Dopaminergic modulation of motor network compensatory mechanisms in Parkinson's disease.


Journal

Human brain mapping
ISSN: 1097-0193
Titre abrégé: Hum Brain Mapp
Pays: United States
ID NLM: 9419065

Informations de publication

Date de publication:
15 10 2019
Historique:
received: 15 02 2019
revised: 28 05 2019
accepted: 27 06 2019
pubmed: 11 7 2019
medline: 21 4 2020
entrez: 11 7 2019
Statut: ppublish

Résumé

The dopaminergic system has a unique gating function in the initiation and execution of movements. When the interhemispheric imbalance of dopamine inherent to the healthy brain is disrupted, as in Parkinson's disease (PD), compensatory mechanisms act to stave off behavioral changes. It has been proposed that two such compensatory mechanisms may be (a) a decrease in motor lateralization, observed in drug-naïve PD patients and (b) reduced inhibition - increased facilitation. Seeking to investigate the differential effect of dopamine depletion and subsequent substitution on compensatory mechanisms in non-drug-naïve PD, we studied 10 PD patients and 16 healthy controls, with patients undergoing two test sessions - "ON" and "OFF" medication. Using a simple visually-cued motor response task and fMRI, we investigated cortical motor activation - in terms of laterality, contra- and ipsilateral percent BOLD signal change and effective connectivity in the parametric empirical Bayes framework. We found that decreased motor lateralization persists in non-drug-naïve PD and is concurrent with decreased contralateral activation in the cortical motor network. Normal lateralization is not reinstated by dopamine substitution. In terms of effective connectivity, disease-related changes primarily affect ipsilaterally-lateralized homotopic cortical motor connections, while medication-related changes affect contralaterally-lateralized homotopic connections. Our findings suggest that, in non-drug-naïve PD, decreased lateralization is no longer an adaptive cortical mechanism, but rather the result of maladaptive changes, related to disease progression and long-term dopamine replacement. These findings highlight the need for the development of noninvasive therapies, which would promote the adaptive mechanisms of the PD brain.

Identifiants

pubmed: 31291039
doi: 10.1002/hbm.24710
pmc: PMC6865418
doi:

Substances chimiques

Dopamine Agonists 0
Dopamine VTD58H1Z2X

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4397-4416

Subventions

Organisme : Fondation Leenaards
Pays : International
Organisme : Fondation ROGER DE SPOELBERCH
Pays : International
Organisme : H2020 Future and Emerging Technologies
ID : 720270
Pays : International
Organisme : Partridge Foundation
Pays : International
Organisme : Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
ID : 32003B_135679
Pays : International
Organisme : Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
ID : 32003B_159780
Pays : International
Organisme : Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
ID : NCCR-Synapsy 125759
Pays : International
Organisme : Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
ID : NCCR-Synapsy 565593
Pays : International

Informations de copyright

© 2019 Wiley Periodicals, Inc.

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Auteurs

Maya A Jastrzębowska (MA)

Laboratory of Psychophysics, Brain Mind Institute, School of Life Sciences, École Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
Laboratory for Research in Neuroimaging (LREN), Department of Clinical Neuroscience, Lausanne University Hospital (CHUV) and University of Lausanne (UNIL), Lausanne, Switzerland.

Renaud Marquis (R)

Laboratory for Research in Neuroimaging (LREN), Department of Clinical Neuroscience, Lausanne University Hospital (CHUV) and University of Lausanne (UNIL), Lausanne, Switzerland.
EEG and Epilepsy Unit, University Hospital of Geneva and Faculty of Medicine, Geneva, Switzerland.

Lester Melie-García (L)

Laboratory for Research in Neuroimaging (LREN), Department of Clinical Neuroscience, Lausanne University Hospital (CHUV) and University of Lausanne (UNIL), Lausanne, Switzerland.

Antoine Lutti (A)

Laboratory for Research in Neuroimaging (LREN), Department of Clinical Neuroscience, Lausanne University Hospital (CHUV) and University of Lausanne (UNIL), Lausanne, Switzerland.

Ferath Kherif (F)

Laboratory for Research in Neuroimaging (LREN), Department of Clinical Neuroscience, Lausanne University Hospital (CHUV) and University of Lausanne (UNIL), Lausanne, Switzerland.

Michael H Herzog (MH)

Laboratory of Psychophysics, Brain Mind Institute, School of Life Sciences, École Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.

Bogdan Draganski (B)

Laboratory for Research in Neuroimaging (LREN), Department of Clinical Neuroscience, Lausanne University Hospital (CHUV) and University of Lausanne (UNIL), Lausanne, Switzerland.
Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany.

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