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      Impact of noise on hearing in the military

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      Author(s): ,
      Publication date (Electronic):
      Journal: Military Medical Research
      Publisher: BioMed Central
      Keywords: Hearing loss, Noise-induced, Military personnel, Ear protective devices

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          Abstract

          Hearing plays a vital role in the performance of a soldier and is important for speech processing. Noise-induced hearing loss is a significant impairment in the military and can affect combat performance. Military personnel are constantly exposed to high levels of noise and it is not surprising that noise induced hearing loss and tinnitus remain the second most prevalent service-connected disabilities. Much of the noise experienced by military personnel exceeds that of maximum protection achievable with double hearing protection. Unfortunately, unlike civilian personnel, military personnel have little option but to remain in noisy environments in order to complete specific tasks and missions. Use of hearing protection devices and follow-up audiological tests have become the mainstay of prevention of noise-induced hearing loss. This review focuses on sources of noise within the military, pathophysiology and management of patients with noise induced hearing loss.

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          Tinnitus with a normal audiogram: physiological evidence for hidden hearing loss and computational model.

          Roland Schaette, David McAlpine (2011)
          Ever since Pliny the Elder coined the term tinnitus, the perception of sound in the absence of an external sound source has remained enigmatic. Traditional theories assume that tinnitus is triggered by cochlear damage, but many tinnitus patients present with a normal audiogram, i.e., with no direct signs of cochlear damage. Here, we report that in human subjects with tinnitus and a normal audiogram, auditory brainstem responses show a significantly reduced amplitude of the wave I potential (generated by primary auditory nerve fibers) but normal amplitudes of the more centrally generated wave V. This provides direct physiological evidence of "hidden hearing loss" that manifests as reduced neural output from the cochlea, and consequent renormalization of neuronal response magnitude within the brainstem. Employing an established computational model, we demonstrate how tinnitus could arise from a homeostatic response of neurons in the central auditory system to reduced auditory nerve input in the absence of elevated hearing thresholds.
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            Development of tinnitus-related neuronal hyperactivity through homeostatic plasticity after hearing loss: a computational model.

            Roland Schaette, Richard Kempter (2006)
            Tinnitus, the perception of a sound in the absence of acoustic stimulation, is often associated with hearing loss. Animal studies indicate that hearing loss through cochlear damage can lead to behavioral signs of tinnitus that are correlated with pathologically increased spontaneous firing rates, or hyperactivity, of neurons in the auditory pathway. Mechanisms that lead to the development of this hyperactivity, however, have remained unclear. We address this question by using a computational model of auditory nerve fibers and downstream auditory neurons. The key idea is that mean firing rates of these neurons are stabilized through a homeostatic plasticity mechanism. This homeostatic compensation can give rise to hyperactivity in the model neurons if the healthy ratio between mean and spontaneous firing rate of the auditory nerve is decreased, for example through a loss of outer hair cells or damage to hair cell stereocilia. Homeostasis can also amplify non-auditory inputs, which then contribute to hyperactivity. Our computational model predicts how appropriate additional acoustic stimulation can reverse the development of such hyperactivity, which could provide a new basis for treatment strategies.
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              Efferent feedback minimizes cochlear neuropathy from moderate noise exposure.

              Stéphane F. Maison, Hajime Usubuchi, M. Liberman (2013)
              Although protective effects of the cochlea's efferent feedback pathways have been well documented, prior work has focused on hair cell damage and cochlear threshold elevation and, correspondingly, on the high sound pressure levels (>100 dB SPL) necessary to produce them. Here we explore the noise-induced loss of cochlear neurons that occurs with lower-intensity exposures and in the absence of permanent threshold shifts. Using confocal microscopy to count synapses between hair cells and cochlear nerve fibers, and using measurement of auditory brainstem responses and otoacoustic emissions to assess cochlear presynaptic and postsynaptic function, we compare the damage from a weeklong exposure to moderate-level noise (84 dB SPL) in mice with varying degrees of cochlear de-efferentation induced by surgical lesion to the olivocochlear pathway. Such exposure causes minimal acute threshold shifts and no chronic shifts in mice with normal efferent feedback. In de-efferented animals, there was up to 40% loss of cochlear nerve synapses and a corresponding decline in the amplitude of the auditory brainstem response. Quantitative analysis of the de-efferentation in inner versus outer hair cell areas suggested that outer hair cell efferents are the most important in minimizing this neuropathy, presumably by virtue of their sound-evoked feedback reduction of cochlear amplification. The moderate nature of this acoustic overexposure suggests that cochlear neurons are at risk even in everyday acoustic environments, so the need for cochlear protection is plausible as a driving force in the design of this feedback pathway.
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                Author and article information

                Contributors
                Jenica Su-ern Yong: yong.suern@gmail.com
                De-Yun Wang: de_yun_wang@nuhs.edu.sg
                Journal
                Journal ID (nlm-ta): Mil Med Res
                Journal ID (iso-abbrev): Mil Med Res
                Title: Military Medical Research
                Publisher: BioMed Central (London )
                ISSN (Print): 2095-7467
                ISSN (Electronic): 2054-9369
                Publication date (Electronic): 25 February 2015
                Publication date PMC-release: 25 February 2015
                Publication date Collection: 2015
                Volume: 2
                Electronic Location Identifier: 6
                Affiliations
                Department of Otolaryngology-Head and Neck Surgery, National University Health System, National University of Singapore, Singapore, Singapore
                Article
                Publisher ID: 34
                DOI: 10.1186/s40779-015-0034-5
                PMC ID: 4455974
                PubMed ID: 26045968
                SO-VID: 931ff7e0-7143-4d1a-ae36-d1c8c77c15a9
                Copyright © © Yong and Wang; licensee BioMed Central. 2015
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 16 August 2014
                Date accepted : 30 January 2015
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2015

                Keywords: hearing loss,noise-induced,military personnel,ear protective devices
                Data availability:
                Keywords: hearing loss, noise-induced, military personnel, ear protective devices

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