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L-dopa treatment increases oscillatory power in the motor cortex of Parkinson's disease patients.
NeuroImage: Clinical ( IF 3.4 ) Pub Date : 2020-04-20 , DOI: 10.1016/j.nicl.2020.102255
Chunyan Cao 1 , Dianyou Li 2 , Shikun Zhan 2 , Chencheng Zhang 2 , Bomin Sun 2 , Vladimir Litvak 3
Affiliation  

Parkinson's disease (PD) is a movement disorder caused by dopaminergic neurodegeneration. Levodopa (L-dopa) is an effective medication for alleviating motor symptoms in PD that has been shown previously to reduce subcortical beta (13-30 Hz) oscillations. How L-dopa influences oscillations in the motor cortex is unclear. In this study, 21 PD patients were recorded with magnetoencephalography (MEG) in L-dopa ON and OFF states. Oscillatory components of resting-state power spectra were compared between the two states and the significant effect was localized using beamforming. Unified Parkinson's Disease Rating Scale (UPDRS) III akinesia and rigidity sub-scores for the most affected hemibody were correlated with source power values for the contralateral hemisphere. An L-dopa-induced power increase was found over the central sensors significant in the 18-30 Hz range (F(1,20) > 14.8, PFWE corr < 0.05, cluster size inference with P = 0.001 cluster-forming threshold). Beamforming localization of this effect revealed distinct peaks at the bilateral sensorimotor cortex. A significant correlation between the magnitude of L-dopa induced 18-30 Hz oscillatory motor-cortical power increase and the degree of improvement in contralateral akinesia and rigidity was found (F(2, 19) = 4.9, pone-tailed = 0.02, R2 = 0.2). Power in the same range was also inversely correlated with combined akinesia and rigidity scores in the L-dopa OFF state (F(2, 19) = 9.2, ptwo-tailed = 0.007, R2 = 0.33) but not in the L-dopa ON state (F(2, 19) = 0.27, ptwo-tailed = 0.6, R2 = 0.01). These results suggest that the role of motor cortical beta oscillations in PD is distinct from that of subcortical beta.

中文翻译:


左旋多巴治疗可增加帕金森病患者运动皮层的振荡能力。



帕金森病(PD)是一种由多巴胺能神经变性引起的运动障碍。左旋多巴 (L-dopa) 是一种有效缓解帕金森病运动症状的药物,此前已被证明可以减少皮层下 β (13-30 Hz) 振荡。左旋多巴如何影响运动皮层的振荡尚不清楚。在这项研究中,21 名 PD 患者在左旋多巴开启和关闭状态下进行了脑磁图 (MEG) 记录。比较两种状态之间的静息态功率谱的振荡分量,并使用波束形成来定位显着影响。受影响最严重的半身的统一帕金森病评定量表 (UPDRS) III 运动不能和僵硬子评分与对侧半球的源功率值相关。在 18-30 Hz 范围内发现中央传感器上左旋多巴引起的功率显着增加(F(1,20) > 14.8,PFWE corr < 0.05,簇大小推断 P = 0.001 簇形成阈值)。这种效应的波束形成定位揭示了双侧感觉运动皮层的明显峰值。发现左旋多巴诱导的 18-30 Hz 振荡运动皮质功率增加的幅度与对侧运动不能和僵硬的改善程度之间存在显着相关性(F(2, 19) = 4.9,pone-tailed = 0.02,R2 = 0.2)。在左旋多巴关闭状态下,相同范围内的功率也与运动不能和僵硬的综合评分呈负相关(F(2, 19) = 9.2,ptwo-tailed = 0.007,R2 = 0.33),但在左旋多巴开启状态下则不然状态(F(2, 19) = 0.27,ptwo-tailed = 0.6,R2 = 0.01)。这些结果表明,运动皮质 β 振荡在 PD 中的作用与皮质下 β 振荡的作用不同。
更新日期:2020-04-22
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