Institute of Clinical Neuroscience and Medical Psychology, Heinrich Heine University, Düsseldorf, Germany.
Exp Neurol. 2011 Jun;229(2):324-31. doi: 10.1016/j.expneurol.2011.02.015. Epub 2011 Mar 1.
Increasing evidence suggests that abnormal oscillatory activity in basal ganglia and cortex plays a pivotal role in the pathophysiology of Parkinson's disease. Recordings of local field potentials from subthalamic nucleus of patients undergoing deep brain stimulation have focused on oscillations occurring at frequencies below 100 Hz in the alpha, beta and gamma range and suggested that, in particular, an increase of beta band oscillations underlies slowing of movement in Parkinson's disease. Recent findings showing that the amplitude of high frequency oscillations (>200 Hz) couples with the phase of beta activity have raised the important question about the role of subthalamic high frequency oscillations in Parkinson's disease. To investigate functional characteristics and clinical relevance of high frequency oscillations, we recorded local field potentials from 18 subthalamic nuclei of 9 akinetic-rigid Parkinsonian patients with implanted deep brain stimulation electrodes and still externalised leads before and after intake of levodopa. We identified two distinct bands of high frequency oscillations, one centred around 250 Hz and another one around 350 Hz that show characteristic levodopa dependent amplitude and coupling behaviours. Administration of levodopa changed the power ratio between the two high frequency bands towards the component centred around 350 Hz in all 18 nuclei under study (p<10(-4)). Moreover, this power ratio correlated significantly with the Unified Parkinson's Disease Rating Scale hemibody akinesia/rigidity subscore (r=0.3618, p=0.015), but interestingly not with beta peak power (p=0.1) suggesting that levodopa induced changes in high frequency and beta oscillations are at least potentially independent of each other. Accordingly, a combined parameter composed of power ratio of high frequency oscillations and beta peak power significantly increased the correlation with the motor state (r=0.45, p=0.004). These results indicate that a shift from slower to faster frequencies of the spectrum greater than 200 Hz represents a prokinetic neurophysiological marker underlying levodopa induced motor improvement in Parkinson's disease.
越来越多的证据表明,基底神经节和皮层的异常振荡活动在帕金森病的病理生理学中起着关键作用。对接受深部脑刺激的患者的丘脑底核进行局部场电位记录的研究集中在 alpha、beta 和 gamma 频带下低于 100 Hz 的振荡,并表明,特别是帕金森病运动迟缓的基础是 beta 频带振荡的增加。最近的研究结果表明,高频(>200 Hz)振荡的幅度与 beta 活动的相位耦合,提出了一个重要的问题,即丘脑底核高频振荡在帕金森病中的作用。为了研究高频振荡的功能特征和临床相关性,我们记录了 9 例无动性僵硬帕金森病患者的 18 个丘脑底核的局部场电位,这些患者植入了深部脑刺激电极,并在服用左旋多巴前后仍有外部导联。我们确定了两个不同的高频振荡带,一个中心在 250 Hz 左右,另一个在 350 Hz 左右,它们表现出特征性的左旋多巴依赖性幅度和耦合行为。在所有 18 个研究核中,左旋多巴给药改变了两个高频带之间的功率比,偏向于中心在 350 Hz 的成分(p<10(-4))。此外,该功率比与统一帕金森病评定量表偏瘫运动迟缓/僵硬亚评分显著相关(r=0.3618,p=0.015),但有趣的是与 beta 峰值功率无关(p=0.1),这表明左旋多巴诱导的高频和 beta 振荡变化至少可能彼此独立。因此,由高频振荡和 beta 峰值功率的功率比组成的组合参数与运动状态的相关性显著增加(r=0.45,p=0.004)。这些结果表明,频谱中大于 200 Hz 的较慢到较快频率的转变代表了一种促动神经生理学标记,是左旋多巴诱导帕金森病运动改善的基础。
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