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Misophonia

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Misophonia
Other namesselective sound sensitivity syndrome,[1] misophonic disorder,[2][3] select sound sensitivity syndrome,[4] soft sound sensitivity symptom,[4] sound-rage[4][5][6]
Pronunciation
SpecialtyPsychiatry, clinical psychology, audiology
Complicationssocial isolation, extreme trigger avoidance, relationship difficulties, anxiety (particularly phonophobia), maladaptive coping strategies (including suicidality, aggression, and self-harm)[4][7][8]
Usual onsetVariable (childhood through adulthood), with most common onset in childhood/early adolescence[7]
CausesNeuropsychological and perceptual processing differences of unclear etiology[4][9]
TreatmentMost evidence for specialized forms of cognitive-behavioral therapy,[10][11][12] with extremely limited (case report/series-level) evidence for other psychotherapy modalities, Tinnitus Retraining Therapy, and certain medications.[11][12]

Misophonia (or selective sound sensitivity syndrome) is a disorder of decreased tolerance to specific sounds or their associated stimuli, or cues. These cues, known as "triggers", are experienced as unpleasant or distressing and tend to evoke strong negative emotional, physiological, and behavioral responses not seen in most other people.[8] Misophonia and the behaviors that people with misophonia often use to cope with it (such as avoidance of "triggering" situations or using hearing protection) can adversely affect the ability to achieve life goals, communicate effectively, and enjoy social situations.[4][7] Originating within the field of audiology in 2001,[13] the condition remained largely undescribed in the clinical and research literature until 2013, when a group of psychiatrists at Amsterdam University Medical Center published a detailed misophonia case series and proposed the condition as a "new psychiatric disorder" with defined diagnostic criteria.[14] At present, misophonia is not listed as a diagnosable condition in the DSM-5-TR, ICD-11, or any similar manual,[8][15][16][17] making it difficult for most people with the condition to receive official clinical diagnoses of misophonia or billable medical services. An international panel of misophonia experts has rigorously established a consensus definition of misophonia as a medical condition,[8] and since its initial publication in 2022, this definition has been widely adopted by clinicians and researchers studying the disorder.[18][19]

When confronted with specific "trigger" stimuli, people with misophonia experience a range of negative emotions, most notably anger, extreme irritation, disgust, anxiety, and sometimes rage.[8] The emotional response is often accompanied by a range of physical symptoms (e.g., muscle tension, increased heart rate, and sweating) that may reflect activation of the fight-or-flight response.[8] Unlike the discomfort seen in hyperacusis, misophonic reactions do not seem to be elicited by the sound's loudness but rather by the trigger's specific pattern or meaning to the hearer.[20][21][22] Many people with misophonia cannot trigger themselves with self-produced sounds, or if such sounds do cause a misophonic reaction, it is substantially weaker than if another person produced the sound.[7][8]

Misophonic reactions can be triggered be many different auditory, visual, and audiovisual stimuli,[8] most commonly mouth/nose/throat sounds (particularly those produced by chewing or eating/drinking), repetitive sounds produced by other people or objects, and sounds produced by animals.[7][8] The term misokinesia has been proposed to refer specifically to misophonic reactions to visual stimuli, often repetitive movements made by others.[14][23] Once a trigger stimulus is detected, people with misophonia may have difficulty distracting themselves from the stimulus and may experience suffering, distress, and/or impairment in social, occupational, or academic functioning.[8] Many people with misophonia are aware that their reactions to misophonic triggers are disproportionate to the circumstances,[8] and their inability to regulate their responses to triggers can lead to shame, guilt, isolation, and self-hatred, as well as worsening hypervigilance about triggers, anxiety, and depression.[24][25][26] Studies have shown that misophonia can cause problems in school, work, social life, and family.[18] In the United States, misophonia is not considered one of the 13 disabilities recognized under the Individuals with Disabilities Education Act (IDEA) as eligible for an individualized education plan,[27] but children with misophonia can be granted school-based disability accommodations under a 504 plan.[28]

