Little Simon, Tan Huiling, Anzak Anam, Pogosyan Alek, Kühn Andrea, Brown Peter
Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom.
Sobell Department of Motor Neuroscience & Movement Disorders, UCL Institute of Neurology, London, United Kingdom.
PLoS One. 2013 Dec 20;8(12):e82762. doi: 10.1371/journal.pone.0082762. eCollection 2013.
Parkinson's disease is characterised by excessive subcortical beta oscillations. However, little is known about the functional connectivity of the two basal ganglia across hemispheres and specifically the role beta plays in this. We recorded local field potentials from the subthalamic nucleus bilaterally in 23 subjects with Parkinson's disease at rest, on and off medication. We found suppression of low beta power in response to levodopa (t22 = -4.4, p<0.001). There was significant coherence between the two sides in the beta range in 19 of the subjects. Coherence was selectively attenuated in the low beta range following levodopa (t22 = -2.7; p = 0.01). We also separately analysed amplitude co-modulation and phase synchronisation in the beta band and found significant amplitude co-modulation and phase locking values in 17 and 16 subjects respectively, off medication. There was a dissociable effect of levodopa on these measures, with a significant suppression only in low beta phase locking value (t22 = -2.8, p = 0.01) and not amplitude co-modulation. The absolute mean values of amplitude co-modulation (0.40 ± 0.03) and phase synchronisation (0.29 ± 0.02) off medication were, however, relatively low, suggesting that the two basal ganglia networks may have to be approached separately with independent sensing and stimulation during adaptive deep brain stimulation. In addition, our findings highlight the functional distinction between the lower and upper beta frequency ranges and between amplitude co-modulation and phase synchronization across subthalamic nuclei.
帕金森病的特征是皮质下β振荡过度。然而，关于两个基底神经节跨半球的功能连接，尤其是β在其中所起的作用，我们知之甚少。我们在23名帕金森病患者静息状态下、服药和未服药时，双侧记录了丘脑底核的局部场电位。我们发现左旋多巴可抑制低β功率（t22 = -4.4，p<0.001）。19名受试者两侧在β频段存在显著的相干性。左旋多巴给药后，低β频段的相干性选择性减弱（t22 = -2.7；p = 0.01）。我们还分别分析了β频段的幅度共调制和相位同步，发现未服药时，分别有17名和16名受试者存在显著的幅度共调制和锁相值。左旋多巴对这些指标有不同的影响，仅低β锁相值有显著抑制（t22 = -2.8，p = 0.01），而幅度共调制无显著变化。然而，未服药时幅度共调制（0.40±0.03）和相位同步（0.29±0.02）的绝对平均值相对较低，这表明在适应性深部脑刺激过程中，可能需要分别对两个基底神经节网络进行独立的感知和刺激。此外，我们的研究结果突出了丘脑底核中较低和较高β频率范围之间以及幅度共调制和相位同步之间的功能差异。
