Cerebral Apoplexy (Stroke): Pathogenesis, Pathophysiology and Therapy as Illustrated by Regional Blood Flow Measurements in the Brain

Abstract

Pathophysiological and pathogenetic concepts, particularly in occlusive cerebrovascular disease, are reviewed and discussed with emphasis on the results of current research. Therapy is discussed in the context of these concepts. When focal ischemia, with or without cerebral infarction, is not associated with definable arterial occlusion, studies of regional cerebral blood flow strongly support the thromboembolic theory; the arterial defect is relatively transient and is caused by an embolus or thrombus which rapidly disappears (fragments or is lysed). The treatment of transient ischemic attacks by the administration of anticoagulant or surgical reconstruction of the appropriate artery is discussed. When cerebral infarction is caused by arterial occlusion there is vasomotor paralysis (loss of autoregulation and of reactivity to carbon dioxide). In some instances hypercapnia apparently causes only the vessels in nonaffected brain to dilate so that an increased amount of blood streams to these parts while blood pressure falls in collaterals leading to the focus and blood flow to the infarct is decreased (steal syndrome). If blood flow is decreased to nonaffected brain, by vasoconstriction caused by hyperventilation, increased amounts of blood may be shunted into the infarct (reverse steal) where autoregulation is lost. Vasoconstriction, as a treatment, might be beneficial. However, in patients with severe cerebral infarction no convincing favorable affect has been noted. The potential therapeutic action of hyperventilation in patients with mild cerebral infarction has not been studied. Extensive (global) changes in the cerebral blood flow in cerebral infarction, certain aspects of intracerebral hemorrhage, and the role of hypertension in cerebrovascular disease are also dealt with.