Abstract
Decreased central inhibition, possibly related to hearing loss, may contribute to chronic tinnitus. However, many individuals with normal hearing thresholds report tinnitus, suggesting that the percept in this population may arise from sources other than peripheral deafferentation. One measure of inhibition is sensory gating. Sensory gating involves the suppression of non-novel input, and is measured through cortical auditory evoked potential (CAEP) responses to paired stimuli. In typical gating function, amplitude suppression is observed in the second CAEP response when compared to the first CAEP response, illustrating inhibitory activity. Using this measure, we investigated central inhibitory processes in normal hearing young adults with and without mild tinnitus to determine whether inhibition may be a contributing factor to the tinnitus percept. Results showed that gating function was impaired in the tinnitus group, with the CAEP Pa component significantly correlated with tinnitus severity. Further exploratory analyses were conducted to evaluate variability in gating function within the tinnitus group, and findings showed that high CAEP amplitude suppressors demonstrated gating performance comparable to adults without tinnitus, while low amplitude suppressors exhibited atypical gating function.
Highlights
IntroductionIdiopathic tinnitus, a phantom auditory percept,[1] is an auditory disorder that may be induced by peripheral damage (e.g. hearing loss), but is thought to be sustained centrally.[2] the pathophysiology of tinnitus remains largely unknown, it has been theorized that deafferentation of neural fibers, resulting from cochlear damage, may induce a decrease of inhibition in the central auditory nervous system.[3] Decreased central inhibition can lead to increased spontaneous neural firing rate, neural synchrony, and cortical re-organization.[1] For example, re-organization in the tonotopic map of the auditory cortex has been observed in hearing loss and tinnitus, possibly due to decreased lateral disinhibition as neurons are no longer stimulated by auditory input in the hearing loss region.[1] tinnitus has been reported in adults with clinically normal auditory thresholds.[4] It is unclear as to whether a decrease in central inhibition is related to the tinnitus percept in this population, as there is no clinical indication of cochlear damage present as a possible cause
Idiopathic tinnitus, a phantom auditory percept,[1] is an auditory disorder that may be induced by peripheral damage, but is thought to be sustained centrally.[2]
Due to hypotheses that gating in the frontal cortex may be atypical in tinnitus,[9] as well as a previous study in which we found a frontal region of interest (ROI) to be sensitive to changes in frontal cortical activity,[19] individual frontal ROIs were created from an average of thirteen electrodes (3, 4, 5, 9 or Fp2, 10, 11 or Fz, 12, 15, 16, 18, 19, 22 or Fp1, 23)
Summary
Idiopathic tinnitus, a phantom auditory percept,[1] is an auditory disorder that may be induced by peripheral damage (e.g. hearing loss), but is thought to be sustained centrally.[2] the pathophysiology of tinnitus remains largely unknown, it has been theorized that deafferentation of neural fibers, resulting from cochlear damage, may induce a decrease of inhibition in the central auditory nervous system.[3] Decreased central inhibition can lead to increased spontaneous neural firing rate, neural synchrony, and cortical re-organization.[1] For example, re-organization in the tonotopic map of the auditory cortex has been observed in hearing loss and tinnitus, possibly due to decreased lateral disinhibition as neurons are no longer stimulated by auditory input in the hearing loss region.[1] tinnitus has been reported in adults with clinically normal auditory thresholds.[4] It is unclear as to whether a decrease in central inhibition is related to the tinnitus percept in this population, as there is no clinical indication of cochlear damage present as a possible cause
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
