Abstract

Loudness recruitment is a common symptom of hearing loss induced by cochlear lesions, which is defined as an abnormally fast growth of loudness perception of sound intensity. This is different from hyperacusis, which is defined as “abnormal intolerance to regular noises” or “extreme amplification of sounds that are comfortable to the average individual”. Although both are characterized by abnormally high sound amplification, the mechanisms of occurrence are distinct. Damage to the outer hair cells alters the nonlinear characteristics of the basilar membrane, resulting in aberrant auditory nerve responses that may be connected to loudness recruitment. In contrast, hyperacusis is an aberrant condition characterized by maladaptation of the central auditory system. Peripheral injury can produce fluctuations in loudness recruitment, but this is not always the source of hyperacusis. Hyperacusis can also be accompanied by aversion to sound and fear of sound stimuli, in which the limbic system may play a critical role. This brief review aims to present the current status of the neurobiological mechanisms that distinguish between loudness recruitment and hyperacusis.

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