TY - JOUR
T1 - Age-Related Compensation Mechanism Revealed in the Cortical Representation of Degraded Speech
AU - Anderson, Samira
AU - Roque, Lindsey
AU - Gaskins, Casey R.
AU - Gordon-Salant, Sandra
AU - Goupell, Matthew J.
N1 - Funding Information:
This study was supported by the National Institute on Deafness and Other Communication Disorders of the National Institutes of Health (NIH) under award number R21DC015843 (Anderson) and the National Institute on Aging under award number R01AG051603 (Goupell). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Acknowledgments
Publisher Copyright:
© 2020, Association for Research in Otolaryngology.
PY - 2020
Y1 - 2020
N2 - Older adults understand speech with comparative ease in quiet, but signal degradation can hinder speech understanding much more than it does in younger adults. This difficulty may result, in part, from temporal processing deficits related to the aging process and/or high-frequency hearing loss that can occur in listeners who have normal- or near-normal-hearing thresholds in the speech frequency range. Temporal processing deficits may manifest as degraded neural representation in peripheral and brainstem/midbrain structures that lead to compensation, or changes in response strength in auditory cortex. Little is understood about the process by which the neural representation of signals is improved or restored by age-related cortical compensation mechanisms. Therefore, we used vocoding to simulate spectral degradation to compare the behavioral and neural representation of words that contrast on a temporal dimension. Specifically, we used the closure duration of the silent interval between the vowel and the final affricate /t∫/ or fricative /ʃ/ of the words DITCH and DISH, respectively. We obtained perceptual identification functions and electrophysiological neural measures (frequency-following responses (FFR) and cortical auditory-evoked potentials (CAEPs)) to unprocessed and vocoded versions of these words in young normal-hearing (YNH), older normal- or near-normal-hearing (ONH), and older hearing-impaired (OHI) listeners. We found that vocoding significantly reduced the slope of the perceptual identification function in only the OHI listeners. In contrast to the limited effects of vocoding on perceptual performance, vocoding had robust effects on the FFRs across age groups, such that stimulus-to-response correlations and envelope magnitudes were significantly lower for vocoded vs. unprocessed conditions. Increases in the P1 peak amplitude for vocoded stimuli were found for both ONH and OHI listeners, but not for the YNH listeners. These results suggest that while vocoding substantially degrades early neural representation of speech stimuli in the midbrain, there may be cortical compensation in older listeners that is not seen in younger listeners.
AB - Older adults understand speech with comparative ease in quiet, but signal degradation can hinder speech understanding much more than it does in younger adults. This difficulty may result, in part, from temporal processing deficits related to the aging process and/or high-frequency hearing loss that can occur in listeners who have normal- or near-normal-hearing thresholds in the speech frequency range. Temporal processing deficits may manifest as degraded neural representation in peripheral and brainstem/midbrain structures that lead to compensation, or changes in response strength in auditory cortex. Little is understood about the process by which the neural representation of signals is improved or restored by age-related cortical compensation mechanisms. Therefore, we used vocoding to simulate spectral degradation to compare the behavioral and neural representation of words that contrast on a temporal dimension. Specifically, we used the closure duration of the silent interval between the vowel and the final affricate /t∫/ or fricative /ʃ/ of the words DITCH and DISH, respectively. We obtained perceptual identification functions and electrophysiological neural measures (frequency-following responses (FFR) and cortical auditory-evoked potentials (CAEPs)) to unprocessed and vocoded versions of these words in young normal-hearing (YNH), older normal- or near-normal-hearing (ONH), and older hearing-impaired (OHI) listeners. We found that vocoding significantly reduced the slope of the perceptual identification function in only the OHI listeners. In contrast to the limited effects of vocoding on perceptual performance, vocoding had robust effects on the FFRs across age groups, such that stimulus-to-response correlations and envelope magnitudes were significantly lower for vocoded vs. unprocessed conditions. Increases in the P1 peak amplitude for vocoded stimuli were found for both ONH and OHI listeners, but not for the YNH listeners. These results suggest that while vocoding substantially degrades early neural representation of speech stimuli in the midbrain, there may be cortical compensation in older listeners that is not seen in younger listeners.
KW - aging
KW - cortical
KW - midbrain
KW - perception
KW - vocoding
UR - http://www.scopus.com/inward/record.url?scp=85087711429&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85087711429&partnerID=8YFLogxK
U2 - 10.1007/s10162-020-00753-4
DO - 10.1007/s10162-020-00753-4
M3 - Article
C2 - 32643075
AN - SCOPUS:85087711429
JO - JARO - Journal of the Association for Research in Otolaryngology
JF - JARO - Journal of the Association for Research in Otolaryngology
SN - 1525-3961
ER -