Hyperacusis

Abstract

Hyperacusis is a reduced tolerance to ordinary sounds, in which everyday levels that most listeners find unremarkable are experienced as uncomfortably loud, painful, or threatening. It is not a loss of hearing but a disorder of how sound is perceived and evaluated: many people with hyperacusis have normal audiograms, yet the auditory brain treats moderate inputs as excessive. The dominant explanation is central: when input from a weakened cochlea falls, central auditory structures raise their gain, and that gain over-amplifies sound, so a signal of ordinary strength drives an abnormally large neural response. This article distinguishes hyperacusis from recruitment, misophonia, and phonophobia; describes its loudness, annoyance, fear, and pain forms; explains the central-gain mechanism; sets out how it is measured; and examines why loudness is a cognitive construct entangled with attention, emotion, and tinnitus.

Keywords: hyperacusis, decreased sound tolerance, loudness, central gain

What Hyperacusis Is

*Hyperacusis* is an abnormally reduced tolerance to sound, in which everyday acoustic levels that most people accept without difficulty are perceived as excessively loud, aversive, or painful (Baguley, 2003). The defining feature is a mismatch between the physical intensity of a sound and the reaction it provokes: the clatter of dishes, a child's voice, or the hum of traffic, all comfortably within the range a typical listener ignores, can become intolerable. Crucially, hyperacusis is a disorder of *perception and reaction*, not of *sensitivity* in the audiometric sense. It is not that the person hears faint sounds others cannot; their thresholds for detecting quiet tones are usually normal. What has changed is the growth of loudness and the emotional response to it above threshold (Tyler et al., 2014).

This distinguishes hyperacusis from several conditions with which it is often confused. It is not *recruitment*, the abnormally rapid growth of loudness that accompanies cochlear hearing loss, in which a raised threshold is paired with a normal or near-normal loudness ceiling, compressing the usable range; recruitment is tied to a measurable loss, whereas hyperacusis frequently occurs on a normal audiogram. It is distinct from *misophonia*, a strong aversive or emotional reaction to specific sounds, such as chewing or tapping, defined by the meaning and pattern of the trigger rather than its intensity. And it differs from *phonophobia*, a fear of sound in anticipation of its aversiveness. These conditions overlap and frequently coexist, and together they are increasingly grouped under the umbrella of *decreased sound tolerance* (Pienkowski et al., 2014).

Forms of Hyperacusis

Hyperacusis is not a single experience but a family of reactions to sound, and a widely used clinical scheme distinguishes four forms by the dominant response they provoke (Tyler et al., 2014). These categories are not mutually exclusive; a given person may experience several at once, and they are best read as overlapping dimensions of a reduced tolerance rather than as separate diseases. The value of the distinction is practical: the forms have different mechanisms and respond to different treatments, so naming which reaction predominates guides both explanation and management.

The loudness form is closest to the classical definition and is captured by a steepened loudness-growth function. The annoyance and fear forms foreground the emotional and evaluative side of the reaction, which is why hyperacusis so often travels with anxiety and avoidance. The pain form, in which sound produces a stabbing or burning sensation in the ears at levels far below the roughly 120-decibel threshold at which sound is normally painful, has drawn particular recent attention, and has been linked to a distinct population of type II cochlear afferents that behave as nociceptors, signaling tissue-damaging noise through a non-canonical pathway from the cochlea to the brain (Flores et al., 2015). Because the forms coexist, prevalence estimates vary widely with definition, but population surveys using questionnaires place clinically significant hyperacusis in a small but non-trivial minority of adults (Paulin et al., 2016).

How the Brain Amplifies Sound

The central puzzle of hyperacusis is that hearing can be intact, or even reduced, while the reaction to sound is exaggerated. The leading resolution is the *central gain* model. Sensory systems do not passively relay their input; they adjust their responsiveness to keep their output within a useful range, much as an automatic volume control raises amplification when a signal weakens. When the auditory periphery is damaged or understimulated, whether by noise exposure, ototoxic drugs, or the loss of auditory-nerve synapses, the average input reaching central auditory structures falls. In response, neurons in the auditory brainstem, midbrain, and cortex increase their gain to restore their accustomed firing rate (Auerbach et al., 2014).

