THE PATHOGENESIS OF GAIT HYPOKINESIA IN PARKINSONS-DISEASE
THE PATHOGENESIS OF GAIT HYPOKINESIA IN PARKINSONS-DISEASE
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DOI：
10.1093/brain/117.5.1169
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发表时间：
1994-10-01
期刊：
影响因子：
14.5
通讯作者：
SUMMERS, JJ
中科院分区：
文献类型：
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作者：
MORRIS, ME;IANSEK, R;SUMMERS, JJ
为了确定帕金森病 (PD) 步态运动功能减退的根本缺陷，我们进行了一系列实验，将帕金森病受试者与年龄和身高匹配的对照组进行比较，比较他们在三种条件下调节步长、步频（每分钟步数）这两个参数的能力。在第一种情况下，记录慢速行走、正常行走和快速行走的步态的空间和时间参数。第二个条件将帕金森步态与老年人对照的行走模式进行比较，同时控制两种运动速度：快（首选控制）速度找到慢速（PD首选）速度。在第三种情况下，我们检查了 PD 受试者在其他两个参数（例如速度和节奏）保持在控制值时调节一个参数（例如步幅）的能力。使用脚踏开关步幅分析系统对总共 34 名 PD 受试者和 34 名匹配的对照进行了测试，该系统测量了一系列 10 m 步行试验的步态空间和时间参数。帕金森病受试者在每次实验中都表现出明显的步态运动功能减退。尽管他们保留了以与对照相似的方式改变步态速度的能力，但他们的反应范围却缩小了。在较低速度范围内，PD 受试者可以通过调整步频和较小程度的步幅来改变步行速度。然而，当控制步行速度时，发现 PD 受试者的步幅比对照组大，步频也比对照组高。内部控制机制无法响应针对年龄和身高匹配速度设置的固定步频来升级步幅长度。相比之下，当步幅被设定为与年龄和身高匹配的对照所获得的值时，步频很容易受到外部提示和内部控制机制的调节。结论是，步幅调节是步态运动功能减退的根本问题，PD 受试者表现出的步频相对增加是调节步幅困难的一种补偿机制。这些发现是在基底神经节在产生维持步态序列的内部线索以及与运动康复策略的构建相关的假设作用的背景下讨论的。
To identify the fundamental deficit in gait hypokinesia in Parkinson's disease (PD) we conducted a series of experiments that compared PD subjects with age- and height-matched controls in their capacity to regulate either stride length, cadence (steps per minute) ol both parameters to three conditions. In the first condition the spatial and temporal parameters of gait were documented for slow: normal and fast walking. The second condition compared parkinsonian gait with the walking pattern of elderly controls whilst controlling for two movement speeds: fast (control preferred) speed find slow (PD preferred) speed. In the third condition we examined the ability of PD subjects to regulate one parameter (e.g. stride length) when the other two parameters (e.g. velocity and cadence) were held at control values. A total of 34 PD subjects and 34 matched controls were tested using a footswitch stride analysis system that measured the spatial and temporal parameters of gait for gait for a series of 10 m walking trials. Parkinsonian subjects exhibited marked gait hypokinesia in each of the experiments. Although they retained the capacity to vary their gait velocity in a similar manner to controls, their range of response was reduced. Within the lower velocity range, PD subjects could vary their speed of walking by adjusting cadence and to a lesser extent, stride length. However when the speed of walking was controlled the stride length was found to be shouter and the cadence higher in PD subjects than in controls. Stride length could not be upgraded by internal control mechanisms in response to a fixed cadence set for age and height-matched velocity. In contrast, cadence was readily modulated by external cues and by internal control mechanisms when stride length was fired to the values obtained for age- and height-matched controls. It was concluded that regulation of stride length is the fundamental problem in gait hypokinesia and the relative increase in cadence exhibited by PD subjects is a compensatory mechanism for the difficulty in regulating stride length. These findings are discussed in the context of the hypothesized role of the basal ganglia in generating internal cues for the maintenance of the gait sequence and in relation to the structuring of movement rehabilitation strategies.