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First published online November 7, 2008, 10.2967/jnumed.108.054668
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Journal of Nuclear Medicine Vol. 49 No. 12 2006-2011
© 2008 by Society of Nuclear Medicine

doi: 10.2967/jnumed.108.054668

Clinical Investigation

Changes in Cerebral Glucose Metabolism in Patients with Parkinson Disease with Dementia After Cholinesterase Inhibitor Therapy

Phil Hyu Lee*,1, Seok Woo Yong*,2 and Young-Sil An3

1 Department of Neurology, Yonsei University College of Medicine, Seoul, South Korea; 2 Department of Neurology, Ajou University School of Medicine, Suwon, South Korea; and 3 Department of Nuclear Medicine, Kyung Hee University School of Medicine, Seoul, South Korea

Correspondence: For correspondence or reprints contact: Phil Hyu Lee, Department of Neurology, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, Seoul 120-752, South Korea. E-mail: phisland{at}chol.com

We investigated changes in cerebral glucose metabolism after cholinesterase inhibitor (ChEI) therapy in patients with Parkinson disease dementia (PDD) to determine whether cognitive improvements would be reflected in changes of cerebral metabolic patterns, thus offering insight into the neural substrate of cognitive dysfunction in patients with PDD. Methods: We performed a serial PET study before (baseline) and after ChEI therapy on 10 patients with PDD, using statistical parametric mapping. Additionally, covariance analysis was performed to extract regions in which increased change in regional cerebral metabolism correlated significantly with increased Mini-Mental State Examination scores. Results: The statistical parametric mapping analysis indicated that significantly increased cerebral metabolism after ChEI therapy, compared with at baseline, was most evident in the left angular gyrus extending to the supramarginal area and left superior and middle frontal gyri. Additionally, cerebral metabolism was significantly increased in the right superior frontal and left middle orbitofrontal gyri. In contrast, the right fusiform gyrus showed significantly decreased metabolism after ChEI, compared with at baseline. In the correlation analysis, improvements in Mini-Mental State Examination scores after ChEI treatment were significantly associated with increased cerebral metabolism in the left supramarginal, orbitofrontal, and cingulate areas. Conclusion: Our data suggest that prefrontal and parietal association areas may be relevant structures for the pharmacologic response to ChEI in patients with PDD.

Key Words: neurology • PET • cerebral metabolism • Parkinson disease dementia • cholinesterase inhibitor

* Contributed equally to this work.

COPYRIGHT © 2008 by the Society of Nuclear Medicine, Inc.


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