Decreased tolerance in response to specific every-day sounds (misophonia) is a serious, debilitating disorder that is gaining rapid recognition within the mental health community. Emerging research findings suggest that misophonia may have a unique neural signature. Specifically, when examining responses to misophonic trigger sounds, differences emerge at a physiological and neural level from potentially overlapping psychopathologies. While these findings are preliminary and in need of replication, they support the hypothesis that misophonia is a unique disorder. In this theoretical paper, we begin by reviewing the candidate networks that may be at play in this complex disorder (e.g., regulatory, sensory, and auditory). We then summarize current neuroimaging findings in misophonia and present areas of overlap and divergence from other mental health disorders that are hypothesized to co-occur with misophonia (e.g., obsessive compulsive disorder). Future studies needed to further our understanding of the neuroscience of misophonia will also be discussed. Next, we introduce the potential of neurostimulation as a tool to treat neural dysfunction in misophonia. We describe how neurostimulation research has led to novel interventions in psychiatric disorders, targeting regions that may also be relevant to misophonia. The paper is concluded by presenting several options for how neurostimulation interventions for misophonia could be crafted.

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Background: Misophonia is the inability to tolerate certain aversive, repetitive common sounds. Methods: Using a within-subjects experimental design, twenty-nine participants with misophonia and thirty clinical controls with high emotion dysregulation received inhibitory neurostimulation (1Hz) over a personalized medial prefrontal cortex (mPFC) target functionally connected to the left insula; excitatory neurostimulation (10Hz) over a personalized dorsolateral PFC (dlPFC) target; and sham stimulation over either target. Stimulations were applied while participants were either listening or cognitively downregulating emotions associated with personalized aversive, misophonic, or neutral sounds. Subjective units of distress (SUDS) and psychophysiological measurements (skin conductance response[SCR] and level [SCL], and high-frequency heart rate variability [HF-HRV]) were collected. Results: Compared to controls, participants with misophonia reported higher distress (delta_SUDS = 1.91-1.93, ps <.001) when listening to and when downregulating misophonic distress, although no psychophysiological differences were found. Both types of neurostimulation reduced distress significantly more than sham, with excitatory rTMS providing the most benefit (Cohen d_SUDS= 0.53; d_SCL= 0.14). Excitatory rTMS also enhanced the regulation of emotions associated with misophonic sounds in both groups when measured by SUDS (d_control= 1.28; d_Misophonia= 0.94), and in the misophonia group alone when measured with SCL (d= 0.20). Both types of neurostimulation were well tolerated and feasible to administer. Discussion: Clinical controls and misophonic participants were different in their self-report but not in psychophysiological measures of distress and regulations. Participants reported the lowest misophonic distress when engaging in cognitive restructuring enhanced with high-frequency neurostimulation, a finding that offers insight into the best path forward for misophonia interventions.