Upsala J Med Sci 81: 113-1 18, 1976 Segmental Arterial Spasm in Patients with Total Brain Infarction LARS-ERIK LORELIUS From the Department of Diagnostic Radiology, University Hospital, Uppsala, Sweden ABSTRACT An arteriographic investigation has shown that segmental spasm occurs in a relatively high frequency of patients with total brain infarction (12 of 30), and if spasm at the origin of arterial branches is included, the frequency is still higher (19 of 30). The phenomenon is possibly a sign of changed sympathetic tone, the pathophysiological significance of which is discussed. INTRODUCTION During the last 20 years sporadic reports have been made of wave-like, regular, inconstant luminal variations in arteries at arteriography. This phe- nomenon is usually limited to one segment of the artery and arteriographically it somewhat resembles fibromuscular hyperplasia. It differs from the latter condition, however, by the softness and strict re- gularity of the waves. Furthermore, these waves can be altered or made to disappear completely by another injection of contrast medium, with or without previous injection of a vasodilative agent. The length of the wave in the affected segment is correlated to the diameter of the artery. This ar- teriographic phenomenon will be referred to in the following as a segmental spasm ( S S ) . The first t o report this observation was Ratschow (13). H e believed it to be due to a dysfunction of the vessel, and claimed that occurrence of the phe- nomenon on the arteriogram was related to pain. Wickbom & Bartley (18) found that arterial “spasm” were eliminated by Priscol’ and claimed that a proneness to spasm was more marked in patients with Raynaud’s disease. They also pointed out that the frequency of the phenomenon was inversely proportional to the age of the patient, which they A substance with a moderately effective adrenergic - blocking function. 8-762852 attributed to increasing rigidity of the vessel wall with advancing age. Lindbom (10) reported that spasms could be induced by raising the intra- vascular pressure or by stretching the artery. The term “standing waves” was used by Theander (16), who concluded from measurements on films that the length of the waves in the involved segment was directly related to the diameter of the artery, and also observed that in one case the vessel was wider when stationary waves were noted than when they were absent. From these findings and from physical arguments he considered that the phenomenon could not be due t o spasm but was caused by resonance in the vessel proximal to an occlusion. This theory was questioned by Kohler (9) who made a physico-physiological analysis of the stand- ing wave phenomenon and demonstrated that the arteriographic length of the assumed standing wave in human arteries did not correspond to the luminal variations. Kohler considered that the changes were prob- ably caused by a spastic circular constriction of the arterial wall, and were very likely an artificial phe- nomenon produced by an irritation from the con- trast medium in an especially sensitive vessel. Mayall (11) postulated that the wavy contour was due to the formation of layers between the blood and the contrast medium, with rippling at the inter- face between these layers. This theory was refuted, among other authors, by New (12), who pointed out that the phenomenon could also be perceived with a horizontal roentgen beam. Ishikawa et al. (6, 7) reported a series of arteriographies of the lower ex- tremity, in which accordion-like arterial shadows were present in about 10%. They claimed that this high frequency was related to the fact that the examination was performed with semiflexed legs and under spinal anesthesia, conditions which Upsala J Med Sci 81 114 L . - E . Lorelius n 1 lalal “1 1 15 25 35 45 55 65 age n t spasm 15 25 35 45 age n m a l e 3 1, -- 15 25 35 45 55 6 5 age n female 4 - 1 2” 1 L 15 25 35 45 55 65 W e Fig. 1 . Age distribution in the total material and in the patients with spasm. The type of spasm with regard to pa- tients age and sex. seemed to predispose to longitudinal contraction of the artery. They also pointed out that the phenom- enon persisted after manual compression of the artery proximal to the site of injection. On electrical stimulation of the sympathetic nerves supplying the kidney in the rabbit, Bergquist et al. (2) found lu- minal variations in the