This homeostatic compensation is adaptive up to a point, because it preserves the audibility of faint sounds when the input is degraded. But it has a cost. A gain increase that rescues weak signals will over-amplify strong ones, so that a sound of ordinary intensity now drives an abnormally large neural response, experienced as excessive loudness. The same mechanism has been proposed to generate tinnitus, the perception of sound without an external source, because amplified neural noise can be heard as a phantom tone; this shared origin is why hyperacusis and tinnitus so often occur together (Zeng, 2013). Formal loudness models make the idea quantitative, casting tinnitus as increased central noise and hyperacusis as an increase in the nonlinear gain applied to sound.

The physiological substrate of this gain change is being mapped onto specific circuits and neurochemistry. A recurring theme is a shift in the balance between excitation and inhibition: a reduction in inhibitory neurotransmission, alongside changes in serotonergic and other neuromodulatory systems, would raise the responsiveness of central auditory neurons and steepen the growth of loudness (Knipper et al., 2013). The link to hidden peripheral damage is direct, because the loss of auditory-nerve synapses can reduce the drive to central structures without shifting the audiogram, providing exactly the weakened input that triggers a compensatory gain increase (Schaette & McAlpine, 2011). On this account, hyperacusis is not a fault of the ear letting in too much sound, but of a brain that has turned up its own amplification too far.

Measuring Hyperacusis

Because hyperacusis is defined by reaction rather than detection, measuring it means quantifying tolerance above threshold, not sensitivity at it. The central psychophysical measure is the *loudness discomfort level* (LDL), sometimes called the uncomfortable loudness level: the sound level at which a listener judges a tone or noise to have become uncomfortably loud. In hyperacusis, LDLs are lowered, sometimes dramatically, while detection thresholds remain normal, so the gap between the softest audible sound and the loudest tolerable one, the *dynamic range* of comfortable hearing, is narrowed (Sheldrake et al., 2015). An audiometric profile of normal thresholds with reduced LDLs is the psychoacoustic signature of the disorder, and LDLs measured across frequencies often show the greatest reduction in the mid-to-high range.

Psychoacoustic measures capture the loudness dimension but not the emotional and behavioral impact, which is why self-report questionnaires are central to assessment. The most widely used is the Hyperacusis Questionnaire, a validated instrument that samples the attentional, social, and emotional consequences of sound intolerance and yields a score that has been psychometrically normalized against a general population (Khalfa et al., 2002). Questionnaires and LDLs measure related but distinct things: two people with the same lowered LDL can differ greatly in how much the condition disrupts their lives, because the disruption depends on appraisal and avoidance as much as on loudness itself. Systematic review of assessment and treatment has emphasized that this measurement gap, between the physical reaction and its lived impact, is one of the field's central methodological challenges (Fackrell et al., 2017).

Hyperacusis and Cognition

Hyperacusis belongs in cognitive psychology because *loudness* is not a physical quantity but a perceptual and cognitive construct. The intensity of a sound is fixed by its physics, but the loudness a listener experiences is a judgment the brain constructs, and that judgment is shaped by attention, expectation, and emotional state. This is why the same moderate sound can feel tolerable when a listener is calm and unbearable when they are anxious or fatigued, and why directing attention toward a sound tends to increase its perceived loudness. In hyperacusis, an already steepened loudness-growth function interacts with heightened vigilance for sound, so that attention and loudness feed one another in a self-reinforcing loop (Tyler et al., 2014).

The emotional dimension is not incidental but part of the disorder's core. The fear and annoyance forms are defined by appraisal, and the resulting anticipatory anxiety drives avoidance of sound, which shrinks a person's activities and can compound the problem: prolonged avoidance and the use of ear protection in quiet settings reduce auditory stimulation further, which the central-gain model predicts should increase gain and worsen intolerance. Clinically significant hyperacusis is strongly associated with anxiety and depression, and the severity of the emotional reaction to sound predicts the burden of low mood better than the audiometric measures do (Aazh & Moore, 2017). This is also why hyperacusis is prominent in conditions defined partly by atypical sensory processing: reduced sound tolerance is common in autism, where it is one facet of a broader difference in how sensory input is weighted and regulated (Williams et al., 2021).

