eMedicine Specialties > Neurosurgery > Vascular

Vertebral Artery Atherothrombosis

Author: Mark K Eskandari, MD, Associate Professor, Departments of Radiology and Division of Vascular Surgery, Feinberg School of Medicine, Northwestern University; Attending Surgeon, Division of Vascular Surgery, Northwestern Memorial Hospital; Consulting Staff, Division of Vascular Surgery, Northwestern Medical Faculty Foundation; Consulting Staff, Department of Surgery, Jesse Brown Veterans Affairs Medical Center; Consulting Staff, Department of Surgery, Evanston Northwestern Healthcare
Coauthor(s): Mark D Morasch, MD, Clinical Practice Director, Division of Vascular Surgery, Assistant Professor of Surgery, Department of Surgery, Northwestern University Feinberg School of Medicine
Contributor Information and Disclosures

Updated: Feb 20, 2007

Introduction

Problem

Ischemic mechanisms are either hemodynamic or embolic in nature. For hemodynamic symptoms to occur, significant disease must be present in both of the vertebrals, and compensatory contribution from the anterior circulation via the circle of Willis must be incomplete.

Alternatively, hemodynamic ischemia may occur with proximal subclavian artery stenosis leading to a subclavian-vertebral steal phenomenon. Such pathologic states can result in transient "end-organ" (brainstem, cerebellum, and/or occipital lobes) hypoperfusion. Regardless of the specific pathology, patients usually demonstrate reproducible symptoms following postural or positional changes. Hypoperfusion has also been described in the face of underlying cardiac insufficiency.

In general, ischemia attributable to hemodynamic causes rarely results in infarction. Patients typically present with repetitive, short-lived symptoms, which are more of a nuisance than a danger. However, they are prone to succumb to traumatic injuries resulting from loss of balance.

Embolic causes of vertebrobasilar ischemia may not be as well recognized. However, current estimates suggest that up to a third of vertebrobasilar ischemic episodes are caused by distal embolization from plaques or mural lesions of the subclavian, vertebral, and/or basilar arteries. These patients are at high risk for infarction within the tissues supplied by the posterior circulation. Emboli can arise from atherosclerotic lesions, from intimal defects caused by extrinsic compression or repetitive trauma, and (rarely) from fibromuscular lesions, aneurysms, or dissections. Compared to hemodynamic mechanisms of ischemia, emboli are more likely to cause dangerous infarcts that leave patients with permanent and debilitating strokes.

The manifestations of vertebrobasilar ischemia are varied and vague, often making the diagnosis difficult. A number of medical conditions may mimic vertebrobasilar ischemia, thus confounding the selection of patients in need of posterior circulation treatment. These include inappropriate use of antihypertensive medications, cardiac arrhythmias, anemia, brain tumors, benign vertiginous states, basilar artery migraine, and postsubarachnoid hemorrhage vasospasm.

In contradistinction to carotid disease, vertebrobasilar symptoms are poorly defined. The classic symptoms of vertebrobasilar ischemia are dizziness, vertigo, diplopia, perioral numbness, alternating paresthesia, tinnitus, dysphasia, dysarthria, drop attacks, ataxia, and homonymous hemianopsia (see Image 7). Ischemia affecting the temporo-occipital areas of the cerebral hemispheres and segments of the brainstem and cerebellum characteristically produces bilateral symptoms.

Etiology

Atherosclerosis is the primary etiology, although fibromuscular dysplasia (FMD) is an occasional cause

Pathophysiology

Vertebrobasilar ischemia is certainly less common than internal carotid artery disease, yet it must be diagnosed appropriately because it is a treatable vasculopathy. The most common disease affecting the vertebral artery is atherosclerosis. Less common pathologic processes include trauma, FMD, Takayasu disease, osteophyte compression, dissections, aneurysms, and other arteritides.

Indications

Once the diagnosis of vertebrobasilar ischemia has been confirmed with appropriate imaging, surgical correction may be considered. The mere presence of vertebral artery stenosis in an asymptomatic patient is rarely an indication for surgery. Surgical reconstruction is based on the specific etiology. The indication for surgery in patients with hemodynamic symptoms depends on the ability to demonstrate insufficient blood flow to the basilar artery.

In other words, a single normal-caliber vertebral artery can supply sufficient blood flow into the basilar artery regardless of the status of the contralateral vessel. In this particular subset of patients, surgical intervention is indicated only in the presence of a severely stenotic (>75%) vertebral artery and an equally diseased or occluded contralateral vessel. Surgical reconstruction is not indicated in an asymptomatic patient with the aforementioned radiographic findings because these patients are well compensated from the carotid circulation through the posterior communicating vessels.

In contrast, patients with symptomatic vertebrobasilar ischemia due to emboli are candidates for surgical correction of the offending lesion regardless of the condition of the contralateral vertebral artery. However, as in the hemodynamic group, surgical intervention is not indicated in asymptomatic patients with suggestive radiographic findings.

Relevant Anatomy

Atherosclerosis involving the vertebrobasilar system is known to cause posterior circulation ischemia. The posterior circulation, or vertebrobasilar system, supplies blood to the brainstem, cerebellum, and occipital lobes via paired vertebral arteries. The vertebrals converge beyond the base of the skull and form the basilar artery at the base of the pons. The vertebral artery is arbitrarily segmented into the following four parts:

• V1 - The origin of the vertebral artery arising from the subclavian artery to the point at which it enters the C6 transverse process
• V2 - The segment of the artery within the cervical transverse processes (C6-C2)
• V3 - The extracranial segment between the transverse process of the C2 and the base of the skull as it enters the foramen magnum
• V4 - The intracranial portion beginning at the atlantooccipital membrane and terminating at the formation of the basilar artery

The anterior spinal artery arises from branches off each of the vertebral arteries prior to their convergence to form the basilar artery. Pontine and cerebellar arteries arise from the basilar artery before it bifurcates into the paired posterior cerebral arteries.

Contraindications

As discussed previously, a single normal-caliber vertebral artery can supply sufficient blood flow into the basilar artery regardless of the status of the contralateral vessel. In this particular subset of patients, surgical intervention is indicated only in the presence of a severely stenotic (>75%) vertebral artery and an equally diseased or occluded contralateral vessel. Surgical reconstruction is not indicated in an asymptomatic patient with the aforementioned radiographic findings because these patients are well compensated from the carotid circulation through the posterior communicating vessels.

In contrast, patients with symptomatic vertebrobasilar ischemia due to emboli are candidates for surgical correction of the offending lesion regardless of the condition of the contralateral vertebral artery. However, as in the hemodynamic group, surgical intervention is not indicated in asymptomatic patients with suggestive radiographic findings.

Patients with symptomatic vertebrobasilar ischemia who are not amenable to surgery or investigational endoluminal therapy may be treated medically with long-term anticoagulation to prevent thrombosis.

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