Mechanisms and pathophysiology of the low-level blast brain injury in animal models

The symptoms of primary blast-induced mTBI, posttraumatic stress disorder and depression overlap. Evidence of an organic basis for these entities has been scarce and controversial. We present a review of animal studies demonstrating that low-level blast causes pathophysiological and functional changes in the brain. We monitor a time period from minutes to approximately 1 week after blast exposure from multiple modes (air, underwater, localized and whole body). The most salient findings observed were (1) the peak pressures ( P max) in the brain, elicited from the blast from the firing of military weapons ( P max 23–45 kPa), have a similar magnitude as that registered in air close to the head. Corresponding measurements during the detonation pulse from explosives under water show a P max in the brain, which is only 10% of that in water outside the head. (2) The rise time of the pressure curve is 10 times longer in the brain as compared with the blast in air outside the head during firing of military weapons. (3) The lower frequencies in the blast wave appear to be transmitted more readily to the brain than the higher frequencies. (4) When animals are exposed to low levels of blast, the blast wave appears mostly transmitted directly to the brain during air exposure, not via the thorax or abdomen. (5) Low levels of blast cause brain edema, as indicated by increased bioelectrical impedance, an increase in the intracranial pressure, small brain hemorrhages and impaired cognitive function.