That loudness can be reshaped by experience is not only a source of harm but a basis for treatment. Controlled attenuation and enhancement of the acoustic background can shift loudness perception in either direction, demonstrating that the loudness-growth function is plastic (Formby et al., 2003). This principle underlies sound-based therapies, which use controlled, gradually increasing sound exposure to lower gain and widen tolerance over time, most systematically in tinnitus retraining therapy, which addresses hyperacusis and tinnitus together through counseling and sound enrichment (Jastreboff & Jastreboff, 2000).

Worked Example: Reading the Dynamic Range

Consider an adult who reports that ordinary sounds, a coffee grinder, a ringing phone, become painfully loud, though they have never noticed any difficulty hearing quiet sounds. On testing, their detection threshold at 2000 Hz is 5 dB HL, well within normal limits, but their loudness discomfort level at the same frequency is just 65 dB HL. A typical listener without hyperacusis has an LDL in the region of 100 dB HL. What does this pattern show?

First, the threshold. At 5 dB HL, the softest audible sound is normal, so this is not a hearing loss; the ear detects faint sounds as well as anyone's. Second, the dynamic range. The comfortable listening range is the span between the detection threshold and the loudness discomfort level, which here is 65 minus 5, or 60 dB. In a typical listener the same span is roughly 100 minus 5, or 95 dB. The usable range has therefore been compressed by about 35 dB, more than a third of its normal width. Third, the consequence. Ordinary conversational speech sits around 60 to 65 dB, which for this person now falls at the very top of the tolerable range, precisely at the level that provokes discomfort.

The arithmetic converts two audiometric numbers into the lived complaint. The normal threshold explains why the person, and often their clinicians, may doubt that anything is wrong with their hearing, because the standard pure-tone audiogram is unremarkable. The lowered LDL explains the disability: with a comfortable range compressed to 60 dB, the everyday soundscape that a typical listener navigates with ease repeatedly breaches the ceiling of what this person can tolerate. It is the narrowing of the range above threshold, not any change at threshold, that defines the disorder.

Discussion

Hyperacusis is a clarifying case for cognitive science because it severs two things that intuition binds together: the physical intensity of a sound and the loudness it produces. A disorder in which hearing is intact yet moderate sound is intolerable makes vivid that loudness is a construction of the nervous system, subject to gain control, plasticity, attention, and emotion, rather than a faithful readout of acoustic energy. The central-gain model gives this a concrete mechanism, tying the exaggerated reaction to a homeostatic process that is ordinarily useful and only pathological in excess, and it unifies hyperacusis with tinnitus as two expressions of the same over-amplification (Auerbach et al., 2014; Zeng, 2013).

The account remains incomplete in instructive ways. The central-gain model explains the loudness form well but is a less complete account of the pain form, whose apparent basis in cochlear nociception points to a partly peripheral origin, and of the fear and annoyance forms, which are as much about appraisal as amplification (Pienkowski et al., 2014). The measurement gap between psychoacoustic LDLs and questionnaire-based impact reflects this same divide between the sensory reaction and its cognitive and emotional interpretation. A full theory of hyperacusis will have to connect the gain of auditory neurons to the appraisal systems that decide whether a loud sound is merely loud or genuinely threatening, and that connection is where the disorder stops being purely auditory and becomes a problem of cognition.

Current Directions

The most active current questions concern mechanism and measurement. The pain form of hyperacusis, in which sound produces genuine physical pain at moderate levels, has motivated a search for a dedicated nociceptive pathway from the cochlea, a line of work that would separate a peripheral, pain-based intolerance from the central, loudness-based one and imply different treatments for each (Williams et al., 2021). In parallel, the recognition that reduced sound tolerance is prominent in autism and other neurodevelopmental conditions has broadened hyperacusis from an otological complaint into a marker of how sensory input is regulated across disorders, and has sharpened the need for measures that work across populations who may not report their experience in the same way.

