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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 (PAS) and central auditory system (CAS) components. Postblast PAS pathophysiology has been well documented in both clinical case reports and laboratory investigations. In contrast, blast-induced CAS dysfunction remains understudied 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 nonblast acoustic impulse trauma in adult male Sprague-Dawley rats. An array of audiometric tests were utilized, including distortion product otoacoustic emissions (DPOAE), auditory brain stem responses (ABR), middle latency responses (MLR), and envelope following responses (EFRs). Generally, more severe and persistent postinjury 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/brain stem deficits, respectively. EFRs demonstrated temporal processing impairments suggestive of functional damage to regions in the auditory brain stem 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 pathophysiological role to maladaptive neuroplasticity of PAS origin. Even mild blasts can produce lasting hearing impairments that can be assessed with noninvasive electrophysiology, allowing these measurements to serve as simple, effective diagnostics. NEW &amp; NOTEWORTHY Blasts exposures often produce hearing difficulties. Although cochlear damage typically occurs, the downstream effects on central auditory processing are less clear. Moreover, outcomes were compared between individuals exposed to the blast pressure wave vs. those who experienced the blast noise without the pressure wave. It was found that a single blast exposure produced changes at all stages of the ascending auditory path at least 4 wk postblast, whereas blast noise alone produced largely transient changes.

Differences in postinjury auditory system pathophysiology after mild blast and nonblast acute acoustic trauma