Pathophysiology of stroke.
Therapeutic intervention in acute ischemic stroke must be directed at salvaging damaged, but viable, tissue. Ideally, treatment should start in the initial phase when the ischemic tissue still retains a potential for recovery. Furthermore, ischemic stroke may be associated with "chronic threatening ischemia," in which there is ischemic, but viable, tissue with collateral circulation distal to a stenosed or occluded artery. In chronic threatening ischemia, therapeutic manipulation may improve the clinical situation. Since cerebral vasomotor function is impaired or abolished in acute stroke and chronic threatening ischemia, vasodilator therapy tends to "steal" blood away from the lesion. Vasoconstrictors, by decreasing perfusion in healthy parts of the brain, may improve perfusion in ischemic tissue; it has, however, proved difficult to gain clinical benefit from this therapeutic modality. Converting-enzyme inhibitors may have a place in the management of ischemic stroke as they tend to shift cerebral autoregulation toward lower pressures. Calcium antagonists given acutely in stroke may create a steal effect. Despite this, clinical trials indicate that calcium-antagonist treatment may improve the outcome of stroke patients, possibly by an action on the ischemia-threatened brain cells.
Department of Medicine and Nephrology B, Herlev Hospital, Copenhagen, Denmark.
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D000818:Animals; D001921:Brain / Q000378:metabolism; D002545:Brain Ischemia / Q000503:physiopathology; D002543:Cerebral Hemorrhage / Q000503:physiopathology; D002561:Cerebrovascular Disorders / Q000188:drug therapy / Q000503:physiopathology* / Q000628:therapy; D006801:Humans