Auditory brainstem response demonstrates that reduced peripheral auditory input is associated with self-report of tinnitus.

Tinnitus is one of the predicted perceptual consequences of cochlear synaptopathy, a type of age-, noise-, or drug-induced auditory damage that has been demonstrated in animal models to cause homeostatic changes in central auditory gain. Although synaptopathy has been observed in human temporal bones, assessment of this condition in living humans is limited to indirect non-invasive measures such as the auditory brainstem response (ABR). In animal models, synaptopathy is associated with a reduction in ABR wave I amplitude at suprathreshold stimulus levels. Several human studies have explored the relationship between wave I amplitude and tinnitus, with conflicting results. This study investigates the hypothesis that reduced peripheral auditory input due to synaptic/neuronal loss is associated with tinnitus. Wave I amplitude data from 193 individuals [43 with tinnitus (22%), 150 without tinnitus (78%)], who participated in up to 3 out of 4 different studies, were included in a logistic regression analysis to estimate the relationship between wave I amplitude and tinnitus at a variety of stimulus levels and frequencies. Statistical adjustment for sex and distortion product otoacoustic emissions (DPOAEs) was included. The results suggest that smaller wave I amplitudes and/or lower DPOAE levels are associated with an increased probability of tinnitus.