Hearing difficulties are the most commonly reported disabilities among Veterans. Blast exposures during explosive events likely play a role, given their propensity to directly damage both
peripheral auditory system (PAS) and central
auditory system (CAS) components. Post-blast PAS
pathophysiology has been well-documented in both
clinical case reports and laboratory investigations. In contrast, blast-induced CAS dysfunction remains under-studied, but has been hypothesized to contribute to an array of common Veteran behavioral complaints including learning, memory, communication, and emotional regulation. This investigation compared the effects of acute blast and non-blast acoustic impulse trauma in
adult male Sprague-Dawley rats. An array of audiometric tests were utilized, including
distortion product otoacoustic emissions (DPOAE), auditory
brainstem responses (ABR), middle latency responses (MLR), and envelope following responses (EFR). Generally, more severe and persistent post-injury central auditory
processing (CAP) deficits were observed in blast-exposed animals throughout the auditory neuraxis, spanning from the
cochlea to the cortex. DPOAE and ABR results captured cochlear and auditory nerve /
brainstem deficits, respectively. EFRs demonstrated temporal
processing impairments suggestive of functional damage to regions in the auditory
brainstem and the inferior colliculus. MLRs captured thalamocortical transmission and cortical activation impairments. Taken together, the results suggest blast-induced CAS dysfunction may play a complementary pathophysiologic role to maladaptive
neuroplasticity of PAS origin. Even mild blasts can produce lasting hearing impairments that can be assessed with non-invasive
electrophysiology, allowing these measurements to serve as simple, effective diagnostics.