Biological Engineering Department, Massachusetts Institute of Technology, Cambridge, MA, USA.
Exp Brain Res. 2011 Jun;211(2):277-86. doi: 10.1007/s00221-011-2685-0. Epub 2011 Apr 28.
Previous studies examining discrete movements of Parkinson's disease (PD) patients have found that in addition to performing movements that were slower than those of control participants, they exhibit specific deficits in movement coordination and in sensorimotor integration required to accurately guide movements. With medication, movement speed was normalized, but the coordinative aspects of movement were not. This led to the hypothesis that dopaminergic medication more readily compensates for intensive aspects of movement (such as speed), than for coordinative aspects (such as coordination of different limb segments) (Schettino et al., Exp Brain Res 168:186-202, 2006). We tested this hypothesis on rhythmic, continuous movements of the forearm. In our task, target peak speed and amplitude, availability of visual feedback, and medication state (on/off) were varied. We found, consistent with the discrete-movement results, that peak speed (intensive aspect) was normalized by medication, while accuracy, which required coordination of speed and amplitude modulation (coordinative aspect), was not normalized by dopaminergic treatment. However, our findings that amplitude, an intensive aspect of movement, was also not normalized by medication, suggests that a simple pathway gain increase does not act to remediate all intensive aspects of movement to the same extent. While it normalized movement peak speed, it did not normalize movement amplitude. Furthermore, we found that when visual feedback was not available, all participants (PD and controls) made faster movements. The effects of dopaminergic medication and availability of visual feedback on movement speed were additive. The finding that movement speed uniformly increased both in the PD and the control groups suggests that visual feedback may be necessary for calibration of peak speed, otherwise underestimated by the motor control system.
先前研究帕金森病(PD)患者离散运动的研究发现,PD 患者不仅运动速度比对照组慢,而且在运动协调和准确引导运动所需的感觉运动整合方面也存在特定缺陷。药物治疗后,运动速度恢复正常,但运动的协调性并未恢复正常。这导致了一种假设,即多巴胺能药物更易于补偿运动的密集方面(如速度),而不是补偿协调方面(如不同肢体段的协调)(Schettino 等人,Exp Brain Res 168:186-202, 2006)。我们在手前臂的节律性连续运动上测试了这一假设。在我们的任务中,目标峰值速度和幅度、视觉反馈的可用性以及药物状态(开/关)都发生了变化。我们发现,与离散运动结果一致,药物治疗使峰值速度(密集方面)正常化,而准确性(需要速度和幅度调制的协调)则未通过多巴胺能治疗正常化。然而,我们发现运动幅度(运动的密集方面)也未通过药物治疗正常化,这表明简单的通路增益增加并不能以相同的程度来改善运动的所有密集方面。虽然它使运动峰值速度正常化,但它并没有使运动幅度正常化。此外,我们发现当没有视觉反馈时,所有参与者(PD 和对照组)的运动速度都更快。多巴胺能药物和视觉反馈对运动速度的影响是相加的。PD 组和对照组的运动速度都均匀增加的发现表明,视觉反馈可能是峰值速度校准所必需的,否则运动控制系统会低估峰值速度。