Ghassemi Mehrdad, Lemieux Sarah, Jog Mandar, Edwards Roderick, Duval Christian
Département de Kinanthropologie, Université du Québec à Montréal, C.P. 8888, Succursale Centre-Ville, Bureau #N8250, Montréal, Qué., Canada H3C 3P8.
Brain Res Bull. 2006 May 15;69(5):512-8. doi: 10.1016/j.brainresbull.2006.02.015. Epub 2006 Mar 15.
We investigated the likelihood that bradykinesia coexisted with levodopa-induced dyskinesias (LID) in 10 dyskinetic Parkinson's disease patients (DPD). Their motor performance was compared to that of 10 age/gender-matched non-dyskinetic patients (NDPD) and 10 healthy controls. Whole-body movement (WBM) and rapid alternating movements (RAM) at the wrist were recorded simultaneously using 6-degree of freedom magnetic motion tracker and forearm rotational sensors, respectively. WBM was recorded prior to, and while subjects performed pronation-supination movements of their dominant hand with maximal rotational excursion, and as fast as possible for 10s. RANGE, VELOCITY and IRREGULARITY of pronation-supination cycles were quantified to assess motor performance. Results show that DPD patients had greater WBM than NDPD and controls during rest and RAM performance, as expected. There were no differences in motor performance between DPD and NDPD groups for RANGE and VELOCITY, despite significantly longer disease duration for the DPD group (15.5+/-6.2 years versus 6.6+/-2.6 years). However, both the NDPD and DPD groups showed significantly lower RANGE and reduced VELOCITY compared to controls, suggesting the presence of bradykinesia. For IRREGULARITY, DPD patients showed increased fluctuations in pronation-supination cycle amplitude compared to NDPD and controls. However, the lack of correlation between WBM magnitude and IRREGULARITY within the DPD group (Spearman's rank order, rho = 0.31, p > 0.05), suggests that LID were not the primary cause of increased IRREGULARITY. In conclusion, our results demonstrated that bradykinesia can coexist with dyskinesias, suggestive of distinct neural circuits. Our results also demonstrated that the occurrence of LID is not inevitably accompanied with worsening of motor performance.
我们调查了10例患有运动障碍的帕金森病患者（DPD）中运动迟缓与左旋多巴诱导的运动障碍（LID）共存的可能性。将他们的运动表现与10例年龄和性别匹配的非运动障碍患者（NDPD）以及10名健康对照者进行比较。分别使用6自由度磁运动追踪器和前臂旋转传感器同时记录全身运动（WBM）和手腕的快速交替运动（RAM）。在受试者用优势手进行最大旋转幅度的旋前-旋后运动之前以及运动过程中记录WBM，持续10秒，速度尽可能快。对旋前-旋后周期的范围、速度和不规则性进行量化，以评估运动表现。结果显示，正如预期的那样，DPD患者在休息和进行RAM时的WBM比NDPD和对照组更大。尽管DPD组的病程明显更长（15.5±6.2年对6.6±2.6年），但DPD组和NDPD组在范围和速度方面的运动表现没有差异。然而，与对照组相比，NDPD组和DPD组的范围均显著更低，速度也有所降低，这表明存在运动迟缓。对于不规则性，与NDPD和对照组相比，DPD患者的旋前-旋后周期幅度波动增加。然而，DPD组内WBM幅度与不规则性之间缺乏相关性（Spearman等级相关，rho = 0.31，p>0.05），这表明LID不是不规则性增加的主要原因。总之，我们的结果表明运动迟缓可与运动障碍共存，提示存在不同的神经回路。我们的结果还表明，LID的发生并不必然伴随着运动表现的恶化。
