Summary: New fMRI research challenges earlier claims that misophonia arises from an overly sensitive connection between the auditory cortex and orofacial motor areas of the brain.
Source: Ohio State University
Researchers have, for the first time, mapped the brain regions linked to a less-studied trigger of misophonia—repetitive finger tapping—offering a broader view of how this condition may arise.
Scientists at Ohio State University report results that call into question a leading explanation of misophonia’s neural cause. Misophonia is an aversive reaction to certain sounds that can provoke anger, disgust, and a strong urge to escape. While oral noises such as chewing are commonly reported triggers, not everyone with misophonia responds to those sounds.
Previous work published in The Journal of Neuroscience proposed that misophonia stems from hypersensitive functional connections between the auditory cortex and orofacial motor cortex—brain areas involved in sensing sound and controlling facial and mouth movements. The new study, published in Frontiers in Neuroscience, examined whether that explanation holds when the triggers are non-orofacial sounds, such as finger tapping.
The study used functional MRI to scan 19 adults with a range of self-reported misophonia symptoms, from none to mild. Participants completed three questionnaires assessing misophonia severity, performed tasks in the scanner that activated mouth-related and finger-related motor regions, and were also scanned while resting. The tasks included vocalizing simple syllables to localize orofacial motor activity and repeatedly tapping fingers against the leg to localize hand/finger motor activity.
At rest, participants with higher misophonia scores did show stronger resting-state connectivity between the auditory cortex and a sensorimotor region previously labeled as orofacial—replicating earlier resting-state findings. However, when the researchers defined orofacial cortex using task-based activation from vocalization, that task-defined orofacial region did not show the same heightened connectivity in people with greater misophonia symptoms.
In other words, the region identified by resting-state analysis as an “orofacial” area did not align with the brain area that becomes active during actual mouth and face movements. This mismatch calls into question the assertion that misophonia is driven by supersensitive connections specifically between auditory cortex and true orofacial motor cortex.
Instead, the study found that participants with higher misophonia scores exhibited stronger connectivity between finger-related sensorimotor regions and the insula, a brain area closely tied to emotional experience, including feelings of disgust. Notably, this finger–insula connectivity did not involve the auditory cortex in the same way as previously proposed orofacial-auditory connections.
Lead author Heather Hansen, a doctoral student in psychology at Ohio State, summarized the implication: focusing only on chewing and other mouth sounds gives an incomplete picture of misophonia’s neural basis. These new findings provide neural evidence that repetitive, non-orofacial sounds can be associated with the same aversive emotional responses and that the insula, rather than direct auditory–orofacial coupling, may be a key player.
The researchers used both resting-state-defined regions of interest (rsROIs) and task-defined functional ROIs (fROIs) for orofacial and finger areas, and subdivided those regions according to standard sensorimotor atlases to assess motor specificity. Resting-state analyses partially replicated prior results by revealing increased connectivity between rsROIs and both auditory cortex and insula in people with mild misophonia. But task-based orofacial fROIs did not show the same pattern, while finger fROIs did show increased connectivity with the insula.
Taken together, the data point to a broader neural representation of misophonia that extends beyond an orofacial or mirror-neuron explanation. The presence of enhanced finger-related connectivity with an emotion-linked region supports the idea that misophonia can be triggered by a variety of repetitive sounds, not solely those produced by the mouth or face.
Hansen and her colleagues emphasize that further research is needed to fully understand misophonia’s causes and to develop effective interventions. Their findings suggest researchers and clinicians should consider multiple types of triggers and neural pathways when conceptualizing and treating the condition. For people whose misophonia is provoked by non-oral noises, these results offer validation that their experiences have measurable correlates in the brain.
About this misophonia research news
Author: Jeff Grabmeier
Source: Ohio State University
Contact: Jeff Grabmeier – Ohio State University
Image: The image is in the public domain
Original Research: Open access. “Neural evidence for non-orofacial triggers in mild misophonia” by Heather A. Hansen et al., published in Frontiers in Neuroscience
Abstract
Neural evidence for non-orofacial triggers in mild misophonia
Misophonia, an extreme aversion to certain environmental sounds, is a prevalent but understudied condition affecting roughly 20% of the population. Prior neuroimaging work reported higher resting-state functional connectivity between auditory cortex and a purported orofacial motor cortex in people with misophonia, leading to hypotheses that mirror-neuron-like orofacial circuitry may underlie the disorder.
In this study, the researchers attempted to replicate those findings while also testing whether non-orofacial stimuli elicit similar neural signatures. Nineteen adults with varying levels of misophonia completed resting-state scans and a task-based fMRI paradigm including phoneme articulation (to localize orofacial cortex) and finger-tapping (to localize finger cortex).
Using both resting-state-defined regions (rsROIs) and task-defined functional ROIs (fROIs), the team evaluated connectivity between sensorimotor regions and predefined non-sensorimotor targets. The results replicated increased resting connectivity between rsROIs and both auditory cortex and insula in mild misophonia but showed that the resting-state “orofacial” region did not correspond to task-defined orofacial cortex. Instead, connectivity differences extended across multiple sensorimotor areas, and finger fROIs demonstrated higher connectivity with the insula in participants with greater misophonia.
These findings indicate that misophonia’s neural representation is not restricted to an orofacial/motor origin and support the notion that non-orofacial triggers—such as repetitive finger tapping—are relevant to understanding and treating the condition.