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Levodopa influences striatal activity but does not affect cortical hyper-activity in Parkinson’s disease

Authors

  • K. Martinu,

    1. Functional Neuroimaging Unit, Centre de Recherche, Institut universitaire de Gériatrie de Montréal, 4545 Queen Mary, Montréal, QC, H3W 1W5, Canada
    2. Department of Radiology, Université de Montréal, 2900, boul. Édouard-Montpetit Montréal, QC, H3T 1J4, Canada
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  • C. Degroot,

    1. Functional Neuroimaging Unit, Centre de Recherche, Institut universitaire de Gériatrie de Montréal, 4545 Queen Mary, Montréal, QC, H3W 1W5, Canada
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  • C. Madjar,

    1. Functional Neuroimaging Unit, Centre de Recherche, Institut universitaire de Gériatrie de Montréal, 4545 Queen Mary, Montréal, QC, H3W 1W5, Canada
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  • A. P. Strafella,

    1. Centre for Addiction and Mental Health, 250 College Street, Toronto, ON, M5T 1R8, Canada.
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  • O. Monchi

    1. Functional Neuroimaging Unit, Centre de Recherche, Institut universitaire de Gériatrie de Montréal, 4545 Queen Mary, Montréal, QC, H3W 1W5, Canada
    2. Department of Radiology, Université de Montréal, 2900, boul. Édouard-Montpetit Montréal, QC, H3T 1J4, Canada
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O. Monchi, 1Functional Neuroimaging Unit, as above.
E-mail: oury.monchi@umontreal.ca

Abstract

Motor studies of Parkinson’s disease (PD) have shown cortical hypo-activity in relation to nigrostriatal dopamine depletion. Cognitive studies also identified increased cortical activity in PD. We have previously suggested that the hypo-activity/hyper-activity patterns observed in PD are related to the striatal contribution. Tasks that recruit the striatum in control participants are associated with cortical hypo-activity in patients with PD, whereas tasks that do not result in cortical hyper-activity. The putamen, a structure affected by the neurodegeneration observed in PD, shows increased activation for externally-triggered (ET) and self-initiated (SI) movements. The first goal of this study was to evaluate the effect of levodopa on the putamen’s response to ET and SI movements. Our second goal was to assess the effect of levodopa on the hypo-activity/hyper-activity patterns in cortical areas. Patients with PD on and off levodopa and healthy volunteers performed SI, ET and control finger movements during functional magnetic resonance imaging. Healthy participants displayed significant differences in putamen activity in ET and SI movements. These differences were reduced in patients off medication, with non-task-specific increases in activity after levodopa administration. Furthermore, the ventrolateral prefrontal cortex showed significant increases in activity during SI movements in healthy controls, whereas it was hypo-active in PD. This region showed significantly increased activity during ET movements in patients off medication. Levodopa had no effect on this discrepancy. Our results suggest that dopamine replacement therapy has a non-task-specific effect on motor corticostriatal regions, and support the hypothesis that increases and decreases in cortical activity in PD are related to the mesocortical dopamine pathway imbalance.

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