Jacobs J V, Horak F B
Neurological Sciences Institute, Oregon Health & Science University, 505 NW 185th Avenue, Beaverton, OR 97006-3499, USA.
Neurological Sciences Institute, Oregon Health & Science University, 505 NW 185th Avenue, Beaverton, OR 97006-3499, USA; Department of Neurology, Oregon Health & Science University, Portland, OR, USA; Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR, USA; Department of Biomedical Engineering, Oregon Health & Science University, Portland, OR, USA.
Neuroscience. 2006 Aug 25;141(2):999-1009. doi: 10.1016/j.neuroscience.2006.04.014. Epub 2006 May 18.
Subjects with Parkinson's disease exhibit abnormally short compensatory steps in response to external postural perturbations. We examined whether: (1) Parkinson's disease subjects exhibit short compensatory steps due to abnormal central proprioceptive-motor integration, (2) this proprioceptive-motor deficit can be overcome by visual-motor neural circuits using visual targets, (3) the proprioceptive-motor deficit relates to the severity of Parkinson's disease, and (4) the dysfunction of central dopaminergic circuits contributes to the Parkinson's disease subjects' proprioceptive-motor deficit. Ten Parkinson's disease subjects and 10 matched control subjects performed compensatory steps in response to backward surface translations in five conditions: with eyes closed, with eyes open, to a remembered visual target, to a target without seeing their legs, and to a target while seeing their legs. Parkinson's disease subjects were separated into a moderate group and a severe group based on scores from the Unified Parkinson's Disease Rating Scale and were tested off and on their dopamine medication. Parkinson's disease subjects exhibited shorter compensatory steps than did the control subjects, but all subjects increased their step length when stepping to targets. Compared with the other subject groups, the severe Parkinson's disease subjects made larger accuracy errors when stepping to targets, and the severe Parkinson's disease subjects' step accuracy worsened the most when they were unable to see their legs. Thus, Parkinson's disease subjects exhibited short compensatory steps due to abnormal proprioceptive-motor integration and used visual input to take longer compensatory steps when a target was provided. In severe Parkinson's disease subjects, however, visual input does not fully compensate because, even with a target and unobstructed vision, they still exhibited poor step accuracy. Medication did not consistently improve the length and accuracy of the Parkinson's disease subjects' compensatory steps, suggesting that degeneration of dopamine circuits within the basal ganglia is not responsible for the proprioceptive-motor deficit that degrades compensatory steps in Parkinson's disease subjects.
帕金森病患者在应对外部姿势扰动时会表现出异常短的代偿性步幅。我们研究了以下问题：（1）帕金森病患者出现短代偿性步幅是否是由于中枢本体感觉 - 运动整合异常；（2）这种本体感觉 - 运动缺陷是否可以通过利用视觉目标的视觉 - 运动神经回路来克服；（3）本体感觉 - 运动缺陷是否与帕金森病的严重程度相关；（4）中枢多巴胺能回路功能障碍是否导致帕金森病患者的本体感觉 - 运动缺陷。10名帕金森病患者和10名匹配的对照受试者在五种情况下对向后的表面平移进行代偿性步幅动作：闭眼、睁眼、朝着记忆中的视觉目标步行、朝着看不到自己腿部的目标步行以及朝着能看到自己腿部的目标步行。根据统一帕金森病评定量表的评分，帕金森病患者被分为中度组和重度组，并在服用和停用多巴胺药物的情况下进行测试。帕金森病患者的代偿性步幅比对照受试者短，但所有受试者在朝着目标步行时步幅都会增加。与其他受试者组相比，重度帕金森病患者在朝着目标步行时的准确性误差更大，并且在看不到自己腿部时，重度帕金森病患者的步幅准确性恶化最为明显。因此，帕金森病患者由于本体感觉 - 运动整合异常而表现出短代偿性步幅，并且在有目标时利用视觉输入采取更长的代偿性步幅。然而，在重度帕金森病患者中，视觉输入并不能完全代偿，因为即使有目标且视野不受阻碍，他们的步幅准确性仍然很差。药物治疗并不能持续改善帕金森病患者代偿性步幅的长度和准确性，这表明基底神经节内多巴胺回路的退化并非帕金森病患者代偿性步幅退化的本体感觉 - 运动缺陷的原因。
