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.

Extracellular signal-regulated kinase (ERK) is a member of the family of mitogen-activated protein kinases (MAPKs) and coordinately regulates a multitude of cellular processes. In response to a variety of extracellular stimuli, phosphorylation of both threonine and tyrosine residues activates ERK. Recent evidence indicates that ERK is activated in response to cellular stress such as acoustic trauma. However, the specific role of ERK isoforms in auditory function is not fully understood. Here, we show that the isoform ERK2 plays an important role in regulating hair cell (HC) survival and noise-induced hearing loss (NIHL) in mice (C57BL/6J). We found that conditional knockout mice deficient for Erk2 in the inner ear HCs had hearing comparable to control mice and exhibited no HC loss under normal conditions. However, we found that these knockout mice were more vulnerable to noise and had blunted recovery from NIHL compared to control mice. Furthermore, we observed a significantly lower survival rate of inner hair cells in these mice compared to control mice. Our results indicate that ERK2 plays important roles in the survival of HC in NIHL.

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Purpose of the Study: The present study aimed to compare the voice quality after each type of cordectomy with that after radiotherapy (RT) or chemoradiotherapy (CRT) for early glottic carcinoma. Procedures: The GRBAS perceptive scale [consisting of 5 domains: grade (G), roughness (R), breathiness (B), asthenia (A), and strain (S)], aerodynamic tests and acoustic analyses, and the Voice Handicap Index questionnaire were evaluated for 58 laser cordectomy cases and 40 RT or CRT cases. Multiple comparison tests were conducted between each type of cordectomy and RT or CRT. Results: No statistical difference was found between type I/II cordectomy and RT for T1 glottic carcinoma (T1RT), whereas T1RT showed a significantly better outcome than type III cordectomy (G score: p = 0.016, maximum phonation time: p < 0.01, mean flow rate: p < 0.01). Type IV cordectomy was equivalent to RT or CRT for T2 glottic carcinoma (T2RT/CRT), while types V and VI showed a worse voice quality than T2RT/CRT (G score: p = 0.038 to type VI, B score: p = 0.025 to type V and p = 0.032 to type VI, A score: p = 0.017 to type VI). Conclusions: Voice quality after laser cordectomy differs according to the type of cordectomy. Surgeons should inform patients about the expected voice quality after each treatment modality.

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Although an enormous number of animal studies on blast-induced traumatic brain injury (bTBI) have been conducted, there still remain many uncertain issues in its neuropathology and mechanisms. This is partially due to the complex and hence difficult experimental environment settings, e.g., to minimize the effects of blast winds (tertiary mechanism) and to separate the effects of brain exposure and torso exposure. Since a laser-induced shock wave (LISW) is free from dynamic pressure and its energy is spatially well confined, the effects of pure shock wave exposure (primary mechanism) solely on the brain can be examined by using an LISW. In this study, we applied a set of four LISWs in the impulse range of 15–71 Pa·s to the rat brain through the intact scalp and skull; the interval between each exposure was ~5 s. For the rats, we conducted locomotor activity, elevated plus maze and forced swimming tests. Axonal injury in the brain was also examined by histological analysis using Bodian silver staining. Only the rats with exposure at higher impulses of 54 and 71 Pa·s showed significantly lower spontaneous movements at 1 and 2 days post-exposure by the locomotor activity test, but after 3 days post-exposure, they had recovered. At 7 days post-exposure, however, these rats (54 and 71 Pa·s) showed significantly higher levels of anxiety-related and depression-like behaviors by the elevated plus maze test and forced swimming test, respectively. To the best of the authors' knowledge, there have been few studies in which a rat model showed both anxiety-related and depression-like behaviors caused by blast or shock wave exposure. At that time point (7 days post-exposure), histological analysis showed significant decreases in axonal density in the cingulum bundle and corpus callosum in impulse-dependent manners; axons in the cingulum bundle were found to be more affected by a shock wave. Correlation analysis showed a statistically significant correlation between the depression like-behavior and axonal density reduction in the cingulum bundle. The results demonstrated the dependence of behavior deficits and axonal injury on the shock wave impulse loaded on the brain.

Recently, the number of blast injuries of the inner ear has increased in the general population. In blast-induced inner ear injury, a shock wave (SW) component in the blast wave is considered to play an important role in sensorineural hearing loss. However, the mechanisms by which an SW affects inner ear tissue remain largely unknown. We aimed to establish a new animal model for SW-induced inner ear injury by using laser-induced SWs (LISWs) on rats. The LISWs were generated by irradiating an elastic laser target with 694-nm nanosecond pulses of a ruby laser. After LISW application to the cochlea through bone conduction, auditory measurements revealed the presence of inner ear dysfunction, the extent of which depended on LISW overpressure. A significantly lower survival rate of hair cells and spiral ganglion neurons, as well as severe oxidative damage, were observed in the inner ear exposed to an LISW. Although considerable differences in the pressure characteristics exist between LISWs and SWs in real blast waves, the functional and morphological changes shown by the present LISW-based model were similar to those observed in real blast-induced injury. Thus, our animal model is expected to be useful for laboratory-based research of blast-induced inner ear injury.