Central Gain Control in Tinnitus and Hyperacusis

Abstract

Sensorineural hearing loss induced by noise or ototoxic drug exposure reduces the neural activity transmitted from the cochlea to the central auditory system. Despite a reduced cochlear output, neural activity from more central auditory structures is paradoxically enhanced at suprathreshold intensities. This compensatory increase in the central auditory activity in response to the loss of sensory input is referred to as central gain enhancement. Enhanced central gain is hypothesized to be a potential mechanism that gives rise to hyperacusis and tinnitus, two debilitating auditory perceptual disorders that afflict millions of individuals. This review will examine the evidence for gain enhancement in the central auditory system in response to cochlear damage. Further, it will address the potential cellular and molecular mechanisms underlying this enhancement and discuss the contribution of central gain enhancement to tinnitus and hyperacusis. Current evidence suggests that multiple mechanisms with distinct temporal and spectral profiles are likely to contribute to central gain enhancement. Dissecting the contributions of these different mechanisms at different levels of the central auditory system is essential for elucidating the role of central gain enhancement in tinnitus and hyperacusis and, most importantly, the development of novel treatments for these disorders.

Somatic Tinnitus

“…The increased prevalence of somatic modulation found by the authors in hyperacusis patients could be due to increased peripheral somatic activation or central hypersensitivity to somatic inputs. The latter is supported by neurophysiological findings that show increased sensitivity to multisensory stimuli in patients with hyperacusis, which may be linked to a hypervigilance network [80][81][82][83][84] . Also, Schecklmann 79 and Gilles 85 found worse tinnitus and depression scores in patients with hyperacusis than in those without.…”

Pump Up the Volume: Could Excessive Neural Gain Explain Tinnitus and Hyperacusis?

“…Reviews of neural gain mechanisms in the auditory system have focused on cellular and molecular mechanisms [Auerbach et al, 2014] or on the current understanding of tinnitus from human and animal studies [Eggermont and Roberts, 2014], while others have provided an overview including clinical implications [Jastreboff and Hazell, 1993;Norena, 2011]. Here we focus on (i) evidence for changes in neural gain in the auditory system of animals, (ii) physiological and perceptual changes in adult human listeners following an acute period of enhanced acoustic stimulation and/or deprivation, (iii) physiological evidence of excessive neural gain in tinnitus and hyperacusis patients, and (iv) the relevance of neural gain in the clinical treatment of tinnitus and hyperacusis.…”

Coexistance of tinnitus and hyperacusis in individuals with auditory dys-synchrony: A single case study

“…Notably, this neuronal recalibration can result in an enhancement of incoming sensory signals, which may increase the loudness intolerance and hyperacusis which often accompanies hearing loss (27). Hence, the Central Gain Model accounts for both tinnitus and hyperacusis.…”

“…Despite reduced output from the cochlea, there will be enhancement in neural activity in central auditory structures at suprathreshold levels (27). Tinnitus and hyperacusis, while triggered by cochlear damage, result from a maladaptation of the central auditory system to this peripheral dysfunction (26).…”