396 STROKE VOL 14, No 3, MAY-JUNE 1983

4. Bevan JA, Bevan RD: Sympathetic control of the rabbit basilar artery. In Owman C, Edvinsson L (eds) Neurogenic Control of Brain Circulation, Oxford, Pergamon Press, Vol. 30. 285-294, 1977

5. Falck B, Hillarp NA, Thieme G, Torp A: Fluorescence of catecho­lamines and related compounds condensed with formaldehyde. J Histochem Cytochem 10: 348-354, 1962

6. Lindvall O, Bjorklund A: The glyoxcylic acid fluorescence histo-chemical method: A detailed account of the methodology for the visualization of central catecholamine neurons. Histochem 39: 97-127, 1974

7. Bevan RD, Tsuru H: Functional and structural changes in the rabbit

THE OCCURRENCE OF CEREBRAL INSUFFI­CIENCY in the subclavian steal syndrome is well known, and was described by several authors as main­ly regarding the vertebrobasilar system.1^1 Later, Lord et al5 proved statistically that discontinuity of the circle of Willis is the principal factor activating these symp­toms in this syndrome. On the other hand, the numer­ous clinical signs of the subclavian steal syndrome described up till now are thought to be due to addition­al coexistent atherosclerotic extra- and intracranial le­sions in the same patient.5

The importance and variety of collaterals and their task in the hemodynamics of the subclavian steal syn­drome was stressed in some reports.5-7 The role of the carotid system, which is included among these collat­erals, has always been overshadowed by the well known vertebro-vertebral shunt.7 Thus, little is known about probable clinical signs that might occur when the carotid system acts as an unusual collateral pathway in that syndrome.

We therefore intend to discuss a case of left subcla­vian steal syndrome with presenting signs of transient ischemic attacks of the region supplied by the left internal carotid artery. We found it interesting to relate these symptoms to the internal carotid system as an unusual collateral network in this case, as well as with the absence of coexistent demonstrable atherosclerotic lesions of that artery and its branches.

From *the Departments of Neurology, tRadiology and ^Psychiatry, Assaf Harofeh Governmental Hospital, Zerifin, Israel.

Address correspondence to: Dr. Emil Goldenberg, Department of Neurology, Assaf Harofeh Hospital, Zerifin 70300, Israel.

Received May 28, 1982: revision accepted December 23, 1982.

ear artery following sympathetic denervation. Circ Res 49: 478-485, 1981

8. Hart MN, Heistad DD, Brody MJ: Effect of chronic hypertension and sympathetic denervation on wall/lumen ratio of cerebral ves­sels. Hypertension 2: 419-428, 1980

9. Hermsmeyer K, Aprigliano O: Cellular mechanisms of the neuro­tropic influence in vascular muscle. In Bevan J, Godfraind T, Maxwell R, Vanhoutte P (eds) Vascular Neuroeffector Mecha­nisms, New York, Raven Press, 365-367, 1980

10. Goldberg AL, Jablecki C, Li JB: Effects of use and disuse on amino acid transport and protein turnover in muscle. Ann NY Acad Sci 228: 190-201, 1974

Case Report A right handed 52 year old man was examined in the

emergency room because of difficulties of speech and subjective weakness and tingling sensations involving the right side of his face and right extremities. As reported by his family, the onset was abrupt, about two hours prior to hospitalization.

The neurological examination revealed a fully alert athletic man, with hypotonic mild weakness of the right arm and leg, a positive Chaddock sign in the right, and an obvious right central facial weakness. On examining his speech, a nominal aphasia was noted which caused him tension and anxiety. The examina­tion of the optic discs was essentially normal, except for slight arteriosclerotic changes; spontaneous venous pulsations were observed bilaterally. The remainder of the cranial nerves were normal and meningeal signs were absent. A perceptible difference was felt on pal­pation between the carotid pulses (Rt > Lt) without bruits. The arterial blood pressure was 160/80 mm Hg in the right arm and 110/70 mm Hg on left. A distinct systolic murmur was heard in the left supraclavicular fossa. No murmurs were audible over the precordial area. Otherwise, the physical examination was nor­mal. At this stage the patient was given intravenous Rheomacrodex (Dextran 40) and transferred from the emergency room to the ward. On neurological exami­nation three hours later, these findings disappeared with a complete recovery of the right hemiparesis and aphasia.

