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帕金森病中的步态运动迟缓:控制步态协同作用的运动程序的改变。

Gait bradykinesia in Parkinson's disease: a change in the motor program which controls the synergy of gait.

作者信息

Warabi Tateo, Furuyama Hiroyasu, Sugai Eri, Kato Masamichi, Yanagisawa Nobuo

机构信息

Clinical Brain Research Laboratory, Department of Neurology, Sapporo Yamanoue Hospital, Toyokura Memorial Hall, Yamanote 6-9-1-1, Nishi-ku, Sapporo, Hokkaido, 063-0006, Japan.

Department of Neurology, School of Medicine, Shinshu University, Matsumoto, Japan.

出版信息

Exp Brain Res. 2018 Jan;236(1):43-57. doi: 10.1007/s00221-017-5106-1. Epub 2017 Oct 27.

Abstract

This study examined how gait bradykinesia is changed by the motor programming in Parkinson's disease. Thirty-five idiopathic Parkinson's disease patients and nine age-matched healthy subjects participated in this study. After the patients fixated on a visual-fixation target (conditioning-stimulus), the voluntary-gait was triggered by a visual on-stimulus. While the subject walked on a level floor, soleus, tibialis anterior EMG latencies, and the y-axis-vector of the sole-floor reaction force were examined. Three paradigms were used to distinguish between the off-/on-latencies. The gap-task: the visual-fixation target was turned off; 200 ms before the on-stimulus was engaged (resulting in a 200 ms-gap). EMG latency was not influenced by the visual-fixation target. The overlap-task: the on-stimulus was turned on during the visual-fixation target presentation (200 ms-overlap). The no-gap-task: the fixation target was turned off and the on-stimulus was turned on simultaneously. The onset of EMG pause following the tonic soleus EMG was defined as the off-latency of posture (termination). The onset of the tibialis anterior EMG burst was defined as the on-latency of gait (initiation). In the gap-task, the on-latency was unchanged in all of the subjects. In Parkinson's disease, the visual-fixation target prolonged both the off-/on-latencies in the overlap-task. In all tasks, the off-latency was prolonged and the off-/on-latencies were unsynchronized, which changed the synergic movement to a slow, short-step-gait. The synergy of gait was regulated by two independent sensory-motor programs of the off- and on-latency levels. In Parkinson's disease, the delayed gait initiation was due to the difficulty in terminating the sensory-motor program which controls the subject's fixation. The dynamic gait bradykinesia was involved in the difficulty (long off-latency) in terminating the motor program of the prior posture/movement.

摘要

本研究探讨了帕金森病中运动编程如何改变步态迟缓。35例特发性帕金森病患者和9例年龄匹配的健康受试者参与了本研究。在患者注视视觉固定目标(条件刺激)后,视觉开启刺激触发自主步态。当受试者在水平地面行走时,检测比目鱼肌、胫前肌肌电图潜伏期以及足底与地面反作用力的y轴矢量。使用三种范式来区分关/开潜伏期。间隙任务:视觉固定目标关闭;在开启刺激开始前200毫秒(产生200毫秒间隙)。肌电图潜伏期不受视觉固定目标影响。重叠任务:在视觉固定目标呈现期间开启刺激(200毫秒重叠)。无间隙任务:固定目标关闭且开启刺激同时开启。比目鱼肌强直性肌电图后肌电图暂停的开始被定义为姿势(终止)的关潜伏期。胫前肌肌电图爆发的开始被定义为步态(启动)的开潜伏期。在间隙任务中,所有受试者的开潜伏期均未改变。在帕金森病中,视觉固定目标在重叠任务中延长了关/开潜伏期。在所有任务中,关潜伏期延长且关/开潜伏期不同步,这将协同运动改变为缓慢、短步幅步态。步态的协同作用由关和开潜伏期水平的两个独立感觉运动程序调节。在帕金森病中,步态启动延迟是由于终止控制受试者注视的感觉运动程序存在困难。动态步态迟缓与终止先前姿势/运动的运动程序困难(关潜伏期长)有关。

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