Central gain control in tinnitus and hyperacusis.

Summary

Sensorineural hearing loss from noise or ototoxic drugs reduces the neural activity sent from the cochlea, yet activity in more central auditory structures is paradoxically enhanced at suprathreshold intensities, 'central gain enhancement'. This review examines the evidence for that enhancement after cochlear damage, the candidate cellular and molecular mechanisms, and how the enhancement may give rise to hyperacusis and tinnitus. It concludes that multiple mechanisms with distinct temporal and spectral profiles contribute at different levels of the pathway.

Key findings

• Despite reduced cochlear output, central auditory activity is paradoxically enhanced at suprathreshold levels.
• This compensatory increase is termed central gain enhancement.
• Multiple mechanisms with distinct temporal and spectral profiles act at different levels of the pathway.
• Dissecting those mechanisms is framed as essential for developing treatments.