Tinnitus and Cochlear Neural Degeneration: Unveiling Association in Adults with Normal Audiograms
A new groundbreaking study revealed the connection between peripheral neural deficits' biomarkers and tinnitus, suggesting Cochlear Neural Degeneration (CND) as a potential trigger for central hyperactivity. The study results were published in the journal Scientific Reports.
Sensorineural hearing loss in adults is commonly linked to complaints such as tinnitus, decreased tolerance to sound levels, and challenges in hearing amid noisy environments. Approximately 10–15% of adults globally experience tinnitus, with 2–4% facing severe impacts. Sleep deprivation, social isolation, anxiety, and depression, adversely affect work performance, resulting in a severe decline in the quality of life. Current therapies focus on distress relief, lacking a cure until the biological origins of tinnitus are understood. Hence researchers conducted a large cohort study of normal-hearing participants with minimal loss at extended high frequencies (≤ 20 dB HL) and extracted, under computer control, peripheral and central markers from both auditory evoked potentials and auditory efferent reflexes.
This study enrolled English-speaking participants aged 18–72. Inclusion criteria ensured good health, normal ear function, and proficiency in English. Participants were categorized based on self-reported tinnitus experiences, including those without tinnitus, those with temporary episodes, and those with continuous perception. Audiometric evaluations assessed hearing thresholds at standard and extended high frequencies. Auditory assessments involved auditory brainstem responses/electrocochleography and middle-ear muscle reflex measurements. In-depth characterization included threshold analysis, electrocochleography waveform processing, and middle-ear muscle reflex strength computation. This approach aimed to comprehensively investigate the association between cochlear neural deficits and tinnitus.
Results:
Self-report of chronic tinnitus was significantly associated with
(1) reduced cochlear nerve responses,
(2) weaker middle-ear muscle reflexes,
(3) stronger medial olivocochlear efferent reflexes, and
(4) hyperactivity in the central auditory pathways.
Thus, the present study revealed the connection between peripheral neural deficits' biomarkers and tinnitus, suggesting Cochlear Neural Degeneration (CND) as a potential trigger for central hyperactivity. Future psychophysical measures may help interpret the underlying pathology and clarify CND's role in central hyperactivity development. In a noise-damaged mouse model, neurotrophin overexpression or supplementation can promote the regeneration of connections, offering insights into potential therapeutic strategies in humans. Developing diagnostic assays for CND is crucial to identify candidates for future treatments and assess efficacy in rebuilding the damaged inner ear and potentially reversing the tinnitus percept.
Further reading: Vasilkov, V., Caswell-Midwinter, B., Zhao, Y. et al. Evidence of cochlear neural degeneration in normal-hearing subjects with tinnitus. Sci Rep 13, 19870 (2023). https://doi.org/10.1038/s41598-023-46741-5