The expression of misophonia symptoms varies, as does their severity, which can range from mild and sub-clinical to severe and highly disabling.[2][8] The reported prevalence of clinically significant misophonia varies widely across studies due to the varied populations studied and methods used to determine whether a person meets diagnostic criteria for the condition.[29] But three studies that used probability-based sampling methods estimated that 4.6–12.8% of adults may have misophonia that rises to the level of clinical significance.[30][31][32] Misophonia symptoms are typically first observed in childhood or early adolescence, though the onset of the condition can be at any age.[7][8] Treatment primarily consists of specialized cognitive-behavioral therapy,[11] with limited evidence to support any one therapy modality or protocol over another and some studies demonstrating partial or full remission of symptoms with this or other treatment, such as psychotropic medication.[12]

Terminology and origins of the concept

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Pawel Jastreboff and Margaret M. Jastreboff coined the term "misophonia" in 2001 with the assistance of Guy Lee,[33][34] introducing it in their article "Hyperacusis",[35] with further explanation in the International Tinnitus and Hyperacusis Society's ITHS Newsletter.[13]

"Misophonia" comes from the Ancient Greek words μῖσος (IPA: /mîː.sos/), meaning "hate", and φωνή (IPA: /pʰɔː.nɛ̌ː/), meaning "voice" or "sound", loosely translating to "hate of sound", and was coined to differentiate the condition from other forms of decreased sound tolerance, such as hyperacusis (hypersensitivity to certain frequencies and volume ranges) and phonophobia (fear of sounds).[6][36][13]

The term "misophonia" was first used in a peer-reviewed journal in 2002.[37] Before that, the disorder was more commonly called "selective sound sensitivity syndrome", or "4S", a term coined by audiologist Marsha Johnson.[18] Other names formerly used for the condition include "soft sound sensitivity symptom", "select sound sensitivity syndrome", "decreased sound tolerance", and "sound-rage".[4]

In their seminal 2013 case series of patients with misophonia, Schröder and colleagues coined the term "misokinesia" (a term analogous to misophonia translating to "hatred of movement")[14] to describe misophonia-like reactions that occur when people are "triggered" by specific repetitive visual stimuli, such as another person's foot shaking, fingers tapping, or gum chewing.[23] Other authors have proposed "Conditioned Aversive Response Disorder" (C.A.R.D.) as a more suitable name, which seeks to incorporate both auditory and non-auditory aspects of misophonia/misokinesia into a single condition.[38]

Adopting DSM-5-like terminology, some research groups have also advocated the term "misophonic disorder"[2] to distinguish clinically significant and disabling misophonia from what they term "misophonic reactions" (i.e., sub-clinical manifestations of misophonia that do not cause marked distress or substantially impair a person's daily life, relationships, or activities).[2]

Notably, of the above terms, only "misophonia" is widely used by researchers, clinicians, and sufferers of the condition. It is the primary term used for the condition in mainstream journalistic coverage[39][40][41][42] and by the primary philanthropic agency funding research into it (The Misophonia Research Fund [MRF]),[43] and the term selected for use in an (MRF-funded) project to derive a field-wide consensus definition of the condition for clinical and research use.[8]

Signs and symptoms

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Misophonia is a disorder of sound tolerance characterized by extreme and disproportionate emotional reactions to specific sounds (or less commonly, visual stimuli) in one's environment, termed "triggers."[8] Trigger stimuli are experienced as extremely unpleasant or distressing and tend to evoke a "misophonic reaction" that consists of both unpleasant negative emotions (i.e., extreme irritation, anger, anxiety, or disgust; less commonly rage or panic) and increased sympathetic arousal(manifested in physical symptoms such as muscle tension, increased heart rate, and sweating).[7][8]

Trigger stimuli are highly varied and sometimes idiosyncratic, but certain stimuli such as chewing and other oronasal sounds are among the most commonly reported triggers in both clinically referred and population-based samples.[7][8] The Duke Misophonia Questionnaire,[44] a commonly used misophonia symptom measure, groups misophonia triggers into the following categories:

