Abstract
Cognitive deficits following traumatic brain injury are the result of structural and neurochemicdal changes. Differential diagnosis of impaired cognition should include consideration of preinjury factors, injury-specific factors, and early pharmacologic management, which can have potentially adverse effects on later cognitive functioning. The primary treatment strategy for cognitive dysfunction is the removal of agents that are known or presumed to have adverse cognitive effects. In this article, the use of catecholamine agonists, cholinergic agonists, opiate antagonists, neuropeptides, nootropes, and other agents is discussed. The use of pharmacologic agents to facilitate cognition has thus far been disappointing.
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