A Review of the Neurobiological Mechanisms that Distinguish Between Loudness Recruitment and Hyperacusis

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.

Figure 1

Loudness models for normal subjects, patients with loudness recruitment, and patients with hyperacusis (Cox, 1997). The maximum discomfort threshold for a normal person is 100 dB HL. Patients with loudness recruitment have a largely unchanged maximum discomfort threshold, although they often have sensorineural deafness, while some patients with hyperacusis have an increased hearing threshold, the maximum discomfort threshold falls to 70–80 dB instead, thus the range of hearing tolerance is significantly reduced.

Figure 2

Diagram of Loudness recruitment classification and hyperacusis. N – normal individuals, A – abnormal patients.

Figure 3

Input-output curve for normal ear and loudness recruitment ear at different frequencies.