  • People making mouth sounds while eating or drinking (e.g., chewing, crunching, slurping).
  • People making nasal/throat sounds (e.g., sniffing, sneezing, nose-whistling, coughing, throat-clearing).
  • People making mouth sounds when not eating (e.g., making the "tsk" sound, heavy breathing, snoring, whistling).
  • People making repetitive sounds (e.g., typing, tapping nails on table, pen clicking, writing, construction work, using machinery).
  • Rustling or tearing objects (e.g., paper, plastic).
  • Speech sounds (e.g., "p" sounds, hissing "s" sounds, someone speaking with a lisp, high-pitched voices).
  • Body or joint sounds (e.g., snapping fingers, cracking joints, jaw clicking).
  • Rubbing sounds (e.g., hands on pants, hands against one another, Styrofoam rubbing together).
  • Stomping or loud walking (e.g., heels clicking, flip flops, etc.).
  • Muffled sounds (e.g., voices separated by a wall, TV/music in another room).
  • People talking in the background (e.g., phone calls in public, many people talking at once).
  • Repetitive or continuous sounds not made by a person (e.g., clock ticking, air conditioner humming, water running).
  • Animals making repetitive sounds (e.g., licking, chirping, barking, eating, drinking).
  • Seeing someone making or about to make a sound that bothers you, even if you can't hear it (e.g., seeing someone reach into a bag of chips, seeing someone eating on TV with the volume off).

Although less well studied, reported visual triggers in misokinesia include another person's repetitive movements (foot/leg shaking, arms swinging, hands rubbing together, hair twirling, fidgeting), as well as the sight of an auditory trigger that one cannot actually hear (such as someone chewing with their mouth open or tapping their fingers on a desk).[7][8][23]

Reactions to triggers can range from mild (extreme irritation, anxiety, disgust, and/or physical discomfort) to severe (anger, rage, hatred, fear, panic, and/or profound emotional distress).[8] A number of physical symptoms may also accompany the misophonic response, including muscle tension, increased heart rate, sweating, and a feeling of pressure in one's body.[7][8][18] Other idiosyncratic physical and cognitive symptoms are also possible.[7][18]

The five dimensions of cognitive-behavioral responses to "triggers," as empirically derived from the "S-Five" (another commonly used misophonia questionnaire),[45][46] are as follows:

  • Internalizing appraisals such as self-critical thoughts, feeling guilty about one's reactions, and feeling ashamed for reacting to triggers
  • Externalizing appraisals such as blaming others for making triggering sounds, feeling that others are being selfish or disrespectful, and believing that specific sounds are "just bad manners" and should never be made by anyone
  • Anxiety/avoidance responses such as isolating oneself, moving away from the sound, or limiting opportunities to avoid potential trigger exposure
  • Feeling threatened/overwhelmed such as feeling trapped, having thoughts of helplessness, or panicking when one can't escape a trigger
  • Aggressive outbursts such as yelling, screaming, pushing, hitting, throwing things, or (rarely in adults) becoming physically violent

People with misophonia, particularly adults, are typically aware that their emotional reactions and behaviors in response to triggers are disproportionate to the situation,[18] and this frequently causes some degree of internal conflict due to a desire to suppress these reactions.[24]

The first misophonic reaction typically occurs when a person is young, often between the ages of 9 and 13.[7] But misophonia can have an onset at any age, with cases as young as two years old and a number of adult-onset cases reported in the literature.[18][7] The initial misophonic reaction will often originate from someone in a close relationship or a pet.[47]

Fear and anxiety associated with trigger sounds can cause people with this condition to avoid important social and other interactions that may expose them to these sounds.[7] This avoidance and other behaviors can make it harder for them to achieve their goals and enjoy interpersonal interactions.[6][26] It can also have a significant adverse effect on their careers and relationships.[18] Many people with misophonia experience worsening mental health, and some develop psychopathology secondary to their misophonia, including depression, anxiety, phonophobia, self-harm behaviors, and suicidality.[18][26][48][49]

Mechanism

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Misophonia's mechanism is not yet fully understood, and all proposed causes of the disorder are hypothesized based on a combination of clinical observation and the limited existing empirical research.[4] Although misophonia is a disorder of sound tolerance, work to date has not typically demonstrated any peripheral audiologic abnormalities in people with the condition,[50][51][52] suggesting that any "auditory" abnormalities may be caused by a dysfunction of the central auditory system or other parts of the brain that govern "higher-order" perceptor or cognition, rather than the ears per se.[17]

