Pathophysiology of cerebral infarction.
Evidence available at present from animal studies indicates that the flow of blood can be restored to ischemic zones in the brain as long as 24 hours after the onset of ischemia, and that such reperfusion could result in the restoration of function of neurons that have not been functioning during the period of ischemia. However, reperfusion also can cause worsening of ischemic cerebral edema resulting in increased neurological disability or death. Adequate measures for control of cerebral edema will be necessary if surgical intervention is to become an effective therapy for acute ischemic cerebral infarcts.
D000818:Animals; D001929:Brain Edema / Q000209:etiology / Q000503:physiopathology; D002415:Cats; D002560:Cerebrovascular Circulation; D002561:Cerebrovascular Disorders / Q000503:physiopathology; D004195:Disease Models, Animal; D004569:Electroencephalography; D000882:Haplorhini; D006801:Humans; D002542:Intracranial Embolism and Thrombosis / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D007427:Intracranial Pressure; D007511:Ischemia / Q000503:physiopathology; D009474:Neurons / Q000502:physiology