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Abnormal Auditory Gain in Hyperacusis: Investigation with a Computational Model

Hyperacusis is a frequent auditory disorder that is characterized by abnormal loudness perception where sounds of relatively normal volume are perceived as too loud or even painfully loud. As hyperacusis patients show decreased loudness discomfort levels (LDLs) and steeper loudness growth functions,...

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Autores principales: Diehl, Peter U., Schaette, Roland
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4502361/
https://www.ncbi.nlm.nih.gov/pubmed/26236277
http://dx.doi.org/10.3389/fneur.2015.00157
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author Diehl, Peter U.
Schaette, Roland
author_facet Diehl, Peter U.
Schaette, Roland
author_sort Diehl, Peter U.
collection PubMed
description Hyperacusis is a frequent auditory disorder that is characterized by abnormal loudness perception where sounds of relatively normal volume are perceived as too loud or even painfully loud. As hyperacusis patients show decreased loudness discomfort levels (LDLs) and steeper loudness growth functions, it has been hypothesized that hyperacusis might be caused by an increase in neuronal response gain in the auditory system. Moreover, since about 85% of hyperacusis patients also experience tinnitus, the conditions might be caused by a common mechanism. However, the mechanisms that give rise to hyperacusis have remained unclear. Here, we have used a computational model of the auditory system to investigate candidate mechanisms for hyperacusis. Assuming that perceived loudness is proportional to the summed activity of all auditory nerve (AN) fibers, the model was tuned to reproduce normal loudness perception. We then evaluated a variety of potential hyperacusis gain mechanisms by determining their effects on model equal-loudness contours and comparing the results to the LDLs of hyperacusis patients with normal hearing thresholds. Hyperacusis was best accounted for by an increase in non-linear gain in the central auditory system. Good fits to the average patient LDLs were obtained for a general increase in gain that affected all frequency channels to the same degree, and also for a frequency-specific gain increase in the high-frequency range. Moreover, the gain needed to be applied after subtraction of spontaneous activity of the AN, which is in contrast to current theories of tinnitus generation based on amplification of spontaneous activity. Hyperacusis and tinnitus might therefore be caused by different changes in neuronal processing in the central auditory system.
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spelling pubmed-45023612015-07-31 Abnormal Auditory Gain in Hyperacusis: Investigation with a Computational Model Diehl, Peter U. Schaette, Roland Front Neurol Neuroscience Hyperacusis is a frequent auditory disorder that is characterized by abnormal loudness perception where sounds of relatively normal volume are perceived as too loud or even painfully loud. As hyperacusis patients show decreased loudness discomfort levels (LDLs) and steeper loudness growth functions, it has been hypothesized that hyperacusis might be caused by an increase in neuronal response gain in the auditory system. Moreover, since about 85% of hyperacusis patients also experience tinnitus, the conditions might be caused by a common mechanism. However, the mechanisms that give rise to hyperacusis have remained unclear. Here, we have used a computational model of the auditory system to investigate candidate mechanisms for hyperacusis. Assuming that perceived loudness is proportional to the summed activity of all auditory nerve (AN) fibers, the model was tuned to reproduce normal loudness perception. We then evaluated a variety of potential hyperacusis gain mechanisms by determining their effects on model equal-loudness contours and comparing the results to the LDLs of hyperacusis patients with normal hearing thresholds. Hyperacusis was best accounted for by an increase in non-linear gain in the central auditory system. Good fits to the average patient LDLs were obtained for a general increase in gain that affected all frequency channels to the same degree, and also for a frequency-specific gain increase in the high-frequency range. Moreover, the gain needed to be applied after subtraction of spontaneous activity of the AN, which is in contrast to current theories of tinnitus generation based on amplification of spontaneous activity. Hyperacusis and tinnitus might therefore be caused by different changes in neuronal processing in the central auditory system. Frontiers Media S.A. 2015-07-15 /pmc/articles/PMC4502361/ /pubmed/26236277 http://dx.doi.org/10.3389/fneur.2015.00157 Text en Copyright © 2015 Diehl and Schaette. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Diehl, Peter U.
Schaette, Roland
Abnormal Auditory Gain in Hyperacusis: Investigation with a Computational Model
title Abnormal Auditory Gain in Hyperacusis: Investigation with a Computational Model
title_full Abnormal Auditory Gain in Hyperacusis: Investigation with a Computational Model
title_fullStr Abnormal Auditory Gain in Hyperacusis: Investigation with a Computational Model
title_full_unstemmed Abnormal Auditory Gain in Hyperacusis: Investigation with a Computational Model
title_short Abnormal Auditory Gain in Hyperacusis: Investigation with a Computational Model
title_sort abnormal auditory gain in hyperacusis: investigation with a computational model
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4502361/
https://www.ncbi.nlm.nih.gov/pubmed/26236277
http://dx.doi.org/10.3389/fneur.2015.00157
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