The "neurophysiological" (Jastreboff) model

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The first mechanistic theory of misophonia, proposed by Jastreboff and Jastreboff in 2014,[53][54] is based on the authors' clinical experience and little empirical data. This model, which the authors call the "neurophysiological model",[54] seeks to contrast misophonia with hyperacusis, another disorder of sound tolerance that primarily manifests as excessive loudness perception (or the experience of physical pain in one's ears or head) in response to soft or moderate-intensity everyday sounds.[19][55] The Jastreboffs' neurophysiological model posits that the fundamental difference between misophonia and hyperacusis is that decreased sound tolerance in hyperacusis is closely coupled to the physical properties of the sound stimulus (i.e., intensity, frequency) while, in misophonia, decreased tolerance of "trigger" sounds has little to do with acoustic properties (beyond louder sounds perhaps being easier to perceive and respond to)[54] and arguably depends almost exclusively on the meaning of the sound(s) to a given person.[53][54][56] Its creators have used this model to explain certain aspects of the misophonia phenotype, such as that most people with misophonia do not present with peripheral hearing loss and that context (including whether a trigger is produced by oneself) plays a large role in response to a trigger sound.[54][56]

Although entirely speculative and not based on any empirical neuroscientific data on misophonia, the "neurophysiologic" model also postulates several putative neural mechanisms for the condition from a systems neuroscience perspective.[56] Namely, when processing a trigger stimulus, the brain's central auditory system is thought to have enhanced functional connections with its limbic and autonomic control areas, and downstream overactivity of these areas is theorized to be responsible for the excessive emotional responses and certain physical symptoms of the condition, respectively.[54] These preliminary neuroscientific hypotheses form the basis of the Jastreboffs' signature intervention for sound tolerance conditions (Tinnitus Retraining Therapy, an unproven combination of structured counseling and sound therapy originally developed for tinnitus and now available in modified form to treat misophonia).[53][56]

Notably, there has been relatively little empirical support for the central neuroscientific hypotheses of the neurophysiologic model. Although there has been a relative lack of neuroimaging research on misophonia thus far, functional connectivity between auditory cortical and limbic or autonomic control areas is not typically increased either at rest or during the experience of trigger sound perception.[9] Though many of these same limbic and autonomic control areas may still be relevant in the pathophysiology of misophonia (with anterior insula being one of the most strongly implicated nodes thus far),[9] recent reviews of human neuroimaging research in this condition[9][57] indicate that (a) their activation may be driven by other pathways than simple auditory→limbic or auditory→limbic→autonomic hyper-connectivity and (b) additional structures outside of the Jastreboffs' model (such as premotor cortex)[58] may play a central role in this disorder. The "neurophysiologic" model has also been criticized by other theorists for its vagueness and unwillingness to specify the specific neural structures/processes involved in the "limbic system" portion of the model, as well as its inability to account for non-sound trigger stimuli.

The "action perception" (Berger-Gander-Kumar) model

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A more recently developed model of misophonia was published by neuroscientist Sukhbinder Kumar and colleagues at the University of Iowa in 2024.[57] This model, not formally named by the authors but termed the "action perception" model of misophonia by other researchers using it[59] (alternatively the Berger-Gander-Kumar model), sought to build on the shortcomings of earlier models[53][3] by (a) explicitly incorporating the most up-to-date empirical findings in the behavioral, clinical and neuroimaging literature on misophonia, (b) providing coherent explanations for the presence of non-auditory (i.e., visual) and multi-sensory trigger stimuli, and (c) considering perspectives from social cognitive theory and social neuroscience in the broader theory. Although the action perception model is consistent with many of the findings in the misophonia neuroimaging literature, it is important to note that it was generated specifically to explain those findings and therefore represents something of a "just-so story" until its predictions can be empirically validated.[57][60][61]

Based on what is known from neuroimaging and behavioral studies of misophonia, the action perception model conceptualizes the disorder as follows:[57]

