (1-3) (9-11). 78 Rahman, Iacob General considerations in lumbar spinal stenosis 1893 – first decompressive laminectomy: Lane in England did a to relieve a woman of cauda equina syndrome caused by spinal stenosis (1-3) (9-11) 1900 - connexion between lumbo- sciatalgic pain and nerve compression was first remarked by Sachs B and Fraenkel J. (12) 1945 Sarpyener M.A. reveal congenital stricture of the spinal canal (14) 1948 Van Gelderen C. suggest that ligamentum flavum hypertrophy could be a possible cause of lumbar spinal stenosis reffering to two clinical observations. (1-3) (10-11) 1954 –Verbiest H.A. A. – a holland surgeon, defined first the clinical syndrome of lumbar stenosisin seven patients who had bilateral radicular pain and motor and sensory disturbances in the legs, caused by standing and walking and made first the difference between “narrow” and “shrink”.(15). He also remarked clinical signs in congenital lumbar spinal stenosis justified by mechanical nerve compression at saccoradiculography (16). (16)(115)(16) 1955 - Schlesinger (cited by 11) and 1972 - Epstein et al. (17) reported some cases and described the clinical and radiographic findings of facet syndrome. They pointed out the importance of the height of the intervertebral foramen on plain radiographs in narrow lateral recess cases. Since then several authors recognized and described lateral recess stenosis and lateral entrapment syndrome (18-20). In the 1960s and 1970s spinal stenosis began to be recognized as an impairing condition, also during the 1970s and 1980s, many case reports showed successful surgical treatment rates, but these were based on subjective assessment by surgeons. 1974 Kirkaldy-Willis P. Paine K, Cauchoix J, et al. precise the anathomo-pathological aspects in LSS and made correlation with clinical signs (21). 1978 Porter and colleagues discovered that individuals who experience back pain and other symptoms are likely to have smaller spinal canals than those who are asymptomatic (22) 1982 Rothman reported that a normal sized lumbar canal is rarely encountered in persons with either disc disease or those requiring a de-roofing (laminectomy) procedure (23). 1992, Johnsson, Rosén and Udén described the natural history of LSS (24) and concluded that a reasonable treatment optionfor lumbar stenosis is observation. Another investigators appreciate that significant neurologic deterioration is rare: 70% of patients reported no significant change in symptoms, 15% showed significant improvement, whereas 15% showed some deterioration (25)(26). Frequency LSS are frequent, the incidence of this condition has been reported to be 8–11% of population, generally occurs in the sixth or seventh decade of life, except congenital; in the 4th decade to men in central lumbar stenosis, in the 5-6 th decades to women in lateral stenosis. LSS is more frequent to woman: ratio woman/men: 3/1 to 5/1400,000 (30). 400,000 Americans are estimated to have spinal stenosis with increased incidence with the expansion of life-expectancy (3). Romanian Neurosurgery (2015) XXIX (XXII) 1: 77 - 84 79 For residents Generally LSS are 5 times less frequent as lumbar disc hernia. No clear correlation exists between the symptoms of stenosis and race, occupation, sex or body type; the anvergure of the degenerative process which cannot be prevented by diet, exercise or lifestyle (1-3). The anvergure of the problem is expanding: americans are estimated to have spinal stenosis with increased incidence with the expansion of life-expectancy, especially by increasing place of neuroimagistic procedures; prevalence 1 case at 1000 persons (27). Ubiquitous degeneration associated with aging may lead to stenosis of the spinal canal, especially along the lumbar spine. As a result of the changing societal age structure, the incidence of symptomatic lumbar spinal stenosis is increasing exponentially. Inpatients older than 60, lumbar spinal stenosis is found on magnetic resonance imaging in more than 20% of cases (28). Older patients’ desires for mobility and functionality, combined with improved perioperative management, have resulted in a situation where surgical intervention is being increasingly considered. In the United States, the incidence of surgery has increased eight-fold from 1979 to 1992 (29) and