Citation

Algattas H, Huang JH. Int. J. Mol. Sci. 2013; 15(1): 309-341.

Affiliation

School of Medicine and Dentistry, University of Rochester Medical Center, 601 Elmwood Ave, Box 441, Rochester, NY 14642, USA. jason_huang@urmc.rochester.edu.

Copyright

(Copyright © 2013, Molecular Diversity Preservation International)

DOI

10.3390/ijms15010309

PMID

24381049

Abstract

Traumatic Brain Injury (TBI) affects a large proportion and extensive array of individuals in the population. While precise pathological mechanisms are lacking, the growing base of knowledge concerning TBI has put increased emphasis on its understanding and treatment. Most treatments of TBI are aimed at ameliorating secondary insults arising from the injury; these insults can be characterized with respect to time post-injury, including early, intermediate, and late pathological changes. Early pathological responses are due to energy depletion and cell death secondary to excitotoxicity, the intermediate phase is characterized by neuroinflammation and the late stage by increased susceptibility to seizures and epilepsy. Current treatments of TBI have been tailored to these distinct pathological stages with some overlap. Many prophylactic, pharmacologic, and surgical treatments are used post-TBI to halt the progression of these pathologic reactions. In the present review, we discuss the mechanisms of the pathological hallmarks of TBI and both current and novel treatments which target the respective pathways.

Language: en