Citation

Bramlett H, Dietrich WD. J. Neurotrauma 2014; 32(23): 1834-1848.

Affiliation

University of Miami, Neurological Surgery , 1095 NW 14th Terrace , Miami, Florida, United States , 33136 ; HBramlett@med.miami.edu.

Copyright

(Copyright © 2014, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2014.3352

PMID

25158206

Abstract

Traumatic brain injury (TBI) is a significant clinical problem with few therapeutic interventions successfully translated to the clinic. Increased importance on the progressive and long-term consequences of traumatic brain injury have been emphasized both in the experimental and clinical literature. 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. 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. Recently, the increased incidence in age-dependent neurodegenerative diseases in this patient population has also been emphasized. 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. The current article will review many of these pathophysiological mechanisms that may be important targets for limiting the chronic consequences of TBI.

Language: en