Pathophysiology of dystonia: Through the lens of Mark Hallett.

Dystonia was originally framed as a basal ganglia disorder, yet the mechanisms linking abnormal basal ganglia output to its defining clinical features have remained uncertain. Over four decades, Mark Hallett approached this problem by posing deceptively simple mechanistic questions and addressing them through careful physiological investigation, progressively reshaping the conceptual understanding of dystonia. Across these investigations, the concept of dystonia evolved from abnormalities of muscle activation toward broader concepts of motor control and network dysfunction. Emerging evidence suggested that dystonia reflects abnormal regulation within distributed sensorimotor networks, where impaired inhibition, abnormal premotor influences, altered sensory modulation, and dysregulated plasticity interact across cortical and subcortical circuits. In this framework, dystonia is not simply excessive movement, but a failure of the mechanisms that normally refine and shape motor behaviour. At the same time, Hallett consistently emphasized the heterogeneity of dystonia and cautioned against overgeneralization. By considering individual dystonic entities on their own terms, his work provides more than a catalogue of physiological findings: it offers a coherent framework for understanding how abnormal physiological processes may become acquired and stabilized within motor networks. The persistence of dystonia despite diverse treatments suggests that the decisive factor may lie not in outward phenomenology, but in the durability of network modification itself. Understanding how such pathological motor memories are maintained-and how they might be safely reversed-remains central to future therapeutic progress.