The past history of our patient revealed a mild dia­betes of four years duration and a previous transient episode of right unilateral weakness and speech distur-

Unusual Clinical Signs in Left Subclavian Artery Occlusion: Clinical and Angiographic Correlation

E. GOLDENBERG, M.D.,* A. ARLAZOROFF, M.D.,* M. PAJEWSKI, M.D.,t

AND C. L. CARPEL, M.D.t

SUMMARY A case of left subclavian steal syndrome with transient ischemic attacks of left carotid artery distribution is presented. An attempt to explain this uncommon symptomatology is based on a rare patent cervical arterial network, stealing blood from the left common carotid artery and supplying the distal portion of the obstructed left subclavian artery.

Stroke, Vol 14, No. 3, 1983

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LEFT SUBCLAVIAN ARTERY OCCLUSlOWGoldenberg et al. 397

FIGURE 1. Complete proximal obstruction of the left subclavi­an artery, with normal cervical portion of both carotid arteries, and dilatation of the rt. vertebral artery.

bances, which occurred one month prior to hospitaliza­tion and was of short duration. No complaints of ische­mic heart disease, arterial hypertension, nor venereal disease were elicited from the history. His father ap­parently died from a stroke and the mother disappeared in the holocaust. Our patient was a heavy smoker but took no alcohol. It should be pointed out that he changed his job six months prior to his two neurologi­cal episodes, when he began to work as a heavy truck driver.

On the first day of hospitalization his EEG tracing was normal, except for bursts of slow wave activity in the left hemisphere which appeared only on pressure over the right carotid artery. This manoeuver was per­formed after ophthalmodynamometry revealed bilater­al normal values. On brain scanning, both static and dynamic studies were normal. These tests were repeat­ed two weeks later with identical results. Routine labo­ratory tests, ECG, plain skull and chest X Rays were within normal limits. A slightly elevated fasting blood sugar was noted. The antinuclear factor was negative, complement fixation, protein electrophoresis and total lipids were also normal. Cardiological investigation

FIGURE 3. Short anastomotic branch between left deep cervi­cal artery and probably left vertebral artery.

including ECG holter monitoring and echocardiog­raphy revealed no pathology. Angiography performed two days after admission showed

1. a complete proximal obstruction of the left sub­clavian artery, normal cervical segments of both carotid arteries, and a dilatation of the right ver­tebral artery (fig. 1),

2. an intact intracranial carotid system (fig. 2), 3. marked dilatation of the left external occipital

artery, with retrograde flow in the left deep cer­vical artery (fig. 2), with a short anastomotic branch between this artery and (probably) the vertebral artery (fig. 3).

4. Late reversed flow in the left vertebral artery (fig- 4).

Due to the presence of this obvious steal from the left common carotid artery additional to the classic right-left vertebral steal, we performed the Javid test; pres­sure on the left carotid artery abolished the left radial pulse. A brain CT done three days after angiography failed to show any evidence of cerebral infarction or a space occupying lesion. There was no dilatation of the ventricular system or the subarachnoidal space.

The patient was transferred to the department of vascular surgery, where he underwent an Axillo-Axil-lary by-pass. Follow up for a year and a half reveals a

FIGURE 2. Intact left intracranial carotid system, dilatation of the left external occipital artery, retrograde opacification of left deep cervical artery. FIGURE 4. Late retrograde filling of left vertebral artery.

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398 STROKE V O L 14, No 3, MAY-JUNE 1983

complete improvement. His EEG tracing remains nor­mal, even on pressure over the carotid artery.

Discussion There is no doubt about the presence of a classical

vertebro-vertebral shunt in this patient, in view of the dilatation of the right vertebral artery and the late retro­grade filling of the left vertebral artery. This shunt did not produce any sign of vertebrobasilar insufficiency probably because the circle of Willis was intact.5 On the other hand, we observed an arterial collateral pat­tern with a steal of blood from the left common carotid artery via the left external occipital to the deep cervical artery.7 It is of roentgenological interest to stress the direct feeding of the distal left subclavian artery by the deep cervical artery. This pattern is less frequent than the direct feeding of the subclavian by the vertebral, which in turn benefits from branches of the deep cervi­cal artery.7 In our patient there is only one visible anastomosis between these two arteries. This relative­ly uncommon7 arterial collateral pattern i.e. "steal­ing" blood from the left common carotid artery may have a primary function in the etiology of the clinical syndrome.

Our opinion is based on: 1. The positive Javid test as mentioned above,

proving the relationship between the left carotid and the left radial pulse.

2. The occurrence of left hemispheric slow wave pattern in the EEG during pressure on the right carotid artery proves the relative incapacity of the left carotid artery to feed alone its ipsilateral hemisphere.8 The absence of any arteriographic demonstrable narrowing or arteriosclerotic le­sions in that artery reinforces the fact that part of its flow takes part in the steal dynamics.

