From a clinical perspective, this work suggests a pathophysiological framework for deconstructing the complex social and emotional symptoms that characterise FTD syndromes. Such symptoms are difficult to measure using conventional neuropsychological tests, and may only be elicited by naturalistic social interactions: dynamic motor physiological surrogates might index both the affective dysfunction of patients’ daily lives and the underlying disintegration of culprit neural networks38. These physiological metrics might facilitate early disease detection and tracking over a wider spectrum of severity than is currently possible and enable socio-emotional assessment in challenging clinical settings (such as aphasia), especially since our results suggest that (in contrast to explicit emotion recognition) automatic motor reactivity may be relatively insensitive to semantic deficits. Our findings further suggest that such metrics are not simply ciphers of reduced cognitive capacity but may help stratify broad disease groupings (such as the heterogeneous bvFTD syndrome) and at the same time, may capture mechanisms that transcend traditional syndromic boundaries. We therefore propose that the paradigm of emotional sensorimotor reactivity may yield a fresh perspective on FTD nosology and candidate novel biomarkers of FTD syndromes. Looking forward, this paradigm suggests a potential strategy for biofeedback-based retraining of emotional responsiveness, perhaps in conjunction with disease-modifying therapies79.