4.5 Article

Dopaminergic modulation of the default mode network in Parkinson's disease

Journal

EUROPEAN NEUROPSYCHOPHARMACOLOGY
Volume 20, Issue 11, Pages 784-792

Publisher

ELSEVIER
DOI: 10.1016/j.euroneuro.2010.07.001

Keywords

Parkinson's disease; Dopamine; Brain deactivation; fMRI; Posterior cingulate; Medial prefrontal cortex

Funding

  1. Health Ministry, Hospital Protocol of Clinical Research
  2. Institut de Recherches Internationales Servier (IRIS)

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Default mode network (DMN) is characterized by a deactivation of several cortical areas (including medial prefrontal cortex and posterior cingulate cortex) during goal-directed experimental tasks. Few findings are reported on DMN and the involvement of dopaminergic medication on this network in Parkinson's disease (PD). To evaluate the effect of levodopa on DMN deactivation, we conducted a randomized, crossover, placebo-controlled experiment consisting of two fMRI assessments in fourteen non-demented, non-depressed PD patients compared to thirteen healthy volunteers. They received either acute doses of levodopa or placebo in two fMRI sessions. Brain deactivation was evaluated during a facial emotion recognition task. While the control subjects showed a classical brain deactivation pattern during the emotional task, the PD patients taking placebo only deactivated the ventral medial prefrontal cortex. Patients failed to deactivate the posterior midline and lateral parts of DMN network. After levodopa administration, this network was restored conjointly with the improvement of motor dysfunction in PD patients. The levodopa effect on DMN is probably the consequence of a beneficial dopamine (DA) medication effect which leads to a fine tuning of the dopamine level in the motor part of striatum, resulting to a global improvement of physical state of PD patients and consequently an increased attentional resource to external stimuli. The absence of medial prefrontal deactivation impairment may suggest a preserved mesocortical DA system in these patients. (C) 2010 Elsevier B.V. and ECNP. All rights reserved.

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