• D Devos and L Defebvre.
• Department of Neurology and Movement Disorders, EA2683, IFR114, CHRU of Lille, Lille, France. d-devos@chru-lille.fr
• Prog. Brain Res. 2006 Jan 1;159:331-49.

AbstractIn the early stages of Parkinson's disease (PD), impaired motor preparation has been related to a decrease in the latency of mu rhythm event-related desynchronisation (ERD) compared with control subjects, suggesting hypo activation of the contralateral, primary sensorimotor (PSM) cortex. Following movement, a decrease in amplitude of beta rhythm ERS was observed over the same region and thought to be related to impairment in cortical deactivation. By monitoring ERD/ERS, we aimed (i) to extend to advanced PD the observations made in less-advanced parkinsonism and (ii) to test the effect of acute L-Dopa, internal pallidal or subthalamic stimulation on these abnormalities. For the clinical evaluation the motor score of UPDRS decreased by about 60% under subthalamic stimulation and following acute L-Dopa administration and by 40% under internal pallidal stimulation. The following concurrent ERD/ERS changes under subthalamic stimulation and L-Dopa were observed: a marked increase in mu ERD latency during movement preparation over contralateral central region; an increase in mu ERD during movement execution over bilateral central regions; a decrease in mu ERD latency over bilateral frontocentral region and an increase in beta ERS over contralateral central region after movement. On the contrary, mu ERD latency was not improved under internal pallidal stimulation. Changes of mu and beta rhythm parameters seemed to be inversely correlated with bradykinesia. Mu rhythm ERD latency and the beta ERS amplitude further decreased in advanced PD compared with early stages, suggesting greater impairment of cortical activation/deactivation as the disease progresses and a partial restoration in relation to clinical improvement under treatments. Consequently, it appears that L-Dopa and deep brain stimulation partially restored the normal patterns of cortical oscillatory activity in PD, possibly by decreasing the low frequency hyper synchronisation at rest. This mechanism could be involved at the basal ganglia level in the sensorimotor integration implicated in the movement control.

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