By Julia Campbell, Au.D., Ph.D.
Tinnitus, or the perception of sound where none is present, has been estimated to affect approximately 15 percent of adults. Unfortunately, there is no cure for tinnitus, nor is there an objective measure of the disorder, with professionals relying instead upon patient report.
There are several theories as to why tinnitus occurs, with one of the more prevalent hypotheses involving what is termed decreased inhibition. Neural inhibition is a normal function throughout the nervous system, and works in tandem with excitatory neural signals for accomplishing tasks ranging from motor output to the processing of sensory input. In sensory processing, such as hearing, both inhibitory and excitatory neural signals depend on external input.
For example, if an auditory signal cannot be relayed through the central auditory pathways due to cochlear damage resulting in hearing loss, both central excitation and inhibition may be reduced. This reduction in auditory-related inhibitory function may result in several changes in the central nervous system, including increased spontaneous neural firing, neural synchrony, and reorganization of cortical regions in the brain. Such changes, or plasticity, could possibly result in the perception of tinnitus, allowing signals that are normally suppressed to be perceived by the affected individual. Indeed, tinnitus has been reported in an estimated 30 percent of those with clinical hearing loss over the frequency range of 0.25 to 8 kilohertz (kHz), suggesting that cochlear damage and tinnitus may be interconnected.
However, many individuals with clinically normal hearing report tinnitus. Therefore, it is possible that in this specific population, inhibitory dysfunction may not underlie these phantom perceptions, or may arise from a different trigger other than hearing loss.
One measure of central inhibition is sensory gating. Sensory gating involves filtering out signals that are repetitive and therefore unimportant for conscious perception. This automatic process can be measured through electrical responses in the brain, termed cortical auditory evoked potentials (CAEPs). CAEPs are recorded via electroencephalography (EEG) using noninvasive sensors to record electrical activity from the brain at the level of the scalp.
In healthy gating function, it is expected that the CAEP response to an initial auditory signal will be larger in amplitude when compared with a secondary CAEP response elicited by the same auditory signal. This illustrates the inhibition of repetitive information by the central nervous system. If inhibitory processes are dysfunctional, CAEP responses are similar in amplitude, reflecting decreased inhibition and the reduced filtering of incoming auditory information.
Due to the hypothesis that atypical inhibition may play a role in tinnitus, we conducted a study to evaluate inhibitory function in adults with normal hearing, with and without mild tinnitus, using sensory gating measures. To our knowledge, sensory gating had not been used to investigate central inhibition in individuals with tinnitus. We also evaluated extended high-frequency auditory sensitivity in participants at 10, 12.5, and 16 kHz—which are frequencies not included in the usual clinical evaluation—to determine if participants with mild tinnitus showed hearing loss in these regions.
Tinnitus severity was measured subjectively using the Tinnitus Handicap Index. This score was correlated with measures of gating function to determine if tinnitus severity may be worse with decreased inhibition.
Our results, published in Audiology Research on Oct. 2, 2018, showed that gating function was impaired in adults with typical hearing and mild tinnitus, and that decreased gating was significantly correlated with tinnitus severity. In addition, those with tinnitus did not show significantly different extended high-frequency thresholds in comparison to the participants without tinnitus, but it was found that better hearing in this frequency range related to worse tinnitus severity.
This result conflicts with the theory that hearing loss may trigger tinnitus, at least in adults with typical hearing, and may indicate that these individuals possess heightened auditory awareness, although this hypothesis should be directly tested.
Overall, it appears that central inhibition is atypical in adults with typical hearing and tinnitus, and that this is not related to hearing loss as measured in clinically or non-clinically tested frequency regions. The cause of decreased inhibition in this population remains unknown, but genetic factors may play a role. We are currently investigating the use of sensory gating as an objective clinical measure of tinnitus, particularly in adults with hearing loss, as well as the networks in the brain that may underlie dysfunctional gating processes.
2016 Emerging Research Grants scientist Julia Campbell, Au.D., Ph.D., CCC-A, F-AAA, 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.
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