Devos D, Defebvre L
Department of Neurology and Movement Disorders, EA2683, IFR114, CHRU of Lille, Lille, France.
Prog Brain Res. 2006;159:331-49. doi: 10.1016/S0079-6123(06)59022-3.
In 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.
在帕金森病（PD）早期，与对照受试者相比，运动准备受损与μ节律事件相关去同步化（ERD）潜伏期缩短有关，提示对侧初级感觉运动（PSM）皮层激活不足。运动后，在同一区域观察到β节律事件相关同步化（ERS）幅度降低，认为与皮层失活受损有关。通过监测ERD/ERS，我们旨在（i）将在病情较轻的帕金森综合征中所做的观察扩展到晚期PD，以及（ii）测试急性左旋多巴、苍白球内侧部或丘脑底核刺激对这些异常的影响。对于临床评估，丘脑底核刺激和急性左旋多巴给药后，统一帕金森病评定量表（UPDRS）运动评分下降约60%，苍白球内侧部刺激后下降40%。在丘脑底核刺激和左旋多巴作用下，观察到以下同时发生的ERD/ERS变化：运动准备期间对侧中央区域μ ERD潜伏期显著增加；运动执行期间双侧中央区域μ ERD增加；运动后双侧额中央区域μ ERD潜伏期缩短，对侧中央区域β ERS增加。相反，苍白球内侧部刺激下μ ERD潜伏期未改善。μ和β节律参数的变化似乎与运动迟缓呈负相关。与早期相比，晚期PD中μ节律ERD潜伏期和β ERS幅度进一步降低，提示随着疾病进展，皮层激活/失活受损更严重，而治疗后临床改善与之相关的部分恢复。因此，似乎左旋多巴和深部脑刺激部分恢复了PD中皮层振荡活动的正常模式，可能是通过减少静息时的低频超同步化。这种机制可能在基底神经节水平参与了运动控制中涉及的感觉运动整合。