On the clinical side, the priority is evidence. A scoping review of interventions for hyperacusis in adults found that while sound therapy, cognitive behavioral therapy, and counseling are widely used, the trial evidence supporting them remains thin, and it called for standardized outcome measures and controlled studies to establish what actually works (Fackrell et al., 2017). Refining questionnaires and loudness-discomfort measures so that they capture both the sensory reaction and its emotional burden, and can serve as reliable trial endpoints, is a continuing effort, because without agreed measures the effectiveness of treatment cannot be settled (Aazh & Moore, 2017).

Common Misconceptions

Hyperacusis means unusually good or sharp hearing.

It is not heightened sensitivity to faint sounds; detection thresholds are typically normal. What is abnormal is the growth of loudness and the reaction to sound above threshold (Baguley, 2003).

Hyperacusis is the same as recruitment.

Recruitment is the rapid loudness growth that accompanies a measurable cochlear hearing loss, whereas hyperacusis commonly occurs on a normal audiogram and reflects central over-amplification (Tyler et al., 2014).

Hyperacusis and misophonia are the same thing.

Misophonia is an aversive reaction to specific trigger sounds regardless of their loudness, defined by meaning and pattern, while hyperacusis is driven by intensity; they overlap but are distinct (Pienkowski et al., 2014).

Wearing ear protection constantly is the safe response.

Overusing hearing protection in ordinary quiet reduces auditory stimulation, which the central-gain model predicts should further raise gain and worsen intolerance (Auerbach et al., 2014).

Glossary

Annoyance hyperacusis.

The form of hyperacusis dominated by irritation and negative emotional appraisal of sound rather than by pain or perceived loudness alone.

Central gain.

The homeostatic increase in the responsiveness of central auditory neurons that compensates for weakened peripheral input and, in excess, over-amplifies ordinary sound.

Decreased sound tolerance.

The umbrella term covering hyperacusis, misophonia, and phonophobia, reflecting their frequent overlap in reduced tolerance to sound.

Dynamic range.

The span of sound levels between the detection threshold and the loudness discomfort level; it is narrowed in hyperacusis while the threshold stays normal.

Fear hyperacusis.

The form dominated by anxiety and anticipatory avoidance of sound; it overlaps with phonophobia.

Hyperacusis.

A reduced tolerance to ordinary environmental sound, in which everyday levels are perceived as intolerably loud, painful, or threatening.

Loudness discomfort level (LDL).

The sound level at which a listener judges a sound to have become uncomfortably loud; lowered in hyperacusis. Also called the uncomfortable loudness level.

Loudness-growth function.

The relationship between physical sound level and perceived loudness; it is abnormally steep in the loudness form of hyperacusis.

Loudness.

The perceived intensity of a sound; a construct of the nervous system that depends on gain, attention, and emotion, not only on physical sound level.

Misophonia.

A strong aversive or emotional reaction to specific sounds, such as chewing, defined by the identity of the trigger rather than its loudness.

Pain hyperacusis.

The form in which sound produces physical pain or discomfort in the ears at levels well below the normal pain threshold, possibly reflecting cochlear nociception.

Phonophobia.

A fear of sound in anticipation of its aversiveness, driving avoidance; a component of the fear form of decreased sound tolerance.

Recruitment.

The abnormally rapid growth of loudness that accompanies cochlear hearing loss, in which a raised threshold pairs with a near-normal loudness ceiling; distinct from hyperacusis.

Tinnitus retraining therapy (TRT).

A management approach combining directive counseling with sound enrichment, used to reduce the impact of tinnitus and hyperacusis together.

Tinnitus.

The perception of sound without an external source; it frequently co-occurs with hyperacusis and is attributed to the same central over-amplification.

Key Researchers

Hashir Aazh

An audiologist and clinical researcher on tinnitus and hyperacusis rehabilitation who documented the strong association between reduced sound tolerance and depression, showing that the emotional reaction to sound predicts mood burden better than audiometric measures.
ORCID - Google Scholar

David M. Baguley

(1961-2022). A professor of hearing sciences at the University of Nottingham and president of the British Tinnitus Association whose foundational reviews defined hyperacusis for a generation of clinicians and set the agenda for its study.
In Memoriam

Sylvie Hébert

A researcher at the Université de Montréal who studies the psychophysics of loudness, tinnitus, and hyperacusis and their links to stress, connecting the auditory reaction to sound with physiological and emotional regulation.
Faculty page

