Devos D, Labyt E, Cassim F, Bourriez J L, Reyns N, Touzet G, Blond S, Guieu J D, Derambure P, Destée A, Defebvre L
Department of Neurology, EA2683, Lille University Medical Centre, France.
Eur J Neurosci. 2003 Oct;18(7):1884-8. doi: 10.1046/j.1460-9568.2003.02925.x.
In Parkinson's disease, poor motor performance (resulting primarily from abnormal cortical activation during movement preparation and execution) may also be due to impaired sensorimotor integration and defective cortical activity termination of the ongoing movement, thus delaying preparation of the following one. Reduced movement-related synchronization of the beta rhythm in Parkinson's disease compared to controls has been put forward as evidence for impaired postmovement cortical deactivation. We assessed the effects of subthalamic deep brain stimulation and l-dopa on beta rhythm synchronization over the premotor and primary sensorimotor cortex. Ten advanced patients performed self-paced wrist flexion in four conditions according to the presence or not of stimulation and l-dopa. Compared to without treatment, the motor score improved by approximately 60%; the beta synchronization was present over the contralateral frontocentral region and increased significantly over the contralateral central region under stimulation and under l-dopa, with a maximal effect when both treatments were associated. Our advanced patients displayed very focused and attenuated beta rhythm synchronization which, under stimulation, increased over the contralateral premotor and primary sensorimotor cortex. Stimulation and l-dopa both partly restored postmovement cortical deactivation in advanced Parkinson's disease, although the respective mechanisms probably differ. They may improve bradykinesia and cortical deactivation by reestablishing movement-related somatosensory processing at the end of the movement through the basal ganglia into the cortex.
在帕金森病中，运动表现不佳（主要源于运动准备和执行过程中异常的皮质激活）也可能是由于感觉运动整合受损以及正在进行的运动的皮质活动终止存在缺陷，从而延迟了下一个运动的准备。与对照组相比，帕金森病患者β节律与运动相关的同步性降低，这被认为是运动后皮质失活受损的证据。我们评估了丘脑底核深部脑刺激和左旋多巴对运动前区和初级感觉运动皮质β节律同步性的影响。10名晚期患者根据是否存在刺激和左旋多巴，在四种情况下进行了自主节奏的腕部屈曲。与未治疗相比，运动评分提高了约60%；在刺激和左旋多巴作用下，对侧额中央区出现β同步化，对侧中央区β同步化显著增加，两种治疗联合时效果最大。我们的晚期患者表现出非常集中且减弱的β节律同步化，在刺激下，对侧运动前区和初级感觉运动皮质的β节律同步化增加。刺激和左旋多巴都部分恢复了晚期帕金森病患者运动后的皮质失活，尽管各自的机制可能不同。它们可能通过在运动结束时通过基底神经节重新建立与运动相关的体感处理并传入皮质，来改善运动迟缓及皮质失活。
