Mitochondrial damage in traumatic CNS injury

With over 1.5 million injuries every year, traumatic brain injury (TBI) has become an almost ubiquitous phenomenon in our country. As this disorder can be present without any outward sign of physical damage and the victims are usually cognitively impaired (i.e., not vocal), it has become a largely silent epidemic (Jennett 1998; Thurman et al. 1999; Jager et al. 2000; CDC 2003; Langlois et al. 2006). Current advancements in medicine have allowed patients who would have previously succumbed to their wounds, to survive long after their initial injury. Also, there is a growing population of individuals who sustain a mild to moderate TBI who do not seek treatment (∼25%), and often develop prolonged and chronic neurological symptoms (CDC 2003). The growing injured population has presented our society with an enormous economic and social burden, as these patients are commonly unable to properly reintegrate in to their previous professional and social networks. They become exceedingly dependent on family and social outreach programs to live their daily lives which cause their health care costs to total tens of billion dollars per year (Langlois et al. 2006). Although there are limited treatment options designed to allow people to survive their injuries, consisting of minimizing acute brain edema, decreasing intracranial pressure, and the prevention of peripheral complications, there is no current treatment to attenuate or recover the loss of neural tissue (Hatton 2001).