A4 Hypercusis and Misophonia: Abnormal Sensitivity to Sound

Topic

In individuals with abnormal sound sensitivity, sound traveling along the central auditory pathway toward the auditory cortex undergoes processing that deviates from the norm: the central auditory pathway assigns the sound greater importance than its actual physical intensity warrants. This excessive assignment can stem from two distinct mechanisms that converge on the central auditory pathway. The first is deafferentation: when peripheral hearing loss reduces the signal reaching the central auditory pathway, the pathway reacts by increasing its own gain to compensate for the lost signal. The second mechanism is maladaptive neuroplasticity: the central auditory pathway establishes or reinforces connections with structures that do not typically play a major role in processing ordinary sounds—a process that occurs without necessarily involving peripheral hearing loss.

When deafferentation increases the gain of the central auditory pathway, the effect goes beyond merely compensating for the lost signal; it also excessively amplifies sounds that are transmitted normally. Consequently, sounds of everyday intensity begin to elicit a neural response equivalent to what was previously triggered only by much more intense sounds. This excessive gain in the central auditory pathway lowers the threshold of discomfort—the intensity level at which a sound ceases to be tolerable and becomes painful or unbearable. The higher the gain in the central auditory pathway, the lower the discomfort threshold becomes, because progressively less actual physical intensity is required to produce the same internal response that previously demanded a much louder sound. This pathological reduction in the discomfort threshold is known as hyperacusis: sounds of normal, everyday intensity are perceived as excessively loud or even painful. Maladaptive neuroplasticity, in contrast, does not operate by generally increasing the gain of the central auditory pathway; instead, it links the central auditory pathway to circuits that generate strong emotional reactions. Consequently, a specific sound is no longer processed merely as a sound but also triggers a response of aversion, anger, or anxiety. This reinforced connection between the central auditory pathway and emotional circuits causes very specific—and otherwise low-intensity—sounds, such as chewing or breathing, to trigger a disproportionate reaction; this reaction depends not on the sound's loudness, but on the nature of the sound itself. This disproportionate activation of emotional circuits in response to specific sounds is known as misophonia. Unlike hyperacusis, misophonia does not lower the threshold for discomfort regarding sound in general; rather, it concentrates the abnormal reaction on a limited set of trigger sounds.

Both hyperacusis and misophonia ultimately manifest as the same abnormal sound sensitivity described at the beginning of this model: the central auditory pathway—whether due to the excessive gain caused by deafferentation or the emotional connections resulting from maladaptive neuroplasticity—ceases to process everyday sounds as neutral stimuli. Instead, it transforms them into sources of distress, either because they are perceived as excessively loud or because they are emotionally intolerable.

Since the abnormal sound sensitivity described in this model depends not on whether a sound is objectively harmful but on how the central auditory pathway processes it, none of the available interventions work by reducing the sound's physical intensity. Desensitization involves exposing the individual—gradually and in a controlled manner—to sounds of increasing intensity, allowing the central auditory pathway to readjust its discomfort threshold upward and, over time, reduce the excessive gain that sustains hyperacusis. Retraining therapy combines that same gradual exposure with work aimed at weakening the connection between the central auditory pathway and emotional circuits—a particularly relevant approach when the abnormal sound sensitivity involves a component of misophonia. Controlled hearing protection, meanwhile, limits the use of earplugs or earmuffs to strictly necessary situations; this is because constant protection against sound further reduces the signal reaching the central auditory pathway and—through the same mechanism of deafferentation described earlier—can ultimately increase central gain rather than alleviate it.

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