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Neurology 2003;60:1744-1749
© 2003 American Academy of Neurology

Effects of levodopa on motor sequence learning in Parkinson’s disease

A. Feigin, MD, M. F. Ghilardi, MD, M. Carbon, MD, C. Edwards, MA, M. Fukuda, MD, V. Dhawan, PhD, C. Margouleff, C. Ghez, MD and D. Eidelberg, MD

From the Center for Neurosciences (Drs. Feigin, Carbon, Fukuda, Dhawan, Margouleff, and Eidelberg, C. Edwards), North Shore–Long Island Jewish Research Institute, and Department of Neurology (Drs. Feigin, Fukuda, Dhawan, Margouleff, and Eidelberg), North Shore University Hospital, Manhasset, and New York University School of Medicine, New York, and Center for Neurobiology and Behavior (Drs. Ghilardi and Ghez), Motor Control Laboratory, Columbia College of Physicians and Surgeons, New York, NY.

Address correspondence and reprint requests to Dr. A. Feigin, Center for Neurosciences, North Shore–Long Island Jewish Research Institute, 350 Community Dr., Manhasset, NY 11030; e-mail: asfeigin{at}aol.com

Background: Dopaminergic therapy with levodopa improves motor function in PD patients, but the effects of levodopa on cognition in PD remain uncertain.

Objective: To use H215O and PET to assess the effect of levodopa infusion on motor sequence learning in PD.

Methods: Seven right-handed PD patients were scanned "on" and "off" levodopa while performing a sequence learning task. The changes in learning performance and regional brain activation that occurred during this intervention were assessed.

Results: During PET imaging, levodopa infusion reduced learning performance as measured by subject report (p < 0.05). This behavioral change was accompanied by enhanced activation during treatment in the right premotor cortex and a decline in the ipsilateral occipital association area (p < 0.01). Levodopa-induced changes in learning-related activation responses in the occipital association cortex correlated with changes in learning indexes (p < 0.01).

Conclusions: Levodopa treatment appears to have subtle detrimental effects on cognitive function in nondemented PD patients. These effects may be mediated through an impairment in brain activation in occipital association cortex.




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