Marlies Knipper

An auditory neuroscientist at the University of Tübingen whose work on the molecular neurobiology of hearing disorders traced how shifts in excitation, inhibition, and neuromodulation underlie the central changes of tinnitus and hyperacusis.
Faculty page

Brian C. J. Moore

(b. 1946). An emeritus professor of auditory perception at the University of Cambridge and a leading psychoacoustician whose work on loudness and its measurement underpins the modern understanding of how loudness perception goes awry in hyperacusis.
Faculty page - Google Scholar - Wikipedia

Richard J. Salvi

An auditory neuroscientist at the University at Buffalo and director of its Center for Hearing and Deafness who advanced the central-gain account of tinnitus and hyperacusis through studies of auditory plasticity after cochlear insult.
Faculty page

Richard S. Tyler

An audiologist at the University of Iowa whose two-part review of hyperacusis organized the field around the loudness, annoyance, fear, and pain forms and framed its definitions, measurement, mechanisms, and treatment.
Faculty page

Fan-Gang Zeng

A hearing scientist and engineer at the University of California, Irvine whose active loudness model formalized tinnitus as increased central noise and hyperacusis as increased nonlinear gain, giving the central account a quantitative form.
ORCID - Faculty page - Google Scholar

Frequently Asked Questions

What is hyperacusis?

Hyperacusis is a reduced tolerance to ordinary sound, in which everyday levels that most people find unremarkable are experienced as uncomfortably loud, painful, or threatening. It is a disorder of loudness perception and reaction rather than of hearing sensitivity (Baguley, 2003).

Does hyperacusis mean I have hearing loss?

Not usually. Most people with hyperacusis have normal or near-normal detection thresholds; the abnormality is in how loudness grows above threshold, so the standard pure-tone audiogram often looks unremarkable (Sheldrake et al., 2015).

How is hyperacusis different from misophonia?

Misophonia is an aversive reaction to specific trigger sounds, such as chewing or tapping, defined by what the sound is rather than how loud it is, whereas hyperacusis is driven by sound intensity. They overlap and often coexist under the umbrella of decreased sound tolerance (Pienkowski et al., 2014).

What causes hyperacusis?

The leading explanation is central gain: when input from the ear weakens, the auditory brain increases its amplification to compensate, and that heightened gain over-amplifies ordinary sound. Reduced inhibition and changes in neuromodulation are thought to underlie the shift (Auerbach et al., 2014; Knipper et al., 2013).

Why do hyperacusis and tinnitus so often occur together?

Both are attributed to the same central over-amplification: increased gain that over-responds to real sound produces hyperacusis, while amplified neural noise heard as a phantom tone produces tinnitus (Zeng, 2013).

How is hyperacusis measured?

Two complementary ways: the loudness discomfort level, the sound level judged uncomfortably loud, which is lowered in hyperacusis; and validated questionnaires such as the Hyperacusis Questionnaire, which capture its attentional, social, and emotional impact (Khalfa et al., 2002; Sheldrake et al., 2015).

Is hyperacusis linked to anxiety and depression?

Yes. Clinically significant hyperacusis is strongly associated with anxiety and depression, and the severity of the emotional reaction to sound predicts the burden of low mood better than the audiometric measures do (Aazh & Moore, 2017).

Can hyperacusis be treated?

Because loudness perception is plastic, sound-based therapies use controlled, gradually increasing exposure to widen tolerance, often alongside counseling and cognitive behavioral therapy. These are widely used, though controlled trial evidence for them is still limited (Formby et al., 2003; Fackrell et al., 2017).

