Faist M, Xie J, Kurz D, Berger W, Maurer C, Pollak P, Lücking C H
Department of Clinical Neurology and Neurophysiology, University of Freiburg, Germany.
Brain. 2001 Aug;124(Pt 8):1590-600. doi: 10.1093/brain/124.8.1590.
The fundamental disturbance of the parkinsonian gait is the reduction in walking velocity. This is mainly due to reduction in stride length, while cadence (steps/min) is slightly enhanced. Treatment with L-dopa increases stride length while cadence is unchanged. Chronic stimulation of the thalamus has no effect on Parkinsonian gait. The efficacy of electrical stimulation of the subthalamic nucleus (STN) on gait in advanced Parkinson's disease has been clearly demonstrated clinically. The aim of the present study was to quantify the changes in gait measures induced by STN stimulation and L-dopa and to assess possible differential or additive effects. Eight Parkinson's disease patients (mean +/- SD age 48.1 +/- 7.3 years) with chronic bilateral STN stimulation (mean duration of disease 13.3 +/- 2.4 years, mean stimulation time 15.4 +/- 10.6 months) and 12 age-matched controls were investigated. Subjects walked on a special treadmill with a closed-loop ultrasound control system that used the subject's position to adjust treadmill speed continuously for the actual walking velocity. In an appropriate crossover design, spatiotemporal gait measures and leg joint angle movements were assessed for at least 120 stride cycles in four treatment conditions: with and without stimulation and with and without a suprathreshold dose of L-dopa. With STN stimulation, there were increases of almost threefold in mean walking velocity (from 0.35 to 0.96 m/s) and stride length (from 0.34 to 0.99 m). Cadence remained constant. The range of motion of the major leg joints also increased. L-Dopa alone had a slightly weaker effect, with an increase in walking velocity to 0.94 m/s and in stride length to 0.92 m at a similar cadence. These increased values were in the range of those for healthy age-matched subjects performing the same task. The combination of both treatments further increased the mean walking velocity to 1.19 m/s and stride length to 1.20 m at an unchanged cadence. However, not all patients receiving STN stimulation improved further when they also received L-dopa. These results demonstrate that chronic bilateral STN stimulation, like treatment with L-dopa, improves walking velocity by increasing stride length without changing cadence. STN stimulation almost exclusively affects mechanisms involved in the control of spatial gait measures rather than rhythmicity. The gait measures obtained with STN stimulation alone are in the range of control subjects.
帕金森步态的根本障碍是步行速度降低。这主要是由于步幅减小,而步频(步/分钟)略有增加。左旋多巴治疗可增加步幅,而步频不变。丘脑慢性刺激对帕金森步态无影响。临床已明确证实,丘脑底核(STN)电刺激对晚期帕金森病步态的疗效。本研究的目的是量化STN刺激和左旋多巴引起的步态测量变化,并评估可能的差异或叠加效应。研究了8例接受慢性双侧STN刺激的帕金森病患者(平均年龄±标准差48.1±7.3岁,平均病程13.3±2.4年,平均刺激时间15.4±10.6个月)和12例年龄匹配的对照组。受试者在配备闭环超声控制系统的特殊跑步机上行走,该系统利用受试者的位置根据实际步行速度连续调整跑步机速度。采用适当的交叉设计,在四种治疗条件下评估时空步态测量和腿部关节角度运动,每种条件下至少测量120个步幅周期:有刺激和无刺激,以及有和无超阈值剂量的左旋多巴。STN刺激时,平均步行速度(从0.35米/秒增至0.96米/秒)和步幅(从0.34米增至0.99米)几乎增加了三倍。步频保持不变。主要腿部关节的活动范围也增加了。单独使用左旋多巴的效果稍弱,在相似步频下,步行速度增至0.94米/秒,步幅增至0.92米。这些增加的值与执行相同任务的年龄匹配健康受试者的值范围相当。两种治疗方法联合使用可使平均步行速度在步频不变的情况下进一步增至1.19米/秒,步幅增至1.20米。然而,并非所有接受STN刺激的患者在同时接受左旋多巴治疗时都能进一步改善。这些结果表明,慢性双侧STN刺激与左旋多巴治疗一样,通过增加步幅而不改变步频来提高步行速度。STN刺激几乎只影响参与空间步态测量控制的机制,而非节律性。单独使用STN刺激获得的步态测量值在对照组受试者的范围内。