Increased prefrontal activation to misophonic triggers in misophonia
Poster No:
670
Submission Type:
Abstract Submission
Authors:
Jasmine Tan1,2, Sergio Osorio1,2, Grace Levine1,2, Seppo Ahlfors3,2, Julie Arenberg4, Tal Kenet1,2
Institutions:
1Department of Neurology, Harvard Medical School, Massachusetts General Hospital, Boston, MA, 2Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Boston, MA, 3Department of Radiology, Harvard Medical School, Massachusetts General Hospital, Boston, MA, 4Department of Audiology, Harvard Medical School, Mass. Eye and Ear, Boston, MA
First Author:
Jasmine Tan, PhD
Department of Neurology, Harvard Medical School, Massachusetts General Hospital|Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital
Boston, MA|Boston, MA
Department of Neurology, Harvard Medical School, Massachusetts General Hospital|Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital
Boston, MA|Boston, MA
Co-Author(s):
Sergio Osorio, PhD
Department of Neurology, Harvard Medical School, Massachusetts General Hospital|Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital
Boston, MA|Boston, MA
Department of Neurology, Harvard Medical School, Massachusetts General Hospital|Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital
Boston, MA|Boston, MA
Grace Levine
Department of Neurology, Harvard Medical School, Massachusetts General Hospital|Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital
Boston, MA|Boston, MA
Department of Neurology, Harvard Medical School, Massachusetts General Hospital|Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital
Boston, MA|Boston, MA
Seppo Ahlfors, PhD
Department of Radiology, Harvard Medical School, Massachusetts General Hospital|Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital
Boston, MA|Boston, MA
Department of Radiology, Harvard Medical School, Massachusetts General Hospital|Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital
Boston, MA|Boston, MA
Julie Arenberg, PhD, CCC-A
Department of Audiology, Harvard Medical School, Mass. Eye and Ear
Boston, MA
Department of Audiology, Harvard Medical School, Mass. Eye and Ear
Boston, MA
Tal Kenet, PhD
Department of Neurology, Harvard Medical School, Massachusetts General Hospital|Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital
Boston, MA|Boston, MA
Department of Neurology, Harvard Medical School, Massachusetts General Hospital|Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital
Boston, MA|Boston, MA
Introduction:
Misophonia is a disorder of abnormal emotional reactions to specific sensory stimuli, and in particular auditory stimuli. Such stimuli, known as misophonic "triggers", are often sounds made by the body, like chewing or breathing, and may seem innocuous but can elicit anger, disgust, stress and anxiety for people suffering from misophonia (Vitoratou et al., 2021). Misophonic triggers have been shown to activate the salience network in people with misophonia (Kumar et al., 2017; Schröder et al., 2019), yet relatively little is known about the cortical underpinnings of misophonia. In this study, we used magnetoencephalography (MEG) to measure activation during an auditory spatial attention task.
Methods:
Participants performed a classic auditory oddball paradigm while attending to the cued ear, and were instructed to ignore sounds in the non-cued ear. The sounds in the non-cued ear consisted of the same standard tones as in the cued ear, and two categories of deviant tones. One category consisted of novel stimuli such as claps or clinks that were rated as benign by participants ("distractors"), while the other category consisted of sounds that were selected to trigger misophonia in each individual participant, such as chewing ("triggers"). We hypothesized that while all deviant sounds in the un-cued ear will elicit involuntary "bottom-up" attention, the misophonia-specific trigger sounds will also lead to cortical activation related to emotional reactions not experienced by non-misophonic distractor sounds. Participants with self-reported misophonia were assessed by an audiologist to rule out other primary auditory processing disorders, and were included only if they met the misophonia criteria on the misophonia specific S-Five Questionnaire, which measures number of misophonic triggers and intensity of reaction to these triggers (Vitoratou et al., 2021). Thus far, MEG data has been acquired from 5 (out of a target of 40) misophonia participants (mean age = 24.2, SD = 4.27) and 2 healthy controls (mean age = 25.11, SD = 2,23). Individual cortical surfaces were obtained from structural T1 MRI images, and BEM head models were computed. We used sLORETA-MNE source modelling to extract responses in source (cortical) space for each participant. Visual inspection of source space activations showed that peak activation to the misophonic trigger sounds followed an initial activation in response to the sound, which was not condition specific, and localized to the anterior regions of the prefrontal cortex (PFC), with some participants showing peak activation in the orbitofrontal cortex and others showing peak activation in the inferior frontal gyrus (IFG). After plotting grand-averaged source activations, the time window of 380-480ms after stimulus onset showed the largest difference in activation between the distractors and triggers conditions. sLORETA activation in this time window was then averaged to be compared across condition and group.
Results:
In misophonic participants, the mean activation to misophonic triggers in the prefrontal ROIs was higher (in arbitrary units, mean = 22.7, SD = 7.12) than the mean activation to distractors that were not triggers (mean = 17.6, SD = 4.16). The two matched controls did not show any notable difference in mean activation to the misophonic triggers (mean = 12.4, SD = 3.52) versus the non-misophonic distractors (mean = 16.1, SD = 1.30).
Conclusions:
These findings add support for the involvement of the prefrontal regions in the neural basis of misophonia. While the orbitofrontal cortex has been posited to relate to a failure of emotional reappraisal (Cerliani & Rouw, 2020), the left inferior frontal gyrus has yet to be linked to misophonia (Neacsiu et al., 2022). The left IFG has been linked to interpersonal emotion regulation, which may be relevant to the social aspect of being distressed by sounds made by others (Grecucci et al., 2013).
Disorders of the Nervous System:
Psychiatric (eg. Depression, Anxiety, Schizophrenia) 1
Emotion, Motivation and Social Neuroscience:
Emotion and Motivation Other
Novel Imaging Acquisition Methods:
MEG 2
Perception, Attention and Motor Behavior:
Attention: Auditory/Tactile/Motor
Keywords:
Affective Disorders
DISORDERS
Hearing
MEG
Psychiatric Disorders
Source Localization
Systems
1|2Indicates the priority used for review
Provide references using author date format
Grecucci, A.(2013). Reappraising social emotions: The role of inferior frontal gyrus, temporo-parietal junction and insula in interpersonal emotion regulation. Frontiers in Human Neuroscience, 7(SEP), 52765.
Kumar, S. (2017). The Brain Basis for Misophonia. Current Biology, 27(4), 527–533.
Neacsiu, A. D. (2022). The neurobiology of misophonia and implications for novel, neuroscience-driven interventions. Frontiers in Neuroscience, 16(July), 1–23.
Schröder, A. (2019). Misophonia is associated with altered brain activity in the auditory cortex and salience network. Scientific Reports, 9(1).
Vitoratou, S. (2021). Listening to People with Misophonia: Exploring the Multiple Dimensions of Sound Intolerance Using a New Psychometric Tool, the S-Five, in a Large Sample of Individuals Identifying with the Condition. Psych 2021, Vol. 3, Pages 639-662, 3(4), 639–662.