الفهرس 
Review of LiteratureOnly 14 pages are availabe for public view
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Abstract
The adult brain is extremely vulnerable to various kinds of insults weather, traumatic, degenerative or ischemic which ultimately results in loss of neurological function.
Cerebral ischemia is initiated by cessation of blood flow to the brain as in cardiac arrest or decreased brain perfusion as in intra-operative severe hypotension or carotid endarterectomy.
Oxygen and glucose deprivation result in activation of N-methylD-aspartate receptors leading to massive accumulation of glutamate which stimulates various calcium influx processes. The released calcium results in membrane depolarization, activation of lipases and proteases.
The activation of lipases initiates membrane hydrolyses with consequent release of hydrogen peroxide, superoxides and preoxynitrite. These free radicals cause neuronal damage and subsequent neuronal loss manifested three days after ischemia.
In addition apoptotic cell death continues to occur for several weaks following the ischemic insult. Furthermore, delayed inflammatory reaction, and inicroglial infiltration take place.
Various neuroprotective strategies have been tried to reduce brain damage and ameliorate associated functional deficits. Among these are the use of anti-glutametergic agents like Dizoclipine, calcium channel blockers, sodium channel blockers, Gamma arninobutyric acid agonists,
tioxidants and hypothermia.