[Event-related desynchronization and Parkinson disease. Importance in the analysis of the phase of preparation for movement].
This study was aimed at determining the spatiotemporal distribution of event-related desynchronization (ERD) during self-paced voluntary movement in order to establish the interest of this method for the analysis of movement programming in Parkinson's disease. Desynchronization of mu rhythm was recorded 2 s before to 0.5 s after right then left self-paced voluntary wrist flexions from 11 leads covering the primary sensorimotor cortex (central), supplementary motor area (frontocentral) and parietal cortex (parietocentral). Recordings were obtained from ten control subjects, ten patients treated for Parkinson's disease (bilateral symptoms) and 20 patients presenting with right or left hemiparkinsonism before and after chronic administration of L-dopa. In the control group, ERD started over the contralateral primary sensorimotor cortex 1,750 ms before movement and was bilateral just before performance of the movement. In both treated and de novo Parkinson's disease groups, decrease in ERD latency (1,000 to 1,250 ms before movement) was only observed when movements were performed with the akinetic hand and corresponded to a decrease in motor cortical activity. This confirmed that programming of movement is affected in Parkinson's disease. Earlier ERD with central ipsilateral distribution were also observed, suggesting that other cortical areas might be activated to compensate for dysfunction of movement programming and to increase the level of cortical activity required for performance of the movement. The administration of L-dopa to de novo hemiparkinsonians patients resulted in increased ERD latency over contralateral and ipsilateral central areas. As in the treated Parkinson's disease group, frontocentral ERD could also be recorded. L-dopa would thus partially restore the affected motor programmation and modulate cortical activation in both supplementary motor area and primary motor cortex, the later receiving more afferences from basal ganglia.
Defebvre
L
L
Service de neurophysiologie clinique, CHRU de Lille, France.
Derambure
P
P
Bourriez
J L
JL
Destée
A
A
Guieu
J D
JD
D000978:Antiparkinson Agents / Q000627:therapeutic use; D016022:Case-Control Studies; D003344:Cortical Synchronization; D004569:Electroencephalography; D006801:Humans; D007980:Levodopa / Q000627:therapeutic use; D008875:Middle Aged; D009068:Movement / Q000502:physiology*; D010300:Parkinson Disease / Q000188:drug therapy / Q000503:physiopathology*; D014836:Volition / Q000502:physiology*
D000978:Antiparkinson Agents; D007980:Levodopa