Independently of the angiographic findings, three oth­er pathological processes, which may present with transient ischemic attacks, were considered as possible causes of the patient's symptomatology.

1. Angiographically not identified small ulcer­ations or thrombi could have been present in the left carotid system. This possibility was men­tioned by De Weese and Lipschik,9 who found normal angiograms in such cases, especially when performed weeks after the transient ische­mic attack. Such processes should have been identified in the angiography performed two days after the last attack in our patient, as they diappear quickly.

2. Angiography may be completely normal in cere­bral embolism of cardiac origin.10' " This possi­bility was ruled out on cardiologic investigation and lack of signs of embolism in other parts of the body.

3. Hemispheric deep lacunar infarcts with normal angiogram may cause transient ischemic at­tacks.10 Normal isotope brain scan and CT can­not rule out this diagnosis. Therefore the possi­bility cannot be rejected. Even if proved

however, such infarcts could occur as a result of carotid insufficiency due to the shunting to the subclavian artery, in the absence of any other potential risk factors.

Although the acceptance of neurological symptoms as a direct result of exercising the involved arm is an important diagnostic aid in subclavian steal syn­drome,1 this fact should not be regarded as a "sine qua non." It is well known that Fields et al reported the oral communication of E. J. Wylie in 1971,12 who was able to produce this phenomenon in only two patients out of approximately fifty. Solti et al, found this phe­nomenon in four of their eight patients with cerebral insufficiency and subclavian steal syndrome.13 In our patient, we did not elicit a clear history of exercising with the arm related to his symptoms. It should be noted however, that transient episodes of focal cerebral insufficiency occurred after the patient changed his work to a field involving significant use of the arms.

Considering the complete relief of symptoms fol­lowing the Axillo-Axillary by-pass and maintenance of the normal pattern in the EEG even following pres­sure on the right carotid artery, we believe that among the other possibilities mentioned here above, the most logical explanation is the occurrence of the transient left hemispheric syndrome due to the steal from the left carotid artery.

References 1. North RR, Fields WS, De Bakey MD, et al: Brachial-basilar insuf­

ficiency syndrome. Neurology 12: 810-820, 1962 2. Siekert RG, Millikan CH, Whisnant JP: Reversed blood flow in the

vertebral arteries. Annals of Internal Medicine 61: 64-72, 1964 3. Mc Dowell HA: Surgical correction of vertebral steal followed by

contralateral retrograde vertebral flow. Annals of Surgery 168: 154-156. 1968

4. Heyman A, Young WG Jr, Dillon M, Goree JA et al: Cerebral ischemia caused by occlusive lesions of the subclavian or innomi­nate arteries. Arch of Neurol 10: 581-589, 1964

5. Lord RSA, Adar R, Stein RL: Contribution of the circle of Willis to the subclavian steal syndrome. Circ 40: 871-878, 1969

6. Newton TH, Wylie EJ: Collateral circulation associated with oc­clusion of the proximal subclavian and innominate arteries. Amer J Roentgenology 91: 394-405, 1964

7. Labauge R, Crouset G, Castan P: L'exploration angiographique des hemodetournements dans les arteres du cou a destinee cere-brale. J de Radiol Electrorol Med Nuc 50: 200-210, 1969

8. Hughes RR: An introduction to clinical electroencephalography. Bristol, John Wright and Sons Ltd. page 68, 1961

9. De Weese JA, May AG, Lipchik EO, et al: Anatomic and hemody­namic correlations in carotid arterial stenosis. Stroke 1: 149-157, 1970

10. Pessin MS, Duncan GW, Mohr JP, et al: Clinical and angiographic features of carotid transient ischemic attacks. N Eng J Med 296: 358-362, 1977

11. Marshal J, Wilkinson IMS: The pathogenosis of carotid transient ischemic attacks in patients with normal angiograms. Brain 94: 359^02, 1971

12. Fields WS, Lemak NA: Joint Study of Extracranial arterial occlu­sion. VII Subclavian steal A review of 168 cases. JAMA 222: 1139-1143, 1972

13. Solti F, Iskum M, Papp S, et al: The regulation of cerebral blood circulation in subclavian steal syndrome. Circ 42: 1185-1191, 1970

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E Goldenberg, A Arlazoroff, M Pajewski and C L Carpelcorrelation.

Unusual clinical signs in left subclavian artery occlusion: clinical and angiographic

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1983 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.14.3.396

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