There are no treatments for reducing morbidity and mortality after traumatic brain injury. Only management of secondary effects, such as edema and hemorrhage, are performed to limit the spread of damage. Despite lack of treatment, some patients live after extensive cortical trauma and recover some behavioral functions with time. The processes underlying such recovery are poorly understood. Recent work indicating that recovery of function after unilateral cortical injury can be accelerated or slowed by drug treatment has important theoretical and clinical implications. In addition, such an investigation may provide some insight into the processes of spontaneous recovery and support the classic, but controversial hypothesis of a diaschisis - a functional depression of brain areas remote from but connected to the primary lesion - which may contribute to subsequent symptoms or cause death. We will directly determine if such functional depressions occur after injury and if they are changed by drug treatment. We will test this hypothesis using a cortical contusion model or ablation of sensorimotor cortex in rats to determine the role of the catecholamines in recovery after brain injury. The sequalae following brain injury is complex. To develop a scientific treatment, an understanding of mechanisms underlying recovery of function is required. This is best achieved via empirical investigation, utilizing converging operations. To achieve this goal, we propose experiments utilizing behavioral tests, lesion procedures, liquid chromatography, and pharmacology to better understanding mechanisms by which drugs may influence recovery from brain injury. Data from these studies may compliment one another and have important implications for theories of recovery of function.
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