Very High-Frequency Hearing Loss and Tinnitus: Is There a Link?

By Julia Campbell, Au.D., Ph.D.

Tinnitus is theorized to possibly arise from decreased central inhibition related to cochlear damage, or hearing loss. A reduction in inhibition function would allow signals that are normally suppressed to be perceived, resulting in tinnitus. However, many individuals with clinically typical hearing also present with tinnitus.

In our earlier study, results indicated that despite an apparently intact peripheral auditory system, inhibitory function was atypical and significantly related to tinnitus severity among a population reporting mild tinnitus. With central inhibition lowered, signals that are typically dampened are able to be perceived, potentially resulting in tinnitus. Our paper also showed the utility of measuring central inhibition through cortical auditory evoked potentials (CAEPs), which are electrical responses in the brain that reveal levels of central inhibition.

Given the prior study’s results, we thought it is possible that hearing loss within extended high-frequency thresholds (10, 12.5, and 16 kilohertz), which are not typically assessed in the clinic, may negatively impact inhibitory function and subsequent gating measures.

For our follow-up research, published in the American Journal of Audiology on April 22, 2019, we examined the role of both extended high-frequency thresholds and sensory gating dysfunction, a measure of central inhibition abnormality, in typical-hearing adults with and without tinnitus. Results suggest that extended high-frequency thresholds do not correlate with CAEP amplitude gating indices—in other words, high-frequency hearing loss was not associated with decreased central inhibition.

CAEP gating waveforms in A) a typical-hearing subject without tinnitus and B) a typical-hearing subject with tinnitus. The solid line represents the CAEP response to the first stimulus (S1) in a tonal pair, and the dashed the CAEP response to the se…

CAEP gating waveforms in A) a typical-hearing subject without tinnitus and B) a typical-hearing subject with tinnitus. The solid line represents the CAEP response to the first stimulus (S1) in a tonal pair, and the dashed the CAEP response to the second stimulus (S2) in a tonal pair. Typical gating is observed when CAEP S2 amplitude is lower compared with CAEP S1 amplitude (A). Atypical gating occurs when CAEP S2 amplitude is equal to or larger than CAEP S1 amplitude (B).

However, we found an unexpected relationship in the tinnitus group: Those with better (lower) thresholds also presented with worse tinnitus. We believe this finding may be due to typical-hearing adults with better high-frequency hearing to be more aware of internal auditory signals, and thus perceive tinnitus. However, further research is needed to investigate this hypothesis.

In addition, atypical gating performance was observed in adults with a Tinnitus Handicap Inventory score over 6, which may demonstrate that tinnitus severity must reach a certain point in order for central gating deficits to be observed, or vice versa. A hierarchical multiple regression showed both extended high-frequency thresholds and atypical gating function to account for a significant 49 percent of tinnitus severity.

Therefore, auditory gating appears to be a useful objective measure for tinnitus severity, at least in adults with clinically typical hearing. It also appears that the testing of extended high-frequency thresholds is warranted in this population, to be used in combination with CAEP amplitude gating indices. Our laboratory is now conducting studies investigating the utility of auditory gating as a clinical tool for the objective assessment of tinnitus severity in adults with hearing loss.

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2016 Emerging Research Grants scientist Julia Campbell, Au.D., Ph.D., CCC-A, FAAA, received the Les Paul Foundation Award for Tinnitus Research. She is an assistant professor in communication sciences and disorders in the Central Sensory Processes Laboratory at the University of Texas at Austin. If you are interested in participating in this research, email julia.campbell@austin.utexas.edu.

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