Current Concepts of Cerebrovascular Disease — Stroke Vertebrobasilar Disease Time for a New Strategy

VERTEBROBASILAR ischemia is a common disorder which is now frequently diagnosed by medical students, house officers, practitioners, and consultants alike. Although brainstem softening was recognized in the 19th century, the underlying pathology was not understood until the classic report of Kubik and Adams in 1946.' These authors called attention to the clinical features in patients discovered at postmortem to have had an occlusion of the basilar artery and emphasized the abrupt onset and very poor prognosis of this condition. After Fisher reported that transient ischemic attacks frequently occurred in patients with occlusion of the internal carotid artery and, in fact, that they warned of an impending stroke, Denny-Brown, Siekert, Millikan, Fang, Williams, and others called attention to similar transient ischemic episodes related to disease of the posterior circulation. The term "vertebrobasilar insufficiency" was born. Treatment for this newly described condition began in the 1950's with enthusiastic use of anticoagulant therapy as a result of a number of clinical trials, all of which were uncontrolled. Also, in all of these trials vertebrobasilar disease was considered as a single entity. Most studies revealed a small measure of benefit from anticoagulant treatment when large groups of patients were studied. Clinicians are still debating the indications for anticoagulant therapy in patients with vertebrobasilar ischemia. Since the 1950's, a number of therapies have been used for posterior circulation ischemia. Surgically created extracranial-intracranial shunts (usually occipital to posterior inferior cerebellar artery) have been tried in a small number of patients; the indications for this procedure remain uncertain. Some investigators have advocated carotid endarterectomy for patients with vertebrobasilar ischemia and coexistent carotid stenosis; when formally studied, carotid surgery offered little or no benefit in a group of patients with this combination of findings. Antiplatelet aggregating agents, e.g., aspirin, sulfinpyrazone, and