NOVEL PHARMACOLOGICAL STRATEGIES IN THE TREATMENT OF EXPERIMENTAL TRAUMATIC BRAIN INJURY - 1998

The mechanisms underlying secondary or delayed cell death following tr aumatic brain injury are poorly understood. Recent evidence from exper imental models suggests that widespread neuronal loss is progressive a nd continues in selectively vulnerable brain regions for months to yea rs after the initial insult. The mechanisms underlying delayed cell de ath are believed to result, in part, from the release or activation of endogenous ''autodestructive'' pathways induced by the traumatic inju ry. The development of sophisticated neurochemical, histopathological and molecular techniques to study animal models of TBI have enabled re searchers to begin to explore the cellular and genomic pathways that m ediate cell damage and death, This new knowledge has stimulated the de velopment of novel therapeutic agents designed to modify gene expressi on, synthesis, release, receptor or functional activity of these patho logical factors with subsequent attenuation of cellular damage and imp rovement in behavioral function. This article represents a compendium of recent studies suggesting that modification of post-traumatic neuro chemical and cellular events with targeted pharmacotherapy can promote functional recovery following traumatic injury to the central nervous system.