Hyperacusis is a complex auditory disorder involving an abnormal sensitivity to sound, where low to moderate sound levels may be perceived as excessively loud or painful, despite being tolerable to individuals with normal hearing. (Auerbach et al., 2014 and Williams et al., 2021).
The definition of hyperacusis can vary, but most commonly it refers to an increased loudness perception of everyday sounds (loudness hyperacusis) or a lowered pain threshold from sounds to the point that everyday sounds cause physical pain in the ears and surrounding areas (pain hyperacusis).
Hyperacusis differs from misophonia, which involves strong negative emotions like anger and disgust triggered by specific sounds, and from phonophobia, which is an ongoing and irrational fear of certain sounds. However, these other types of sound intolerance can sometimes happen alongside hyperacusis. (Williams et al., 2021).
Loudness hyperacusis
Loudness hyperacusis causes people to perceive sounds at typical listening levels as overwhelmingly loud compared to those without the condition. (Tyler et al., 2014).
“A consensus is emerging in the auditory neuroscience literature that hyperacusis may be associated with a sustained and persistent increase in central auditory gain” (Fackrell et. al. 2017). The central gain model suggests that when the cochlea is damaged, the brain compensates by increasing neural gain, or “turning up the volume”, in the central auditory system to make up for the reduced input from the ear. This heightened sensitivity causes the brain to respond more strongly to sound, even when the actual auditory signals are weaker. Extensive research in both animal and human studies supports this theory, showing that brain regions such as the auditory cortex, midbrain, and thalamus exhibit abnormally elevated sound-evoked activity in individuals with loudness hyperacusis. This exaggerated brain response is believed to underline the hypersensitivity to everyday sounds that defines loudness hyperacusis (Auerbach et al., 2014).
It has also been suggested that a disrupted serotonin system may contribute to hyperacusis. This idea comes from Marriage and Barnes (1995), who noticed hyperacusis in patients with neurological conditions like PTSD and depression, both associated with serotonin imbalance. Since serotonin is believed to influence both the strength of auditory signals and how we subjectively experience sound (Thompson et al., 1994), they proposed it could also be involved in hyperacusis. However, this theory is currently difficult to verify through scientific studies (Marriage and Barnes, 1995).
Pain hyperacusis (noxacusis)
Pain hyperacusis, also known as noxacusis (Liu et al., 2015 and Beers Wood et al., 2024), occurs when a person experiences pain from sounds at much lower volumes than those that typically cause pain in people with normal hearing, which is usually around 120 decibels (Tyler et al., 2014).
The type of pain can differ from person to person, ranging from a dull ache or burning feeling to sharp, stabbing, or throbbing pain. Compared to loudness hyperacusis, individuals with pain hyperacusis tend to have a more severe clinical profile, as individuals report more frequent setbacks, less progress in symptom relief over time, more severe comorbid headache disorders, and lower benefits from sound therapy (Williams et al., 2021).
Current explanations for the neural basis of pain hyperacusis suggest that it may involve various parts of the auditory system, including the middle ear, the inner ear, and the central auditory pathways.
Noreña et al. (2018) suggest that sound-induced pain and related symptoms, like ear fullness, tinnitus, and dizziness, may start with problems in the tensor tympani muscle of the middle ear. After acoustic shock or trauma, this muscle can become overactive or damaged, leading to an energy shortage. Without enough energy (ATP), the muscle struggles to relax, causing a buildup of lactic acid that triggers pain-sensitive nerves. This can create a cycle of pain and inflammation. The model also connects this process to pain spreading to the face, scalp, and neck through the trigeminal nerve, which controls the tensor tympani muscle. Conditions like whiplash and jaw dysfunction may also affect this muscle and contribute to ear-related pain.
Some researchers suggest that Type II cochlear nerve fibers, which are not involved in hearing, may function as pain sensors in the inner ear. These fibers are similar to pain-sensing C fibers in the body and might carry pain signals to the brain when the inner ear is damaged. After injury, a large release of ATP can make these fibers overly sensitive. Once sensitized, they may start reacting to even small amounts of ATP released during normal hearing, potentially causing pain in response to everyday sounds (Liu et.al., 2015 and Flores et al., 2016).
Extensive research in animal models shows that injury to the peripheral auditory system can cause elevated neural responses along the central auditory pathway, which may contribute to heightened sound sensitivity. While this mechanism, known as increased central gain, is commonly linked to loudness hyperacusis, there is limited empirical support connecting it directly to sound-induced pain. However, persistent stimulation or irritation of peripheral nerves may lead to central sensitization, which could potentially involve the central auditory system in the development of pain hyperacusis (Jahn et al., 2025).
