Pseudo subclavian steal syndrome: Case report

Highlights

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  We hereby report a case which closely mimicked signs and symptoms of Subclavian Steal syndrome.

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  On further analysis, etiology was found to be due to congenital vascular malformations and atherosclerotic changes in the internal carotid artery.

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  We could not find similar reported cases in literature.

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  The figures are updated to clarify the clinical findings.

Abstract

Introduction

Vertebrobasilar insufficiency (VBI) is a condition that results from restricted blood flow to the posterior portions of the brain, which are primarily served by the vertebral and basilar arteries. It is the most common cause of vertigo in the elderly and is usually accompanied by impaired vision and sensation. Congenital abnormalities, atherosclerosis, stroke and/or trauma may all lead to decreased vertebrobasilar circulation. A syndrome called Subclavian Steal Syndrome (SSS), which manifests with similar neurological symptoms but with a different pathophysiology, may also cause VBI.

Case presentation

A middle-aged female presented with gradual onset fainting and vertigo attacks. Cardiac, auditory and autonomic etiologies were investigated and excluded. Clinical findings and presentation were highly suggestive of subclavian steal. However, subsequent CT angiography showed normal subclavian arteries. Instead, findings included a persistent right trigeminal artery (PTA), stenosis of the right proximal internal carotid artery, atresis of the left vertebral artery and distal segment of right vertebral artery, congenitally compromised changes in vertebral circulation (bilateral absence of the posterior communicating arteries (PCOMs)) and an absent anterograde vertebrobasilar circulation. Symptoms resolved after carotid endarterectomy.

Discussion

Due to the absence of a normally developed posterior circulation, the PTA was the main source of blood supply for the patient. Development of recent artheromatous changes in the right internal carotid artery, however, resulted in decreased blood through PTA, further compromising posterior circulation. This resulted in vertebrobasilar insufficiency, and manifested in symptomology similar to SSS.

Conclusions

This clinical encounter illustrates the relative contribution of anatomical and vasoocclusive factors in closely mimicking symptoms of subclavian steal syndrome.