Warabi Tateo, Furuyama Hiroyasu, Sugai Eri, Kato Masamichi, Yanagisawa Nobuo
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.
Exp Brain Res. 2018 Jan;236(1):43-57. doi: 10.1007/s00221-017-5106-1. Epub 2017 Oct 27.
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.
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。