3 February 2012
Martinu K,
Degroot C,
Madjar C,
Strafella AP,
Monchi O
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.
