T raumatic brain injury (TBI) produces both acute and more chronic consequences that lead to permanent disabilities that increase long-term mortality and reduced life expectation. The current article will review many of these pathophysiological mechanisms that may be important targets for limiting the chronic consequences of TBI. Pathomechanisms felt to be active in the acute and long-term consequences of TBI include excitotoxicity, apoptosis, inflammatory events, seizures, demyelination, white matter pathology, as well as decreased neurogenesis. Recently, the increased incidence in age-dependent neurodegenerative diseases in this patient population has also been emphasized. In models of mild, moderate, and severe TBI, histopathological and behavioral studies have emphasized the progressive nature of the initial traumatic insult and the involvement of multiple pathophysiological mechanisms, including sustained injury cascades leading to prolonged motor and cognitive deficits. Thus, there is a need for a better understanding of the chronic consequences of TBI, with the ultimate goal of developing novel therapeutic interventions to treat the devastating consequences of brain injury. Increased importance on the progressive, long-term consequences of TBI have been emphasized, both in the experimental and clinical literature. Traumatic brain injury (TBI) is a significant clinical problem with few therapeutic interventions successfully translated to the clinic.
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