Relevant conflicts of interest/financial disclosures: Nothing to report.
Version of Record online: 29 APR 2011
Copyright © 2011 Movement Disorder Society
Volume 26, Issue 8, pages 1451–1457, July 2011
How to Cite
Kapogiannis, D., Mooshagian, E., Campion, P., Grafman, J., Zimmermann, T. J., Ladt, K. C. and Wassermann, E. M. (2011), Reward processing abnormalities in Parkinson's disease. Mov. Disord., 26: 1451–1457. doi: 10.1002/mds.23701
Funding for this work came exclusively from the Clinical Neuroscience Program of the National Institute of Neurological Disorders and Stroke and the Intramural Research Program of the National Institute on Aging (to Dr. Kapogiannis), National Institutes of Health, and the Center for Neuroscience and Regenerative Medicine at the Uniformed Service University of the Health Sciences, via the Henry Jackson foundation (to Dr. Mooshagian).
Full financial disclosures and author roles may be found in the online version of this article.
- Issue online: 21 JUL 2011
- Version of Record online: 29 APR 2011
- Manuscript Accepted: 7 FEB 2011
- Manuscript Revised: 6 JAN 2011
- Manuscript Received: 1 OCT 2010
- transcranial magnetic stimulation;
- motor cortex
The primary motor cortex is important for motor learning and response selection, functions that require information on the expected and actual outcomes of behavior. Therefore, it should receive signals related to reward. Pathways from reward centers to motor cortex exist in primates. Previously, we showed that gamma aminobutyric acid–A–mediated inhibition in the motor cortex, measured by paired transcranial magnetic stimulation, changes with expectation and uncertainty of money rewards generated by a slot machine simulation. We examined the role of dopamine in this phenomenon by testing 13 mildly affected patients with Parkinson's disease, off and on dopaminergic medications, and 13 healthy, age-matched controls. Consistent with a dopaminergic mechanism, reward expectation or predictability modulated the response to paired transcranial magnetic stimulation in controls, but not in unmedicated patients. A single dose of pramipexole restored this effect of reward, mainly by increasing the paired transcranial magnetic stimulation response amplitude during low expectation. Levodopa produced no such effect. Both pramipexole and levodopa increased risk-taking behavior on the Iowa Gambling Task. However, pramipexole increased risk-taking behavior more in patients showing lower paired transcranial magnetic stimulation response amplitude during low expectation. These results provide evidence that modulation of motor cortex inhibition by reward is mediated by dopamine signaling and that the physiological state of the motor cortex changes with risk-taking tendency in patients on pramipexole. The cortical response to reward expectation may represent an endophenotype for risk-taking behavior in patients on agonist treatment. © 2011 Movement Disorder Society