Understanding the brain injury mechanisms of primary blast exposure
Blast brain injury research has largely focused on the pressure transmission of the blast wave to the head. However, the large dynamic pressures can also cause high head accelerations. The injury mechanisms and sequelae from shock waves and head accelerations may not be the same, but both may be significant contributors to the overall pathology. In this study, we examine two immunohistochemical markers of axonal injury from blast exposures with varying head accelerations to anaesthetised ferrets. The immunohistochemical marker for neurofilament compaction, RM014 stained approximately 1,000 times more tissue area than the marker for impaired axonal transport, β-APP. .This trend in positive reactivity was most apparent in the large white matter tracts. The positive relationships between their immunoreactivities and impulse were similar, but RM014 had a slightly greater dependence on head acceleration than β-APP. Another observation was that the positive staining for the two axonal injury markers did not always occur in the same anatomical regions. The different injury patterns witnessed for the two markers highlight the complexity of blast brain injury compared with blunt neurotrauma. This study demonstrates that the accelerative aspect of the exposure event may contribute to the injury outcome.
