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      Hidden hearing loss, cochlear synaptopathy and occupational noise Translated title: Pérdida auditiva oculta, sinaptopatía coclear y ruido ocupacional

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          Abstract

          Abstract Introduction: Cochlear synaptopathy after noise exposure (CSNE) is defined as the transient or permanent functional damage to the ribbon synapsis of the inner hair cells of the cochlea. This article has the objective of comment the usefulness of early identification of the hidden hearing loss after CSNE based on audiological markers and in changes in the clinical methodology in clinical groups for its searching. Method: Review of related literature in scientific databases and narrative description of results. Results: CSNE results in a hidden hearing loss in patients with normal pitch audiogram, mainly workers or individuals exposed to high noise levels. The main studies of identification have been performed mainly in groups of students from college or musicians. Conclusions: Is necessary adjustments in hearing health policy for an wide early identification of CSNE in at risk populations for the identification of the hidden hearing loss and fight for its damage regulation.

          Translated abstract

          Resumen Introducción: La sinaptopatía coclear por exposición a ruido (SCER) es definida como una alteración funcional transitoria o permanente de las sinapsis en cinta de las células pilosas internas de la cóclea. Este artículo tiene el objetivo de comentar la utilidad de la identificación temprana de la pérdida auditiva oculta por SCER basado en marcadores audiológicos y en la metodología usada en grupos clínicos para su búsqueda. Método: Revisión de la literatura relacionada en bases científicas y la narración descriptiva de los resultados. Resultados: La SCER produce una pérdida auditiva oculta en pacientes con audiograma normal, principalmente obreros o individuos expuestos a niveles de ruido intenso. Los principales estudios de identificación de la SCER han sido realizados principalmente en estudiantes universitarios o en músicos. Conclusiones: Son necesarios ajustes en la política de salud auditiva para una amplia identificación temprana de la SCER en las poblaciones en riesgo para la pérdida auditiva oculta y luchar por una regulación del daño.

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          Adding insult to injury: cochlear nerve degeneration after "temporary" noise-induced hearing loss.

          Overexposure to intense sound can cause temporary or permanent hearing loss. Postexposure recovery of threshold sensitivity has been assumed to indicate reversal of damage to delicate mechano-sensory and neural structures of the inner ear and no persistent or delayed consequences for auditory function. Here, we show, using cochlear functional assays and confocal imaging of the inner ear in mouse, that acoustic overexposures causing moderate, but completely reversible, threshold elevation leave cochlear sensory cells intact, but cause acute loss of afferent nerve terminals and delayed degeneration of the cochlear nerve. Results suggest that noise-induced damage to the ear has progressive consequences that are considerably more widespread than are revealed by conventional threshold testing. This primary neurodegeneration should add to difficulties hearing in noisy environments, and could contribute to tinnitus, hyperacusis, and other perceptual anomalies commonly associated with inner ear damage.
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            Tinnitus with a normal audiogram: physiological evidence for hidden hearing loss and computational model.

            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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              Toward a Differential Diagnosis of Hidden Hearing Loss in Humans

              Recent work suggests that hair cells are not the most vulnerable elements in the inner ear; rather, it is the synapses between hair cells and cochlear nerve terminals that degenerate first in the aging or noise-exposed ear. This primary neural degeneration does not affect hearing thresholds, but likely contributes to problems understanding speech in difficult listening environments, and may be important in the generation of tinnitus and/or hyperacusis. To look for signs of cochlear synaptopathy in humans, we recruited college students and divided them into low-risk and high-risk groups based on self-report of noise exposure and use of hearing protection. Cochlear function was assessed by otoacoustic emissions and click-evoked electrocochleography; hearing was assessed by behavioral audiometry and word recognition with or without noise or time compression and reverberation. Both groups had normal thresholds at standard audiometric frequencies, however, the high-risk group showed significant threshold elevation at high frequencies (10–16 kHz), consistent with early stages of noise damage. Electrocochleography showed a significant difference in the ratio between the waveform peaks generated by hair cells (Summating Potential; SP) vs. cochlear neurons (Action Potential; AP), i.e. the SP/AP ratio, consistent with selective neural loss. The high-risk group also showed significantly poorer performance on word recognition in noise or with time compression and reverberation, and reported heightened reactions to sound consistent with hyperacusis. These results suggest that the SP/AP ratio may be useful in the diagnosis of “hidden hearing loss” and that, as suggested by animal models, the noise-induced loss of cochlear nerve synapses leads to deficits in hearing abilities in difficult listening situations, despite the presence of normal thresholds at standard audiometric frequencies.
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                Author and article information

                Journal
                mesetra
                Medicina y Seguridad del Trabajo
                Med. segur. trab.
                Escuela Nacional de Medicina del Trabajo. Instituto de Salud Carlos III (Madrid, Madrid, Spain )
                0465-546X
                1989-7790
                June 2023
                : 69
                : 271
                : 100-107
                Affiliations
                [4] Mexico City orgnameNational Institute of Rehabilitation orgdiv1Laboratory of Cognitive Neurophysiology México
                [3] Mexico City orgnameUniversidad Nacional Autónoma de México orgdiv1School of Medicine Mexico
                [1] Mexico City orgnameNational Institute of Rehabilitation orgdiv1Laboratory of Central Auditory Processes México
                [2] Mexico City orgnameInstituto Mexicano del Seguro Social orgdiv1Department of Health in Work Mexico
                Article
                S0465-546X2023000200004 S0465-546X(23)06927100004
                10.4321/s0465-546x2023000200004
                ba5ae427-06f0-4467-84fa-d93cacb1f967

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

                History
                : 26 January 2023
                : 29 November 2022
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 19, Pages: 8
                Product

                SciELO Spain


                Pérdida auditiva oculta,Occupational noise,Sinaptopatía coclear,Ruido ocupacional,Hidden hearing loss,Cochlear synaptopathy

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