RESUMO
OBJECTIVE: To evaluate whether cochlear synaptopathy is a common pathophysiologic cause of tinnitus in individuals with normal audiograms. STUDY DESIGN: Prospective study. SETTING: Tertiary referral center. METHODS: 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 90âdB nHL click stimuli in quiet conditions; 2) the latency shift of wave V with 80âdB nHL click stimuli in background noise, varying from 40âdB HL to 70âdB HL; and 3) uncomfortable loudness levels (UCLs) at 500âHz and 3000âHz pure tones. RESULTS: 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 500âHz or 3000âHz between TEs and NTEs, but the UCLs were lower in TEs (mean 111.3âdB or 104.1âdB) and NTEs (mean 109.4âdB or 100.6âdB) than in control ears (mean 117.9âdB or 114.1âdB, pâ<â0.017). No subject met our criteria for cochlear synaptopathy or increased central gain in terms of all three parameters. CONCLUSION: 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.