What is Hyperacusis?
In 1938, H. B. Pearlman originally coined the term “hyperacusis” when he was studying facial paralysis, describing it as an “increased sensitivity to sound” (para. 1). Over the ensuing decades, as more research delved into hyperacusis, a variety of new and sometimes conflicting definitions emerged, encompassing terms such as “heightened awareness, hypersensitivity, loudness, discomfort, hyperresponsiveness, intolerance, phonophobia, irritability, misophonia, annoyance, fear, and pain” (Tyler et al., 2014, p. 403). These diverse definitions can make comprehending the intricate and multifaceted nature of hyperacusis a challenging task. Fortunately, Dr. Richard Tyler and his colleagues at the University of Iowa conducted a comprehensive literature review of previous hyperacusis research with the aim of categorizing its various subtypes. They identified four distinct subtypes: loudness, annoyance, fear, and pain, which can affect individuals singularly or in tandem.
The initial subtype, known as loudness hyperacusis, is characterized by an amplified perception of sound, resulting in noises being perceived as significantly louder than what a healthy auditory system would typically register (Tyler et al., 2014, p. 403). Individuals afflicted with this subtype may exhibit a spectrum of reactions, spanning from mild discomfort in response to ordinary noise levels to being fully disabled. In severe cases, for instance, the sound of a dropped pen may be perceived as a gunshot, running tap water might sound like a waterfall, and even quiet whispers can be experienced as piercing screams.
Pollard (2019) reports that the prevailing consensus attributes loudness hyperacusis to the central gain model (para. 11), which Auerbach et al. (2014) explain results from a malfunction in the central auditory system due to noise or ototoxic drug-induced sensorineural hearing loss. They say that this malfunction leads to reduced neural activity from the cochlea to the central auditory system, consequently causing an amplification of perceived sound levels (p. 1-2). It’s important to note that while this is the primary theory explaining the development of loudness hyperacusis, it has not been definitively confirmed, and there may be other mechanisms involved.
Annoyance and Fear Hyperacusis
Tyler et al. (2014) elaborate on two distinct forms of hyperacusis, which are rooted in emotional reactions to sound rather than physical sensations. The first is annoyance hyperacusis, which is a reaction to certain sounds that can result in “irritation, anxiety, and tension” (p. 404, as cited in Urnau & Tochetto, 2011). For instance, sounds like babies crying, traffic noise, leaf blowers, and so on could trigger these emotional responses. Although many people find certain sounds annoying, those with annoyance hyperacusis find unpleasant sounds to be far more “pervasive or persistent” (Tyler et al., 2014, p. 404) compared to the general population.
The second emotional subtype is fear hyperacusis, which is characterized by a strong aversion to particular sounds, leading to anticipatory responses in those affected; this could manifest itself as actively avoiding places where these sounds are likely to occur (Tyler et al., 2014, p. 404). For example, an individual with fear hyperacusis might avoid crowded restaurants due to the fear of sudden loud noises like clattering dishes or loud conversations. It is worth noting that these two forms of hyperacusis often coexist and can often develop following experiences with loudness or pain hyperacusis (Salvi et al., 2022, p. 2).
Pain Hyperacusis (Noxacusis)
Finally, it’s essential to highlight that pain hyperacusis, also known as noxacusis, stands as the least investigated and least comprehensively understood subtype of hyperacusis (Pollard, 2019, para, 1). According to Tyler et al. (2014), this condition causes individuals to experience ear pain in response to sound levels significantly below the typical pain threshold, beginning at 120 decibels (p. 404). Ordinary sounds, such as birds chirping, people conversing, or music playing, can elicit pain in individuals grappling with noxacusis. A recent survey conducted by Williams et al. (2021) reveals that those afflicted with pain hyperacusis generally describe their pain as a burning, stabbing, aching, or throbbing sensation, which may occur either immediately after exposure to noise or at times hours later (para. 27). Furthermore, the survey found that compared to loudness hyperacusis, those with pain hyperacusis reported ”a higher frequency of temporary symptom exacerbations (i.e., “setbacks”), less perceived symptom improvement over time, more severe comorbid headache disorders, and reduced benefit from sound therapy (para. 3).
Research into the mechanisms causing this debilitating pain is in its early phases, but there are several theories on how it may occur. To start, it is possible that loudness hyperacusis at catastrophic levels could cause sounds to be so loud for individuals that they are perceived as painful (Auerbach et al., 2014, p. 1). A second possible mechanism could be abnormal contractions of the tensor tympani muscle after an acoustic shock or trauma that have the potential to cause a series of issues, including pain hyperacusis (Norena et al., 2018, para. 19). Thirdly, Liu et al. (2015) propose that recently discovered type II afferent neurons within the inner ear may become activated due to cochlear damage, resulting in sounds becoming noxious (p. 14723). Pain hyperacusis is a highly complex phenomenon, and it is likely that various mechanisms, both known and unknown, contribute to the pain experienced by those afflicted with it.
Gaining insights into the various subtypes of hyperacusis serves as a crucial foundation for directing research efforts aimed at uncovering the underlying mechanisms and developing effective treatments for these conditions. Equally important is the need for individuals with hyperacusis to acquaint themselves with these subtypes because it will give them a precise understanding of their condition and facilitate more effective management strategies. While a complete understanding of hyperacusis and its mechanisms is still far from complete, this comprehensive literature review offers a strong foundation for future research endeavours.
Auerbach, B. D., Rodrigues, P. V., & Salvi, R. J. (2014). Central gain control in tinnitus and hyperacusis. Frontiers in Neurology, 5, 206, 1-21. https://doi.org/10.3389/fneur.2014.00206.
Liu, C., Glowatzki, E., & Fuchs, P. A. (2015). Unmyelinated type II afferent neurons report cochlear damage. Proceedings of the National Academy of Sciences, 112(47), 14723–14727. https://doi.org/10.1073/pnas.1515228112.
Noreña, A. J., Fournier, P., Londero, A., Ponsot, D., & Charpentier, N. (2018). An integrative model accounting for the symptom cluster triggered after an acoustic shock. Trends in Hearing, 22. https://doi.org/10.1177/2331216518801725.
Perlman, H. B. (1938). LXXIX hyperacusis. Annals of Otology, Rhinology & Laryngology, 47(4), 947–953. https://doi.org/10.1177/000348943804700408.
Pollard, B. (2019). Unraveling the mystery of hyperacusis with pain. ENT & Audiology News, 7(6). https://www.entandaudiologynews.com/features/audiology-features/post/unravelling-the-mystery-of-hyperacusis-with-pain.
Salvi, R., Chen, G.-D., & Manohar, S. (2022). Hyperacusis: Loudness intolerance, fear, annoyance and pain. Hearing Research, 426, 108648–108648. https://doi.org/10.1016/j.heares.2022.108648.
Tyler, R. S., Pienkowski, M., Roncancio, E. R., Jun, H. J., Brozoski, T., Dauman, N., 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., Suzman, E., & Woynaroski, T. G. (2021). A Phenotypic Comparison of Loudness and Pain Hyperacusis: Symptoms, Comorbidity, and Associated Features in a Multinational Patient Registry. American journal of audiology, 30(2), 341–358. https://doi.org/10.1044/2021_AJA-20-00209.