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

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

doi:10.1093/braincomms/fcaa052

Mikkel C Vinding, Panagiota Tsitsi + Show 5 more

Open Access

https://doi.org/10.1093/braincomms/fcaa052

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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.

Highlights

Parkinson’s disease is a neurodegenerative disease that, most often, initially manifests with motor symptoms such as tremor, rigidity, and bradykinesia
We explored whether beta burst characteristics vary within Parkinson’s patients because of dopaminergic medication; and as a third aim, explored whether beta burst characteristics were related to symptom severity in Parkinson’s disease
When the Parkinson’s patients were OFF medication showed a 6-17% lower beta burst rate compared to healthy controls

Summary

Introduction

Parkinson’s disease is a neurodegenerative disease that, most often, initially manifests with motor symptoms such as tremor, rigidity, and bradykinesia. The dopamine loss leads to widespread functional changes in brain activity; for instance, throughout the basal ganglia-thalamic-cortical network, oscillatory activity in the beta band (13–30 Hz) exhibits systematic disease-related changes in Parkinson’s disease (Jenkinson and Brown, 2011). Increased beta power in the STN and the basal ganglia has further been linked to increased severity of bradykinesia and rigidity in Parkinson’s patients (Kühn et al, 2006; Martin et al, 2018). Disease-related changes in the beta band are found in STN and basal ganglia in Parkinson’s patients but is present in the cortex, from where brain activity can be recorded non-invasively while patients are at rest, using magnetoencephalography (MEG) and electroencephalography (EEG)

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