Brainstem Correlates of Tinnitus and Hyperacusis in Normal-Hearing Listeners: Distinct Neural Signatures Linked to Cochlear Nerve Degeneration

OBJECTIVES: To determine how cochlear nerve degeneration (CND) relates to tinnitus and sound hypersensitivity in normal-hearing listeners, and whether these symptoms are associated with distinct patterns of central gain within the auditory brainstem. DESIGN: In a cohort of normal-hearing adults with normal audiometric thresholds (≤20 dB HL from 0.25 to 8 kHz) and mean extended high-frequency thresholds ≤20 dB HL, we recorded click-evoked electrocochleography (ECochG) and assessed sound sensitivity using the Hyperacusis Handicap Questionnaire (HHQ). To separate peripheral from central contributions, we used a frequency-based filtering approach that exploits differences in the temporal properties of auditory generators along the ascending pathway, applying a high-frequency filter (470 to 3000 Hz) to derive peripheral auditory nerve measures and a low-frequency filter (3.3 to 470 Hz) to isolate slower brainstem components. Mixed-effects and sequential regression analyses were used to examine associations between ECochG markers, tinnitus status, and HHQ scores. RESULTS: High-pass ECochG responses showed that both tinnitus and elevated HHQ scores were independently associated with reduced peripheral amplitudes, consistent with CND. In high-pass waveforms, cochlear nucleus gain was selectively elevated in participants with tinnitus, regardless of HHQ score. In contrast, low-pass responses revealed that a later brainstem component, and its amplitude relative to the earlier component, were increased in participants with high HHQ scores, independent of tinnitus status. Sequential regression analyses indicated that the effects of peripheral neural loss on tinnitus and on sound sensitivity overlapped only partially, with each symptom not fully accounting for the other. CONCLUSIONS: In normal-hearing listeners, tinnitus and hyperacusis share a common peripheral correlate in CND but exhibit distinct brainstem gain signatures. These findings suggest that tinnitus and sound hypersensitivity reflect dissociable forms of central compensation to cochlear nerve injury.