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(Kumar et al., 2021) proposed that misophonia has a primarily motor basis, centered on hyperactivity within orofacial mirror neurons in the ventral premotor cortex (PMv). In this model, triggering sounds, particularly oral/nasal sounds such as chewing, activate mirror neurons that simulate the observed action, producing an aversive response. The critical neural abnormality lies in increased resting-state connectivity between auditory cortex (planum temporale) and orofacial PMv. Non-orofacial triggers are not considered independently represented; instead, they are theorized to arise secondarily through associative learning once the orofacial trigger system is established. Thus, the model is relatively specific: misophonia is driven by aberrant mirroring of mouth-related actions.

In contrast, Hansen et al. (2022) argue for a broader sensorimotor-insular connectivity model. While they replicate increased connectivity involving PMv, they demonstrate that the effect is not confined to this mirror-neuron region but extends across primary motor (M1), primary somatosensory (S1), and dorsal premotor cortex (PMd). Moreover, they show that finger-related motor and somatosensory regions exhibit differential insula connectivity in individuals with higher misophonia scores. This finding suggests that non-orofacial triggers (e.g., finger-tapping, typing) may have direct neural representations rather than being acquired through associative learning. Instead of a narrowly defined orofacial mirror dysfunction, Hansen’s model proposes a distributed sensorimotor network interacting with the insula, implicating broader action–sound representations in misophonia. (Hansen et al., 2022)