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Vol. 64, No. 2, 2010
Issue release date: August 2010
Section title: Original Paper
Eur Neurol 2010;64:65–73
(DOI:10.1159/000315036)

Cerebral Glucose Metabolism of Parkinson’s Disease Patients with Mild Cognitive Impairment

Lyoo C.H. · Jeong Y. · Ryu Y.H. · Rinne J.O. · Lee M.S.
Departments of aNeurology and bRadiology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, and cDepartment of Brain and Bioengineering, KAIST, Daejeon, Korea; dTurku PET Center, University of Turku, Turku, Finland

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 3/14/2010
Accepted: 5/11/2010
Published online: 7/1/2010

Number of Print Pages: 9
Number of Figures: 3
Number of Tables: 2

ISSN: 0014-3022 (Print)
eISSN: 1421-9913 (Online)

For additional information: http://www.karger.com/ENE

Abstract

Background: Half of Parkinson’s disease (PD) patients with mild cognitive impairment (MCI) develop dementia. We studied topographic distribution of cerebral hypometabolism in PD with different types of MCI. Methods: This study included 61 nondemented PD patients and 14 age-matched controls. PD patients were grouped into normal cognition (PD-NC, n = 20), single amnestic (PD-SA, n = 12), single nonamnestic (PD-SN, n = 11), and multidomain MCI (PD-MD, n = 18). Using [18F]-fluorodeoxy-glucose PET, cerebral glucose metabolism of MCI groups was compared with that of controls and the PD-NC group. Results: In comparison with controls, PD-NC and PD-SA groups showed no hypometabolic brain areas. However, the PD-SN group showed hypometabolism in parieto-temporo-occipital cortices. The PD-MD group showed widespread hypometabolism that predominantly involved parieto-occipital cortices. In comparison with the PD-NC group, only the PD-MD group showed hypometabolism in lateral frontal, cingulate, and parieto-temporo-occipital cortices. Conclusions: The distribution of hypometabolic brain areas of the PD-MD group suggests that PD-MD seems to be caused by a common pathology with PD dementia. PD-SA and PD-SN seem to be caused by very mild or topographically heterogeneous cerebral dysfunction. Longitudinal clinical and neuroimaging studies are needed to define whether PD patients with single domain MCI progress to PD-MD and finally to dementia.


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 3/14/2010
Accepted: 5/11/2010
Published online: 7/1/2010

Number of Print Pages: 9
Number of Figures: 3
Number of Tables: 2

ISSN: 0014-3022 (Print)
eISSN: 1421-9913 (Online)

For additional information: http://www.karger.com/ENE


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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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