Is executive control used to compensate for involuntary movements in levodopa-induced dyskinesia?

摘要

Levodopa (L-dopa)-induced dyskinesia (LID) emerge in the majority of PD patients after long-term L-dopa treatment. LID most often coincide with the maximal antiparkinsonian effect of L-dopa ("peak dose or ondyskinesias") and are mainly choreiform in nature. Though the precise mechanism responsible for the development of LID is still unclear, the pathophysiology apparently involves a change in the firing patterns that signal between the basal ganglia and the cortex, leading to overactivation of motor frontal areas. Two recent neuroimaging studies published in this journal provide new information about the relationship between cortical function and LID.