Steiner Leon Amadeus, Neumann Wolf-Julian, Staub-Bartelt Franziska, Herz Damian M, Tan Huiling, Pogosyan Alek, Kuhn Andrea A, Brown Peter
Department of Neurology, Charité, Campus Virchow Klinikum, University Medicine Berlin, Berlin, Germany.
Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
Mov Disord. 2017 Aug;32(8):1183-1190. doi: 10.1002/mds.27068. Epub 2017 Jun 22.
Exaggerated oscillatory activity in the beta frequency band in the subthalamic nucleus has been suggested to be related to bradykinesia in Parkinson's disease (PD). However, studies seeking correlations between such activity in the local field potential and motor performance have been limited to the immediate postoperative period, which may be confounded by a stun effect that leads to the temporary alleviation of PD deficits.
Local field potentials were recorded simultaneously with motor performance in PD patients several months after neurostimulator implantation. This was enabled by the chronic implantation of a pulse generator with the capacity to record and transmit local field potentials from deep brain stimulation electrodes. Specifically, we investigated oscillatory beta power dynamics and objective measures of bradykinesia during an upper limb alternating pronation and supination task in 9 patients.
Although beta power was suppressed during continuously repeated movements, this suppression progressively diminished over time in tandem with a progressive decrement in the frequency and amplitude of movements. The relationship between changes within local field potentials and movement parameters was significant across patients, and not present for theta/alpha frequencies (5-12 Hz). Change in movement frequency furthermore related to beta power dynamics within patients.
Changes in beta power are linked to changes in movement performance and the sequence effect of bradykinesia months after neurostimulator implantation. These findings provide further evidence that beta power may serve as a biomarker for bradykinesia and provide a suitable substrate for feedback control in chronic adaptive deep brain stimulation. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
有研究表明,帕金森病(PD)患者丘脑底核的β频段振荡活动增强与运动迟缓有关。然而,关于局部场电位中的这种活动与运动表现之间相关性的研究仅限于术后即刻,这可能会受到“休克效应”的干扰,该效应会导致PD症状暂时缓解。
在神经刺激器植入数月后的PD患者中,同时记录局部场电位和运动表现。这是通过长期植入具有记录和传输来自深部脑刺激电极的局部场电位能力的脉冲发生器实现的。具体而言,我们在9名患者的上肢交替旋前和旋后任务中,研究了振荡β功率动态变化和运动迟缓的客观指标。
尽管在持续重复运动期间β功率受到抑制,但随着时间的推移,这种抑制作用逐渐减弱,同时运动的频率和幅度也逐渐减小。局部场电位变化与运动参数之间的关系在患者中具有显著性,而在θ/α频率(5 - 12Hz)时不存在这种关系。此外,运动频率的变化与患者体内的β功率动态变化有关。
神经刺激器植入数月后,β功率的变化与运动表现的变化以及运动迟缓的序列效应相关。这些发现进一步证明β功率可能作为运动迟缓的生物标志物,并为慢性适应性深部脑刺激中的反馈控制提供合适的基础。© 2017作者。《运动障碍》由Wiley Periodicals, Inc.代表国际帕金森和运动障碍协会出版。