Vertebrobasilar Ischemia: Embolic |
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and Low-Flow Mechanisms |
Ramon Berguer
A 51-year-old male experienced over a period of 6 months a major stroke and several transient ischemic attacks (TIAs) of vertebrobasilar distribution. The original episode consisted of loss of balance, loss of coordination, and loss of the left visual field whiledrivinga bus, which resultedin a road accident. Since then, he hadexperienced four additional episodes of aphasia and paraparesis lasting for 4–5 h. A diagnosis of vertebral artery dissection was made at the local hospital and he was placed on Coumadin. Concomitant diagnoses were hypertension, non-insulin-dependent diabetes, and hypercholesterolemia. In spite of adequate international normalized ratio (INR) levels, his symptoms continued and he was referred to us.
On admission, magnetic resonance imaging (MRI) showed right occipital and left cerebellar infarctions (Fig. 34.1).
Question 1
The work-up of this patient presenting with symptoms of vertebrobasilar ischemia and MR evidence of infarction in the posterior circulation territory must include:
A. CT scan of the brain B. Carotid-vertebral duplex
C. Electroencephalogram (EEG) D. Arteriogram
E. Echocardiogram
R. Berguer
Cardiovascular Center, The University of Michigan, Ann Arbor, MI, USA
G. Geroulakos and B. Sumpio (eds.), Vascular Surgery, |
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DOI: 10.1007/978-1-84996-356-5_34, © Springer-Verlag London Limited 2011 |
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Fig. 34.1 MRI showing cerebellar and brainstem infarctions
Question 2
The etiology of infarction in the posterior circulation territory is:
A. Distal embolization of atheromatous material from vertebral or basilar artery lesions B. Arrhythmia
C. Bilateral carotid disease in patients with absent vertebral arteries D. Traumatic or spontaneous dissection of the vertebral artery
E. Transient drop in central aortic pressure in a patient with severe bilateral stenoses of both vertebral arteries
An arteriogram showed a 60% stenosis in the fourth portion of the right vertebral artery, and a tenuous, incomplete (dissected) left vertebral artery, which, at the level of C1, became a normal artery and, higher up, joined with the opposite vertebral artery (Fig. 34.2). A diagnosis of embolizing dissection of the left vertebral artery was made. Because the dissection was not responsive to medical therapy, the patient underwent a bypass from the left internal carotid to the left (suboccipital) vertebral artery using a saphenous vein.1 The proximal vertebral site of the embolizing dissection was ligated above C1, immediately below the distal anastomosis of the carotid-vertebral bypass (Fig. 34.3). The patient did well from this operation and stopped having symptoms. His anticoagulation was discontinued. He remains asymptomatic after 5 years of follow-up.
Question 3
Once the objective diagnosis of vertebral artery dissection is made in a patient with vertebrobasilar symptoms the next step is:
34 Vertebrobasilar Ischemia: Embolic and Low-Flow Mechanisms |
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Fig. 34.2 Arteriogram: dissection of the left vertebral artery, which is occluded from its origin to C4 (lower arrow), dissected and partially occluded from C4 to C1 (between arrows), and normal distal to C1 (Reprinted from Berguer1, © 1999, with permission from The Society for Vascular Surgery)
A. Anticoagulation with heparin, then Coumadin
B. Stenting of the dissection followed by antiplatelet therapy
C. Surgical bypass of the dissected segment with ligation of the proximal vertebral artery
34.1 Commentary
Dissection of the vertebral artery may occur spontaneously or result from trauma.2–6 The traumatic event is usually an exaggerated extension or rotation of the neck as may occur during sports and deceleration injuries. Clinical presentation of dissection of the vertebral artery starts with pain over the posterolateral aspect of the neck irradiating to the nuchal area. There may be an interval of several days between the initial pain, announcing the dissection, and the development of clinical symptoms. The latter are ischemic manifestations of the dissection and appear in 60–90% of patients after an interval of several days, usually 1–2 weeks. In order to visualize the lesion, a carotid-vertebral duplex would not provide a discriminating datum to help in the decision on the management of our patient because it could only detect a concomitant carotid atheroma, which
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Fig. 34.3 Postoperative carotid arteriogram showing a saphenous vein bypass from the distal cervical internal carotid to the vertebral artery beyond C1 (Reprinted from Berguer1, © 1999, with permission from The Society for Vascular Surgery)
has never been shown to be the source of infarction in the cerebellum or brain stem. The dissected segment of the artery can be visualized by MRA, CTA or arteriography. The latter will provide in addition the information about the carotid arteries that you would have derived from the carotid-vertebral duplex. [Q1: D, E] [Q2: A, D] The visualization of the target territories (brain stem, cerebellum and often occipital lobes) is best done with MRI. The dense bone surrounding the brain stem creates resolution artifacts in the CT scan.
The treatment of symptomatic vertebral artery dissection is empirical with systemic anticoagulation. Patients with posterior fossa symptoms should undergo MRI before starting anticoagulation to rule out a subarachnoid hemorrhage. The latter may occur following dissection and rupture of the fourth (intracranial) segment of the vertebral artery.
Anticoagulation is empirically used for the treatment of symptomatic dissection because the ischemia that follows is usually the consequence of embolization from the double channel, not a low-flow effect. The fear of distal extension of the dissection with anticoagulants has prompted some leading experts to give antiplatelet therapy to patients