Pathophysiology of the inner ear after blast injury caused by laser-induced shock wave.

Katsuki Niwa,Akihiro Shiotani,Kunio Mizutari,Yasushi Satoh,Shunichi Sato,Satoko Kawauchi,Yasushi Kobayashi,Takeshi Matsunobu,Takaomi Kurioka,Toshiyasu Matsui

doi:10.1038/srep31754

Abstract

The ear is the organ that is most sensitive to blast overpressure, and ear damage is most frequently seen after blast exposure. Blast overpressure to the ear results in sensorineural hearing loss, which is untreatable and is often associated with a decline in the quality of life. In this study, we used a rat model to demonstrate the pathophysiological and structural changes in the inner ear that replicate pure sensorineural hearing loss associated with blast injury using laser-induced shock wave (LISW) without any conductive hearing loss. Our results indicate that threshold elevation of the auditory brainstem response (ABR) after blast exposure was primarily caused by outer hair cell dysfunction induced by stereociliary bundle disruption. The bundle disruption pattern was unique; disturbed stereocilia were mostly observed in the outermost row, whereas those in the inner and middle rows stereocilia remained intact. In addition, the ABR examination showed a reduction in wave I amplitude without elevation of the threshold in the lower energy exposure group. This phenomenon was caused by loss of the synaptic ribbon. This type of hearing dysfunction has recently been described as hidden hearing loss caused by cochlear neuropathy, which is associated with tinnitus or hyperacusis.

Highlights

Was associated with so-called “hidden hearing loss,” which is implicated in tinnitus and hyperacusis
We have demonstrated a novel animal model of sensorineural hearing loss (SNHL)
The degree of the ABR threshold elevation we observed in this study was very similar to the sensorineural hearing loss in human subjects recovered from blast injuries in real bombing situations[6]

Summary

Introduction

Was associated with so-called “hidden hearing loss,” which is implicated in tinnitus and hyperacusis (diminished sound-level tolerance). After LISW exposure, the ABR threshold at the exposed ear (right side) was immediately elevated in the high and middle energy groups, with significant elevation remaining up to 28 days after exposure (2.25 and 2.5 J/cm[2]; Fig. 2b,c). The ABR threshold was not elevated in the 2.0 J/cm[2] group, the ABR wave I amplitude was significantly decreased from immediately after LISW exposure up to 28 days after exposure (Fig. 2d), which was similar to the higher energy groups (Fig. 2e,f).

Results

Conclusion