The goal of this study was to identify the effects of auditory deprivation (age-related hearing loss) and auditory stimulation (history of hearing aid use) on the neural registration of sound across two stimulus presentation conditions: (1) equal sound pressure level and (2) equal sensation level.
We used a between-groups design, involving three groups of 14 older adults (n = 42; 62 to 84 years): (1) clinically defined normal hearing (≤25 dB from 250 to 8000 Hz, bilaterally), (2) bilateral mild–moderate/moderately severe sensorineural hearing loss who have never used hearing aids, and (3) bilateral mild–moderate/moderately severe sensorineural hearing loss who have worn bilateral hearing aids for at least the past 2 years.
There were significant delays in the auditory P1-N1-P2 complex in older adults with hearing loss compared with their normal hearing peers when using equal sound pressure levels for all participants. However, when the degree and configuration of hearing loss were accounted for through the presentation of equal sensation level stimuli, no latency delays were observed. These results suggest that stimulus audibility modulates P1-N1-P2 morphology and should be controlled for when defining deprivation and stimulus-related neuroplasticity in people with hearing loss. Moreover, a history of auditory stimulation, in the form of hearing aid use, does not appreciably alter the neural registration of unaided auditory evoked brain activity when quantified by the P1-N1-P2.
When comparing auditory cortical responses in older adults with and without hearing loss, stimulus audibility, and not hearing loss–related neurophysiological changes, results in delayed response latency for those with age-related hearing loss. Future studies should carefully consider stimulus presentation levels when drawing conclusions about deprivation- and stimulation-related neuroplasticity. Additionally, auditory stimulation, in the form of a history of hearing aid use, does not significantly affect the neural registration of sound when quantified using the P1-N1-P2–evoked response.
1Department of Psychological and Brain Sciences, Washington University, St Louis, Washington, USA
2Department of Speech and Hearing Sciences, University of Washington, Washington, USA
3Department of Cognitive and Information Sciences, University of California, Merced, California, USA.
Received January 15, 2018; accepted December 7, 2018.
K.S.M designed and performed experiments, analyzed data, and wrote the article; K.C.B performed experiments, analyzed data, and wrote the article; K.L.T assisted in the design of the experiments and wrote the article.
This work was supported by grants T32-DC005361 (to K.S.M. and K.C.B) and F30-DC10297 (to K.S.M.) from NIH and grant from American Academy of Audiology Student Investigator Research Grant (to K.S.M.).
Kelly L. Tremblay is on the board of trustrees for the Hearing Loss Association of America and is the founder of Lend an Ear. The other authors have no conflicts of interest to disclose.
Portions of this article were presented at the 7th International and Interdisciplinary Research Conference on Aging and Speech Communication, November 6, 2017, Tampa, FL, and the 41st Annual MidWinter Meeting of the Association for Research in Otolaryngology, February 12, 2018.
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Address for correspondence: Katrina (Kate) S. McClannahan, Department of Psychological and Brain Sciences, Washington University in St. Louis, 1 Brookings Dr, Campus Box 1125, St. Louis, MO 63130, USA. E-mail: email@example.com
Online date: Februray 11, 2019