To evaluate whether cochlear synaptopathy is a common pathophysiologic cause of tinnitus in individuals with normal audiograms.
Tertiary referral center.
We enrolled 27 subjects with unilateral tinnitus and normal symmetric hearing thresholds, and 27 age- and sex-matched control subjects with normal symmetric hearing thresholds. We measured 1) the amplitudes of waves I and V with 90 dB nHL click stimuli in quiet conditions; 2) the latency shift of wave V with 80 dB nHL click stimuli in background noise, varying from 40 dB HL to 70 dB HL; and 3) uncomfortable loudness levels (UCLs) at 500 Hz and 3000 Hz pure tones.
There were no significant differences in the wave V/I amplitude ratio or the latency shift in wave V with increasing noise levels among the tinnitus ears (TEs), nontinnitus ears (NTEs), and control ears. There were no significant differences in UCLs at 500 Hz or 3000 Hz between TEs and NTEs, but the UCLs were lower in TEs (mean 111.3 dB or 104.1 dB) and NTEs (mean 109.4 dB or 100.6 dB) than in control ears (mean 117.9 dB or 114.1 dB, p
< 0.017). No subject met our criteria for cochlear synaptopathy or increased central gain in terms of all three parameters.
Based on these results for UCL, increased central gain is a major mechanism of tinnitus in humans with normal audiograms. However, this compensatory mechanism for reduced auditory input may originate from other pathophysiologic factors rather than from cochlear synaptopathy.