Recovery of brain function following ischemia.
Experimental evidence conveys clear suggestions that early reperfusion following at least focal cerebral ischemia in the primate is accompanied by a return of function demonstrably suspended during the ischemic period. Complete and permanent arrest of the cerebral circulation has been known within seconds to lead to depression of brain electrical activity, and within minutes to gross disruption of the normal energy metabolism with failure of ionic homeostatic mechanisms. There is irreversible cell change and death within 5 to 10 minutes. Very much more protracted periods of ischemia have been shown more recently to be associated with potential viability of neuronal function, and in clinical neurosurgery we have known for years that patients with established cerebral vascular occlusion and a dense neurological deficit may show quite evident improvement over months or years. In these protracted recoveries, the potential for re-learning in nervous circuits may play a part, but in more acute circumstances, for example in the progressive recovery from vasospasm, re-learning is clearly not a factor, and this demonstrates quite evidently that neurons at one moment apparently non-functioning, can again within a few minutes recover function even after hours of apparent suppression. The experimental evidence is fairly well known. In this symposium and elsewhere we have presented a model of experimental occlusion of the middle cerebral artery in primates demonstrating irreversible recovery of electrical function after some 20 minutes of middle cerebral artery occlusion, and reversible recovery of ionic homeostasis after periods of up to an hour.(ABSTRACT TRUNCATED AT 250 WORDS)
Gough-Cooper Department of Neurological Surgery, Institute of Neurology, London, U.K.
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D000328:Adult; D001921:Brain / Q000503:physiopathology; D001925:Brain Damage, Chronic / Q000503:physiopathology*; D001929:Brain Edema / Q000503:physiopathology; D002545:Brain Ischemia / Q000503:physiopathology*; D002544:Cerebral Infarction / Q000503:physiopathology; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009460:Neurologic Examination; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology; D009435:Synaptic Transmission / Q000502:physiology*