Morris M E, Iansek R, Matyas T A, Summers J J
Geriatric Research Unit, Kingston Centre, Cheltenham, Australia.
Brain. 1996 Apr;119 ( Pt 2):551-68. doi: 10.1093/brain/119.2.551.
Results of our previous studies have shown that the slow, shuffling gait of Parkinson's disease patients is due to an inability to generate appropriate stride length and that cadence control is intact and is used as a compensatory mechanism. The reason for the reduced stride length is unclear, although deficient internal cue production or inadequate contribution to cortical motor set by the basal ganglia are two possible explanations. In this study we have examined the latter possibility by comparing the long-lasting effects of visual cues in improving stride length with that of attentional strategies. Computerized stride analysis was used to measure the spatial (distance) and temporal (timing) parameters of the walking pattern in a total of 54 subjects in three separate studies. In each study Parkinson's disease subjects were trained for 20 min by repeated 10 m walks set at control stride length (determined from control subjects matched for age, sex and height), using either visual floor markers or a mental picture of the appropriate stride size. Following training, the gait patterns were monitored (i) every 15 min for 2 h; (ii) whilst interspersing secondary tasks of increasing levels of complexity; (iii) covertly, when subjects were unaware that measurement was taking place. The results demonstrated that training with both visual cues and attentional strategies could maintain normal gait for the maximum recording time of 2 h. Secondary tasks reduced stride length towards baseline values as did covert monitoring. The findings confirm that the ability to generate a normal stepping pattern is not lost in Parkinson's disease and that gait hypokinesia reflects a difficulty in activating the motor control system. Normal stride length can be elicited in Parkinson's disease using attentional strategies and visual cues. Both strategies appear to share the same mechanism of focusing attention on the stride length. The effect of attention appears to require constant vigilance to prevent reverting to more automatic control mechanisms.
我们之前的研究结果表明，帕金森病患者缓慢、拖沓的步态是由于无法产生合适的步长，且其节奏控制完好，并被用作一种补偿机制。步长缩短的原因尚不清楚，尽管内部线索产生不足或基底神经节对皮质运动设定的贡献不足是两种可能的解释。在本研究中，我们通过比较视觉线索和注意力策略在改善步长方面的长期效果，来检验后一种可能性。在三项独立研究中，共对54名受试者使用计算机化步幅分析来测量步行模式的空间（距离）和时间（时间安排）参数。在每项研究中，帕金森病受试者以控制步长（根据年龄、性别和身高匹配的对照受试者确定）进行重复10米步行训练20分钟，训练方式为使用视觉地面标记或合适步幅大小的心理图像。训练后，对步态模式进行监测：（i）每15分钟监测一次，持续2小时；（ii）在穿插进行复杂度不断增加的次要任务时进行监测；（iii）在受试者 unaware that measurement was taking place（此处原文有误，推测可能是“unaware that measurement was being taken”，即“未意识到正在进行测量”）时进行隐蔽监测。结果表明，视觉线索训练和注意力策略训练都能在最长2小时的记录时间内维持正常步态。次要任务会使步长缩短至基线值水平（隐蔽监测时也是如此）。这些发现证实，帕金森病患者产生正常步行模式的能力并未丧失，步态运动不能反映出激活运动控制系统存在困难。使用注意力策略和视觉线索可在帕金森病患者中引发正常步长。两种策略似乎都具有将注意力集中在步长上的相同机制。注意力的作用似乎需要持续保持警觉，以防止恢复到更自动的控制机制。
