Cortical beta burst dynamics are altered in Parkinson's disease but normalized by deep brain stimulation

NeuroImage

Olesia Korsun¹  Jukka Nenonen²  Mia Liljeström³  Jussi Nurminen⁴  Hanna Renvall⁴  Eero Pekkonen⁴  K. Amande M. Pauls⁵  Jan Kujala⁶ 

[1] BioMag Laboratory, HUS Medical Imaging Center, University of Helsinki, Aalto University, and Helsinki University Hospital, Helsinki, Finland;Corresponding author at: BioMag Laboratory, HUS Medical imaging Center, Helsinki University Hospital, Haartmaninkatu, 00290 Helsinki, Finnland.;Department of Neuroscience and Biomedical Engineering, Aalto University School of Science, Aalto University, Helsinki, Finland;BioMag Laboratory, HUS Medical Imaging Center, University of Helsinki, Aalto University, and Helsinki University Hospital, Helsinki, Finland;Department of Neurology, Helsinki University Hospital and Department of Clinical Neurosciences (Neurology), University of Helsinki, Helsinki, Finland;Megin Oy, Espoo, Finland;

关键词: Parkinson's disease;    Magnetoencephalography;    Beta burst;    Deep brain stimulation;    Oscillatory activity;    Resting state;   

DOI  :  

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown