The brain basis of “hatred of sound:” Misophonia

“Munch, munch, munch.”

For most of us, the sounds of our lunch date chewing or a coworker clicking their pen are everyday components of an auditory landscape that go largely unnoticed. But for others, these seemingly mundane sounds are painfully unpleasant to the point of eliciting uncontrollable irritation or rage. There is ongoing disagreement as to whether this hatred of sound, termed misophonia, should be recognized as a legitimate psychiatric disorder, and many sufferers continue to shamefully hide their extreme emotional responses to common sounds. But a recent surge in interest in misophonia is encouraging many to acknowledge that they suffer from the condition, and some medical professionals to accept that this reaction to otherwise neutral auditory stimuli reflects a veritable disorder. A flurry of research, aimed to characterize its behavioral manifestations and outline diagnostic criteria, has appeared over the past decade, though few studies have sought to determine the neural underpinnings of misophonia.

Characterizing the “hatred of sound”

Since “misophonia” was first coined in the early 2000’s, efforts have been made to characterize its symptoms through patient interview. Although its prevalence remains uncertain due to its still relative obscurity, studies suggest that it typically strikes in adolescence, affects men and women equally, and may occur in much as 20% of the population. The most commonly reported trigger sounds include eating, breathing or repetitive behaviors like typing or pen clicking. Hearing such sounds often evokes uncontrollable irritation, disgust or anger, which the individual recognizes as socially inappropriate. Therefore, the misophonic may try to suppress any outward reaction, with few acting upon their urges with verbal or physical aggression. These aversive responses in fact manifest as measurable physiological arousal. Compared to healthy controls, misophonic individuals have excessive skin conductance responses to auditory stimuli, and the magnitude of these skin responses correlates with how distressing the participants perceive the sounds.

An undiagnosed disorder?

The symptoms of misophonia largely overlap with other clinically accepted psychiatric disorders, including obsessive compulsive disorder (OCD), post-traumatic stress disorder, and various phobias. Some individuals reporting misophonic symptoms also have comorbid psychiatric conditions such as attention-deficit hyperactivity disorder, hypochondria, OCD, or eating disorders. Although some experts advise that misophonia be identified as a unique psychiatric disorder, it has yet to be included in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). Miren Edelstein, a graduate student at the University of California San Diego who researches misophonia, explains that

“The uncertainty surrounding the official status of misophonia as a discrete disorder stems from the fact that it does indeed have some similarities with other existing conditions. However, while some misophonics definitely do suffer from some of these other existing conditions, many do not and report no other ailments whatsoever. Because of this variation, I don’t believe another existing disorder can completely account for the specific constellation of symptoms present in misophonia.”

The misophonic brain

Despite an advancing understanding of the psychological and behavioral manifestations of misophonia, little research has attempted to clarify its neurobiological bases. Researchers suspect that misophonia is not a primary auditory disorder, but rather stems from aberrant attentional or emotional processing later in the brain’s auditory system. There is preliminary support for this explanation from one small EEG study. In an oddball auditory paradigm, misophonic participants showed a smaller N1 evoked potential than controls elicited by unexpected auditory tones, whereas the “pre-attentive” P1 component showed no group difference. The N1 is involved in early attention and detecting sensory changes, suggesting that abnormal attentional signaling early in the auditory processing stream may contribute to misophonia. Interestingly, an altered N1 peak has also been associated with impulsivity, drug abuse and bipolar disorder.

Recently, researchers used fMRI to examine brain activity in misophonic individuals while they listened to sounds that were neutral, unpleasant or characteristic misophonia triggers. The misophonics rated the trigger sounds as more distressing than the unpleasant or neutral sounds, whereas normal controls rated trigger and unpleasant sounds as similarly annoying, confirming a selective intolerance for triggers by misophonics. Critically, the misophonics showed greater activation in the insula than controls during trigger sounds, and this activity increased with greater reported distress. Furthermore, functional connectivity between the insula and other brain regions involved in attention and emotion was altered in misophonics when listening to trigger sounds. Although the insula has been promiscuously implicated in a plethora of cognitive processes, its proposed functions include internal awareness of one’s body and emotional states. Though preliminary, these findings suggest that misophonia is associated with pathological activation of a brain network supporting interception. Edelstein, who was not involved in this study, comments “There was a huge gap in the literature until recently. I think this study was a triumphant effort towards gleaning neurophysiological insights on misophonia and its findings fit nicely into the narrative emerging from behavioral research on misophonia.”

It has also been proposed that altered brain connectivity underlying misophonia may be similar to that occurring in synesthesia, a condition in which one sensory stimulus evokes sensation in a different modality (e.g., the letter “A” is associated with the color red). Faulty enhanced neural connections could theoretically lead to abnormal associations amongst sensory and emotional brain regions in misophonia, although this hypothesis remains untested.

Pacifying sound distress

Given the novelty of misophonia, effective therapies have been inadequately assessed. However, there is some support for the use of cognitive behavioral therapy and conditioning retraining. Hopefully, with further research into both its psychological profile and neurobiological underpinnings, misophonia will gain both greater social acceptance and effective treatment options.

References

Bruxner G. (2016). ‘Mastication rage’: a review of misophonia – an under-recognised symptom of psychiatric relevance? Australas Psychiatry. 24(2):195-7. doi:10.1177/1039856215613010

Edelstein M, Brang D, Rouw R, Ramachandran V (2013). Misophonia: physiological investigations and case descriptions. Front Hum Neurosci. 7:296. doi: 10.3389/fnhum.2013.00296

Jastreboff MM, Jastreboff PJ. (2001). Components of decreased sound tolerance: hyperacusis, misophonia, phonophobia. ITHS Newsletter. 2:5-7

Kluckow H, Telfer J, Abraham S. (2014). Should we screen for misophonia in patients with eating disorders? A report of three cases. Int J Eat Disord. 47(5):558-61. doi:10.1002/eat.22245

Kumar S et al. (2017). The Brain Basis for Misophonia. Curr Biol. 27(4):527-33. doi:10.1016/j.cub.2016.12.048

Schroder A, Vulink N, Denys D. (2013). Misophonia: Diagnostic Criteria for a New Psychiatric Disorder. PLOS One. 8(1):e54706. doi:10.1371/journal.pone.0054706

Schroder A et al. (2014). Diminished N1 auditory evoked potentials to oddball stimuli in misophonia patients. Front Behav Neurosci. 8:123. doi:10.3389/fnbeh.2014.00123

Wu MS, Lewin AB, Murphy TK, Storch EA. Misophonia: Incidence, Phenomenology, and Clinical Correlates in an Undergraduate Student Sample. J Clin Psychol. 70(10):944-1007. doi: 10.1002/jclp.22098

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Any views expressed are those of the author, and do not necessarily reflect those of PLOS.

Emilie Reas received her PhD in Neuroscience from UC San Diego, where she used fMRI to study memory. As a postdoc at UCSD, she currently studies how the brain changes with aging and disease. In addition to her tweets for @PLOSNeuro she is @etreas.