Two causes of ischemic stroke stand out: atherosclerotic–thrombotic disease of the cerebral or extracerebral vessels, and cerebral embolism. An understanding of the biology of these two processes is essential for the analysis of the clinical, laboratory, and imaging features of stroke and its treatment. All other causes of vascular occlusion taken together, account for far fewer strokes. These alternative causes are also important and they are accorded sections later in the chapter.
This is the most common cause of ischemic strokes and of all the types of stroke, cerebral embolism develops most rapidly, “like a bolt out of the blue.” As a rule, the full-blown picture evolves within seconds, exemplifying the idealized temporal profile of a stroke. Although the abruptness with which the stroke develops and the lack of prodromal symptoms point strongly to embolism, the diagnosis is based on the total clinical circumstance. Embolism always merits careful consideration in young persons, in whom atherosclerosis, discussed below, is less common. Only occasionally does the problem unfold more gradually, over many hours, with some fluctuation of symptoms. Possibly, in these cases the embolus initiates a propagating thrombotic process in the occluded vessel.
In most cases, the embolic material consists of a fragment that has broken away from a thrombus within the heart or independently from the endocardial surface of a cardiac chamber or valve (“cardioembolic”). Somewhat less frequently, the source is intraarterial from the distal end of a thrombus within the lumen of an occluded or severely stenotic carotid or vertebral artery (“artery-to-artery embolus”), or a clot that originates in the systemic venous system and passes through an aperture in the heart walls, for example, patent foramen ovale, or the origin of an embolus may be from large atheromatous plaques in the aorta. Thrombotic or infected material (endocarditis) that adheres to the aortic or mitral heart valves and breaks free are also well-appreciated sources of embolism, as are clots originating on prosthetic heart valves. Embolism caused by fat, tumor cells (atrial myxoma), fibrocartilage, amniotic fluid, or air enters into the differential diagnosis of stroke only in special circumstances.
The embolus usually becomes arrested at a bifurcation or other site of natural narrowing of the lumen of an intracranial vessel. The resultant infarction is pale, hemorrhagic, or mixed; hemorrhagic infarction nearly always indicates embolism, as noted originally by Fisher and Adams in an obscure abstract and elaborated in their 1987 chapter in Furlan’s book (although venous occlusion can do the same). Any region of the brain may be affected, the territories of the middle cerebral artery, particularly the superior division, being most frequently involved. The two cerebral hemispheres are approximately equally affected. Large embolic clots can block large vessels, while smaller fragments reach vessels as small as 0.2 mm in diameter, usually with inconsequential effects. The embolic material may remain arrested and plug the lumen solidly, but more often it breaks into fragments that enter smaller vessels so that even careful pathologic examination fails to reveal their final location. In this instance, the clinical effects may abate. Because of the rapidity with which embolic occlusion develops, useful collateral influx does not become established. Thus, sparing of the brain territory distal to the site of occlusion is usually not as evident as in thrombosis that develops more slowly.