Acute Inflammatory Response in Rodent Brain and Blood Following a Blast Induced Traumatic Brain Injury

Abstract : The predominant cause of neurotrauma among the military population is exposure to a blast wave. The shockwave produced by an explosive device can travel through the brain causing mild brain damage without any visible signs of injury. There has been a lot of interest in the role blast exposure plays in mild traumatic brain injury (TBI) and how this may link to the clinical features of the injury. TBI is a very complex disorder that is characterized by primary and secondary injury mechanisms (Loane and Faden, 2010). The primary injury mechanism is due to direct damage to the brain cells occurring at the time of the initial impact producing a series of biochemical processes which then result in the secondary brain injury. Secondary brain injury develops within minutes and can last up to months and includes a variety of processes among which is the initiation of inflammatory and immune responses (Frugier et al. 2010; Morganti-Kossman et al. 2007). The development of secondary injury events provides a window of opportunity for therapeutic intervention to prevent progressive tissue damage and loss of function after injury (Kumar and Loane, 2012; Loane and Faden, 2010).