  • Sensory information about any stimulus travels from the ear (eye in the case of visual information) through lemniscal/non-lemniscal auditory pathways (or analogous visual pathways) to arrive at and be processed by primary and higher-level auditory cortex (visual cortex).
  • Information is transmitted from a sensory cortex (auditory or visual) to the (pre)motor cortex to form a motor representation of a given action (putatively related to the human "mirror neuron" system).[57]
  • Under pathological conditions (e.g., when an individual with misophonia hears a sound that "triggers" them):
    • The strength or quality of the "motor representation" may be fundamentally different than in non-misophonic people, as demonstrated by hyperactivity of regions responsible for creating these representations.[58][62]
    • The aberrant motor representation conveys an abnormally strong signal to the (anterior) insular cortex, which is then hyperactive relative to non-misophonic controls.[58][63]
    • Although it is less clear whether this pathway is aberrant or hyperactive due to mixed/limited empirical findings,[57] the insula communicates this signal to (a) the amygdala (putatively responsible for the extreme emotional responses during a misophonic reaction) and (b) autonomic control centers such as the periaqueductal gray and several hypothalamic nuclei (putatively responsible for physiologic aspects of a misophonic reaction, such as changes in heart rate, skin conductance, and potentially other subjective symptoms of being triggered).
  • Though the action perception model denotes the "information flow" through the central nervous system as unidirectional, the authors note that more complex bidirectional interactions between the various nodes of the implicated brain network are likely.[57]

The action perception model represents a major advance over previous theoretical work in this area, particularly in its ability to comprehensively explain the neuroimaging data on misophonia published before 2024, when the theory was first proposed.[57] Additionally, by focusing on higher-order "motor representations" of objects/actions that are abstracted from their initial sensory information and represented in association cortex (i.e., motor/premotor and limbic areas), the model can be applied to both the auditory and non-auditory triggers of misophonia (i.e., misokinesia) just as easily.[57] The action perception model also explains certain clinical features of misophonia well, such as the extreme context-specificity of the condition, given that the perceived (even if incorrectly perceived) source of the sound[64] and whether the source can be identified[65] appear to be among the largest drivers of the severity of a given misophonic reaction.[57] Last, although still largely speculative, the action perception model provides an explanation for the peculiar observation that many people with misophonia (46.7% of this population in a recent study by Kumar's group)[66] engage in mimicry (deliberate or unconscious imitation of the trigger sound). As the anterior insula is engaged when counter-imitating an action (i.e., performing the opposite of the imitated movement),[67] Kumar and colleagues theorize that this mimicry conveys an "error signal" that helps inhibit the hyperactive insular cortex involved in the triggering process, thereby reducing the intensity of the misophonic response.[57][66]

Despite its success in explaining findings in the misophonia literature, the action perception model's predictions are largely untested, and many aspects of the model rely on empirical studies with substantial methodological limitations.[57] The basic neural mechanisms of action perception, mimicry, and the role (if any) of the "human mirror neuron system" within a broader social cognition framework in non-clinical populations must be further explored.[57] The role of other comorbid conditions, particularly those such as autism that are known to both affect social cognition and cooccur with misophonia at exceptionally high rates,[59][68] is also an area for future research to support the model.[57] The action perception model is not established fact but a plausible explanation that requires further evidential support.

Diagnosis

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In 2022, clinical and scientific leaders convened to create a consensus definition of misophonia,[8] agreeing that it is a disorder of decreased tolerance to specific sounds and their associated stimuli. Before this consensus definition was reached, scholars and clinicians debated how to describe and define misophonia, which has limited comparison of study cohorts and hampered the development of standard diagnostic criteria.[8]

Misophonia is distinguished from hyperacusis, which is not specific to a given sound and does not involve a similar strong reaction, and from phonophobia, which is a fear of loud sounds,[47] but it may occur with either.[69] There are no standard diagnostic criteria,[15][47] and many doctors are unaware of the disorder.[8]

Studies show that misophonia often has related comorbid conditions, including anxiety disorders, post-traumatic stress disorder,[70] OCD,[71][72][73] and depressive disorders.[74][75] Some research supports the belief that misophonia is genetic, but more research is needed.[76] It appears that misophonia can occur on its own or along with other health, developmental, and psychiatric problems.[8] When attempting to diagnose a patient with misophonia, doctors sometimes mistake its symptoms for an anxiety disorder, bipolar disorder, or obsessive-compulsive disorder.[8]

Despite misophonia's relative phenotypic distinctiveness, it has been suggested that it belongs to the spectrum of obsessive-compulsive-and-related disorders.[77][16][18] Indeed, distinguishing certain elements of misophonia from those of obsessive-compulsive disorder and obsessive-compulsive personality disorder may be difficult, as many features often overlap.[78][79][80][81][82]

