Posterior Circulation: Large Artery Occlusive Disease and Embolism

Introduction

In many respects, strokes involving the posterior circulation parallel those of the anterior circulation. Ischemic infarcts may be due to atherothrombosis of large arteries, lacunes from occlusion of small penetrating arteries, or embolism from either the heart or proximal vascular sites. Unlike those of the anterior circulation, however, the vessels of the posterior circulation are more difficult to study by noninvasive means. Carotid stenosis in the neck, for example, can be easily assessed by duplex ultrasound, but similar disease in the extracranial vertebral artery may require angiography for reliable detection. The complexity of structures in the brain stem also makes localization of infarction more difficult. Nevertheless, certain clinical patterns help localize the lesions and suggest which vessels are involved . These clinical findings aid the physician in determining the most likely mechanism of stroke and the most appropriate therapy.

Vascular Anatomy of the Posterior Circulation

Vessels comprising the posterior circulation include the vertebral arteries arising from the subclavian arteries, three paired cerebellar arteries, the basilar artery, and two posterior cerebral arteries (PCAs) arising from the top of the basilar artery ( Fig. 81.1 ). The structures supplied by these vessels include the brain stem, cerebellum, thalamus, medial temporal lobes, and occipital lobes. There are two types of vessels that supply the brain stem and cerebellum. Long circumferential arteries such as the cerebellar arteries run superficially and supply the lateral brain stem and the cerebellar hemispheres. Smaller penetrating arteries arise from the dorsal surface of the basilar artery and supply the basis pontis and medial portions of the brain stem. These smaller arteries do not have collaterals and occlusions of these vessels result in brain stem lacunes.

Posterior circulation ischemia may cause slurred speech, motor weakness, sensory change, and visual loss, similar to that found with anterior circulation stroke. Clinical features pointing to brain stem or cerebellar ischemia, however, are vertigo, nystagmus, gait or limb ataxia, double vision, bilateral motor weakness, and coma ( Table 81.1 ). Findings such as aphasia, hemineglect, and higher-order sensory loss (astereognosis, agraphesthesia) are more commonly seen in anterior circulation ischemia.

Subclavian Artery Disease

Atherosclerosis of the subclavian artery also commonly involves the origin of the vertebral artery. “Subclavian steal” refers to a condition in which there is severe stenosis or occlusion of the subclavian artery proximal to the origin of the vertebral artery. Low pressure in the subclavian artery distal to the lesion leads to “stealing” of blood from the vertebral artery . Angiography in this situation shows normal antegrade blood flow in the right vertebral artery, but reversed flow down the left vertebral artery into the subclavian artery.

On examination of a patient with left subclavian steal, for example, one may find a left supraclavicular bruit and decreased amplitude or delay of the left radial pulse. Occasionally patients have symptoms such as dizziness, parethesias, blurred vision, and ataxia, but many have no symptoms at all. Exercise of the affected arm is said to precipitate symptoms (by drawing off more blood into the arm), but this is actually a rare finding. Although patients may have transient neurological symptoms, the risk of stroke is small. Many patients with subclavian stenosis are asymptomatic, and the condition is an incidental finding on examination.

Vertebral Artery Origin Disease

Atherosclerotic disease of the vertebral artery origin (VAO) is common in patients with peripheral vascular disease, but because of difficulty in noninvasive detection of these lesions, the natural history of VAO stenosis is uncertain. If both vertebral arteries are of good caliber, then occlusion of one extracranial vertebral artery can be asymptomatic. On the other hand, in some patients one vertebral artery is either very small, occluded, or ends before connecting with the basilar artery (an anatomical variant). In these individuals with “basilarization” of the remaining vertebral artery, disease in this artery can produce symptoms similar to basilar artery stenosis.

Atherosclerosis of the VAO can lead to transient ischemic attacks (TIAs) or stroke in a manner parallel to a carotid artery stenosis in the neck . Spells may be hemodynamic in nature (particularly if the other vertebral artery is small or diseased) or due to platelet fibrin emboli from the site of atherosclerosis. Patients have TIAs with dizziness, ataxic gait, slurred speech, transient weakness or numbness of the extremities, and diplopia. If the extracranial vertebral artery thromboses, a clot may break off and embolize into the intracranial circulation, causing stroke. An embolus typically lodges in the intracranial vertebral artery (ICVA), at the apex of the basilar artery, or in a PCA.

Patients with VAO stenosis and TIAs often respond to antiplatelet therapy (e.g., aspirin or clopidogrel). Those with continued spells on antiplatelet agents can be treated with anticoagulation with warfarin, but the benefit of long-term anticoagulation in this setting is uncertain. Anticoagulants are often used in patients with acute vertebral artery thrombosis to prevent propagation of the clot or distal embolism. These patients can be treated with warfarin for several months and then switched to aspirin, because by that time the thrombus has probably organized and poses less of a threat for embolism. For patients with vertebral origin stenosis who have continued TIAs despite medical treatment, the stenosis can be treated by endovascular means, typically with a stent placement . Case series suggest that this is a relatively safe procedure with resolution of TIAs, but no large, randomized clinical trial has been performed to compare the long-term outcome of stenting with medical therapy alone.