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Everyday sounds can feel unbearably loud or physically painful for people with hyperacusis, a complex disorder that may require tailored, cautious care.

 

Hyperacusis is a disorder in which everyday sounds are experienced as uncomfortable or intolerable. For some people, sounds feel unbearably loud; for others, sounds trigger physical pain. Although these symptoms are closely related and often occur together, research increasingly suggests that Loudness hyperacusis and pain hyperacusis (also called Noxacusis) represent distinct but overlapping clinical phenotypes.

This article summarises key points from my presentation at the 2025 Academy of Research Conference to clarify how these two forms of hyperacusis are similar, how they differ and why these distinctions matter.

Defining loudness and pain hyperacusis

Loudness hyperacusis is generally characterised by an abnormal perception of sound intensity. Sounds that most people perceive as tolerable (e.g. birds chirping, running water or traffic noise) are perceived as unbearably loud to someone with loudness hyperacusis [1]. Pain hyperacusis, in contrast, occurs when everyday sounds cause physical pain. Individuals with pain hyperacusis typically describe sensations such as burning, stabbing, throbbing or pinching triggered by sound exposure. It is important to understand that these symptoms are experienced as genuine bodily pain and can be quite debilitating, sometimes spreading beyond the ear to the head, face, neck or even elsewhere in the body [2].

 

 

How common are sound hypersensitivity disorders?

Studies suggest that as many as 17% of the general population reports sensitivity or intolerance to everyday sounds [3]. However, precise prevalence estimates for pain and loudness hyperacusis subtypes are not yet available.

What is clear is that loudness and pain hyperacusis frequently co-occur. In a large group of adults with hyperacusis, nearly four out of five reported symptoms of both pain and loudness hyperacusis [4]. About two-thirds primarily experienced pain hyperacusis, while roughly one-third primarily experienced loudness hyperacusis [4]. While this high degree of overlap may suggest that the disorders share underlying mechanisms, individual differences in dominant symptom profiles point toward meaningful clinical phenotypes that should be evaluated and addressed on a case-by-case basis.

Shared symptoms and comorbidities

Individuals with either subtype of hyperacusis often experience similar associated conditions [2,4]. Common comorbidities include tinnitus, headaches or migraines, mental health conditions (e.g. anxiety, depression) and hearing difficulties (e.g. hearing loss, difficulty hearing speech-in-noise, sound distortion). These shared features reinforce the idea that loudness and pain hyperacusis are closely related rather than entirely separate disorders.

Pain hyperacusis as a more severe phenotype

Despite similar symptoms and comorbidities, the overall burden of illness appears to be greater in pain hyperacusis [2,4]. People with pain hyperacusis often report more severe symptoms, less spontaneous improvement in symptoms over time, greater functional impairment and more frequent and intense symptom ‘setbacks’ or flare-ups. Setbacks may follow sound exposure, illness, stress or other triggers [4]. These differences are clinically important because they imply that pain hyperacusis may require different management strategies and a more cautious therapeutic approach.

Proposed mechanisms: from ear to brain

Current theories of hyperacusis involve multiple levels of the auditory system, from the middle and inner ear to the brainstem and auditory cortex [4]. One widely studied framework is the central gain theory. According to this model, reduced or altered input from the auditory periphery leads the central auditory system to ‘turn up the volume’, amplifying sound-evoked neural responses. This increased central gain can result in heightened loudness perception, sound-related distress and tinnitus. Central gain mechanisms are thought to play a major role in loudness hyperacusis and may also contribute to pain hyperacusis.

It has also been suggested that pain hyperacusis may involve dysfunction of the middle and/or inner ears. Proposed middle ear mechanisms of pain hyperacusis focus on the tensor tympani muscle and trigeminal nerve. Overactivity, involuntary contractions or overload of the tensor tympani muscle may trigger inflammation and activate the trigeminal nerve. Sensory and nociceptive signals from the trigeminal nerve are integrated in the brainstem and cortex, potentially leading to widespread pain responses to sound in the middle ear, head and neck regions.

