Apathy scores in Parkinson’s disease relate to EEG components in an incentivized motor task

Author:

Lee Soojin1ORCID,Song Esther12,Zhu Maria13,Appel-Cresswell Silke14,McKeown Martin J14ORCID

Affiliation:

1. Pacific Parkinson’s Research Centre, The University of British Columbia , Vancouver, BC V6T 2B5 , Canada

2. Department of Psychiatry, The University of British Columbia , Vancouver, BC V6T 2A1 , Canada

3. Department of Medicine, The University of British Columbia , Vancouver, BC V6T 1Z3 , Canada

4. Division of Neurology, Department of Medicine, The University of British Columbia , Vancouver, BC V6T 2B5 , Canada

Abstract

Abstract Apathy is one of the most prevalent non-motor symptoms of Parkinson’s disease and is characterized by decreased goal-directed behaviour due to a lack of motivation and/or impaired emotional reactivity. Despite its high prevalence, the neurophysiological mechanisms underlying apathy in Parkinson’s disease, which may guide neuromodulation interventions, are poorly understood. Here, we investigated the neural oscillatory characteristics of apathy in Parkinson’s disease using EEG data recorded during an incentivized motor task. Thirteen Parkinson’s disease patients with apathy and 13 Parkinson’s disease patients without apathy as well as 12 healthy controls were instructed to squeeze a hand grip device to earn a monetary reward proportional to the grip force they used. Event-related spectral perturbations during the presentation of a reward cue and squeezing were analysed using multiset canonical correlation analysis to detect different orthogonal components of temporally consistent event-related spectral perturbations across trials and participants. The first component, predominantly located over parietal regions, demonstrated suppression of low-beta (12–20 Hz) power (i.e. beta desynchronization) during reward cue presentation that was significantly smaller in Parkinson’s disease patients with apathy compared with healthy controls. Unlike traditional event-related spectral perturbation analysis, the beta desynchronization in this component was significantly correlated with clinical apathy scores. Higher monetary rewards resulted in larger beta desynchronization in healthy controls but not Parkinson’s disease patients. The second component contained gamma and theta frequencies and demonstrated exaggerated theta (4–8 Hz) power in Parkinson’s disease patients with apathy during the reward cue and squeezing compared with healthy controls (HCs), and this was positively correlated with Montreal Cognitive Assessment scores. The third component, over central regions, demonstrated significantly different beta power across groups, with apathetic groups having the lowest beta power. Our results emphasize that altered low-beta and low-theta oscillations are critical for reward processing and motor planning in Parkinson’s disease patients with apathy and these may provide a target for non-invasive neuromodulation.

Funder

John Nichol Chair in Parkinson’s Research

Canadian Institutes of Health Research

Publisher

Oxford University Press (OUP)

Reference77 articles.

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