• M Charles Liberman and Sharon G Kujawa.
• Department of Otology and Laryngology, Harvard Medical School, Boston MA, USA; Eaton-Peabody Laboratories, Massachusetts Eye & Ear Infirmary, Boston MA, USA.
• Hear. Res. 2017 Jun 1; 349: 138-147.

AbstractCommon causes of hearing loss in humans - exposure to loud noise or ototoxic drugs and aging - often damage sensory hair cells, reflected as elevated thresholds on the clinical audiogram. Recent studies in animal models suggest, however, that well before this overt hearing loss can be seen, a more insidious, but likely more common, process is taking place that permanently interrupts synaptic communication between sensory inner hair cells and subsets of cochlear nerve fibers. The silencing of affected neurons alters auditory information processing, whether accompanied by threshold elevations or not, and is a likely contributor to a variety of perceptual abnormalities, including speech-in-noise difficulties, tinnitus and hyperacusis. Work described here will review structural and functional manifestations of this cochlear synaptopathy and will consider possible mechanisms underlying its appearance and progression in ears with and without traditional 'hearing loss' arising from several common causes in humans.Copyright © 2017 Elsevier B.V. All rights reserved.

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