Physiological measurements of acoustic trauma following blast-induced traumatic brain injury (TBI) in laboratory mice

Abstract

Exposure to a high intensity blast from the detonation of improvised explosive devices (IEDs) can lead to a traumatic brain injury (TBI) and concurrent trauma to major auditory structures. Research on whether this trauma is permanent or temporary has been inconclusive due to heterogeneity of injury acquisition. A blast wave system that generates consistent and controllable blast waves has been developed, allowing for investigation into the co-morbidity of auditory damage and TBI. In this study, the effects of blast exposure on auditory brainstem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs) in male and female mice were measured. ABRs and DPOAEs were collected prior to exposure to a blast to represent the baseline auditory capacity of each individual subject. Mice were tested at 3, 30, and 90 days after the exposure to capture initial trauma and the degree of recovery. A shift in ABRs and DPOAEs thresholds was observed in post-exposure mice, indicating trauma to central and peripheral auditory systems. Following the 90 day tests, brains and cochleae were collected for further analysis. [Work supported by R01DC016641.]Exposure to a high intensity blast from the detonation of improvised explosive devices (IEDs) can lead to a traumatic brain injury (TBI) and concurrent trauma to major auditory structures. Research on whether this trauma is permanent or temporary has been inconclusive due to heterogeneity of injury acquisition. A blast wave system that generates consistent and controllable blast waves has been developed, allowing for investigation into the co-morbidity of auditory damage and TBI. In this study, the effects of blast exposure on auditory brainstem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs) in male and female mice were measured. ABRs and DPOAEs were collected prior to exposure to a blast to represent the baseline auditory capacity of each individual subject. Mice were tested at 3, 30, and 90 days after the exposure to capture initial trauma and the degree of recovery. A shift in ABRs and DPOAEs thresholds was observed in post-exposure mice, indicating trauma to central and periphe...