Properties (15)
Id 42952cc2-724f-41a1-b611-8c8862138461
Year 2022
Abstract Misophonia, an extreme aversion to certain environmental sounds, is a highly prevalent yet understudied condition plaguing roughly 20% of the general population. Although neuroimaging research on misophonia is scant, recent work showing higher resting-state functional connectivity (rs-fMRI) between auditory cortex and orofacial motor cortex in misophonia vs. controls has led researchers to speculate that misophonia is caused by orofacial mirror neurons. Since orofacial motor cortex was defined using rs-fMRI, we attempted to theoretically replicate these findings using orofacial cortex defined by task-based fMRI instead. Further, given our recent work showing that a wide variety of sounds can be triggering (i.e., not just oral/nasal sounds), we investigated whether there is any neural evidence for misophonic aversion to non-orofacial stimuli. Sampling 19 adults with varying misophonia from the community, we collected resting state data and an fMRI task involving phoneme articulation and finger-tapping. We first defined “orofacial” cortex in each participant using rs-fMRI as done previously, producing what we call resting-state regions of interest (rsROIs). Additionally, we functionally defined regions (fROIs) representing “orofacial” or “finger” cortex using phoneme or finger-tapping activation from the fMRI task, respectively. To investigate the motor specificity of connectivity differences, we subdivided the rsROIs and fROIs into separate sensorimotor areas based on their overlap with two common atlases. We then calculated rs-fMRI between each rsROI/fROI and a priori non-sensorimotor ROIs. We found increased connectivity in mild misophonia between rsROIs and both auditory cortex and insula, theoretically replicating previous results, with differences extending across multiple sensorimotor regions. However, the orofacial task-based fROIs did not show this pattern, suggesting the “orofacial” cortex described previously was not capturing true orofacial cortex; in fact, using task-based fMRI evidence, we find no selectivity to orofacial action in these previously described “orofacial” regions. Instead, we observed higher connectivity between finger fROIs and insula in mild misophonia, demonstrating neural evidence for non-orofacial triggers. These results provide support for a neural representation of misophonia beyond merely an orofacial/motor origin, leading to important implications for the conceptualization and treatment of misophonia.
Cssclasses
  • purpleRed
Aliases
  • (Hansen et al., 2022)
Import Date 02-21-2026
Dv Authors Heather A. Hansen, Patricia Stefancin, Andrew B. Leber, Zeynep M. Saygin,
Dv Initial Source Misophonia MOC
Dv Status #status/reviewed
Dv Limitations • Small sample size (n = 19). • Mild misophonia sample; not severe clinical cases. • Resting-state connectivity cannot establish directionality or causality.
Dv Future Directions • Examine clinical/severe misophonia populations. • Further investigate posterior insula contributions. • Expand beyond orofacial-centric conceptualizations of misophonia.
Dv Relevance • good source on fMRI methods for miso. • shows neural evidence for existence on non-orofacial triggers in miso, suggesting more neural representations for miso beyond just orofacial l/motor regions. • could be considered a counter to the Kumar motor model
Dv Statistics • Group main effect (HMAT rsROI): F(1,408)=53.345, p=1.481×10⁻¹². • PMv–Planum Temp.: t(17)=2.556, p=0.020, pHB=0.082. • PMv–Posterior Insula: t(17)=2.934, p=0.009, pHB=0.037. • Posterior Insula–S1/M1/PMd rsROIs: t(17)=2.542–2.876, pHB≤0.037. • Posterior Insula correlations (rsROIs): r=0.51–0.70, pHB≤0.036. • fROI group × fROI interaction (HMAT): F(1,816)=8.201, p=0.004. • Freesurfer finger fROI–Posterior Insula: t(17)=2.882, p=0.010, pHB=0.041. • No significant A1 connectivity differences.
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Neural evidence for non-orofacial triggers in mild misophonia

Status:: #status/reviewed

Metadata

Abstract
Background/Purpose Background-
• Misophonia affects ~20% of the population; neural mechanisms understudied.
• Prior fMRI studies implicated anterior insula, auditory cortex, amygdala, and functional connectivity abnormalities.
• Kumar et al. (2021) proposed a “motor basis of misophonia,” reporting increased rs-connectivity between planum temporale and orofacial ventral premotor cortex (PMv).
• Prior work restricted misophonia to oral/nasal triggers.
• Evidence indicates triggers extend beyond orofacial sounds.
• Previous ROIs defined via resting-state connectivity; potential circularity and lack of functional validation.

