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.