Brain ischemia results from the occlusion of cervicocranial vessels or hypoperfusion to the brain caused by various processes: atherothrombosis, embolism, or hemodynamic abnormalities.


Atherothrombosis occurs in the large cervicocranial arteries in the neck and head and small penetrating arteries. In this condition, a localized thrombus is formed in situ on an atherosclerotic arterial narrowing; it impedes distal blood flow and causes ischemia and ensuing infarction of the brain tissue supplied by the artery. The neurological symptoms and signs depend on the location of the brain vessel affected.


In brain embolism, a brain artery is suddenly blocked by embolic material, which is usually a thrombus that developed more proximally in the heart (cardiogenic), aorta, proximal arteries (intra-arterial), or venous system (paradoxical). These donor sites give rise to various types of particulate matter (white platelet-fibrin and red erythrocyte-fibrin thrombi, cholesterol crystals, fragments of atherosclerotic plaques, calcific fragments of valves and plaques, air, fat, myxomatous tumor fragments, bacterial vegetations), which then travel within the cervicocranial arteries to reach a recipient site. If the embolic material lodges for very long at a recipient site, the resulting hypoperfusion causes an infarct that often becomes hemorrhagic when the embolus moves or fragments and reperfusion occurs. The clinical findings depend on the location of the recipient brain artery affected.


Critically lowered blood flow to the brain (too severe to be compensated by cerebral autoregulation mechanisms) caused by cardiac pump failure or hypovolemia causes a global decrease in cerebral blood flow. During such episodes, most patients are hypotensive. This condition causes infarction in the border zones between the major cerebral arteries (so-called watershed infarction) as well as widespread bilateral cerebral dysfunction. The major zones of damage are between the anterior and middle cerebral arteries, and between the middle and posterior cerebral arteries in the parieto-occipital regions of the cerebral hemispheres (Fig. 45-1 (Figure Not Available) ). Loss of vision, decreased alertness, and weakness affecting predominantly the shoulder, hand, and thigh result.

Figure 45-1 (Figure Not Available) In heart (pump) failure and watershed infarction, (A) normal pump and arterial circulation do not occur; instead, due to (B) low pump pressure and border-zone ischemia, water goes to the center of hoses (arteries) and stippled areas show poor flow. In contrast, with (C) "blocked hose" and middle cerebral artery infarction, water flow is deficient in the center of stfstippled area). (Adapted from Caplan LR: Stroke. Clinical Approach. Boston, Butterworth-Heineman, 1993.)

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