in 2007 37,598 people were treated surgically for lumbar stenosis in the US, totally a bill of 1.65 billion dollars (25) (26). LSS - classifications Anatomical classification (1-3) (31-33): LSS are defined by the anterior-posterior diameter less than 15 mm (normal value 15-25 mm) and lateral recess less than 3 mm. It’s to be remarked that adult cross section lumbar spinal area (av. 194 sq mm) are similar to those seen of 4 years old. LSS could be (figure 1): segmentary (2 levels 45%, 1 level 37%, 3 levels 17%) or diffuse; - central, 10% due to hypertrophic spurring, bony projection or ligamentum flavum/laminar thickening - clover leaf (“fleur de lis”): laminar thickening with subsequent postero-lateral bulging - medial - secondary to IAP hypertrophy - lateral recess and foraminal stenosis 45%, secondary to SAP hypertrophy - mixed 45% A B C D E 80 Rahman, Iacob General considerations in lumbar spinal stenosis F G Figure 1 - LSS - modified after (1)(32): A normal aspect, B short pedicles reducing the antero-posterior diameter, C central stenosis, articular process are disposed in sagittal plane, D clover leaf central stenosis, E severe stenosis macroscopic aspect, F different shapes of spinal canal in spinal stenosis, G didactic schema in central stenosis Aetiological classification (1-3) (10) (11) (21) (22) (30) 1. Congenital stenosis (narrowed lumbar channel) – described by Sarpyener at childrens (14), Verbiest in adults (8), are rare, occurring in only 5-9 % of cases. Congenital lumbar stenosis could be idiopathic or concomitent with anatomical variants: partial or total LSS; unilateral asymmetric, with discontinuity in stenosis; normal lumbar segment between 2 stenotic segments; normal central lumbar canal with lateral recess stenosis or associated with sacral stenosis. Anatomically lumbar constitutional stenosis are related to short pedicles, and short, thick, vertical lamae; sometimes medial articular part are in contact with spinous process, short interspinous and interlamae spaces, the antero-posterior diameteris ≤ 15 mm and interpedicular diameter has cvasinormal dimmension or < of 25 mm. Generally congenital stenosis are insufficient to generate clinical symptoms, but able to decompensate by secondary lesions (35) (36): - dysplastic lesions: achondroplasic, acromesomelic, arterio-hepatic, diastrophic, osteo glophonic nanism, hypochondroplasic, thanatophoric, Smith-McCort syndrome, Weill-Marchesani syndrome, Gordon syndrome – all spinal canal could be stenotic - dysostotic lesions: cheiro-lumbar, Gorlin baso celullar naevomatose, Wyers & Thier syndrome, acrodysostose A rare cause of lumbar canal stenosis are idiopathic lumbar epidural lipomatosis (37). 2. Secondary (acquired) stenosis (shrink lumbar channel): - nonspecific: degenerative changes more frequent in aged persons related to hypertrophic frequent asymmetric articular process; include central canal and lateral recess stenosis from posterior disc protrusion, zygapophyseal joint and ligamentum flavum hypertrophy/calcification, degenerative spondylolisthesis – characterized by forward displacement of a vertebra due to disc and facet degeneration (38), synovial cysts, lumbar epidural varices (39), lumbo-sacral transitional vertebra; degenerative process stages responsible for dysfunction, instability - specific: -traumatic Romanian Neurosurgery (2015) XXIX (XXII) 1: 77 - 84 81 For residents - systemic processes include: Paget disease, fluorosis, acromegaly, ankylosing spondylitis, renal osteodystrophy, neoplastic, infectious, lipomatous epiduritis of Cushing disease, tabetic arteriopaty - iatrogenic changes result following surgical procedures such as laminectomy, fusion, discectomy, malpositioned osseous grafts used for osteosynthesis 3. Combined congenital and degenerative - in several cases generally degenerative stages made symptomatic a constitutional lumbar stenosis. Pathophysiology of LSS LSS is a slow, fluctuent progression disease, occur in all affected individuals. LSS is more frequent on L3-L4 and L4-L5, segments; several patho-physiological mechanisms could be related to this condition. No clear correlation exists between the symptoms of stenosis and race, occupation, sex, body type. The degenerative process cannot be prevented by diet, exercise or