Misophonia
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.
[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] 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.
[7][8] The term misokinesia has been proposed to refer specifically to misophonic reactions to visual stimuli, often repetitive movements made by others.
[37] Before that, the disorder was more commonly called "selective sound sensitivity syndrome", or "4S", a term coined by audiologist Marsha Johnson.
[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.
as a more suitable name, which seeks to incorporate both the respective auditory and non-auditory aspects of misophonia and 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).
"[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] There may also be a feeling of unwanted sexual arousal, similar to the obsessive-compulsive complex known as groinal response,[44][45] upon encountering the trigger stimulus.
[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][18] The five dimensions of cognitive-behavioral responses to "triggers", as empirically derived from the "S-Five" (another misophonia questionnaire that was used in the first large-scale prevalence study of the condition in the UK),[51][52][53] are as follows: 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.
[18][26][55][56] 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.
[60] An unpublished study suggests a genetic locus is associated with responses to a single question asking about the misophonic symptom of experiencing rage to sounds of people chewing.
[63][65] 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.
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][66] 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)[67] may play a central role in this disorder.
[66][69][70] Based on what is known from neuroimaging and behavioral studies of misophonia, the action perception model conceptualizes the disorder as follows:[66] The action perception model arguably represents a major advance over previous theoretical work in this area, particularly in its ability to explain the neuroimaging data on misophonia published before 2024, when the theory was first proposed.
[66] 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.
[66] 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)[74] 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),[75] 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.
[66] 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.
[66] The role of other co-occurring conditions, particularly those such as autism that are known to both affect social cognition and cooccur with misophonia at exceptionally high rates,[68][76] is also an area for future research to explore and test the model.
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.
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.
[18][90] It has been suggested that assessment should involve collection of multiple sources of data, such as patient case histories, interviews, audiological examination, and self-report tools.
[107][108] One specific phenomenon observed to this end with clomipramine in at least one instance is reduced electrodermal reactivity to innocuous auditory stimuli.
