Abstract

Fast rhythms excess is a hallmark of Parkinson’s Disease (PD). To implement innovative, non-pharmacological, neurostimulation interventions to restore cortical-cortical interactions, we need to understand the neurophysiological mechanisms underlying these phenomena. Here, we investigated effective connectivity on source-level resting-state electroencephalography (EEG) signals in 15 PD participants and 10 healthy controls. First, we fitted multivariate auto-regressive models to the EEG source waveforms. Second, we estimated causal connections using Granger Causality, which provide information on connections’ strength and directionality. Lastly, we sought significant differences connectivity patterns between the two populations characterizing the network graph features—i.e., global efficiency and node strength. Causal brain networks in PD show overall poorer and weaker connections compared to controls quantified as a reduction of global efficiency. Motor areas appear almost isolated, with a strongly impoverished information flow particularly from parietal and occipital cortices. This striking isolation of motor areas may reflect an impaired sensory-motor integration in PD. The identification of defective nodes/edges in PD network may be a biomarker of disease and a potential target for future interventional trials.

Highlights

  • Parkinson’s disease (PD) main clinical features are motor symptoms, which have a causal factor in dopamine depletion in the basal ganglia circuit [1]

  • Controls showed a higher number of connections; almost all of them, regardless of their origin, were directed to bilateral central regions

  • The diagonal elements of the matrix are set to zero, since they represent connections from a regions of interest (ROIs) to itself. (c,d) Grand-average percentage matrices for (c) controls (d) and PD participants: values in the matrix are reported as the result of the ratio, e.g., 0.77 = 100 which corresponds to 77%

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Summary

Introduction

Parkinson’s disease (PD) main clinical features are motor symptoms, which have a causal factor in dopamine depletion in the basal ganglia circuit [1]. This degenerative process translates in abnormally fast oscillatory activity expressed in the cortico-basal loop, with frequencies ranging up to 200–250 Hz [2]. At scalp level, this activity may be only recorded as beta frequency, due to the impedance and attenuation processes to which the travelling signal undergoes while passing through brain tissue, cerebrospinal fluid and bone. Effective connectivity studies the direct influence that one cortical area may exerts over another and describes the direction of the interaction

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