Tinnitus and Auditory Perception After a History of Noise Exposure: Relationship to Auditory Brainstem Response Measures

Objectives: To determine whether auditory brainstem response (ABR) wave I amplitude is associated with measures of auditory perception in young people with normal distortion product otoacoustic emissions (DPOAEs) and varying levels of noise exposure history. Design: Tinnitus, loudness tolerance, and speech perception ability were measured in 31 young military Veterans and 43 non-Veterans (19 to 35 years of age) with normal pure-tone thresholds and DPOAEs. Speech perception was evaluated in quiet using Northwestern University Auditory Test (NU-6) word lists and in background noise using the words in noise (WIN) test. Loudness discomfort levels were measured using 1-, 3-, 4-, and 6-kHz pulsed pure tones. DPOAEs and ABRs were collected in each participant to assess outer hair cell and auditory nerve function. Results: The probability of reporting tinnitus in this sample increased by a factor of 2.0 per 0.1 µV decrease in ABR wave I amplitude (95% Bayesian confidence interval, 1.1 to 5.0) for males and by a factor of 2.2 (95% confidence interval, 1.0 to 6.4) for females after adjusting for sex and DPOAE levels. Similar results were obtained in an alternate model adjusted for pure-tone thresholds in addition to sex and DPOAE levels. No apparent relationship was found between wave I amplitude and either loudness tolerance or speech perception in quiet or noise. Conclusions: Reduced ABR wave I amplitude was associated with an increased risk of tinnitus, even after adjusting for DPOAEs and sex. In contrast, wave III and V amplitudes had little effect on tinnitus risk. This suggests that changes in peripheral input at the level of the inner hair cell or auditory nerve may lead to increases in central gain that give rise to the perception of tinnitus. Although the extent of synaptopathy in the study participants cannot be measured directly, these findings are consistent with the prediction that tinnitus may be a perceptual consequence of cochlear synaptopathy. ACKNOWLEDGMENTS: The authors thank Drs. Brad Buran and Charlie Liberman for their helpful comments on the study and article. This research was supported by the Department of Veterans Affairs, Veterans Health Administration, Rehabilitation Research and Development Service: Award No. C1484-M (to N.F.B.) and C9230-C [to National Center for Rehabilitative Auditory Research (NCRAR)]. N.F.B. designed and performed the experiments, analyzed the data, and wrote the article. D.K.-M. aided in the design of the experiments and provided critical revision. G.P.M. provided statistical analysis and critical revision. The opinions and assertions presented are private views of the authors and are not to be construed as official or as necessarily reflecting the views of the Veterans Administration (VA) or the Department of Defense. The authors have no conflicts of interest to disclose. Address for correspondence: Naomi F. Bramhall, VA RR&D National Center for Rehabilitative Auditory Research (NCRAR), 3710 SW US Veterans Hospital Road, P5-NCRAR, Portland, OR 97239, USA. E-mail: naomi.bramhall@va.gov Received April 28, 2017; accepted November 16, 2017. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and text of this article on the journal’s Web site (www.ear-hearing.com). Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

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