Department of Neurology, Leipzig University Medical Center, Leipzig, Germany.
Method and Development Group Brain Networks, Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany.
J Neurophysiol. 2022 Jun 1;127(6):1606-1621. doi: 10.1152/jn.00541.2021. Epub 2022 May 11.
Bradykinesia is a cardinal motor symptom in Parkinson's disease (PD), the pathophysiology of which is not fully understood. We analyzed the role of cross-frequency coupling of oscillatory cortical activity in motor impairment in patients with PD and healthy controls. High-density EEG signals were recorded during various motor activities and at rest. Patients performed a repetitive finger-pressing task normally, but were slower than controls during tapping. Phase-amplitude coupling (PAC) between β (13-30 Hz) and broadband γ (50-150 Hz) was computed from individual EEG source signals in the premotor, primary motor, and primary somatosensory cortices, and the primary somatosensory complex. In all four regions, averaging the entire movement period resulted in higher PAC in patients than in controls for the resting condition and the pressing task (similar performance between groups). However, this was not the case for the tapping tasks where patients performed slower. This suggests the strength of state-related β-γ PAC does not determine Parkinsonian bradykinesia. Examination of the dynamics of oscillatory EEG signals during motor transitions revealed a distinctive motif of PAC rise and decay around press onset. This pattern was also present at press offset and slow tapping onset, linking such idiosyncratic PAC changes to transitions between different movement states. The transition-related PAC modulation in patients was similar to controls in the pressing task but flattened during slow tapping, which related to normal and abnormal performance, respectively. These findings suggest that the dysfunctional evolution of neuronal population dynamics during movement execution is an important component of the pathophysiology of Parkinsonian bradykinesia. Our findings using noninvasive EEG recordings provide evidence that PAC dynamics might play a role in the physiological cortical control of movement execution and may encode transitions between movement states. Results in patients with Parkinson's disease suggest that bradykinesia is related to a deficit of the dynamic regulation of PAC during movement execution rather than its absolute strength. Our findings may contribute to the development of a new concept of the pathophysiology of bradykinesia.
运动徐缓是帕金森病（PD）的主要运动症状，但其病理生理学尚不完全清楚。我们分析了皮质振荡活动的频域耦合在 PD 患者和健康对照者运动障碍中的作用。在各种运动和休息期间记录高密度 EEG 信号。患者正常进行重复手指按压任务，但比对照组在敲击时慢。在运动前皮质、初级运动皮质和初级躯体感觉皮质以及初级躯体感觉复合体的个体 EEG 源信号中计算了β（13-30 Hz）和宽带γ（50-150 Hz）之间的相位-振幅耦合（PAC）。在所有四个区域中，对整个运动周期进行平均处理，结果表明在休息状态和按压任务下，患者的 PAC 高于对照组（组间表现相似）。然而，在患者较慢的敲击任务中并非如此。这表明与状态相关的β-γ PAC 的强度并不能决定帕金森运动徐缓。对运动转换过程中振荡 EEG 信号的动力学进行检查，发现 PAC 上升和下降的独特模式出现在按压开始周围。这种模式也出现在按压结束和缓慢敲击开始时，将这种特殊的 PAC 变化与不同运动状态之间的转换联系起来。在按压任务中，患者的转换相关 PAC 调制与对照组相似，但在缓慢敲击时变平，分别与正常和异常表现相关。这些发现表明，运动执行过程中神经元群体动力学的功能障碍演变是帕金森运动徐缓病理生理学的一个重要组成部分。我们使用非侵入性 EEG 记录的研究结果提供了证据，表明 PAC 动力学可能在运动执行的生理皮质控制中发挥作用，并可能对运动状态之间的转换进行编码。帕金森病患者的结果表明，运动徐缓与运动执行期间 PAC 动态调节的缺陷有关，而不是其绝对强度。我们的发现可能有助于提出运动徐缓病理生理学的新概念。