Classification

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The diagnosis of misophonia is not recognized in the DSM-5-TR or the ICD-11, and it is not classified as a hearing or psychiatric disorder.[47] It may be a form of sound–emotion synesthesia, and has parallels with some anxiety disorders.[17] A 2022 structured study of prominent researchers resulted in the creation of the consensus definition of misophonia, determining that misophonia should be classified as a disorder, and not a symptom of another condition or syndrome.[8] During the early phase of research on misophonia, it was defined by different criteria with variable methods used to diagnose and assess symptom severity. As a result of lack of consensus about how to define and evaluate misophonia, comparisons between study cohorts were difficult, measurement tools were not psychometrically well-validated, and the field could not rigorously assess the efficacy of different treatment approaches. The creation of the definition serves as the foundation of future diagnostic criteria and validated diagnostic tools, and brings cohesion to the diverse and interdisciplinary misophonia research and clinical communities.[8]

Management

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Health care providers generally try to help people cope with misophonia by recognizing what the person is experiencing and working on coping strategies.[47] A majority of smaller studies done on the subject have focused on the use of tinnitus retraining therapy, cognitive behavioral therapy and exposure therapy, which is believed to decrease the person's awareness of their trigger sounds.[6] These treatment approaches have not been sufficiently studied to determine their effectiveness.[6][36] Other possible treatment options have been theorized by researchers, including acceptance-based approaches and mindfulness.[6] Ultimately, it is speculated that treatment methods may vary significantly in effectiveness from patient to patient.[6]

Minimal research has been conducted on the possible effects of neuromodulation and pharmacologic treatments. A study published in 2022 suggests that some forms of misophonia treatment may vary in effectiveness based on the preference of each patient, particularly in cases of parents with children who have misophonia.[83] In addition, the use of propranolol has also been found to be helpful in some patients.[84]

Clomipramine has anecdotally been found to be of use in at least a certain subset of people suffering from disorders allied with hyperacusis;[85] given its success in the treatment of obsessive-compulsive disorder, it may have a place in the treatment of misophonia,[86] which appears to have parallels with both conditions. Clomipramine does appear to have a distinct potential mediating effect on auditory-tone processing.[87][88] One specific phenomenon observed to this end with clomipramine in at least one instance is reduced electrodermal reactivity to innocuous auditory stimuli.[89]

Whether pindolol (a beta-blocker with similar action to propranolol and augmentative therapeutic effects in obsessive-compulsive disorder[90]) and certain selective serotonin reuptake inhibitors (e.g., fluvoxamine, escitalopram, fluoxetine) can also prove effective in the treatment of misophonia likewise remains to be seen.

Large-scale research has not yet been conducted, but observation of coping strategies people with misophonia use has shown some consistent results.[6] People with misophonia often cope by avoiding distressing situations or distracting themselves from such situations,[91] for example by using earplugs or headphones, mimicking trigger sounds, and playing music.[92]

Sequent repatterning therapy

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Image of Sequent Repatterning logo
The SRT process is associated with this logo, registered in 2019

Sequent Repatterning therapy for misophonia (SRT) is based on the idea that emotional responses are learned and consolidated over time, rather than innate, which makes it a form of cognitive behavioral therapy.[93] Development of this therapy began in 2012 when researcher Christopher Pearson applied aspects of hypnotherapy, parts work therapy, and NLP to create a therapy model for misophonia. He presented his work to the International Association of Neuropsychotherapy in 2017 and an article, "Reviewing Misophonia and its Treatment",[94] was published in International Journal of Neuropsychotherapy later that year. Pearson also contributed to the proposals for diagnostic criteria for misophonia, published in Frontiers.[95] Sequent Repatterning practitioners apply these diagnostic steps when assessing potential clients. Sequent Repatterning Therapy is not generally accepted by the clinical community and has not been shown to be an effective therapy for misophonia, which has not been shown to be caused by habituation. Habituation-based therapies often exacerbate symptoms instead of easing them.

