Cassim François, Labyt Etienne, Devos David, Defebvre Luc, Destée Alain, Derambure Philippe
Service de Neurophysiologie clinique, Hôpital Roger-Salengro, CHRU de Lille, 59037 Lille Cedex, France.
Epileptic Disord. 2002 Dec;4 Suppl 3:S31-45.
The functions of oscillations within the basal ganglia are poorly understood. We discuss in the present paper, the possible physiological or pathological roles of oscillatory activities within the basal ganglia, and their relationship to cortical oscillations. Three aspects are presented: 1. What do we know from animal studies? 2. What do we know from neurophysiological studies in parkinsonian patients? 3. What is the effect of L-dopa treatment and electrical stimulation within basal ganglia circuits on cortical oscillations? Animal studies suggest that neuronal oscillations are spontaneously generated within the basal ganglia system, especially from the GPE and the subthalamic nucleus (STN), but are mainly synchronized by cortical activity via the striatal inputs. Dopamine depletion results in a global increase of oscillations within the whole basal ganglia system, particularly in the GP-NST network. Oscillations within the basal ganglia may, in part, be related to tremor since they are enhanced, especially in the globus pallidus internus (GPI) and the STN, in human and animal dopaminergic depletion. However, they also play a role in the physiology of movement as revealed by coherence analysis between cortex, muscles and GPI/STN in parkinsonian patients undergoing deep brain stimulation. It is known that the basal ganglia may influence cortico-muscular oscillations such as the Piper rhythm and other rhythms in the beta band. In off-drug parkinsonian patients, low frequency oscillations (4-10 Hz) are favoured, presumably resulting in bradykinesia and low force. When medically (Ldopa) or surgically (deep brain stimulation) treated, these low frequency oscillations are replaced by high frequency (70 Hz) oscillations that are important for motor programs to be correctly executed. Studies of cortical reactivity related to planning of voluntary movement in parkinsonian patients provide evidence that it is possible to influence cortical reactivity through the basal ganglia system.
基底神经节内振荡的功能目前还知之甚少。在本文中,我们讨论了基底神经节内振荡活动可能的生理或病理作用,以及它们与皮层振荡的关系。文章主要从三个方面进行阐述:1. 我们从动物研究中了解到了什么?2. 我们从帕金森病患者的神经生理学研究中了解到了什么?3. 基底神经节回路中的左旋多巴治疗和电刺激对皮层振荡有什么影响?动物研究表明,神经元振荡在基底神经节系统内自发产生,尤其是从外侧苍白球(GPE)和丘脑底核(STN),但主要通过纹状体输入由皮层活动同步。多巴胺耗竭导致整个基底神经节系统内振荡的整体增加,特别是在苍白球 - 丘脑底核网络中。基底神经节内的振荡可能部分与震颤有关,因为在人类和动物多巴胺能耗竭时,它们会增强,尤其是在内侧苍白球(GPI)和STN中。然而,正如在接受深部脑刺激的帕金森病患者中,通过皮层、肌肉和GPI/STN之间的相干分析所揭示的那样,它们在运动生理学中也发挥着作用。已知基底神经节可能会影响皮层 - 肌肉振荡,如派珀节律和β波段中的其他节律。在未服药的帕金森病患者中,低频振荡(4 - 10Hz)占优势,这可能导致运动迟缓及力量不足。在接受药物(左旋多巴)或手术(深部脑刺激)治疗后,这些低频振荡会被高频(70Hz)振荡所取代,而高频振荡对于正确执行运动程序很重要。对帕金森病患者与自主运动计划相关的皮层反应性的研究表明,有可能通过基底神经节系统影响皮层反应性。