Department of Neurology, Helsinki University Hospital and Department of Clinical Neurosciences (Neurology), University of Helsinki, Helsinki, Finland; BioMag Laboratory, HUS Medical Imaging Center, University of Helsinki, Aalto University, and Helsinki University Hospital, Helsinki, Finland.
BioMag Laboratory, HUS Medical Imaging Center, University of Helsinki, Aalto University, and Helsinki University Hospital, Helsinki, Finland; Department of Neuroscience and Biomedical Engineering, Aalto University School of Science, Aalto University, Helsinki, Finland.
Neuroimage. 2022 Aug 15;257:119308. doi: 10.1016/j.neuroimage.2022.119308. Epub 2022 May 13.
Exaggerated subthalamic beta oscillatory activity and increased beta range cortico-subthalamic synchrony have crystallized as the electrophysiological hallmarks of Parkinson's disease. Beta oscillatory activity is not tonic but occurs in 'bursts' of transient amplitude increases. In Parkinson's disease, the characteristics of these bursts are altered especially in the basal ganglia. However, beta oscillatory dynamics at the cortical level and how they compare with healthy brain activity is less well studied. We used magnetoencephalography (MEG) to study sensorimotor cortical beta bursting and its modulation by subthalamic deep brain stimulation in Parkinson's disease patients and age-matched healthy controls. We show that the changes in beta bursting amplitude and duration typical of Parkinson's disease can also be observed in the sensorimotor cortex, and that they are modulated by chronic subthalamic deep brain stimulation, which, in turn, is reflected in improved motor function at the behavioural level. In addition to the changes in individual beta bursts, their timing relative to each other was altered in patients compared to controls: bursts were more clustered in untreated Parkinson's disease, occurring in 'bursts of bursts', and re-burst probability was higher for longer compared to shorter bursts. During active deep brain stimulation, the beta bursting in patients resembled healthy controls' data. In summary, both individual bursts' characteristics and burst patterning are affected in Parkinson's disease, and subthalamic deep brain stimulation normalizes some of these changes to resemble healthy controls' beta bursting activity, suggesting a non-invasive biomarker for patient and treatment follow-up.
过度的丘脑下核β振荡活动和增加的β频带皮质-丘脑下核同步性已成为帕金森病的电生理特征。β振荡活动不是紧张性的，而是以“爆发”的短暂幅度增加的形式发生。在帕金森病中，这些爆发的特征发生了改变，特别是在基底神经节中。然而，皮质水平的β振荡动力学及其与健康大脑活动的比较研究较少。我们使用脑磁图（MEG）研究了帕金森病患者和年龄匹配的健康对照组的感觉运动皮质β爆发及其对丘脑下核深部脑刺激的调制。我们表明，帕金森病典型的β爆发幅度和持续时间的变化也可以在感觉运动皮质中观察到，并且可以被慢性丘脑下核深部脑刺激调制，这反过来又反映在行为水平上运动功能的改善。除了单个β爆发的变化外，与对照组相比，它们彼此之间的时间关系在患者中也发生了改变：在未经治疗的帕金森病中，爆发更加聚类，发生“爆发的爆发”，并且与较短的爆发相比，较长的爆发的再爆发概率更高。在主动深部脑刺激期间，患者的β爆发类似于健康对照组的数据。总之，个体爆发的特征和爆发模式都受到帕金森病的影响，而丘脑下核深部脑刺激可以使其中一些变化正常化，类似于健康对照组的β爆发活动，这表明这是一种用于患者和治疗随访的非侵入性生物标志物。
