Oscillatory and non-oscillatory features of the magnetoencephalic sensorimotor rhythm in Parkinson’s disease

Abstract

Parkinson’s disease (PD) is associated with changes in neural activity in the sensorimotor alpha and beta bands. Using magnetoencephalography (MEG), we investigated the role of spontaneous neuronal activity within the somatosensory cortex in a large cohort of early- to mid-stage PD patients (N = 78) on Parkinsonian medication and age- and sex-matched healthy controls (N = 60) using source reconstructed resting-state MEG. We quantified features of the time series data in terms of oscillatory alpha power and central alpha frequency, beta power and central beta frequency, and 1/f broadband characteristics using power spectral density. Furthermore, we characterised transient oscillatory burst events in the mu-beta band time-domain signals. We examined the relationship between these signal features and the patients’ disease state, symptom severity, age, sex, and cortical thickness. PD patients and healthy controls differed on PSD broadband characteristics, with PD patients showing a steeper 1/f exponential slope and higher 1/f offset. PD patients further showed a steeper age-related decrease in the burst rate. Out of all the signal features of the sensorimotor activity, the burst rate was associated with increased severity of bradykinesia, whereas the burst duration was associated with axial symptoms. Our study shows that general non-oscillatory features (broadband 1/f exponent and offset) of the sensorimotor signals are related to disease state and oscillatory burst rate scales with symptom severity in PD.

Coordinated reset stimulation of plastic neural networks with spatially dependent synaptic connections

“…Parkinson’s disease is accompanied by synaptic reorganization ( Fan et al, 2012 ; Miguelez et al, 2012 ; Chu et al, 2017 ; Pamukcu et al, 2020 ; Madadi Asl et al, 2022 ) and changes of neuronal activity ( Hammond et al, 2007 ; Neumann et al, 2016 ; Vinding et al, 2024 ) in several brain areas. The severity of motor symptoms, such as bradykinesia and rigidity, correlates with excessive neuronal synchrony (see, e.g., Hammond et al, 2007 ; Neumann et al, 2016 ).…”