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刺激苍白球内侧部是否通过激活抑制性轴突来控制运动障碍?

Does stimulation of the GPi control dyskinesia by activating inhibitory axons?

作者信息

Wu Y R, Levy R, Ashby P, Tasker R R, Dostrovsky J O

机构信息

Second Department of Neurology, Chang-Gung Memorial Hospital, Taipei, Taiwan.

出版信息

Mov Disord. 2001 Mar;16(2):208-16. doi: 10.1002/mds.1046.

DOI:10.1002/mds.1046
PMID:11295772
Abstract

A 69-year-old woman with Parkinson's disease and levodopa-induced dyskinesias had a deep brain stimulation (DBS) electrode inserted into the right globus pallidus internus (GPi). During the operation, the GPi was mapped with dual microelectrode recordings. Stimulation through one microelectrode in GPi inhibited the firing of GPi neurons recorded with another microelectrode 600--1,000 microm distant. The inhibition could be obtained with pulse widths of 150 micros and intensities as low as 10 microA. Single stimuli inhibited GPi neurons for approximately 50 ms. Trains of 300 Hz stimuli inhibited GPi neuron firing almost completely. Postoperatively, stimulation through macroelectrode contacts located in the posterior ventral pallidum controlled the patient's dyskinesias. The effect could be obtained with pulse widths of 50 micros and frequencies as low as 70--80 Hz. We postulate stimulation of the ventral pallidum controls dyskinesias by activating large axons which inhibit GPi neurons.

摘要

一名患有帕金森病和左旋多巴诱导的异动症的69岁女性,将深部脑刺激(DBS)电极插入右侧内侧苍白球(GPi)。手术过程中,通过双微电极记录对GPi进行了图谱绘制。通过GPi中的一个微电极进行刺激,抑制了距离600 - 1000微米远的另一个微电极记录的GPi神经元的放电。使用150微秒的脉冲宽度和低至10微安的强度即可获得这种抑制作用。单个刺激抑制GPi神经元约50毫秒。300赫兹刺激序列几乎完全抑制了GPi神经元的放电。术后,通过位于苍白球腹后部的宏电极触点进行刺激,控制了患者的异动症。使用50微秒的脉冲宽度和低至70 - 80赫兹的频率即可获得这种效果。我们推测,刺激苍白球腹侧通过激活抑制GPi神经元的大轴突来控制异动症。

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