Heinrichs-Graham Elizabeth, Kurz Max J, Becker Katherine M, Santamaria Pamela M, Gendelman Howard E, Wilson Tony W
Department of Psychology, University of Nebraska, Omaha, Nebraska; Center for Magnetoencephalography, University of Nebraska Medical Center, Omaha, Nebraska;
Center for Magnetoencephalography, University of Nebraska Medical Center, Omaha, Nebraska; Department of Physical Therapy, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, Nebraska;
J Neurophysiol. 2014 Oct 1;112(7):1739-47. doi: 10.1152/jn.00383.2014. Epub 2014 Jul 9.
Parkinson's disease (PD) is a progressive debilitating neurodegenerative disorder clinically manifest by motor, posture and gait abnormalities. Human neurophysiological studies recording local field potentials within the subthalamic nucleus and scalp-based electroencephalography have shown pathological beta synchrony throughout the basal ganglia-thalamic-cortical motor network in PD. Notably, suppression of this pathological beta synchrony by dopamine replacement therapy or deep-brain stimulation has been associated with improved motor function. However, due to the invasive nature of these studies, it remains unknown whether this "pathological beta" is actually stronger than that observed in healthy demographically matched controls. We used magnetoencephalography to investigate neuronal synchrony and oscillatory amplitude in the beta range and lower frequencies during the resting state in patients with PD and a matched group of patients without neurological disease. Patients with PD were studied both in the practically defined drug "OFF" state, and after administration of dopamine replacements. We found that beta oscillatory amplitude was reduced bilaterally in the primary motor regions of unmedicated patients with PD compared with controls. Administration of dopaminergic medications significantly increased beta oscillatory activity, thus having a normalizing effect. Interestingly, we also found significantly stronger beta synchrony (i.e., hypersynchrony) between the primary motor regions in unmedicated patients with PD compared with controls, and that medication reduced this coupling which is in agreement with the intraoperative studies. These results are consistent with the known functionality of the basal ganglia-thalamic-cortical motor circuit and the likely consequences of beta hypersynchrony in the subthalamic nucleus of patients with PD.
帕金森病（PD）是一种进行性使人衰弱的神经退行性疾病，临床上表现为运动、姿势和步态异常。对人类进行的神经生理学研究记录了丘脑底核内的局部场电位以及基于头皮的脑电图，结果显示在帕金森病患者的整个基底神经节 - 丘脑 - 皮质运动网络中存在病理性β同步化。值得注意的是，多巴胺替代疗法或深部脑刺激对这种病理性β同步化的抑制与运动功能改善相关。然而，由于这些研究具有侵入性，目前尚不清楚这种“病理性β”是否实际上比在人口统计学匹配的健康对照者中观察到的更强。我们使用脑磁图来研究帕金森病患者和一组无神经系统疾病的匹配患者在静息状态下β频段及更低频率的神经元同步性和振荡幅度。对帕金森病患者在实际定义的药物“关”状态下以及给予多巴胺替代药物后进行了研究。我们发现，与对照组相比，未用药的帕金森病患者初级运动区的双侧β振荡幅度降低。给予多巴胺能药物可显著增加β振荡活动，从而产生归一化作用。有趣的是，我们还发现，与对照组相比，未用药的帕金森病患者初级运动区之间的β同步性（即超同步性）显著更强，并且药物治疗减少了这种耦合，这与术中研究结果一致。这些结果与基底神经节 - 丘脑 - 皮质运动回路的已知功能以及帕金森病患者丘脑底核中β超同步化的可能后果相符。
