The thrombotic stroke syndrome, which represents the result of low blood flow and related phenomena, develops in one of several ways. There may be a single episode, but typically the whole stroke evolves over a few minutes or hours. Characteristic is a “stuttering” or intermittent progression of neurologic deficits. This is a starkly different profile from the abrupt onset of stroke that characterizes the embolic mechanism discussed earlier in the chapter. In thrombosis, a partial stroke may occur and even recede temporarily for several hours, after which there is rapid progression to the completed deficit—or several fleeting episodes may be followed by a longer one and, hours or a day or two later, by a major stroke. Several parts of the body may be affected at once or only one part, such as a limb or one side of the face, the other parts becoming involved serially in step-like fashion until the stroke is fully developed. Or, spells of weakness or involuntary movement of a hand or arm or dimness of vision, lasting 5 to 10 min, occur spontaneously or are brought on by standing or walking. Each of the partial attacks may reproduce the profile of the stroke in miniature. In other words, the principle of intermittency seems to characterize the thrombotic process.
Also somewhat characteristic of atherothrombotic events in many, but not all cases, is the occurrence of the stroke during sleep; the patient awakens paralyzed, either during the night or in the morning. Unaware of any difficulty, he may arise and fall helplessly to the floor with the first step. This is the story given by many patients with thrombotic strokes, as well as by a number with embolic strokes.
Most deceptive are the few instances, in which the neurologic disorder evolves very gradually, over several days or longer (“slow stroke”). One’s first impulse is to make a diagnosis of brain tumor, abscess, or subdural hematoma. Careful analysis of the course of the illness will disclose an uneven, saltatory progression. There are also cases in which the evolution of a thrombotic stroke is evenly progressive over a period of days. It is also likely that the abrupt development of a thrombus on an atherosclerotic plaque can cause a fairly sudden or at least rapid evolution of stroke, thereby simulating embolus but this is not characteristic.
Atheromatous plaques preferentially form at branching points and curves of the cerebral arteries. The most frequent sites are (1) in the internal carotid artery at its origin from the common carotid; (2) in the cervical part of the vertebral arteries or at their origins at the subclavian vessels, and at their junction to form the basilar artery; (3) in the stem or at the main bifurcation of the middle cerebral arteries; (4) in the proximal posterior cerebral arteries as they wind around the midbrain; and (5) in the proximal anterior cerebral arteries as they pass anteriorly and curve over the corpus callosum. The last two sites are far less frequent than the first three. It is less frequent for the cerebral arteries to develop significant plaques that develop into strokes beyond their first major branching after the circle of
Willis. Also, it is unusual for the cerebellar and ophthalmic arteries to show atheromatous involvement. The common carotid and vertebral arteries at their origins are additional frequent sites of atheromatous deposits, but because of abundant collateral arterial pathways, occlusions at these sites are less commonly associated with cerebral ischemia as discussed further on. There is tendency for persons of Asian origin to have intracranial atherosclerosis in contrast to the extracranial variety.