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首页> 外文期刊>NeuroImage: Clinical >Dopaminergic therapy in Parkinson's disease decreases cortical beta band coherence in the resting state and increases cortical beta band power during executive control
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Dopaminergic therapy in Parkinson's disease decreases cortical beta band coherence in the resting state and increases cortical beta band power during executive control

机译:帕金森氏病的多巴胺能疗法可降低静息状态下皮质β带的连贯性并在执行控制过程中增加皮质β带的功率

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It is not yet well understood how dopaminergic therapy improves cognitive and motor function in Parkinson's disease (PD). One possibility is that it reduces the pathological synchronization within and between the cortex and basal ganglia, thus improving neural communication. We tested this hypothesis by recording scalp electroencephalography (EEG) in PD patients when On and Off medication, during a brief resting state epoch (no task), and during performance of a stop signal task that is thought to engage two partially overlapping (or different) frontal-basal-ganglia circuits. For resting state EEG, we measured pair-wise coherence between scalp electrodes in several frequency bands. Consistent with previous studies, in the Off medication state, those patients with the greatest clinical impairment had the strongest coherence, especially in the beta band, indicating pathological over-synchronization. Dopaminergic medication reduced this coherence. For the stop signal task, On vs. Off medication increased beta band power over right frontal cortex for successful stopping and over bilateral sensorimotor cortex for going, especially for those patients who showed greater clinical improvement. Thus, medication reduced pathological coherence in beta band at rest and increased task related beta power for two potentially dissociable cortico-basal ganglia circuits. These results support the hypothesis that dopaminergic medication in PD improves neural communication both at rest and for executive and motor function. Highlights ? EEG measured in PD while On/Off medication during rest and an executive control task. ? Dopaminergic therapy reduces pathological locking jointly with clinical improvement. ? Medication increases beta power during successful stopping over right frontal cortex.
机译:尚不清楚多巴胺能疗法如何改善帕金森氏病(PD)的认知和运动功能。一种可能性是它减少了皮质与基底神经节之间以及之间的病理同步,从而改善了神经沟通。我们通过记录PD患者开和关药物时,短暂的静息状态时期(无任务)以及执行停止信号任务(被认为参与两个部分重叠(或不同)的停止信号任务)期间记录的头皮脑电图(EEG),验证了这一假设)额叶基底神经节回路。对于静止状态的脑电图,我们测量了几个频带中头皮电极之间的成对相干性。与以前的研究一致,在非药物治疗状态下,那些临床损害最大的患者具有最强的连贯性,尤其是在β谱带中,这表明病理性过度同步。多巴胺能药物减少了这种连贯性。对于停止信号任务,开或关药物可增加右额叶皮层的β带功率,以成功停止,并增加双侧感觉运动皮层的通行能力,特别是对于那些表现出更大临床改善的患者。因此,对于两个潜在的可分离的皮质基底神经节回路,药物可降低静止时β带的病理学连贯性,并增加与任务相关的β能量。这些结果支持以下假设:PD中的多巴胺能药物可改善静止状态以及执行和运动功能的神经沟通。强调 ?在休息和执行控制任务期间开/关用药期间,PD中的EEG值已测量。 ?多巴胺能疗法可减少病理锁定并改善临床状况。 ?在成功停止右额叶皮层期间,药物可增加β能量。

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