Postural instability is a major disabling feature in Parkinson’s disease (PD). We quantified the organization of leg and trunk muscles into synergies stabilizing the center of pressure (COP) coordinate within the uncontrolled manifold hypothesis in levodopa-naïve patients with PD and age-matched control subjects. The main hypothesis was that changes in the synergic control of posture are present early in the PD process even before levodopa exposure. Eleven levodopa-naïve patients with PD and 11 healthy controls performed whole-body cyclical voluntary sway tasks and a self-initiated load-release task during standing on a force plate. Surface electromyographic activity in 13 muscles on the right side of the body was analyzed to identify muscle groups with parallel scaling of activation levels (M-modes). Data were collected both before (“off-drug”) and approximately 60 min after the first dose of 25/100 carbidopa/levodopa (“on-drug”). COP-stabilizing synergies were quantified for the load-release task. Levodopa-naïve patients with PD showed no COP-stabilizing synergy “off-drug”, whereas controls showed posture-stabilizing multi-M-mode synergy. “On-drug”, patients with PD demonstrated a significant increase in the synergy index. There were no significant drug effects on the M-mode composition, anticipatory postural adjustments, indices of motor equivalence, or indices of COP variability. The results suggest that levodopa-naïve patients with PD already show impaired posture-stabilizing multi-muscle synergies that may be used as promising behavioral biomarkers for emerging postural disorders in PD. Moreover, levodopa modified synergy metrics differently in these levodopa-naïve patients compared to a previous study of patients on chronic antiparkinsonian medications (Falaki et al. in J Electromyogr Kinesiol 33:20–26, 2017a), suggesting different neurocircuitry involvement.

姿势不稳定是帕金森病 (PD) 的主要致残特征。我们将腿部和躯干肌肉的组织量化为协同作用，在未接受过左旋多巴的 PD 患者和年龄匹配的对照受试者中，在不受控制的流形假设内稳定压力中心 (COP) 坐标。主要假设是，姿势协同控制的变化出现在 PD 过程的早期，甚​​至在左旋多巴暴露之前。11 名未接受过左旋多巴治疗的帕金森病患者和 11 名健康对照者在站在测力板上时进行了全身周期性自愿摇摆任务和自我启动的负载释放任务。分析了身体右侧 13 块肌肉的表面肌电活动，以识别具有平行缩放激活水平（M 模式）的肌肉群。在第一次服用 25/100 卡比多巴/左旋多巴之前（“停药”）和大约 60 分钟后（“服用药物”）收集数据。对负载释放任务的 COP 稳定协同作用进行了量化。未接受左旋多巴治疗的 PD 患者在“停药”状态下没有表现出稳定 COP 的协同作用，而对照组则表现出稳定姿势的多 M 模式协同作用。“用药期间”，PD 患者表现出协同指数显着增加。药物对 M 模式组成、预期姿势调整、运动等效指数或 COP 变异指数没有显着影响。结果表明，未接受过左旋多巴治疗的帕金森病患者已经表现出姿势稳定多肌肉协同作用受损，这可以作为帕金森病中新出现的姿势障碍的行为生物标志物。此外，与先前对慢性抗帕金森病药物患者的研究相比，左旋多巴对这些未使用过左旋多巴的患者的协同指标的修改有所不同（Falaki 等人，J Electromyogr Kinesiol 33:20-26, 2017a），这表明不同的神经回路参与。