Occlusion of the distal intracranial portion of the internal carotid artery (the “T”)—for example, by an embolus—produces a clinical picture like that of middle cerebral artery occlusion: contralateral hemiplegia, hemihypesthesia, and aphasia (with involvement of the dominant hemisphere). When the anterior cerebral territory is included, there are additional clinical features of leg paralysis as described further on. Patients with such large infarctions are usually immediately drowsy or stuporous because of an ill-defined effect on the reticular activating system.
Headache, located as a rule above the eyebrow, on the side of the infarction, may occur with thrombosis or embolism of the carotid artery, but cranial pain is not invariable and is usually mild. The headache associated with occlusion of the middle cerebral artery tends to be more lateral, at the temple; that of posterior cerebral occlusion is located in or behind the eye.
When the circulation of one carotid artery has been incompletely compromised, reducing blood flow in both the middle and anterior cerebral territories on that side, the zone of maximal ischemia lies between the two vascular territories (“cortical watershed”) or, alternatively, in the deep portions of the hemisphere between the territories of the lenticulostriate branches and the penetrating vessels from the convexity (“internal” or “deep watershed”). The infarction in the first instance occupies a region in the high parietal and frontal cortex and the adjacent subcortical white matter. Its size depends upon the adequacy of collateral vessels. Weakness tends to involve the shoulder and hip more than the hand and face. With long-standing carotid stenosis, the cortical watershed zone shifts downward toward the perisylvian portions of the middle cerebral artery territory, even to the extent that a stroke may weaken facial movement or cause a nonfluent aphasia. With impaired perfusion of the deep watershed, infarctions of varying size are situated in the subfrontal and subparietal portions of the centrum semiovale.
The situation can be somewhat different in cases of total circulatory collapse from cardiac arrest, in which perfusion fails not only in the watershed areas between the middle and anterior cerebral arteries but also between the middle and posterior cerebral arteries. Bilateral infarctions are then situated within a zone that extends in a sickle-shaped strip of variable width from the cortical convexity of the frontal lobe through the high parietal lobe, to the occipitoparietal junction. Deeper infarctions also occur, but they more often take the form of contiguous extensions of the just described cortical infarction into the subjacent white matter. There may appear to be several separate infarctions after hypoperfusion states, but these often turn out to be radiographically visible portions of a larger border-zone lesion.
The internal carotid artery also supplies the optic nerve and retina. For this reason, transient monocular blindness occurs prior to the onset of stroke in 10 to 25 percent of cases of symptomatic carotid occlusion. Yet central retinal artery ischemia is a relatively rare manifestation of carotid artery occlusion, presumably because of efficient collateral supply in the globe.
Signs of carotid occlusion include transient monocular blindness or visual loss or dimness of vision with exercise, after exposure to bright light, or on assuming an upright position; retinal atrophy and pigmentation; atrophy of the iris; peripapillary arteriovenous anastomoses in the retinae; and claudication of jaw muscles. However, the cardinal clinical signs of stenoses, ulcerations, and dissections of the internal carotid artery are TIAs. It is a subject of debate whether these are the result of fibrin platelet emboli or a reduction in blood flow. TIAs were discussed earlier, but here it can be stated again that they represent an important risk factor for stroke.