Zhuang Ping, Li Yongjie, Hallett Mark
Beijing Institute of Functional Neurosurgery, Xuanwu Hospital, Capital University of Medical Sciences, Beijing 100053, China.
Clin Neurophysiol. 2004 Nov;115(11):2542-57. doi: 10.1016/j.clinph.2004.06.006.
To explore the role of abnormal neuronal activity in the basal ganglia and thalamus in the generation of dystonia.
Microelectrode recording was performed in the globus pallidus internus (GPi), ventral thalamic nuclear group ventral oral posterior/ventral intermediate, Vop/Vim) and subthalamic nucleus (STN) in patients with primary dystonia (n=11) or secondary dystonia (n=9) during surgery. Electromyogram (EMG) was simultaneously recorded in selected muscle groups. Single unit analysis and cross-correlations were carried out.
Three hundred and sixty-seven neurons were obtained from 29 trajectories (GPi: 13; Vop/Vim: 12; STN: 4), 87% exhibited altered neuronal activity including grouped discharges in GPi (n=79) and STN (n=37), long-lasting neuronal activity (n=70) and rapid neuronal discharge (n=86) in Vop/Vim. There were neurons in Vop, GPi and STN firing at the same frequency as EMG during dystonia (mean: 0.39 Hz, range 0.12-0.84 Hz). Significant correlations between neuronal activity and EMG at the frequency of dystonia were obtained (GPi: r2=0.7 (n=31), Vop/Vim: r2=0.64 (n=18) and STN: r2=0.86 (n=17)).
Consistent with previous findings of abnormalities observed in Vop/VIM and GPi in relation to dystonia, the present data further show that the altered activity in GPi, specifically in dorsal subregions of GPi, Vop/Vim and STN is likely to be directly involved in the production of dystonic movement. Dystonia-related neuronal activity observed in motor thalamus and basal ganglia nuclei of GPi and STN indicates a critical role of their interactions affecting both indirect and direct pathways in the development of either generalized or focal dystonia.
These data support a central role of the basal ganglia in producing dystonic movements.
探讨基底神经节和丘脑异常神经元活动在肌张力障碍发生中的作用。
在手术过程中，对11例原发性肌张力障碍患者和9例继发性肌张力障碍患者的内侧苍白球（GPi）、丘脑腹侧核群腹嘴后核/腹中间核（Vop/Vim）和丘脑底核（STN）进行微电极记录。同时在选定的肌肉群记录肌电图（EMG）。进行单单位分析和互相关分析。
从29条轨迹中获取了367个神经元（GPi：13个；Vop/Vim：12个；STN：4个），87%的神经元表现出神经元活动改变，包括GPi（n = 79）和STN（n = 37）中的成组放电、Vop/Vim中的持续神经元活动（n = 70）和快速神经元放电（n = 86）。在肌张力障碍期间，Vop、GPi和STN中有神经元与EMG以相同频率放电（平均：0.39 Hz，范围0.12 - 0.84 Hz）。在肌张力障碍频率下，获得了神经元活动与EMG之间的显著相关性（GPi：r2 = 0.7（n = 31），Vop/Vim：r2 = 0.64（n = 18），STN：r2 = 0.86（n = 17））。
与先前关于Vop/VIM和GPi中与肌张力障碍相关的异常发现一致，目前的数据进一步表明，GPi中特别是GPi背侧亚区、Vop/Vim和STN中改变的活动可能直接参与肌张力障碍性运动的产生。在运动丘脑以及GPi和STN的基底神经节核中观察到的与肌张力障碍相关的神经元活动表明，它们之间的相互作用在全身性或局灶性肌张力障碍的发展中对间接和直接通路均发挥关键作用。
这些数据支持基底神经节在产生肌张力障碍性运动中起核心作用。