lifestyle. Acute cauda equina syndrome is rare. Degenerative process stages in LSS are: dysfunction, instability, stabilization and three main factors are responsiblefor the development of ths spinal disorder (1-3) (40): 1. Disk protrusion as a a consequence of disk degeneration of a motion segment leed to height segment loss, lateral recess, neural foramen and central canal narrowing. As a consequence it effects ligamentous laxity with increased segmental mobility, with additional strain especially on the facet joints. This subclinical instability of the segment generate osseous hypertrophy, especially the facet joints, fibrotic hypertrophy of the ligamentum flavum, in addition to folding inwards subsequent to height loss. If these reactive processes do not succeed in stabilizing the segment, disk degeneration, laxity of capsules and ligaments may result in the manifest instability of spondylolisthesis. 2. The position of the spine may generate nerve root compression: the strain imposed by standing is in itself sufficient to result in hyperlordosis of the affected segment, with further protrusion of the ligamentum flavum into the spinal canal. 3. Both arterial ischemia as well as venous factors are implied in mechanical nervous roots compressions. Experimental studies have been made looking on lombar roots during walking, on normal asymptomatic patients and to those patients with claudication by LSS, using microendoscopic techniques, under local anesthesia (41). During walking oxygen roots needs are demanding a supplementary arterial supply. The strain and weight imposed by walking results in decompensation of the vascular flow to the spinal nerves, which is mostly sufficient during rest. If patient is bending anteriorly (figure 2), both the canal diameter and arterial supply is bigger. If that is not enough the patient need to sit down to restablish the normal metabolic situation. Also mechanical pressure on cauda equine is generating venous stasis affecting nervous influx by local demielination and axonal degenerescence. 82 Rahman, Iacob General considerations in lumbar spinal stenosis In extension or walking, narrowing occurs In flexion, the size of the spinal canal increases Figure 2 - LSS – modified after (1) (32): patients walk in flexion and prefer to sit and lean forward In synthesis, in LSS the mechanisms explaining simptomatology are Neural compression: Anterior: - disk protrusion or herniation - osteotic overgrowth: osteophytes Posterior: - lamar& ligamentous hypertrophy (the role of TGF-β1, TIMP-1 and TIMP-2 on hypertrophy of the ligamentumflavum in spinal stenosis patients is a local phenomenon, not systemic)(42) - facet hypertrophy, synovial cyst - spinal lipomatosis, etc Pain mechanisms may be due to: - mechanical: chronic compression of the nerve root in LSS causes compromise of blood flow leading to venous congestion, ischaemia, +/-microcirculation anomalies, intraneural edema. This then leads to the development of periradicular fibrosis. Neurogenic claudication likely arises from increased metabolic demands of the nerve root in the presence of vascular compromise and traction on the adhesed nerve root when lower extremity movement occurs during walking - instability - biochemical component especially by cytochines when disc is involved - nucleus pulposus - inflammatory–arthritis Instability: Defined by White and Panjabi (43): “the loss of the spine’s ability to maintain its Romanian Neurosurgery (2015) XXIX (XXII) 1: 77 - 84 83 For residents patterns of displacement, under physiologic loads so there is no initial or additional neurologic deficit, no major deformity and no incapacitating pain” - mechanical instability without clinical signs - symptomatic instability: intermitent pain + clinical signs of LSS Instability mechanisms are leading and responsible for spondylolisthesis and scoliosis may be due to: - loss of discal integrity - loss of ligamentous integrity - loss of facetal integrity - loss of supportive integrity: - paraspinal and abdominal muscle tone and power Conclusion Pathologic determinants that result in a stenotic canal are protruding discs, ligamentum flavum, facet and lamina hypertrophy, lysthesis, degenerative scoliosis and rotational deformities. 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