Morris M, Iansek R, Matyas T, Summers J
Kingston Centre, Cheltenham, Australia.
Mov Disord. 1998 Jan;13(1):61-9. doi: 10.1002/mds.870130115.
The purpose of this investigation was to clarify abnormalities in the stride length-cadence relation in gait hypokinesia in Parkinson's disease (PD). A second aim was to investigate the effect of levodopa medication on the foot-step pattern. In the first experiment, 20 subjects with idiopathic PD and 20 age-, sex-, and height-matched controls performed a series of 10 m walking trials at cadence rates ranging from 40 steps/min to 180 steps/min. Cadence rates were set by an electronic metronome, and gait patterns were measured by using a footswitch stride-analyzer system. By instructing subjects to concentrate on walking in time to the metronome beat, the baseline stride length could be monitored for a range of velocities with the compensatory effects of cadence removed. Linear-regression analysis revealed that the mean slope for the regression of stride length against cadence was not different from normal in PD, although there was a statistically significant difference in mean intercept between the PD group (0.25) and the control group (0.59); [t (19) = -4.76; p = 0.0001]. The second experiment evaluated the effects of levodopa on stride-length regulation in 10 subjects with idiopathic PD on average 45 min before and after the first morning dose was administered. There was a statistically significant increase in stride length for all cadence rates from premedication to postmedication phases and the maximal stride length was achieved at higher cadence rates after medication. The slope of the regression of stride length against cadence did not alter according to medication status, although the mean intercept was significantly lower before levodopa (-0.06) compared with after levodopa (0.27); [t (9) = -3.83; p = 0.004]. These results suggest that defective scaling of stride length underlies gait disturbance in PD.
本研究的目的是阐明帕金森病（PD）步态运动减少中步幅长度与步频关系的异常。第二个目的是研究左旋多巴药物对脚步模式的影响。在第一个实验中，20名特发性PD患者和20名年龄、性别和身高匹配的对照组在步频从40步/分钟到180步/分钟的范围内进行了一系列10米的步行试验。步频由电子节拍器设定，步态模式通过脚踏开关步幅分析系统进行测量。通过指导受试者专注于跟随节拍器节拍行走，可以在去除步频的代偿作用的情况下，监测一系列速度下的基线步幅长度。线性回归分析显示，PD患者步幅长度与步频回归的平均斜率与正常情况无差异，尽管PD组（0.25）和对照组（0.59）的平均截距存在统计学显著差异；[t（19）=-4.76；p=0.0001]。第二个实验评估了左旋多巴对10名特发性PD患者步幅长度调节的影响，这些患者在首次晨服药物前后平均45分钟进行测量。从用药前阶段到用药后阶段，所有步频下的步幅长度均有统计学显著增加，且用药后在较高步频下达到最大步幅长度。步幅长度与步频回归的斜率并未根据用药状态而改变，尽管左旋多巴用药前的平均截距（-0.06）显著低于用药后（0.27）；[t（9）=-3.83；p=0.004]。这些结果表明，步幅长度的比例失调是PD步态障碍的基础。