"Clinicians are advised not to pressure patients to participate in sound-evoked diagnostic testing or to initiate sound therapy before they feel ready"

Proposed inner ear mechanisms of pain hyperacusis involve type II auditory nerve fibres. Unlike the type I fibres that transmit sound information, type II fibres share similar morphological and neurochemical properties with pain-sensing nerve fibres in the somatic nervous system. It has been suggested that these fibres may be activated when damaged outer hair cells in the inner ear release adenosine triphosphate (ATP), thereby transmitting pain-related information to the central nervous system.

While middle and inner ear theories of pain hyperacusis offer logical biological explanations for why sound might cause physical pain in some individuals, it is important to note that these theories have not yet been validated in animal or human models of hyperacusis.

Special considerations for clinical management of pain hyperacusis

Common interventions for hyperacusis include sound therapy (gradual, controlled sound exposure), counselling, cognitive behavioural therapy (CBT) and, in some cases, surgical or pharmacological treatments. For loudness hyperacusis, sound therapy combined with counselling is often considered the primary form of management [5], although high-quality evidence remains limited.

Very few studies have evaluated the efficacy of these interventions in people with pain hyperacusis. Many individuals with pain hyperacusis therefore seek a variety of methods to alleviate their pain. Recent qualitative work has shown that adults with severe pain hyperacusis often try a wide range of medications (e.g. antidepressants, anticonvulsants, muscle relaxants, cannabinoids or nerve blockers) as well as non-pharmacological approaches such as mindfulness, CBT and sound therapy [4]. However, some report that sound-based interventions provide little benefit or even worsen their pain [2,4]. While more research is needed to understand how to relieve sound-induced pain and prevent setbacks, it appears that sound-based therapies may provoke pain-related symptoms if introduced too aggressively or too early.

In the absence of evidence-based treatments for sound-induced pain, managing pain hyperacusis requires an individualised and empathetic approach. The long-term goal is to help individuals tolerate reasonable levels of everyday sound and return to their desired activities. At the same time, clinicians are advised not to pressure patients to participate in sound-evoked diagnostic testing or to initiate sound therapy before they feel ready. Blanket recommendations to cease ear protection are also not recommended in this population. While excessive sound avoidance may contribute to worsening sensitivity over time, patients with pain hyperacusis often must balance this risk against the reality of living in a world where sound can cause significant pain.

Summary

Loudness and pain hyperacusis share many features and frequently co-exist, but pain hyperacusis appears to represent a more severe and disabling phenotype. Distinguishing between these hyperacusis subtypes is essential for understanding patient experiences and tailoring treatment approaches. Future progress will depend on well-designed clinical trials to identify effective therapies for each subtype and to determine why some individuals respond to treatment while others do not. As research advances, clearer definitions and evidence-based care offer hope for improving quality of life for people living with hyperacusis.

 

 

References

1. Henry JA, Theodoroff SM, Edmonds C, et al. Sound tolerance conditions (hyperacusis, misophonia, noise sensitivity, and phonophobia): definitions and clinical management. Am J Audiol 2022;31(3):513–27.
2. Jahn KN, Kashiwagura ST, Yousuf MS. Clinical phenotype and management of sound-induced pain: insights from adults with pain hyperacusis. J Pain 2025;27:104741.
3. Ren J, Xu T, Xiang T. Prevalence of hyperacusis in the general and special populations: a scoping review. Front Neurol 2021;12:706555.
4. Williams ZJ, Suzman E, Woynaroski TG. A phenotypic comparison of loudness and pain hyperacusis: symptoms, comorbidity, and associated features in a multinational patient registry. Am J Audiol 2021;30:1–18.
5. Jahn KN, Koach CE. Hyperacusis diagnosis and management in the United States: clinical audiology practice patterns. Am J Audiol 2023;32(4):950–61.

 

Declaration of competing interests: None declared.

 

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Kelly N Jahn

AuD, PhD, The University of Texas at Dallas, USA.

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