References

Aazh, H., & Moore, B. C. J. (2017). Factors associated with depression in patients with tinnitus and hyperacusis. American Journal of Audiology, 26(4), 562-569. https://doi.org/10.1044/2017_AJA-17-0008

Auerbach, B. D., Rodrigues, P. V., & Salvi, R. J. (2014). Central gain control in tinnitus and hyperacusis. Frontiers in Neurology, 5, 206. https://doi.org/10.3389/fneur.2014.00206

Baguley, D. M. (2003). Hyperacusis. Journal of the Royal Society of Medicine, 96(12), 582-585. https://doi.org/10.1177/014107680309601203

Fackrell, K., Potgieter, I., Shekhawat, G. S., Baguley, D. M., Sereda, M., & Hoare, D. J. (2017). Clinical interventions for hyperacusis in adults: A scoping review to assess the current position and determine priorities for research. BioMed Research International, 2017, 2723715. https://doi.org/10.1155/2017/2723715

Flores, E. N., Duggan, A., Madathany, T., Hogan, A. K., Márquez, F. G., Kumar, G., Seal, R. P., Edwards, R. H., Liberman, M. C., & García-Añoveros, J. (2015). A non-canonical pathway from cochlea to brain signals tissue-damaging noise. Current Biology, 25(5), 606-612. https://doi.org/10.1016/j.cub.2015.01.009

Formby, C., Sherlock, L. P., & Gold, S. L. (2003). Adaptive plasticity of loudness induced by chronic attenuation and enhancement of the acoustic background. Journal of the Acoustical Society of America, 114(1), 55-58. https://doi.org/10.1121/1.1582860

Jastreboff, P. J., & Jastreboff, M. M. (2000). Tinnitus retraining therapy (TRT) as a method for treatment of tinnitus and hyperacusis patients. Journal of the American Academy of Audiology, 11(3), 162-177. https://doi.org/10.1055/s-0042-1748042

Khalfa, S., Dubal, S., Veuillet, E., Perez-Diaz, F., Jouvent, R., & Collet, L. (2002). Psychometric normalization of a hyperacusis questionnaire. ORL, 64(6), 436-442. https://doi.org/10.1159/000067570

Knipper, M., Van Dijk, P., Nunes, I., Rüttiger, L., & Zimmermann, U. (2013). Advances in the neurobiology of hearing disorders: Recent developments regarding the basis of tinnitus and hyperacusis. Progress in Neurobiology, 111, 17-33. https://doi.org/10.1016/j.pneurobio.2013.08.002

Paulin, J., Andersson, L., & Nordin, S. (2016). Characteristics of hyperacusis in the general population. Noise & Health, 18(83), 178-184. https://doi.org/10.4103/1463-1741.189244

Pienkowski, M., Tyler, R. S., Roncancio, E. R., Jun, H. J., Brozoski, T., Dauman, N., Coelho, C. B., Andersson, G., Keiner, A. J., Cacace, A. T., Martin, N., & Moore, B. C. J. (2014). A review of hyperacusis and future directions: Part II. Measurement, mechanisms, and treatment. American Journal of Audiology, 23(4), 420-436. https://doi.org/10.1044/2014_AJA-13-0037

Schaette, R., & McAlpine, D. (2011). Tinnitus with a normal audiogram: Physiological evidence for hidden hearing loss and computational model. Journal of Neuroscience, 31(38), 13452-13457. https://doi.org/10.1523/JNEUROSCI.2156-11.2011

Sheldrake, J., Diehl, P. U., & Schaette, R. (2015). Audiometric characteristics of hyperacusis patients. Frontiers in Neurology, 6, 105. https://doi.org/10.3389/fneur.2015.00105

Tyler, R. S., Pienkowski, M., Rojas Roncancio, E., Jun, H. J., Brozoski, T., Dauman, N., Coelho, C. B., Andersson, G., Keiner, A. J., Cacace, A. T., Martin, N., & Moore, B. C. J. (2014). A review of hyperacusis and future directions: Part I. Definitions and manifestations. American Journal of Audiology, 23(4), 402-419. https://doi.org/10.1044/2014_AJA-14-0010

Williams, Z. J., He, J. L., Cascio, C. J., & Woynaroski, T. G. (2021). A review of decreased sound tolerance in autism: Definitions, phenomenology, and potential mechanisms. Neuroscience & Biobehavioral Reviews, 121, 1-17. https://doi.org/10.1016/j.neubiorev.2020.11.030

Zeng, F.-G. (2013). An active loudness model suggesting tinnitus as increased central noise and hyperacusis as increased nonlinear gain. Hearing Research, 295, 172-179. https://doi.org/10.1016/j.heares.2012.05.009