Tinnitus

To develop a self-report tinnitus handicap measure that is brief, easy to administer and interpret, broad in scope, and psychometrically robust.

Ever since Pliny the Elder coined the term tinnitus, the perception of sound in the absence of an external sound source has remained enigmatic. Traditional theories assume that tinnitus is triggered by cochlear damage, but many tinnitus patients present with a normal audiogram, i.e., with no direct signs of cochlear damage. Here, we report that in human subjects with tinnitus and a normal audiogram, auditory brainstem responses show a significantly reduced amplitude of the wave I potential (generated by primary auditory nerve fibers) but normal amplitudes of the more centrally generated wave V. This provides direct physiological evidence of "hidden hearing loss" that manifests as reduced neural output from the cochlea, and consequent renormalization of neuronal response magnitude within the brainstem. Employing an established computational model, we demonstrate how tinnitus could arise from a homeostatic response of neurons in the central auditory system to reduced auditory nerve input in the absence of elevated hearing thresholds.

The purpose of the current review is to propose a model highlighting the putative connections between hearing loss and the phantom perception of tinnitus (tinnitus being accompanied by hearing loss in the majority, if not all, subjects). Sensory deprivation is followed by dramatic functional and structural changes in the auditory system. Notably, while cochlear injuries are accompanied by a reduced activity in the cochlear nerve, neural activity is increased at virtually all levels in the central auditory system. We suggest that this central hyperactivity could result from a central gain increase; the general purpose of this gain modulation being to adapt neural sensitivity to the reduced sensory inputs, preserving a stable mean firing and neural coding efficiency. However, maintaining neural homeostasis at all costs, in the event of an auditory system sensory deprivation, could be done at the price of amplifying "neural noise" due to the overall increase of gain (or sensitivity), ultimately resulting in the generation of tinnitus. The clinical implications of this model are also presented. Copyright © 2010 Elsevier Ltd. All rights reserved.