The carotid system consists of three major arteries: the common carotid, internal carotid, and external carotid. As indicated in Fig. 33-1, the right common carotid artery arises at the level of the sternoclavicular notch from the innominate (brachiocephalic) artery, and the left common carotid comes directly from the aortic arch. The common carotid arteries ascend in the neck to the C4 level, just below the angle of the jaw, where each divides into external and internal branches (sometimes the bifurcation is slightly above or below this point). This part of the extracerebral circulation is essential to an understanding of stroke. The carotid vessels are subject to atherosclerotic narrowing, atherothrombotic occlusion, arterial dissection and rarely, other processes such as various forms of vasculitis. There are two ways in which carotid stenosis causes ischemic symptoms; the main one is by the embolization from atherosclerosis and platelet-fibrin material originating in the artery and the less common one is a result of hypoperfusion of the ipsilateral cerebral hemisphere.
Occlusion of the common carotid artery accounts for less than 1 percent of cases of carotid artery syndrome, the remainder being because of disease of the internal carotid artery itself. Nevertheless, the common carotid can be occluded by an atheromatous plaque at its origin in the thorax, more often on the left side. Atherosclerotic stenosis or occlusion of the midportion of the common carotid may also occur years after radiation therapy for laryngeal, thyroid, or other head and neck cancer. If the bifurcation is patent, few if any symptoms may result because retrograde flow from the external carotid maintains internal carotid flow and perfusion of the brain.
The remainder of this discussion is concerned with disease of the internal carotid artery. The territory supplied by this vessel and its main branches is shown in Figs. 33-1 and 33-2. The territory affected by diminished blood flow in the brain in cases of carotid occlusion is highly dependent on the configuration of the circle of Willis. For example, when the anterior communicating artery is very small, the ipsilateral anterior cerebral territory is affected as well. In extreme instances where the circle of Willis provides no communication to the side of an occluded carotid artery, thus isolating the hemisphere from other blood flow, massive infarction involving the anterior two-thirds or all of the cerebral hemisphere results. If the two anterior cerebral arteries arise from a common stem on one side, infarction may occur in the territories of both vessels. The territory supplied by the posterior cerebral artery will also be included if this vessel is supplied by the internal carotid rather than the basilar artery (a configuration that reflects a residual fetal origin of the posterior cerebral artery). The clinical manifestations of atherosclerotic thrombotic disease of this artery are among the most variable of any cerebrovascular syndrome because the internal carotid is not an end vessel. In most individuals, it is in continuity with the vessels of the circle of Willis and those of the orbit, and no part of the brain is completely dependent on it. Therefore, occlusion, which occurs most frequently in the first part of the internal carotid artery immediately beyond the carotid bifurcation, is usually silent.
If one internal carotid artery had been occluded at an earlier time, occlusion of the other may cause bilateral cerebral infarction. The clinical effects in such cases may include coma with quadriplegia and continuous horizontal “metronomic” conjugate eye movements.