Purpose-
• Theoretically replicate Kumar et al. (2021) using rs-defined orofacial cortex.
• Functionally define orofacial cortex using task fMRI and test connectivity.
• Test selectivity of findings to orofacial vs. finger representations.
• Examine broader sensorimotor involvement beyond PMv.
Participants/samples • N = 19 adults (14F, 5M); mean age = 25.6 years.
• Higher misophonia group: n = 7; mean score = 28.7 (range 20.5–37.3); A-MISO-S mean = 7.7.
• Lower misophonia group: n = 12; mean score = 9.6 (range 0–17.7); A-MISO-S mean = 2.2.
• Misophonia composite range: 0–37.3/100.
• Excluded: 1 participant for excessive motion (40.9% censored volumes).
• Motion not significantly different between groups: t(17) = 1.196, p = 0.248.
Measures • Misophonia: MAS-1, MAQ-2, A-MISO-S.
• Psychopathology covariates: OCI-R; DASS-21.
• Resting-state fMRI (10 min; TR = 1000 ms; 580 volumes).
• Articulatory localizer task: phoneme production (“BA GA RA DA”), finger tapping, rest.
Procedures • fROIs defined as top 10% activated voxels (P > T for orofacial; T > P for finger).
• rsROIs defined as top 10% PMv voxels most correlated with planum temporale.
• Additional rsROIs defined in S1, M1, PMd; precentral/postcentral gyri.
• Functional connectivity calculated via Pearson correlation; Fisher z-transformed.
• Mixed ANOVAs; Holm–Bonferroni correction.
Results • Resting-state–defined sensorimotor regions showed increased connectivity with the planum temporale and posterior insula in individuals with higher misophonia scores.
• Connectivity differences were not limited to ventral premotor cortex (PMv), but extended across primary motor (M1), primary somatosensory (S1), and dorsal premotor cortex (PMd).
• Posterior insula connectivity scaled with misophonia severity.
• No differences were observed in primary auditory cortex (A1), indicating effects were not driven by low-level auditory processing.
• When sensorimotor regions were defined using task-based fMRI, orofacial regions did not show selective connectivity differences with planum temporale or insula.
• Instead, finger-related motor and somatosensory regions showed greater connectivity with the posterior insula in individuals with higher misophonia scores.
• Individuals with higher misophonia demonstrated stronger connectivity with finger regions than with orofacial regions.
• Resting-state–defined “orofacial” regions showed minimal task selectivity, indicating they were not strongly specific to orofacial movement.
• Functionally defined ROIs showed clear task selectivity, confirming dissociation between rs-defined and task-defined regions.
Discussion/Limits Conclusion-
• The authors conclude that increased connectivity between sensorimotor cortex and planum temporale/insula can be replicated when using rs-defined ROIs.
• The findings indicate that this connectivity is not selective to ventral premotor cortex.
• The authors conclude that rs-defined “orofacial” cortex is not functionally selective for orofacial action.
• The data support involvement of posterior insula in misophonia.
• The findings indicate connectivity differences extend beyond orofacial representations to finger representations.
• The authors conclude that misophonia cannot be explained solely by an orofacial mirror neuron mechanism.
• The data support a neural representation of misophonia beyond a strictly motor basis.
Limitations:: • Small sample size (n = 19).
• Mild misophonia sample; not severe clinical cases.
• Resting-state connectivity cannot establish directionality or causality.
Future Directions:: • Examine clinical/severe misophonia populations.
• Further investigate posterior insula contributions.
• Expand beyond orofacial-centric conceptualizations of misophonia.
Relevance:: • good source on fMRI methods for miso. 
• shows neural evidence for existence on non-orofacial triggers in miso, suggesting more neural representations for miso beyond just orofacial l/motor regions.
• could be considered a counter to the Kumar motor model
Statistics:: • Group main effect (HMAT rsROI): F(1,408)=53.345, p=1.481×10⁻¹².
• PMv–Planum Temp.: t(17)=2.556, p=0.020, pHB=0.082.
• PMv–Posterior Insula: t(17)=2.934, p=0.009, pHB=0.037.
• Posterior Insula–S1/M1/PMd rsROIs: t(17)=2.542–2.876, pHB≤0.037.
• Posterior Insula correlations (rsROIs): r=0.51–0.70, pHB≤0.036.
• fROI group × fROI interaction (HMAT): F(1,816)=8.201, p=0.004.
• Freesurfer finger fROI–Posterior Insula: t(17)=2.882, p=0.010, pHB=0.041.
• No significant A1 connectivity differences.

Notes

key terms and concepts

Misophonia – decreased sound tolerance to specific sounds or associated stimuli resulting in strong negative emotional, physiological, and behavioral responses not seen in others.

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Hansen 2022 commenting on the specificity of the Kumar orifical motor area claims

Hansen 2022 contradiction of the Kumar model

Hansen 2022 challenge to Kumar’s associative learning explanation for non orofacial triggers in Misophonia

Narrative Contrast- Kumar Motor Model vs. Hansen Sensorimotor Model

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