O201 Interhemispheric processing in hyperkinetic movement disorders

Abstract

Objectives changes in interhemispheric connectivity have been recently studied in Huntington’s Disease (HD), although their significance and temporal relation with clinical features are still debated. We studied interhemispheric connectivity in healthy volunteers, early HD and in patients with idiopathic dystonia. Methods ipsilateral Silent Period (onset latency, iSPOL, and duration, iSPD) and Transcallosal Conduction Time (TCT) from the abductor pollicis brevis (APB) muscle were evaluated. In HD, we correlated TMS data with clinical (UHDRS-I, Disease Burden Index), genetic (CAG-length) and cognitive (UHDRS-II) scores. Results iSPD decreased in HD, paralleled by a significant lengthening of iSPOL and TCT (p Discussion Our results could have implications for the disruption of both sensorimotor integration and voluntary motor control in HD. Before voluntary movements, interhemispheric interactions are responsible for the temporary inhibition of ipsilateral primary motor cortex (M1) and the increased excitability of contralateral one. Concurrently, especially during non-dominant hand movements, enhanced interhemispheric inhibition from the ipsilateral hemisphere suppresses superfluous activation arising from the contralateral cortex. These mutual interactions may be lost in symptomatic HD, thus contributing to hyperkinesias. Significance This is the first study using TMS to assess interhemispheric connectivity in hyperkinetic movement disorders, possibly leading to a better knowledge of disease mechanisms.