Occlusive Cerebrovascular Disease

Introduction
Every year, half a million people in the United States suffer a stroke. Fifteen to 30 percent of these episodes are fatal, making stroke the third leading cause of death in this country. Carotid artery stenosis is responsible for as many as 25% of these strokes in the elderly. Most neurologic events are caused by emboli occluding small cerebral arteries. Emboli from the carotid bifurcation may consist of platelet aggregates that form on irregular or ulcerated surfaces or plaque debris liberated by turbulent flow and intraplaque hemorrhage. Less commonly (fewer than 10% of cases), emboli arise from the heart (eg, mural thrombus or atrial myxoma) or from the aortic arch. Stroke can also be caused by intracerebral hemorrhage (from trauma or a ruptured cerebral aneurysm) or by small vessel occlusive disease in the pons, basal ganglia, and internal capsule of the brain (lacunar infarcts).

A transient ischemic attack (TIA) is defined as the sudden onset of a neurologic deficit that resolves completely within 24 hours. A stroke is a neurologic deficit that persists beyond 24 hours. A single TIA or stroke is associated with a 30% risk of subsequent stroke.

Risk factors for carotid disease include hypertension, diabetes mellitus, hypercholesterolemia, advanced age, smoking, and coronary artery disease.

Clinical Findings
A. Symptoms and Signs

Clinical manifestations of carotid artery occlusive disease include contralateral weakness or sensory loss, expressive aphasia, and amaurosis fugax (transient partial or complete loss of vision in the ipsilateral eye). Vertebrobasilar TIAs are characterized by brain stem and cerebellar symptoms, including dysarthria, diplopia, vertigo, ataxia, and hemiparesis or quadriparesis.

Dizziness and unsteadiness, particularly when associated with a quick change in position, are nonspecific symptoms and more often the result of postural hypotension than of vertebrobasilar insufficiency. Syncope is rarely a manifestation of carotid artery occlusive disease. Rather, it is usually a result of a cardiac arrhythmia.

Occlusive disease of the brachiocephalic arteries may be accompanied by cervical bruits, diminished or absent pulses in the neck or arms, Hollenhorst plaques (bright, refractile cholesterol emboli) in the retinal arteries, or a blood pressure difference between the two arms of more than 10 mm Hg. The common carotid pulsation can be examined qualitatively by palpation at the base of the neck. The presence of superficial temporal artery pulsation confirms patency of the ipsilateral external carotid artery. A carotid bruit is a high-pitched, blowing noise localized in the mid neck close to the angle of the mandible. Heart sounds must be auscultated to make certain that the bruit is not caused by a referred murmur of aortic stenosis. Only 30% of patients with cervical bruits have carotid stenosis greater than 60%. The absence of a bruit also does not preclude the possibility of a hemodynamically significant lesion - thus, bruits are neither sensitive nor specific for carotid occlusive disease. In fact, asymptomatic carotid bruits are stronger predictors of death from coronary artery disease than of death from stroke.