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

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Abstract Parkinson’s disease is characterized by a gradual loss of dopaminergic neurons, which are 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 activity—for example, that the beta band exhibits transient bursts of high-amplitude activity. In an exploratory study we used magnetoencephalography (MEG) to record cortical beta band activity to characterize how spontaneous cortical beta bursts manifest in Parkinson’s patients ON and OFF dopaminergic medication, and compare this to matched healthy controls. From three minutes of MEG data, we extracted the time-course of beta band activity from the sensorimotor cortex and characterized high-amplitude epochs in the signal to test if they exhibited burst like properties. We then compared the rate, duration, inter-burst interval, and peak amplitude of the high-amplitude epochs between the Parkinson’s patients and healthy controls. Our results show that Parkinson’s patients OFF medication had a 6-17% lower beta bursts rate compared to healthy controls, while both the duration and the amplitude of the bursts were the same for Parkinson’s patients and 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 PD can be explained primarily by changes in the underlying burst rate. Importantly, our results also revealed a relationship between beta bursts rate and motor symptom severity in PD: a lower burst rate scaled with increased in severity of bradykinesia and postural/kinetic tremor. Beta burst rate might thus serve as neuromarker for Parkinson’s disease that can help in the assessment of symptom severity in Parkinson’s disease or evaluate treatment effectiveness.
Title: Reduction of spontaneous cortical beta bursts in Parkinson’s disease is linked to symptom severity
Description:
Abstract Parkinson’s disease is characterized by a gradual loss of dopaminergic neurons, which are 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 activity—for example, that the beta band exhibits transient bursts of high-amplitude activity.
In an exploratory study we used magnetoencephalography (MEG) to record cortical beta band activity to characterize how spontaneous cortical beta bursts manifest in Parkinson’s patients ON and OFF dopaminergic medication, and compare this to matched healthy controls.
From three minutes of MEG data, we extracted the time-course of beta band activity from the sensorimotor cortex and characterized high-amplitude epochs in the signal to test if they exhibited burst like properties.
We then compared the rate, duration, inter-burst interval, and peak amplitude of the high-amplitude epochs between the Parkinson’s patients and healthy controls.
Our results show that Parkinson’s patients OFF medication had a 6-17% lower beta bursts rate compared to healthy controls, while both the duration and the amplitude of the bursts were the same for Parkinson’s patients and 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 PD can be explained primarily by changes in the underlying burst rate.
Importantly, our results also revealed a relationship between beta bursts rate and motor symptom severity in PD: a lower burst rate scaled with increased in severity of bradykinesia and postural/kinetic tremor.
Beta burst rate might thus serve as neuromarker for Parkinson’s disease that can help in the assessment of symptom severity in Parkinson’s disease or evaluate treatment effectiveness.

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