renal artery reminiscent of those observed in clinical segmental spasm. Seg- mental spasm has been reported from practically all arterial areas except intracranial and coronary arteries-vital vascular areas in which an arterial spasm would endanger the patient’s life. Segmental spasm has not been reported in patients examined under general anaesthesia. The causative mechanism of the phenomenon has been much discussed but little attention has been paid to its pathologic significance and its possible relation to the patient’s symptoms. Its occurrence has been reported in Raynaud’s disease ( l a ) , Biir- ger’s disease (15) and angiodyskinesia (1, 5, 8). N o uniform group of patients has been presented, how- ever. In recent years some reports of nonocclusive ischemia in the small intestine in association with cardiovascular shock have been published (19,20). Siegelmann et al. (14) demonstrated spasm of the superior mesenteric artery in the dog in, various types of cardiovascular shock in angiographic in- vestigations; this spasm was located at the origin of arterial branches, and caliber variations were found in the main trunk or branches of the superior mesenteric artery. We have observed segmental spasm at some arteriographies in our clinic. A relatively large num- ber of these cases have been patients with total brain infarction, For this reason we have re- examined a series of arteriograms from patients with this conditions. MATERIAL AND METHODS (1) A retrospective investigation was performed on ab- dominal arteriograms from 36 patients with clinical signs of total brain infarction (areflexia, hypothermia, per- sistent respiratory arrest as tested by a 3-min apnoea test; isoelectric EEG on two occasions in each patient). On these patients cerebral 4 vessel-angiography was per- formed to establish the diagnosis and renal aortography in order to survey the renal circulation with a view to pos- Fig. 2. Patient 14, a woman aged 38 years. Total cerebral infarction following intoxication. A semi-selective arterio- gram clearly shows segmental spasm in the right renal artery. The patient was having an isoprenaline drip in- fusion at the time of the examination. Upsala J Med Sci81 Arterial spasm in brain death 115 Fig. 3. Patient 21, a man aged 42 years. Total cerebral infarction following an operation for subdural hematoma. Selective angiography of the superior mesenteric artery. No drugs were given during the examination. Note that in addition to segmental spasm there is a distinct spasm at the origin of arterial branches. sible kidney donation. Six patients with atherosclerosis were excluded. Of the remaining 30 patients, 14 were women and 16 men. The age and sex distributions are shown in Fig. 1. (2) Clinical data were obtained from the case journals. The pulse, blood pressure and temperature were recorded regularly. (3) Clinico-chemical blood analysis of PO,, pH and PCO,, using a blood gas analyzer at 37°C (Instrumentation Lab. Incorp., no. 313), were performed within 24 hours following the roentgen examination. HCO, was measured at 37°C with a microcapillary technique on a radiometer p R meter 22 (Radiometer, Copenhagen). Na+ and K+ were determined by flame photometry (IL 343 Flame Photometer, Instrumentation Lab. Inc., Lexington, Mass., USA). These data were also obtained from the case journals. Cerebral 4 vessel-arteriography was performed by the Seldinger technique, using a grey Odman-Ledin catheter with side-holes, introduced through the femoral artery. The tip of the catheter lay in the ascending aorta. At renal aortography 30 ml Angiografin was injected at the level of the origins of the renal arteries, i.e. with the catheter tip located at L 1. All injections were given at a pressure of 5 kp per cmz, using a Cisal I1 pressure syr- inge. The exposure frequency during the renal aorto- graphy was 3 frames per sec for 3 sec, followed by 1 frame every other sec for 8 sec. At selective arteriography of the superior mesenteric artery 25 ml Angiografin was in- jected at a pressure of 3 kp per cm2; the exposure fre- quency was 2 frames per sec for 5 sec and 1 frame every other sec for 10 sec. This selective arteriography was per- formed in patients 21 to 30, with the exception of patient 27. At all arteriographies the ECG, injection time and ex- posure were registered with a Mingograf E n 81 or Mingo- graf 800 direct recorder. The film-focus distance