Epidemiology

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Research is still being conducted on misophonia's global prevalence, but a 2023 study found its prevalence in the UK to be around 18%.[96] This study has been cited in popular outlets, including BBC,[97] Medscape,[98] and Medical Xpress.[99] Studies of misophonia's global prevalence have found it to be as low as 5% and as high as 20%.[96] Its prevalence and severity seem to be similar across genders.[96] In the U.S., it is estimated that 3% of people are affected by misophonia. But in multiple studies, it was determined misophonia may be underdiagnosed (it is not yet an officially diagnosable condition), as it is correlated with other auditory disruptions; 92% of patients who are hyperaware of sounds also have misophonia.[18] There is evidence that significant numbers of undergraduate students in some psychology and medical-science departments suffer from misophonia.[100] The University of Nottingham conducted a study of misophonia in one sample of undergraduate medical students.[101] In 2017, similar rates were found in one university in China,[102] suggesting that the disorder is not specific to a culture.

It may be the case that people with misophonia are more likely to have high fluid intelligence.[103]

Associated symptoms

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Some people[who?] have sought to relate misophonia to autonomous sensory meridian response, or auto-sensory meridian response (ASMR), a pleasant form of paresthesia, a tingling sensation that typically begins on the scalp and moves down the back of the neck and upper spine.[104] ASMR is described as the opposite of what can be observed in reactions to specific audio stimuli in misophonia.[105] There are plentiful anecdotal reports of people who claim to have both misophonia and ASMR. Common to these reports is the experience of ASMR in response to some sounds and misophonia in response to others.[105][106][107]

Society and culture

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People who experience misophonia have formed online support groups.[108][14]

In 2016, a documentary about the condition, Quiet Please, was released.[109]

In 2020, a team of misophonia researchers[14] received the Ig Nobel Prize in medicine "for diagnosing a long-unrecognized medical condition".[110]

The 2022 film Tár depicts a conductor with misophonia.[111]

Season 1, episode 4 of Hulu's The Old Man has a brief discussion of misophonia.[112]

Notable cases

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This is a dynamic list and may never be able to satisfy particular standards for completeness. You can help by adding missing items with reliable sources.

See also

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References

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  1. ^ Sanchez TG, Silva FE (2017). "Familial misophonia or selective sound sensitivity syndrome : evidence for autosomal dominant inheritance?". Brazilian Journal of Otorhinolaryngology. 84 (5): 553–559. doi:10.1016/j.bjorl.2017.06.014. PMC 9452240. PMID 28823694.
  2. ^ a b c d Möllmann A, Heinrichs N, Illies L, Potthast N, Kley H (28 March 2023). "The central role of symptom severity and associated characteristics for functional impairment in misophonia". Frontiers in Psychiatry. 14: 1112472. doi:10.3389/fpsyt.2023.1112472. PMC 10086372. PMID 37056403.
  3. ^ a b Norena A (14 February 2024). "Did Kant suffer from misophonia?". Frontiers in Psychology. 15. doi:10.3389/fpsyg.2024.1242516. ISSN 1664-1078. PMC 10899398. PMID 38420172.
  4. ^ a b c d e f g h Palumbo DB, Alsalman O, De Ridder D, Song JJ, Vanneste S (29 June 2018). "Misophonia and Potential Underlying Mechanisms: A Perspective". Frontiers in Psychology. 9: 953. doi:10.3389/fpsyg.2018.00953. PMC 6034066. PMID 30008683.
  5. ^ Bruxner G (April 2016). "'Mastication rage': a review of misophonia - an under-recognised symptom of psychiatric relevance?". Australasian Psychiatry. 24 (2): 195–197. doi:10.1177/1039856215613010. PMID 26508801. S2CID 7106232.
  6. ^ a b c d e f g h Cavanna AE, Seri S (August 2015). "Misophonia: current perspectives". Neuropsychiatric Disease and Treatment. 11: 2117–2123. doi:10.2147/NDT.S81438. PMC 4547634. PMID 26316758.
  7. ^ a b c d e f g h i j k l m n Potgieter I, MacDonald C, Partridge L, Cima R, Sheldrake J, Hoare DJ (July 2019). "Misophonia: A scoping review of research". Journal of Clinical Psychology. 75 (7): 1203–1218. doi:10.1002/jclp.22771. PMID 30859581.
  8. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa Swedo SE, Baguley DM, Denys D, Dixon LJ, Erfanian M, Fioretti A, et al. (2022). "Consensus Definition of Misophonia: A Delphi Study". Frontiers in Neuroscience. 16: 841816. doi:10.3389/fnins.2022.841816. PMC 8969743. PMID 35368272.
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Further reading

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