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DTIC ADA354090: Multidiscipline Approach to Understanding of Traumatic Brain Injury and the Evaluation of Drugs to Enhance Neurological Recovery After Traumatic Brain Injury.

Head wounds account for almost half of combat deaths and in peacetime traumatic brain injury costs the U.S. Military more than 60M dollars/year. We used the piston impact injury model to produce focal, cortical brain trauma in the anesthetized rat to gain insights into brain injury mechanisms and treatment strategies to help brain injured soldiers. Widespread axonal damage occurred throughout the brain from the focal injury. Neurons cell bodies were often spared about the injury area but their axons and dendrites were severely damaged. Surviving neurons, thus, may be nonfunctional. Free fatty acids, diacylglycerols, and phosphiolipase A2 were elevated widely throughout the brain not only acutely but up to 35 days after injury. Early elevations relate to the acute trauma; sustained elevations probably relate to brain recovery mechanisms. Improvement following brain trauma was biphasic. The early, rapid improvement represents recovery from the acute effects of trauma; the later slower phase possibly represents brain plasticity mechanisms. Neither the platelet activating factor inhibitor (BN52021) nor the calpain inhibitor (MDL 28170) improved the rate or extent of improvement followi

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