was 100 cm in all examinations and the same apparatus was used on all patients included in this investigation. The exposure data were 60-75 kV, 500-600 mA and 0, 10 sec. At the re-examination of the abdominal arteriograms, the renal and superior mesenteric arteries were examined with respect t o segmental spasm and the latter arteries were also examined for spasm at the origins of branches. Spasm at the origins of branches was considered t o be present if at least two of the branches were slightly but clearly narrowed for a very short distance (1-2 mm). RESULTS (1) All examined patients showed clinical signs of total brain infarction, and this was also evident at cerebral 4 vessel-angiography. (2)-The systolic blood pressure was low in all cases (50-100 mmHg). The rectal temperature was also low and varied between 31 and 35.2"C, with the exception of one patient (no. 16), whose tempera- ture was 39°C. This latter measurement was pos- sible wrong. The heart rates varied from 50 t o 150 beats per min at the time of the angiographies. See Tables I and 11. (3) The PO,, PCOz, pH and serum electrolyte values are given in Tables I and 11. At the time of the angiographies the patients were being treated with the drugs listed in Table I. (4) Of the 30 patients, one had segmental spasm in the right renal artery. Eleven had segmental spasm in the superior mesenteric artery or its branches. Sixteen patients had spasm at the origin of two or more branches of the superior mesenteric artery. Nine patients had both segmental spasm and spasm at the origin of arterial branches. (See Tables I and 11). Only in 11 patients was no form of spasm observed. DISCUSSION In 6 patients atheromatosis was noted. These pa- tients were relatively old and none of them showed signs of spasm, possibly because of rigidity of the vessel wall. They were therefore excluded from the subsequent analysis. The reason for the high fre- quency of spasm in patients with total brain infarc- tion can be assumed to be associated with the clini- Upsala J Med S C I 81 + 1 f T ab le I. D at a fo r th e in di vi du al p at ie n ts : a g e, se x, d ia gn os is , d ru gs g iv en , b lo od p re ss u re , h ea rt r at e, te m pe ra tu re a n d c li n ic o- ch em ic al a \ - la bo ra to ry v al u es 2 2 S ys t. H R ? P U nf or tu na te ly t he c as e jo ur na l fo r pa ti en t 1 co ul d no t be f ou nd . S = se gm en ta l sp as m ; B S = sp as m a t or ig in o f br an ch es . D ru gs : a , a tr op in e; b , i ns ul in ; c , i so pr en al in ; d , a nt ib io ti cs ; e , p he ny to in ; f , f ur os em id e; g , c or ti co st er oi ds ; h , c hl or pr om az in e c N o. S ex (y rs ) S S B S D ia gn os is D ru gs (m m H g) m in ) (m m H g) ( m m H g) (m m ol /l ) pH (m m ol /l ) (m m ol /l ) "C f' 2 A ge B P (b ea ts / PO , PC O , H C 0, - N a+ K + T em p. 5 1 d 52 - - ic h em or r 2 0 20 + \ + su bd ur h em at d, g 70 50 - 22 .5 20 7. 5 13 4 3. 1 31 .0 3 8 40 + + fr ac t sk ul l g 90 70 17 2 33 24 7. 46 14 3 5. 7 34 .2 4 0 23 + + fr ac t sk ul l d, g 90 70 15 9 35 28 7. 45 14 4 4. 0 34 .5 16 + + fr ac t sk ul l d7 g 70 60 23 6 21 14 7. 34 13 7 3. 9 32 .8 - su ba ra ch f 70 60 14 1 19 22 7. 55 13 8 3. 9 33 .0 5 P 6 0 34 - 7 0 15 + + su ba ra ch d 70 80 - 21 .5 21 .5 7. 52 15 1 4. 3 34 .8 30 + + su ba ra ch - 90 80 25 6 34 16 7. 43 14 3 3. 7 35 .0 - - su ba ra ch h, c 10 0 15 0 10 8 42 20 7. 27 14 3 4. 0 34 .9 8 6 23 - - fr ac t sk ul l f 90 80 70 37 17 7. 38 13 9 2. 5 33 .7 9 d 10 d 52 11 d 46 - - op tc f, h 50 90 - - - - 13 5 5. 1 35 .2 13 .5 7. 4 12 9 3. 7 34 .2 - - - - 13 0 2. 2 33 .2 53 12 0 30 - in to x ba rb e th yl C 10 0 50 98 19 12 7. 37 15 0 2. 9 32 .6 13 0 38 + - fr ac t sk ul l f, g 70 12 0 16 5 57 23 7. 26 14 8 3. 9 35 .2 14 0 18 24 7. 47 13 2 3. 9 39 .0 e , f , g , h 10 0 10 0 11 9 30 op ic a ne w 15 6 16 0 29 17 6 41 + + su bd ur al h em or r e, f , g , h 80 90 99 41 28 7. 44 14 7 3. 6 33 .4 28 - + fr ac t sk ul l g, h 70 70 10 3 18 21 .5 7. 7 14 8 3. 1 32 .5 op ic h em at - 60 70 - - - - 13 3 6. 1 33 .0 18 0 19 d 41 20 d 23 - + fr ac t sk ul l e, g 90 80 16 4 49 27 .5 7. 21 14 3 3. 3 34 .0 42 + + op s ub d he m at - 80 10 0 10 7 34 33 7. 58 14 6 3. 7 35 .0 - ce r he m or r g 90 60 - - 17 .5 - 14 6 4. 2 32 .0 21 6 22 d 45 + 35 + + su ba ra ch a, d 11 0 80 10 2 33 23 .5 7. 51 13 9 4. 0 31 .5 - su ba ra ch - 90 70 - - 23 .5 - 15 8 4. 1 35 .0 23 0 24 0 40 25 0 22 - + fr ac t s ku ll f 70 60 - - 25 .5 - 15 8 4. 