Head injury is still a major cause of death and disability despite the implementation of aggressive methods of evaluation and intensive care. It is our feeling that if further gains are to be made in improving patient outcome, new efforts must be directed at the basic pathophysiologic processes involved in severe head injury. Based upon extensive data obtained in our laboratories, we have chosen to target our therapeutic efforts at two damaging mechanisms known to be involved with traumatic brain injury (TBI). One therapeutic effort is aimed at the blunting the damaging consequences of oxygen radicals on the cerebral vasculature. The other therapeutic effort focuses on the einhibition of the excitotoxic processes occurring with TBI particularly those involving cholinergic mediated excitation. Specifically, the hypotheses are: 1) the action of free radicals on the cerebral vasculature and the increased excitotoxic influences on neurons contribute significantly to the morbidity and mortality of severe head injury; and 2) quenching of free radicals with PEG-SOD along with the blocking of the effects of excessive excitatory transmitter release with scopolamine can improve the outcome in patients with severe head injury. To prove these hypotheses, we will conduct a randomized controlled clinical trial dividing the patients into one of three groups: 1) a control group, 2) a group given PEG-SOD, and 3) a group given scopolamine. The efficacy of these agents will be determined by looking at the GOS, neurologic, neuropsychologic outcomes, assessment of neuroelectric activity, dynamic ICP studies, indices of vessel el reactivity and biochemical assessment of the effectiveness of the agents that are being used.
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