Search for Electrophysiological Indices of Hidden Hearing Loss
Recent studies in animals indicate that even moderate levels of exposure to noise can damage synaptic ribbons between the inner hair cells and auditory nerve fibers without affecting audiometric thresholds, giving rise to the use of the term “hidden hearing loss” (HHL). Given the pervasive exposure to occupational and recreational noise in the general population, it is likely that individuals afflicted with HHL will go unidentified unless sensitive clinical measures are developed to diagnose this condition. To date, the studies employed to characterize HHL in humans have yielded equivocal results - some studies show wave I amplitude decrement while others show no difference in either Wave I amplitude or the sustained phase-locked activity in the frequency following response (FFR). The main objective of this project is to determine stimulus manipulations that produce electrophysiological changes specific to individuals at risk for HHL. The aim is to develop sensitive clinical electrophysiological metrics for early detection of HHL. We reasoned that synaptopathy associated with HHL may be relatively more susceptible to certain stimulus manipulations that affect synaptic level processes, and will likely produce a greater degradation of responses (recorded from the different levels-inner ear, auditory nerve, and brainstem) in individuals at high risk for HHL compared to controls. The specific stimulus manipulations included sound levels, two different adaptation paradigms (stimulus rate neural adaptation and click train (temporal course and recovery from adaptation) paradigm), ABRs and FFRs (speech token) in noise, and changes in rate of frequency sweep (temporal processes involved in representing frequency change). Consistent with previous studies, there were no differences between the low- and high-risk groups in audiometric thresholds or DPOAE amplitude. The high-risk group had significantly lower Wave I amplitude at high sound levels only and across two different adaptation paradigms with little effect on the responses at higher centers reflecting compensatory mechanisms and/or resilience of later waves to stimulus manipulations. The normalized wave I amplitude change with background noise was smaller for the high-risk group suggesting reduced suppressive masking. Despite reduced wave I amplitude for high-risk group; the high risk group showed no change in rate or click-train induced neural adaptation suggesting that synaptic processes contributing to adaptation remain unaltered; enhanced neural representation of F2 harmonics in quiet as well as background noise; and enhanced representation of rapid tonal sweeps (similar to a dynamic musical note) possibly through corticofugal influence shaped by music experience. These findings suggest that the consequences of music exposure induced synaptopathy reflects a complex interaction of multitude of factors (sound over-exposure, music experience, and homeostatic central compensation. Therefore, there is a need for larger scale datasets with different noise exposure background, longitudinal measurements with an array of behavioral and electrophysiological tests to understand the complex pathogenesis of sound over-exposure damage in normal-hearing individuals.
Krishnan, Purdue University.
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