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NEUROLOGY 2007;68:1062-1068
© 2007 American Academy of Neurology

Cognitive slowing in Parkinson disease is accompanied by hypofunctioning of the striatum

N. Sawamoto, MD, PhD, M. Honda, MD, PhD, T. Hanakawa, MD, PhD, T. Aso, MD, M. Inoue, MD, H. Toyoda, MD, K. Ishizu, MD, PhD, H. Fukuyama, MD, PhD and H. Shibasaki, MD, PhD

From the Human Brain Research Center (N.S., M.H., T.H., T.A., M.I., H.F., H.S.), Kyoto University Graduate School of Medicine, Kyoto, Japan; Nano-Medicine Merger Education Unit (N.S.), Kyoto University, Kyoto, Japan; Department of Cortical Function Disorders (M.H., T.H.), National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan; SORST (M.H.), Japan Science and Technology Agency, Kawaguchi, Japan; Laboratory of Cerebral Integration (H.T.), National Institute for Physiological Sciences, Okazaki, Japan; Department of Nuclear Medicine (H.T., K.I.), Kyoto University Graduate School of Medicine, Kyoto, Japan. Dr. Shibasaki is currently at Takeda General Hospital, Kyoto, Japan.

Address correspondence and reprint requests to Dr. Manabu Honda, Department of Cortical Function Disorders, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-Higashi, Kodaira, Tokyo 187-8502, Japan; e-mail: honda{at}ncnp.go.jp

Objective: To investigate whether cognitive slowing in Parkinson disease (PD) reflects disruption of the basal ganglia or dysfunction of the frontal lobe by excluding an influence of abnormal brain activity due to motor deficits.

Methods: We measured neuronal activity during a verbal mental-operation task with H215O PET. This task enabled us to evaluate brain activity change associated with an increase in the cognitive speed without an influence on motor deficits.

Results: As the speed of the verbal mental-operation task increased, healthy controls exhibited proportional increase in activities in the anterior striatum and medial premotor cortex, suggesting the involvement of the corticobasal ganglia circuit in normal performance of the task. By contrast, patients with PD lacked an increase in the striatal activity, whereas the medial premotor cortex showed a proportional increase.

Conclusions: Although the present study chose a liberal threshold and needs subsequent confirmation, the findings suggest that striatal disruption resulting in abnormal processing in the corticobasal ganglia circuit may contribute to cognitive slowing in Parkinson disease, as is the case in motor slowing.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the March 27 issue to find the title link for this article.

This research is partly funded by Grant-in-Aid for Scientific Research on Priority Areas System study on higher-order brain functions (18020014) and for Young Scientists (B) from the Ministry of Education, Culture, Sports, Science, and Technology of Japan.

Disclosure: The authors report no conflicts of interest.

Received February 10, 2006. Accepted in final form November 27, 2006.


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