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  • SPiN difficulties paper for Pure + pics & SM

    Rights statement: This is the author’s version of a work that was accepted for publication in Hearing Research. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Hearing Research, 364, 2018 DOI: 10.1016/j.heares.2018.03.008

    Accepted author manuscript, 11 MB, PDF-document

    Embargo ends: 9/03/19

    Available under license: CC BY-NC-ND: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License

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Impaired speech perception in noise with a normal audiogram: No evidence for cochlear synaptopathy and no relation to lifetime noise exposure

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E-pub ahead of print
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<mark>Journal publication date</mark>07/2018
<mark>Journal</mark>Hearing Research
Volume364
Number of pages10
Pages (from-to)142-151
<mark>State</mark>E-pub ahead of print
Early online date9/03/18
<mark>Original language</mark>English

Abstract

In rodents, noise exposure can destroy synapses between inner hair cells and auditory nerve fibers (“cochlear synaptopathy”) without causing hair cell loss. Noise-induced cochlear synaptopathy usually leaves cochlear thresholds unaltered, but is associated with long-term reductions in auditory brainstem response (ABR) amplitudes at medium-to-high sound levels. This pathophysiology has been suggested to degrade speech perception in noise (SPiN), perhaps explaining why SPiN ability varies so widely among audiometrically normal humans. The present study is the first to test for evidence of cochlear synaptopathy in humans with significant SPiN impairment. Individuals were recruited on the basis of self-reported SPiN difficulties and normal pure tone audiometric thresholds. Performance on a listening task identified a subset with “verified” SPiN impairment. This group was matched with controls on the basis of age, sex, and audiometric thresholds up to 14 kHz. ABRs and envelope-following responses (EFRs) were recorded at high stimulus levels, yielding both raw amplitude measures and within-subject difference measures. Past exposure to high sound levels was assessed by detailed structured interview. Impaired SPiN was not associated with greater lifetime noise exposure, nor with any electrophysiological measure. It is conceivable that retrospective self-report cannot reliably capture noise exposure, and that ABRs and EFRs offer limited sensitivity to synaptopathy in humans. Nevertheless, the results do not support the notion that noise-induced synaptopathy is a significant etiology of SPiN impairment with normal audiometric thresholds. It may be that synaptopathy alone does not have significant perceptual consequences, or is not widespread in humans with normal audiograms.