References
Auerbach BD, Rodrigues PV, Salvi RJ. Central gain control in tinnitus and hyperacusis. Front Neurol. 2014 Oct 24;5:206. doi: 10.3389/fneur.2014.00206. PMID: 25386157; PMCID: PMC4208401.
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 Jun 14;30(2):341-358. doi: 10.1044/2021_AJA-20-00209. Epub 2021 Apr 20. PMID: 33877881; PMCID: PMC8642094.
Tyler RS, Pienkowski M, Roncancio ER, Jun HJ, Brozoski T, Dauman N, Dauman N, Andersson G, Keiner AJ, Cacace AT, Martin N, Moore BC. A review of hyperacusis and future directions: part I. Definitions and manifestations. Am J Audiol. 2014 Dec;23(4):402-19. doi: 10.1044/2014_AJA-14-0010. PMID: 25104073.
Fackrell K, Potgieter I, Shekhawat GS, Baguley DM, Sereda M, Hoare DJ. Clinical Interventions for Hyperacusis in Adults: A Scoping Review to Assess the Current Position and Determine Priorities for Research. Biomed Res Int. 2017;2017:2723715. doi: 10.1155/2017/2723715. Epub 2017 Oct 9. PMID: 29312994; PMCID: PMC5654244.
Marriage J, Barnes NM. Is central hyperacusis a symptom of 5-hydroxytryptamine (5-HT) dysfunction? The Journal of Laryngology & Otology. 1995;109(10):915-921. doi:10.1017/S0022215100131676
Thompson, G.C., Thompson, A.M., Garrett, K.M. and Britton, B.H. (1994), Serotonin and serotonin receptors in the central auditory system. Otolaryngology–Head and Neck Surgery, 110: 93-102. https://doi.org/10.1177/019459989411000111
Noreña AJ, Fournier P, Londero A, Ponsot D, Charpentier N. An Integrative Model Accounting for the Symptom Cluster Triggered After an Acoustic Shock. Trends Hear. 2018 Jan-Dec;22:2331216518801725. doi: 10.1177/2331216518801725. PMID: 30249168; PMCID: PMC6156190.
Liu C, Glowatzki E, Fuchs PA. Unmyelinated type II afferent neurons report cochlear damage. Proc Natl Acad Sci U S A. 2015 Nov 24;112(47):14723-7. doi: 10.1073/pnas.1515228112. Epub 2015 Nov 9. PMID: 26553995; PMCID: PMC4664349.
Flores EN, Duggan A, Madathany T, Hogan AK, Márquez FG, Kumar G, Seal RP, Edwards RH, Liberman MC, García-Añoveros J. A non-canonical pathway from cochlea to brain signals tissue-damaging noise. Curr Biol. 2015 Mar 2;25(5):606-12. doi: 10.1016/j.cub.2015.01.009. Epub 2015 Jan 29. PMID: 25639244; PMCID: PMC4348215.
Jahn, K. N., Kashiwagura, S. T., & Yousuf, M. S. (2025). Clinical phenotype and management of sound-induced pain: Insights from adults with pain hyperacusis. The Journal of Pain, 27. doi:10.1016/j.jpain.2024.104741
Auerbach et al., 2014: https://pubmed.ncbi.nlm.nih.gov/25386157/
Williams et al., 2021: https://pubmed.ncbi.nlm.nih.gov/33877881/
Tyler et al., 2014: https://pubmed.ncbi.nlm.nih.gov/25104073/
Fackrell et al. 2017: https://pubmed.ncbi.nlm.nih.gov/29312994/
Marriage and Barnes, 1995. https://www.cambridge.org/core/journals/journal-of-laryngology-and-otology/article/abs/is-central-hyperacusis-a-symptom-of-5hydroxytryptamine-5ht-dysfunction/A332CA05FE82AFC10327C823B4EED7DF
Thompson et al. 1994: https://aao-hnsfjournals.onlinelibrary.wiley.com/doi/10.1177/019459989411000111
Noreña et al. 2018: https://pubmed.ncbi.nlm.nih.gov/30249168/
Liu et al. 2015: https://pubmed.ncbi.nlm.nih.gov/26553995/
Flores et al. 2016: https://pubmed.ncbi.nlm.nih.gov/25639244/
Jahn et al 2025: https://pubmed.ncbi.nlm.nih.gov/39586560/