Reduction of spontaneous cortical beta bursts in Parkinson's disease is linked to symptom severity

Mikkel C Vinding; Panagiota Tsitsi; Josefine Waldthaler; Robert Oostenveld; Martin Ingvar; Per Svenningsson; Daniel Lundqvist

doi:10.1093/braincomms/fcaa052

Reduction of spontaneous cortical beta bursts in Parkinson's disease is linked to symptom severity

Brain Commun. 2020 Apr 28;2(1):fcaa052. doi: 10.1093/braincomms/fcaa052. eCollection 2020.

Authors

Mikkel C Vinding¹, Panagiota Tsitsi², Josefine Waldthaler^{2

3}, Robert Oostenveld^{1

4}, Martin Ingvar^{1

5}, Per Svenningsson², Daniel Lundqvist¹

Affiliations

¹ Department of Clinical Neuroscience, NatMEG, Karolinska Institutet, 171 77 Stockholm, Sweden.
² Department of Clinical Neuroscience, Neuro Svenningsson, Karolinska Institutet, Stockholm, Sweden.
³ Department of Neurology, University Hospital Marburg, Marburg, Germany.
⁴ Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, Netherlands.
⁵ Section of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden.

Abstract

Parkinson's disease is characterized by a gradual loss of dopaminergic neurons, which is associated with altered neuronal activity in the beta-band (13-30 Hz). Assessing beta-band activity typically involves transforming the time-series to get the power of the signal in the frequency domain. Such transformation assumes that the time-series can be reduced to a combination of steady-state sine- and cosine waves. However, recent studies have suggested that this approach masks relevant biophysical features in the beta-band-for example, that the beta-band exhibits transient bursts of high-amplitude activity. In an exploratory study, we used magnetoencephalography to record beta-band activity from the sensorimotor cortex, to characterize how spontaneous cortical beta bursts manifest in Parkinson's patients on and off dopaminergic medication, and compare this to matched healthy controls. We extracted the time-course of beta-band activity from the sensorimotor cortex and characterized bursts in the signal. We then compared the burst rate, duration, inter-burst interval and peak amplitude between the Parkinson's patients and healthy controls. Our results show that Parkinson's patients off medication had a 5-17% lower beta bursts rate compared to healthy controls, while both the duration and the amplitude of the bursts were the same for healthy controls and medicated state of the Parkinson's patients. These data thus support the view that beta bursts are fundamental underlying features of beta-band activity, and show that changes in cortical beta-band power in Parkinson's disease can be explained-primarily by changes in the underlying burst rate. Importantly, our results also revealed a relationship between beta burst rate and motor symptom severity in Parkinson's disease: a lower burst rate scaled with increased severity of bradykinesia and postural/kinetic tremor. Beta burst rate might thus serve as a neuromarker for Parkinson's disease that can help in the assessment of symptom severity in Parkinson's disease or in the evaluation of treatment effectiveness.

Keywords: Parkinson’s disease; beta band; beta bursts; bradykinesia; resting-state.