Sensory, Motor and Intrinsic Mechanisms of Thalamic Activity related to Organic and Psychogenic Dystonia.

K Kobayashi, J H Chien, J H Kim, F A Lenz
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引用次数: 6

Abstract

The thalamus is a critical module in the circuit which has been associated with movement disorders including dystonia. This circuit extends from cortex to striatum to pallidum to the thalamic nucleus Ventral Lateral anterior (VLa) to cortex and can be studied by activity recorded during thalamic stereotactic surgery for the treatment of dystonia. Neuronal recordings in the VLa nucleus show low frequency modulation of firing that is correlated with and leads the low frequency modulation of EMG activity; this EMG activity is characteristic of dystonia. Immediately posterior is the Ventral Lateral posterior (VLp) nucleus which, in controls (patients with tremor or chronic pain), is characterized by deep sensory cells which fire at short latency in response to movement of a single joint or to stimulation of deep structures, such as muscles, tendons and joints. In patients with dystonia, neurons with this sensory activity are much more common than in controls and single neurons often respond to movement of multiple joints. In controls operated for the treatment of tremor or chronic pain many neurons in both nuclei are activated during active or involuntary joint movements, such as tremor or dystonia. The active joint movement related to the firing of a cell is usually in the opposite direction to the passive joint movement which causes that cell to fire. This linkage of active or involuntary and passive joint movement is unfocussed in dystonia. The involuntary dystonic joint movement best correlated with firing of a neuron may not activate the neuron when it occurs as a passive movement, while multiple other passive movements will activate the neuron. These linkages may explain the overflow of isolated voluntary activity to multiple other muscles that is seen in dystonia. The activity of either nucleus may have a critical role in dystonia since their disruption by stimulation or lesioning can decrease dystonia.

与器质性和心因性肌张力障碍相关的丘脑活动的感觉、运动和内在机制。
丘脑是神经回路中的一个关键模块,它与包括肌张力障碍在内的运动障碍有关。这个回路从皮层延伸到纹状体,到白球,再到丘脑核腹侧前外侧(VLa)到皮层,可以通过在治疗肌张力障碍的丘脑立体定向手术中记录的活动来研究。VLa核的神经元记录显示放电的低频调制与EMG活动的低频调制相关并导致EMG活动的低频调制;这种肌电图活动是肌张力障碍的特征。紧靠后方的是腹侧外侧后核(VLp),在对照(震颤或慢性疼痛患者)中,其特征是深层感觉细胞在短潜伏期内对单个关节的运动或对深层结构(如肌肉、肌腱和关节)的刺激作出反应。在肌张力障碍患者中,具有这种感觉活动的神经元比对照组常见得多,单个神经元通常对多个关节的运动做出反应。在治疗震颤或慢性疼痛的对照中,两个核中的许多神经元在主动或不自主的关节运动中被激活,如震颤或肌张力障碍。与细胞放电相关的主动关节运动通常与导致细胞放电的被动关节运动方向相反。这种主动或不自主和被动关节运动的联系在肌张力障碍中不集中。与神经元放电最相关的不自主张力障碍关节运动,当它作为被动运动发生时,可能不会激活神经元,而多个其他被动运动将激活神经元。这些联系可以解释肌张力障碍中孤立的随意活动向其他多个肌肉的溢出。任何一个核的活动都可能在肌张力障碍中起关键作用,因为刺激或损伤破坏它们可以减轻肌张力障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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