Misophonia, Misokinesia, and the Brain
New research replicates the brain basis of misophonia.
Posted August 2, 2019 | Reviewed by Ekua Hagan
In the past few years, we have experienced breakthrough research in misophonia. First, we saw Dr. Sukhbinder Kumar’s et al.’s study “The Brain Basis for Misophonia” (2017). This exciting study added compelling evidence that the brains of individuals with misophonia are different from the brains of those without the disorder. Recently, Dr. Arjan Schröder and colleagues at Amsterdam UMC added visual stimuli to a similar study, replicating Dr. Sukhbinder’s results and adding an understanding to the visual elements of misophonia.
The following is an interview with Dr. Arjan Schröder about this study with comments from Dr. Kumar as well:
JB: It is most exciting to see new physiologically and neurologically based research on misophonia! Your study replicates some of Kumar et al.’s 2017 study. Would you explain why, as well as how, your findings impact our overall understanding of misophonia?
Dr. Schröder: In our study, we not only looked at the activated auditory and visual brain regions but also at the different kinds of emotions that could be triggered in misophonia. Importantly, we focused on the key emotions disgust and anger. When we developed our MRI study, we also decided to use audiovisual and not only auditory stimuli. Patients had told us repeatedly that visual input was at least as important to triggering the emotions, so combining audio and video would be more similar to daily situations.
Dr. Kumar comments:
The study used different stimuli than used in our Current Biology study: while the Schröder et al. (2019) study used video as stimuli, our study used sounds only as stimuli. Combining the results of these two fMRI studies shows that the same brain network is involved in misophonia irrespective of the nature of stimuli used. The study replicates our findings of higher activation in anterior insula and anterior cingulate in response to trigger sounds.
JB: Regarding visual stimuli, many people seem to interpret misokinesia as referring to the visual triggers that go along with the auditory trigger sounds. However, “kinesea” refers more to movement. Would you explain what you mean by the term misokinesia in order to clarify for others?
Dr. Schröder: In our first 2013 study in which we tried to describe misophonia symptoms, we noticed the irritation some people experienced when seeing other people repetitively moving (parts of) their limbs, e.g. leg rocking. We therefore coined this misokinesia, i.e. hatred of movement. These didn’t necessarily involve a sound. However, most movements do have some sounds. So the term misokinesia could be used more widely.
JB: In your study, like Dr. Kumar, you also found that there is a difference between typical aversive auditory stimuli and specific misophonia sounds. Would you explain what may account for this difference, both in regard to sounds and the visual triggers that you used?
Dr. Schröder: I think much has to do with context. Many neutral sounds can become salient within a certain context. However, what also strikes me a lot is that most misophonic sounds possess both some sort of repetitiveness and some unpredictability. And this combination can make them more annoying: ‘When will it start? How long will it continue? When will it stop?’
JB: In your study, you do a wonderful job of describing a process by which the salience of particular sounds cause sympathetic nervous system arousal and aversive emotions, which then become associated in memory and consequently increase upon exposure. People often think that if a disorder involves any conditioning component that it is exclusive of any inherent or inborn risk factors. Would you comment on the “nature versus nurture” debate regarding misophonia?
Dr. Schröder: The interplay between nature and nurture, between genes and the environment is such a complex one. Thus to only focus on one part, and neglecting the other, won’t bring us much further in science and healthcare.
JB: You identified the specific emotions anger, disgust, and sadness in your sample in response to typical misophonia auditory and visual stimuli. Each of these emotions may have different neurological correlates and processes. Would you comment on this?
Dr. Schröder: The insula (and ACC) has been implicated in moral assessment of stimuli and the experience of the emotion disgust. I think that’s interesting because both can be linked to the symptoms of misophonia. Obsessive-compulsive personality features might play a role. Different neurocognitive studies have found evidence for increased cognitive inflexibility in OCPD. Thus, when certain sounds are bothersome for a misophonic person, cognitive inflexibility could result in further difficulties disengaging from listening to and ruminating on these sounds.
JB: Misophonia is a complex disorder with many neurological variables, personality variables, etc. One issue that you bring up has to do with insular activity and its relationship to morality assessment. You make a very interesting statement in your paper: “It is possible that patients could have perceived these stimuli as a personal harassment, thus triggering subsequent anger.” If this is the case, do you feel that cross-cultural studies (in which ideations of personal harassment are different) might help to explore this idea?
Dr. Schröder: That’s an interesting idea. I’ve been told that in certain cultures those sounds are not considered as negative sounds during dinner, quite the opposite.
JB: Both your study and Dr. Kumar et al.’s study (2017) refer to interoception (how we sense our internal body responses) as an important function of the salience network. I would imagine that if one had a higher sense of interoception, they might “feel” negative physiological responses (i.e., autonomic nervous system arousal) with more intensity or awareness.
Dr. Schröder: This is an interesting concept for future research.
Dr. Kumar comments: Our Current Biology study provided some initial evidence for this in terms showing that misophonic subjects have higher self-reported scores on questionnaires assessing perception of internal body state. This suggests that misophonic subjects have a different perception of their internal body state even when not stimulated by any trigger stimuli. How this ties into aberrant perceptual/motor response to trigger sounds is not exactly clear. One possible hypothesis is that aberrant perception of internal body response [causes] misophonics generate aberrant expectations about the trigger stimuli. This expectation then drives the response.
JB: You offer what may be the beginning of model for misophonia.
….misophonia involves a conditioned response of anger and physical arousal elicited by human audiovisual triggers; the symptoms are mediated by enhanced reactivity of the salience network in combination with hypervigilance, which is reflected by sensitization of the auditory cortex. You mentioned earlier in your paper that non-human triggers are also found in misophonia but are perhaps not as prevalent. With that in mind, would you sum up your hypothesis in layman’s terms?
Dr. Schröder: I think the core of the triggering sounds are human sounds because those are the sounds we hear the most in our daily lives. However, basically any sound could become salient and connected to a negative experience or emotion, depending on the context.
Dr. Kumar comments: I agree with the outline of the model. I think ‘hypervigilance’ and ‘saliency’ of trigger sounds amount to generating aberrant expectations. This means that there is a strong ‘top-down’ component to the misophonic response in addition to the ‘bottom-up’ (sounds/visual stimuli). I think the future research should start making a distinction between the two types of responses and understanding contributions that each of the type makes in an overall response.
JB: Finally, what do you suggest as the next best steps for misophonia research?
Dr. Schröder: International cooperation is an important one. Especially if you want to dive deeper into the neurobiology (genetics and imaging) you need bigger cohorts. Also, I am interested in the connections with morality, OCPD traits, ASD, and SOR (Sensory Over Responsivity), as well as hyperacusis and tinnitus.
Do you have any new studies in the works, or in mind?
Dr. Schröder: At our institute, we’re constantly improving our treatment and looking at a bigger cohort already.
JB: This is great news! Thank you very much for the interview!
For more information about Dr. Schroder and his publications, please visit the IMRN Advisory Board.
Kumar, S., Tansley-Hancock, O., Sedley, W., Winston, J.S., Callaghan, M.F., Allen, M.,...Griffiths, T.D. (2017). The brain basis for misophonia. Current Biology, 27(4), 527-533. doi:10.1016/j.cub.2016.12.048.
Schröder, A., van Diepen, R., Mazaheri, A., Petropoulos-Petalas, D., Soto de Arnesti, V., Vulink, N., & Denys, D. (2014). Diminished N1 auditory evoked potentials to oddball stimuli in misophonia patients. Frontiers in Behavioral Neuroscience, 8(123). doi:10.3389/fnbeh.2014.00123