Home Research Groundbreaking Research on the Motor Basis for Misophonia

Groundbreaking Research on the Motor Basis for Misophonia

by Misophonia International

An interview with Sukhbinder Kumar and Mercede Erfanian.

Would you describe the major findings of your study, “The motor basis for misophonia” (Journal of Neuroscience, 2021)

In our recent study, we have observed that in misophonia sufferers:

  • The pre-motor cortex that controls the movement of the throat, lips, and the face is involuntarily and automatically over-activated in response to trigger sounds (i.e., chewing, lip-smacking, etc.).
  • The pre-motor cortex and auditory cortex were hyperconnected which led to over-communication between these two brain substrates in response to all sounds.
  • The increased activation of the pre-motor cortex was attributed to emotional distress when confronted with the sound triggers.
  • There was an increased connection between the (ventral) pre-motor cortex and the insula (responsible for emotional processing, interoception, and saliency) at the resting state.
  • We found the same aberrant pattern (hyper-connectivity) between the pre-motor cortex and the visual cortex.

What does this mean?

Our findings suggest that the over-connection between the visual and auditory and pre-motor cortex activates the “mirror system” in the brain of the sufferers.

Would you describe what the mirror system is?

The mirror system is responsible for processing movements of other people in a similar fashion as if we make those movements. For example, people can spontaneously mimic the facial expression of others because of these sensory-motor or “mirror” neurons. Mirror neurons are theorized to influence learning and social behavior. Mirror neurons are the reason we may yawn when we see others yawn or smile if we see another person smile. Mirror neurons are also thought to underlie empathy.

How does this change the traditional view of misophonia?

We used to think that the neural underpinnings of misophonia were limited to auditory parts of the brain and the emotion-processing parts of the brain such as the insula (which is known to represent visceral signals from within the body such as the heart) and the amygdala (which mediates fight/flight response). However, these findings reveal that the route to emotional areas is also via the pre-motor/mirror system.

How does this explain misophonia reactivity?

We are not entirely sure. One hypothesis is that the involuntary activation of the mirror system results in the trigger stimuli being perceived as intruding into the sufferers’ personal space. This may set off the nervous system reactivity. However, more research needs to be done in order to answer this question.

How does misokinesia fit in there? Is it possible that based on the original definition of misokinesia (hatred of movement) that gross motor areas of the brain are also involved? For example, many people describe great aversion when they see someone shaking their leg.

Our work so far has concerned only typical triggers in misophonia. But the model we proposed, in principle, can be extended to explain misokinesia. That is if somebody finds “shaking leg” as triggers, it is likely that it involves hyperactivation of the “leg” motor area in the brain. This needs to be confirmed by further empirical research. Further empirical validation needs further research.

What does this imply in terms of potential therapy?

One important consequence for the potential therapy is that “sounds” in misophonia are not the whole story. In our model, they are only a “medium” via which the action of the trigger person is “mirrored.” The effective therapy, therefore, would, not only concern the auditory part of the brain but also involve the motor part of the brain. More concretely, the therapy should aim to weaken the link between sound and the action which is overly represented in misophonia. Of course, further research is needed to help us define potential therapies.

Would this explain why exposure therapy, for example, has not been successful?

According to these findings, it is possible that the exposure therapy is not efficacious but may also lead to sustained over-activations of the aforementioned brain areas (consequently reinforcing the aberrant functional connections between them).

What are your next steps for research?

I [SK] aim to carry forward the current work in two streams. First, I would like to explore using cost-effective brain measurements such as EEG to show the involvement of “mirror” system in misophonia. Second, I would like to explore the use of non-invasive brain stimulation such as TMS (transcranial magnetic stimulation) to temporarily interrupt the “mirror” system to show its “causal” role in misophonia, in collaboration with other TMS researchers. In addition, I [ME] would like to explore how and why triggers expand into non-orofacial related sounds with specific acoustic parameters (i.e., pattern-based and repetitive).

Thank you both (and thank you to everyone who assisted with this paper) so very much for this interview and for this incredible contribution to misophonia research!


Originally posted on Psychology Today.



The motor basis for misophonia
Sukhbinder Kumar, Pradeep Dheerendra, Mercede Erfanian, Ester Benzaquén, William Sedley, Phillip E. Gander, Meher Lad, Doris E. Bamiou, Timothy D. Griffiths
Journal of Neuroscience 21 May 2021, JN-RM-0261-21; DOI: 10.1523/JNEUROSCI.0261-21.2021

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