On clinical, pathophysiological and neuroanatomical grounds, altered motor recoding might be anticipated to underlie impaired emotional and social signal processing in the frontotemporal dementias (FTD). This diverse group of neurodegenerative diseases manifests as three canonical clinico-anatomical syndromes16; behavioural variant (bvFTD), semantic variant primary progressive aphasia (svPPA) and nonfluent variant primary progressive aphasia (nfvPPA). These broad syndromic groupings encompass various sub-syndromes: in particular, within the heterogeneous bvFTD syndrome at least two major variants can be defined, based on the relative selectivity of right temporal lobe atrophy17,18. Deficits in emotion recognition, empathy and social understanding and behaviour are defining features of bvFTD but integral to all FTD syndromes19–24 and collectively engender substantial distress and care burden25. Impaired facial emotion recognition in bvFTD, svPPA and nfvPPA has been linked to atrophy of an overlapping network of cerebral regions including orbitofrontal cortex, posterior insula and antero-medial temporal lobe23,26, implicated in evaluation of facial emotional expressions and integration with bodily signals27–29. Moreover, various abnormalities of physiological reactivity have been documented in FTD, including changes in resting skin conductance and heart rate variability in bvFTD and altered homeostatic and affective autonomic responses in bvFTD, svPPA and nfvPPA30–36. Patients with bvFTD have been noted to have reduced facial expressivity37 and indeed, deficient volitional imitation of emotional faces38. However, whereas impaired facial EMG reactivity to facial expressions has been linked to emotion processing deficits in Parkinson’s disease39,40, Huntington’s disease41 and schizophrenia42, the motor physiology of emotional reactivity has not been addressed in the FTD spectrum.