The neuromuscular circuit mechanisms of freezing of gait in Parkinson’s disease have received little study. Technological progress enables researchers chronically to sense local field potential activity of the basal ganglia in patients while walking. To study subthalamic activity and the circuit processes of supraspinal contributions to spinal motor integration, we recorded local field potentials, surface EMG of antagonistic leg muscles and gait kinematics in patients while walking and freezing. To evaluate the specificity of our findings, we controlled our findings to internally generated volitional stops. We found specific activation–deactivation abnormalities of oscillatory activity of the subthalamic nucleus both before and during a freeze. Furthermore, we were able to show with synchronization analyses that subthalamo-spinal circuits entrain the spinal motor neurons to a defective timing and activation pattern. The main neuromuscular correlates when turning into freezing were as follows: (i) disturbed reciprocity between antagonistic muscles; (ii) increased co-contraction of the antagonists; (iii) defective activation and time pattern of the gastrocnemius muscle; and (iv) increased subthalamo-muscular coherence with the gastrocnemius muscles before the freeze. Beyond the pathophysiological insights into the supraspinal mechanisms contributing to freezing of gait, our findings have potential to inform the conceptualization of future neurorestorative therapies.

中文翻译：

---

脊髓上对帕金森病患者拮抗抑制缺陷和步态冻结的贡献


帕金森病中步态冻结的神经肌肉回路机制很少得到研究。技术进步使研究人员能够在行走时长期感知患者基底神经节的局部场电位活动。为了研究丘脑底活动和脊髓上对脊髓运动整合的贡献的回路过程，我们记录了患者在行走和冻结时的局部场电位、拮抗腿部肌肉的表面肌电图和步态运动学。为了评估我们研究结果的特异性，我们将研究结果控制在内部生成的意志停止。我们发现在冻结之前和期间丘脑底核振荡活动的特定激活-失活异常。此外，我们能够通过同步分析表明丘脑底脊髓回路使脊髓运动神经元处于有缺陷的时间和激活模式。转为冻结时的主要神经肌肉相关性如下：（i） 拮抗肌之间的互惠性紊乱;（ii） 拮抗剂的共收缩增加;（iii） 腓肠肌的激活和时间模式缺陷;（iv） 冻结前丘脑底肌肉与腓肠肌的连贯性增加。除了对导致步态冻结的脊髓上机制的病理生理学见解外，我们的研究结果还有可能为未来神经修复疗法的概念化提供信息。