AI Article Synopsis

  • The study investigates the link between "hidden hearing loss," cochlear synaptopathy, and tinnitus in individuals with normal hearing by comparing auditory brainstem response (ABR) amplitudes in tinnitus ears (TEs) and non-tinnitus ears (NTEs).
  • Researchers found no significant differences in wave I and wave V amplitudes or uncomfortable loudness levels (UCL) between TEs and NTEs in a sample of tinnitus patients and control subjects.
  • The results suggest that the data do not support the theory of increased central auditory gain due to cochlear synaptopathy in tinnitus patients with normal hearing thresholds, although reduced sound tolerance might indicate some level of synaptopathy between the ears.

Article Abstract

Objective: Recently, "hidden hearing loss" with cochlear synaptopathy has been suggested as a potential pathophysiology of tinnitus in individuals with a normal hearing threshold. Several studies have demonstrated that subjects with tinnitus and normal audiograms show significantly reduced auditory brainstem response (ABR) wave I amplitudes compared with control subjects, but normal wave V amplitudes, suggesting increased central auditory gain. We aimed to reconfirm the "hidden hearing loss" theory through a within-subject comparison of wave I and wave V amplitudes and uncomfortable loudness level (UCL), which might be decreased with increased central gain, in tinnitus ears (TEs) and non-tinnitus ears (NTEs).

Subjects And Methods: Human subjects included 43 unilateral tinnitus patients (19 males, 24 females) with normal and symmetric hearing thresholds and 18 control subjects with normal audiograms. The amplitudes of wave I and V from the peak to the following trough were measured twice at 90 dB nHL and we separately assessed UCLs at 500 Hz and 3000 Hz pure tones in each TE and NTE.

Results: The within-subject comparison between TEs and NTEs showed no significant differences in wave I and wave V amplitude, or wave V/I ratio in both the male and female groups. Individual data revealed increased V/I amplitude ratios > mean + 2 SD in 3 TEs, but not in any control ears. We found no significant differences in UCL at 500 Hz or 3000 Hz between the TEs and NTEs, but the UCLs of both TEs and NTEs were lower than those of the control ears.

Conclusions: Our ABR data do not represent meaningful evidence supporting the hypothesis of cochlear synaptopathy with increased central gain in tinnitus subjects with normal audiograms. However, reduced sound level tolerance in both TEs and NTEs might reflect increased central gain consequent on hidden synaptopathy that was subsequently balanced between the ears by lateral olivocochlear efferents.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5734686PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0189157PLOS

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