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身体姿势稳定时小脑的分区功能。

Compartmentalized cerebellar functions upon the stabilization of body posture.

作者信息

Dichgans J, Fetter M

机构信息

Neurologische Klinik, Universität Tübingen, Germany.

出版信息

Rev Neurol (Paris). 1993;149(11):654-64.

PMID:8091078
Abstract

This paper reviews the features and topodiagnostical meaning of pathological body posture in cerebellar disorders and presents knowledge as to the physiology and pathophysiology of postural disturbances attributed to the cerebellum. Lesions of the spinocerebellar (upper vermal and intermediate) part of the anterior lobe lead to spontaneous anterior-posterior body sway, with a frequency of about 3 Hz with mild or absent ataxia of the upper limbs, but prominent ataxia of the lower limbs. The tremor is provoked by eye closure and by body displacement. Increased gain and poor cerebellar control of the duration and gain of stabilizing reflexes may be the mechanisms of this oscillation. Lesions of the lower (vestibulocerebellar) vermis cause postural ataxia of the head and trunk while sitting, standing, and walking. Postural ataxia is omnidirectional, sometimes of excessive amplitude and contains frequency components below 1 Hz. Dysmetria of the upper and lower limbs is not prominent. Visual stabilization is less than in the other groups of cerebellar patients. Lesions of the cerebellar hemispheres alone, do not cause an increase of postural sway. Lesions of spinocerebellar afferents (Friedreich's disease) lead to a low frequency large amplitude lateral sway with the most of its power below 1.1 Hz. Visual stabilization is preserved. Latencies of early and late EMG responses to sudden displacements are normal in patients with cerebellar disorders. The cerebellum is, therefore, unlikely to be the primary generator of these reflexive responses. On the other hand, the temporal composition of the orderly time sequence of a complex motor program--be it a voluntary act or its postural balancing--is deranged in cerebellar lesions. It is hypothesized that the cerebellum helps to coordinate the timing not only within but also between the single components involved in each subunit of a complex movement in three-dimensional space and that is scales the size and duration of each muscular action. The cerebellum possibly specifies the cortical movement command and sends it back to the motor cortex. The basic structure of a motor program, however, does not seem to be generated within the cerebellum.

摘要

本文综述了小脑疾病中病理性身体姿势的特征和拓扑诊断意义,并介绍了小脑所致姿势障碍的生理学和病理生理学知识。前叶脊髓小脑(上蚓部和中间部)病变导致身体前后自发摆动,频率约为3Hz,上肢共济失调轻微或无,下肢共济失调明显。震颤由闭眼和身体移位诱发。稳定反射的增益增加以及小脑对其持续时间和增益的控制不佳可能是这种振荡的机制。下(前庭小脑)蚓部病变导致坐、站和行走时头部和躯干的姿势性共济失调。姿势性共济失调是全方位的,有时幅度过大,且包含低于1Hz的频率成分。上下肢辨距不良不明显。视觉稳定作用比其他小脑疾病患者小。单纯小脑半球病变不会导致姿势摆动增加。脊髓小脑传入纤维病变(弗里德赖希共济失调)导致低频大幅度侧向摆动,其大部分能量低于1.1Hz。视觉稳定作用保留。小脑疾病患者对突然移位的早期和晚期肌电图反应潜伏期正常。因此,小脑不太可能是这些反射反应的主要产生部位。另一方面,复杂运动程序(无论是随意动作还是其姿势平衡)有序时间序列的时间组成在小脑病变中会紊乱。据推测,小脑不仅有助于协调复杂运动三维空间中每个亚单位单个成分内部的时间,还能协调它们之间的时间,并且能调节每个肌肉动作的大小和持续时间。小脑可能会明确皮层运动指令并将其反馈回运动皮层。然而,运动程序的基本结构似乎不是在小脑中产生的。

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