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May 7, 2008

Reduced dopamine transporter binding in patients with juvenile myoclonic epilepsy

C. Ciumas, MD, PhD, T-B Robins Wahlin, PhD, A. Jucaite, MD, PhD, P. Lindstrom, MD, PhD, C. Halldin, PhD, and I. Savic, MD, PhDAuthors Info & Affiliations
September 9, 2008 issue
71 (11) 788-794
https://doi.org/10.1212/01.wnl.0000316120.70504.d5
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Abstract

Background: Behavioral and cognitive problems are frequently encountered in juvenile myoclonic epilepsy (JME). The underlying mechanisms are unknown. Based on previous data showing that the dopamine system is involved in motor as well as cognitive functions, we tested whether JME may be associated with changes in this system, and if such changes are linked to interictal dysfunctions in these patients.
Method: PET and [11C]PE2I was used to investigate the regional binding potential to the dopamine transporter (DAT) in 12 patients with JME and 12 healthy controls. Binding potential was calculated in the midbrain, substantia nigra, caudate, and putamen. We also tested possible correlations between the respective measures and performance in several neuropsychological tests.
Results: Patients had a reduced binding potential in the substantia nigra and midbrain (p = 0.009 and 0.007), and normal values in the caudate and putamen. They also exhibited impaired psychomotor speed and motor function, which in some tests correlated with DAT binding potential in the midbrain.
Conclusion: Dopamine signaling seems impaired in the target regions for dopaminergic neurons (the striatum and frontal lobe), and related to several interictal dysfunctions in JME. The findings add a new aspect to the pathophysiology of JME.

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Supplementary Material

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File (revised-from-au-at-proofs-appendix_table_e-1.doc)
File (table_e-2_and_e-3.doc)

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Information & Authors

Information

Published In

Neurology®
Volume 71 • Number 11 • September 9, 2008
Pages: 788-794
PubMed: 18463366

Copyright

© 2008.

Publication History

Published online: May 7, 2008
Published in print: September 9, 2008

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Authors

Affiliations & Disclosures

C. Ciumas, MD, PhD
From the Department of Clinical Neuroscience, Division of Neurology (C.C., P.L., I.S.), Department of Neurobiology, Care Sciences and Society (T.-B.R.W.), Karolinska University Hospital, Woman and Child Health (A.J.), and Department of Clinical Neuroscience, Section of Psychiatry (C.H.), Karolinska Institutet, Stockholm; Stockholm Brain Institute (C.C., A.J., P.L., C.H., I.S.), Sweden; and Alzheimer’s Disease Research Unit (T.-B.R.W.), Discipline of Psychiatry, School of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital, Brisbane, Australia.
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T-B Robins Wahlin, PhD
From the Department of Clinical Neuroscience, Division of Neurology (C.C., P.L., I.S.), Department of Neurobiology, Care Sciences and Society (T.-B.R.W.), Karolinska University Hospital, Woman and Child Health (A.J.), and Department of Clinical Neuroscience, Section of Psychiatry (C.H.), Karolinska Institutet, Stockholm; Stockholm Brain Institute (C.C., A.J., P.L., C.H., I.S.), Sweden; and Alzheimer’s Disease Research Unit (T.-B.R.W.), Discipline of Psychiatry, School of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital, Brisbane, Australia.
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A. Jucaite, MD, PhD
From the Department of Clinical Neuroscience, Division of Neurology (C.C., P.L., I.S.), Department of Neurobiology, Care Sciences and Society (T.-B.R.W.), Karolinska University Hospital, Woman and Child Health (A.J.), and Department of Clinical Neuroscience, Section of Psychiatry (C.H.), Karolinska Institutet, Stockholm; Stockholm Brain Institute (C.C., A.J., P.L., C.H., I.S.), Sweden; and Alzheimer’s Disease Research Unit (T.-B.R.W.), Discipline of Psychiatry, School of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital, Brisbane, Australia.
View all articles by this author
P. Lindstrom, MD, PhD
From the Department of Clinical Neuroscience, Division of Neurology (C.C., P.L., I.S.), Department of Neurobiology, Care Sciences and Society (T.-B.R.W.), Karolinska University Hospital, Woman and Child Health (A.J.), and Department of Clinical Neuroscience, Section of Psychiatry (C.H.), Karolinska Institutet, Stockholm; Stockholm Brain Institute (C.C., A.J., P.L., C.H., I.S.), Sweden; and Alzheimer’s Disease Research Unit (T.-B.R.W.), Discipline of Psychiatry, School of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital, Brisbane, Australia.
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C. Halldin, PhD
From the Department of Clinical Neuroscience, Division of Neurology (C.C., P.L., I.S.), Department of Neurobiology, Care Sciences and Society (T.-B.R.W.), Karolinska University Hospital, Woman and Child Health (A.J.), and Department of Clinical Neuroscience, Section of Psychiatry (C.H.), Karolinska Institutet, Stockholm; Stockholm Brain Institute (C.C., A.J., P.L., C.H., I.S.), Sweden; and Alzheimer’s Disease Research Unit (T.-B.R.W.), Discipline of Psychiatry, School of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital, Brisbane, Australia.
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I. Savic, MD, PhD
From the Department of Clinical Neuroscience, Division of Neurology (C.C., P.L., I.S.), Department of Neurobiology, Care Sciences and Society (T.-B.R.W.), Karolinska University Hospital, Woman and Child Health (A.J.), and Department of Clinical Neuroscience, Section of Psychiatry (C.H.), Karolinska Institutet, Stockholm; Stockholm Brain Institute (C.C., A.J., P.L., C.H., I.S.), Sweden; and Alzheimer’s Disease Research Unit (T.-B.R.W.), Discipline of Psychiatry, School of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital, Brisbane, Australia.
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Notes

Address correspondence and reprint requests to Dr. Ivanka Savic, Stockholm Brain Institute, Karolinska Institutet, Dept. of Clinical Neuroscience, Karolinska University Hospital, MR Centre, 171 76 Stockholm, Sweden [email protected]

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