Falletti Marco, Asci Francesco, Zampogna Alessandro, Patera Martina, Pinola Giulia, Centonze Diego, Hallett Mark, Rothwell John, Suppa Antonio
Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy.
IRCCS Neuromed Institute, Pozzilli, Italy.
Mov Disord. 2025 Apr;40(4):727-738. doi: 10.1002/mds.30114. Epub 2025 Jan 8.
Quantitative evidence of levodopa-induced beneficial effects on parkinsonian rigidity in Parkinson's disease (PD) is lacking. Recent research has demonstrated the velocity-dependent nature of objective rigidity in PD and revealed its neural underpinning.
The present study aimed to examine the effect of levodopa on objective rigidity in PD.
Eighteen patients with PD underwent clinical and instrumental evaluations of muscle tone in the OFF and ON states. The clinical assessments focused on rigidity in the most affected upper limb. The biomechanical components of objective rigidity were assessed using robot-assisted wrist extensions at seven angular velocities (5-280°/s). Surface electromyography of the flexor carpi radialis muscle enabled the concurrent evaluation of short- and long-latency stretch reflexes (SLR and LLR).
Levodopa improved the clinical scores of rigidity. Biomechanical measurements showed that levodopa reduced the total and neural components of force but had no effect on viscoelastic components. Levodopa reduced the velocity dependence of the LLRs but did not affect the SLRs. Finally, we found significant clinical-instrumental correlations between levodopa-induced changes and biomechanical and neurophysiological measures of objective rigidity in PD.
Levodopa improved objective rigidity in PD by decreasing its biomechanical neural component as well as the size of LLRs. The beneficial effect of levodopa on biomechanical and neurophysiological features of objective rigidity was related to the specific angular velocity of wrist extensions; that is, the higher the angular velocity, the greater the beneficial impact of levodopa on objective rigidity. These findings allowed the description of a new pathophysiological model of rigidity in PD. © 2025 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
缺乏左旋多巴对帕金森病(PD)患者帕金森氏僵硬有益作用的定量证据。最近的研究表明了PD中客观僵硬的速度依赖性,并揭示了其神经基础。
本研究旨在探讨左旋多巴对PD患者客观僵硬的影响。
18例PD患者在关期和开期接受了肌张力的临床和仪器评估。临床评估集中在受影响最严重的上肢的僵硬情况。使用机器人辅助的腕关节伸展在7种角速度(5-280°/秒)下评估客观僵硬的生物力学成分。桡侧腕屈肌的表面肌电图能够同时评估短潜伏期和长潜伏期牵张反射(SLR和LLR)。
左旋多巴改善了僵硬的临床评分。生物力学测量表明,左旋多巴降低了力的总和及神经成分,但对粘弹性成分没有影响。左旋多巴降低了LLR的速度依赖性,但不影响SLR。最后,我们发现左旋多巴引起的变化与PD中客观僵硬的生物力学和神经生理学测量之间存在显著的临床-仪器相关性。
左旋多巴通过降低其生物力学神经成分以及LLR的大小来改善PD患者的客观僵硬。左旋多巴对客观僵硬的生物力学和神经生理学特征的有益作用与腕关节伸展的特定角速度有关;也就是说,角速度越高,左旋多巴对客观僵硬的有益影响就越大。这些发现有助于描述一种新的PD僵硬病理生理模型。© 2025作者。《运动障碍》由Wiley Periodicals LLC代表国际帕金森和运动障碍协会出版。