Abstract
Ischemic brain injury produced by stroke or cardiac arrest is a major cause of human neurological disability. Steady advances in the neurosciences have elucidated pathophysiological mechanisms of brain ischemia and have suggested many therapeutic approaches directed at specific injury mechanisms to achieve neuroprotection of the acutely ischemic brain. The first portion of this two-part review highlights the differentiating features and pathological mechanisms of focal and global cerebral ischemic injury and summarizes a wealth of recent evidence as to how antagonism of excitatory amino acid neurotoxicity, mediated via NMDA as well as non-NMDA receptors, may offer a means of diminishing the extent of ischemic injury. The Neuroscientist 1:95-103, 1995
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