Functional Trifurcation of the Internal Carotid Artery and its Potential Clinical Significance

Abstract

OME individuals tolerate complete occlusion of the internal carotid artery without experiencing symptoms suggesting focal cerebral ischemia or demonstrating neurologic deficits indicating it. Others may experience a series of minor strokes, and then become asymptomatic. Still others, however, after a series of minor strokes, suddenly have a major stroke from which they may or may not make a satisfactory recovery. A small percentage of such patients will, without prodromal symptoms, suddenly have a major stroke from which they never recover to a significant degree. Although young patients, in general, tolerate interruption of the blood flow through an internal carotid artery better than older patients, widely divergent reactions may occur in patients of apparently comparable cardiovascular status. Actually, the situation may appear paradoxical in that a severe, persistent neurologic deficit with obstruction of the internal carotid artery may develop in a relatively young patient whereas a much older patient may tolerate such obstruction quite well. Undoubtedly, many factors influence a patient's tolerance to obstruction of the internal carotid artery. These include the peripheral blood picture, the blood pressure, the degree of peripheral atheromatosis, the tendency to development of vasospasm, the extent of anastomotic relations between the internal and external carotid arterial systems, the rapidity of occlusion of the artery, and the anatomic pattern of the circle of Willis. Certain chain reactions have been postulated as a common cause of focal cerebral ischemia. For example, if a patient becomes grossly hemiplegic in the presence of partial obstruction of the internal carotid artery by an atheromatous plaque, it may be suggested that embolization of material from the plaque or of a thrombus about the plaque has occurred. This may be postulated to have caused obstruction of the middle cerebral artery and thus have caused the cerebral tissue in its area of distribution to be dependent completely upon collateral flow through the relatively small pial and intracerebral anastomotic vessels with resulting ischemic infarction. It has been theorized that this initial reaction might also produce changes that would cause extensive extravasation of blood into the tissues of the cerebrum. However,