1 31 .0 19 - + op a n ew c, g 10 0 80 12 6 45 22 7. 36 16 5 2. 4 34 .5 - fr ac t sk ul l b 90 70 - - 26 .0 - 15 3 1. 8 31 .5 26 6 27 d 32 + 49 - + fr ac t sk ul l C 80 13 0 - - 26 .0 - 14 5 4. 4 33 .0 90 70 67 34 24 .5 7. 6 15 4 4. 4 33 .2 - - 26 .0 - 16 6 4. 0 34 .0 28 d 29 6 30 30 0 25 - + en ce ph al it is c, d , g 80 80 60 70 78 30 su ba ra ch f, h su ba ra ch f, h 70 80 - - - - - - - - - - + fr ac t sk ul l d , g - Arterial spasm in brain death 117 Table 11. Shows the statistical datas f o r the different groups offindings with respect to arterial bloodpres- sure, heart rate, arterial P O z , PCOz, H C 0 3 - , p H , serum Nu+, K + and body temperature HR BP (beats/ PO, PCO, HCOB- Na+ Kf Temp. (mmHg) min) (mrnHg) (mmHg) (mmol/l) pH (mmol/l) (mmol/l) (“C) ss M n S.D. Range s at origin M n S.D. Range All spasm M n S.D. Range N o spasm M n S.D. Range 86 71 12 12 12 15 70-110 50-100 83 81 7 7 11 22 70-100 60-130 85 75 19 19 12 18 70-110 50-130 76 86 10 10 18 28 50-100 60-120 153 8 64 98-256 115 4 41 67-164 141 12 58 67-256 113 6 36 70-165 29.4 21.9 7.46 144 10 12 10 12 7.6 6.3 0.07 6 19.049.0 12.0-33.0 7.34-7.58 134-153 36.5 24.7 7.47 155 4 7 4 7 13.9 2.2 0.22 11 18.049.0 21.5-26.0 7.21-7.70 143- 31.4 23.0 7.46 148 14 19 14 19 9.8 5.3 0.12 9 18.049.0 12.0-33.0 7.21-7.70 134- 72 72 35.8 20.4 7.38 138 6 7 6 10 12.9 3.9 0.11 9 19.0-57.0 13.5-24.0 7.26-7.55 129-158 cal status. These patients comprise an extreme g r o u p t h e i r higher brain functions have been eliminated and their respiratory centre is out of function. Their blood pressure and body tempera- ture are low, and the heart rate is also usually low. The electrolyte balance is frequently disturbed and artificial ventilation is necessary, entailing a risk of changes in the acid-base status. This retrospective investigation revealed no difference between pa- tients with and those without spasm with respect to blood pressure, temperature, blood gases, blood pH and serum sodium and potassium. Four of five pa- tients treated with a n isoprenaline drip infusion, l l of 13 patients treated with cortisone, and all 6 pa- tients receiving antibiotics had segmental spasm. The material is too small, however to draw any con- clusions from these observations. It is interesting that there appear to be no reports on segmental spasm in children, whereas adoles- cents are well represented in various series. One possible explanation for this is that in children arteriographies are performed under general an- aesthesia, which affects the vascular tone. Preli- minary results of direct nerve recordings in man show that the sympathetic activity in cutaneous 3.7 0.9 12 1.8-5.7 3.7 7 0.7 2 . 4 4 . 4 3.7 0.8 1.8-5.7 19 3.9 1.1 2.2-6.1 10 33.2 12 1.5 3 1.0-35.0 33.2 7 1.2 3 1 .O-34.5 33.2 19 1.3 31.0-35.0 34.6 10 1.8 3 1.5-39.0 nerves is inhibited on induction of anaesthesia (17) with fluothane. A similar anaesthesia might be the reason for the absence of segmental spasm in chil- dren. The sympathetic activity is altered if the im- pulses from higher centers to the vasomotor center are eliminated (3, 4). It is thus possible that the sympathico-adrenal activity in patients with total brain infarction has a completely different profile from that in other individuals; this is possibly to be regarded as dysfunction of the sympathetic nervous system. The simultaneous occurrence of spasm at the origins of branches of the superior mesenteric artery and segmental spasm in the same vascular area supports the theory that segmental spasm is caused by a change in tone of the arterial wall. The high frequency of spasm in a group of patients with total brain infarction may thus mean that segmental spasm is related t o changes in the sympathetic activity of the individual. Applied to clinical routine, the occurrence of segmental spasm may thus, in certain circumstances, be a sign of altered vascular tone, the late effects of which are rela- tively uninvestigated. Thus the phenomenon may imply a change (possibly an increase) of the sym- pathetic tone of the patient. It would be of interest Upsala J M e d S c i 81 118 L . - E . Lorelius to investigate whether in healthy persons this phe- nomenon is a manifestation of a sympathetic dys- function, which could cause changes in the regional blood flow. 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Wickbom, I . & Bartley, 0.: Arterial “spasm” in Upsala J Med Sci 81