Authors: Namitha Jain¹, Shagun Ajmera¹, Gibbeum Kim¹, Howard Berenbaum¹, Fatima Husain¹
¹University of Illinois Urbana-Champaign
Background: Humans are naturally sensitive to emotionally salient sounds, such as screams which signal danger—a response rooted in survival. In individuals with misophonia, however, this sensitivity extends to innocuous sounds, such as chewing or slurping, which trigger intense aversive reactions. Misophonia also shares clinical features with hyperacusis, a condition characterized by heightened sensitivity to sound intensity, making the two difficult to distinguish. The present study examines brain activation patterns in each condition to identify both shared and distinct neural mechanisms.
Method: We recruited 90 participants aged 18–25 and assigned them to four groups based on structured clinical interviews and validated questionnaire scores: misophonia (M), hyperacusis (H), comorbid hyperacusis and misophonia (MH), and controls (C). Participants completed an fMRI task while listening to 90 emotionally-valenced sounds (International Affective Digitized Sounds-2 database) and categorized each as Unpleasant (U), Neutral (N), or Pleasant (P).
Results: Behavioral results showed that the MH group rated more sounds as U than the C and M groups, and fewer as P than the C group. Reaction times did not differ significantly across groups. fMRI data were preprocessed, and first-level contrasts (U>N and P>N) were computed in SPM12. At the group level, the MH group showed greater activation than the C group in the left secondary visual and visual association areas (U>N condition). The MH group exhibited increased activation in the right inferior frontal gyrus relative to the H group (P>N condition). All findings were cluster-level FWE corrected at p<0.05. These results are preliminary, and analyses are ongoing.
Conclusion: Individuals with comorbid misophonia and hyperacusis perceive a broader range of sounds as unpleasant and exhibit increased activity in visual and attentional networks. This heightened sensory-emotional reactivity may reflect a distinct neural profile associated with comorbidity.
