Blast exposure predisposes the brain to increased neurological deficits in a model of blast plus blunt traumatic brain injury.

Soldiers are often exposed to more than one traumatic brain injury (TBI) over the course of their service. In recent years, more attention has been drawn to the increased risk of neurological deficits caused by the 'blast plus' polytrauma, which typically is a blast trauma combined with other forms of TBI. In this study, we investigated the behavioral and neuronal deficits resulting from a blast plus injury involving a mild-moderate blast followed by a mild blunt trauma using the fluid percussion injury model. We identified that the blast injury predisposed the brain to increased cognitive deficits, chronic ventricular enlargement, increased neurodegeneration at acute time points and chronic neuronal loss. Interestingly, a single blast and single blunt injury differed in their onset and manifestation of cognitive and regional neuronal loss. We also identified the presence of cleaved RIP1 from caspase 8 mediated apoptosis in the blunt injury while the blast injury did not activate immediate apoptosis but led to decreased hilar neuronal survival over time.