Send to:

Choose Destination
See comment in PubMed Commons below
Eur Neuropsychopharmacol. 2010 Nov;20(11):784-92. doi: 10.1016/j.euroneuro.2010.07.001. Epub 2010 Jul 31.

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

Author information

  • 1Emotion center, CNRS USR 3246, Paris, France.


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.

Copyright © 2010 Elsevier B.V. All rights reserved.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk