Abstract
There are differences in the temporal and spatial distributions of water and proteins in cerebral edema developing in experimental models of acute cerebral ischemia. Differences in the mechanisms underlying the extravasation of water and proteins may account in part for differences in the responses of ischemic and other types of cerebral edema to therapeutic measures such as the administration of adrenal corticosteroids. Differences between experimental animals and humans, particularly in the sizes of intracranial and cerebrospinal fluid volumes, may make inappropriate the application of results of treatment of experimental models of acute cerebral ischemia to humans with strokes. However, the ultimate goal of the treatment of strokes is not a reduction of edema or an enhancement of cerebral blood flow but the maintenance or restoration of neuronal function, and all therapeutic measures should be assessed by the final neurologic status.
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