Exaggerated basal ganglia beta activity (13–35 Hz) is commonly found in patients with Parkinson’s disease and can be suppressed by dopaminergic medication, with the degree of suppression being correlated with the improvement in motor symptoms. Importantly, beta activity is not continuously elevated, but fluctuates to give beta bursts. The percentage number of longer beta bursts in a given interval is positively correlated with clinical impairment in Parkinson’s disease patients. Here we determine whether the characteristics of beta bursts are dependent on dopaminergic state. Local field potentials were recorded from the subthalamic nucleus of eight Parkinson’s disease patients during temporary lead externalization during surgery for deep brain stimulation. The recordings took place with the patient quietly seated following overnight withdrawal of levodopa and after administration of levodopa. Beta bursts were defined by applying a common amplitude threshold and burst characteristics were compared between the two drug conditions. The amplitude of beta bursts, indicative of the degree of local neural synchronization, progressively increased with burst duration. Treatment with levodopa limited this evolution leading to a relative increase of shorter, lower amplitude bursts. Synchronization, however, was not limited to local neural populations during bursts, but also, when such bursts were cotemporaneous across the hemispheres, was evidenced by bilateral phase synchronization. The probability of beta bursts and the proportion of cotemporaneous bursts were reduced by levodopa. The percentage number of longer beta bursts in a given interval was positively related to motor impairment, while the opposite was true for the percentage number of short duration beta bursts. Importantly, the decrease in burst duration was also correlated with the motor improvement. In conclusion, we demonstrate that long duration beta bursts are associated with an increase in local and interhemispheric synchronization. This may compromise information coding capacity and thereby motor processing. Dopaminergic activity limits this uncontrolled beta synchronization by terminating long duration beta bursts, with positive consequences on network state and motor symptoms.

中文翻译：

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帕金森氏病多巴胺能药物中的Beta爆发动力学

帕金森氏病患者通常会发现过度的基底神经节β活性（13–35 Hz），可以通过多巴胺能药物抑制，其抑制程度与运动症状的改善相关。重要的是，β活性不会持续升高，而是会波动以产生β爆发。在给定的时间间隔内较长的β爆发次数所占的百分比与帕金森氏病患者的临床损害呈正相关。在这里，我们确定β爆发的特征是否取决于多巴胺能状态。在深部脑刺激手术期间临时铅外化过程中，从八名帕金森氏病患者的丘脑下核中记录了局部场电位。在左旋多巴隔夜撤药后和左旋多巴给药后，患者安静地就座。通过应用共同的振幅阈值定义Beta爆发，并比较两种药物条件之间的爆发特征。β爆发的幅度（表示局部神经同步程度）随着爆发持续时间而逐渐增加。左旋多巴的治疗限制了这种发展，导致较短，较低振幅的猝发相对增加。然而，同步不仅限于爆发期间的局部神经种群，而且，当这种爆发在整个半球同时发生时，可以通过双边相位同步来证明。左旋多巴降低了β爆发的可能性和同期爆发的比例。在给定的时间间隔内，较长的beta爆发百分比与运动障碍呈正相关，而短时间的beta爆发百分比则相反。重要的是，猝发持续时间的减少也与运动能力的改善有关。总之，我们证明了长时间的β爆发与局部和半球同步的增加有关。这可能会损害信息编码能力，从而损害电机处理能力。多巴胺能活动通过终止长时间的β爆发来限制这种不受控制的β同步，从而对网络状态和运动症状产生积极影响。猝发持续时间的减少也与运动能力的改善有关。总之，我们证明了长时间的β爆发与局部和半球同步的增加有关。这可能会损害信息编码能力，从而损害电机处理能力。多巴胺能活动通过终止长时间的β爆发来限制这种不受控制的β同步，从而对网络状态和运动症状产生积极影响。猝发持续时间的减少也与运动能力的改善有关。总之，我们证明了长时间的β爆发与局部和半球同步的增加有关。这可能会损害信息编码能力，从而损害电机处理能力。多巴胺能活动通过终止长时间的β爆发来限制这种不受控制的β同步，从而对网络状态和运动症状产生积极影响。