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Published online before print May 7, 2008, doi:10.1212/01.wnl.0000316120.70504.d5)
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NEUROLOGY 2008;71:788-794
© 2008 American Academy of Neurology

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, 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.

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 ivanka.savic-berglund{at}ki.se

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.

Abbreviations: ANOVA = analysis of variance; DA = dopamine; DAT = dopamine transporter; IGE = idiopathic generalized epilepsy; JME = juvenile myoclonic epilepsy; MANOVA = multivariate analysis of variance; ROIs = regions of interest; WM = working memory.


Supplemental data at www.neurology.org

Editorial, page 784

See also page 795

e-Pub ahead of print on May 7, 2008, at www.neurology.org.

Supported by the Swedish Medical Research Council and the Karolinska Institute. Carolina Ciumas received a stipend from Margarethahemmet and the Swedish Epilepsy Society. Sällskapet Barnavard Foundation financially supported Aurelija Jucaite.

Disclosure: The authors report no disclosures.

Received July 17, 2007. Accepted in final form January 3, 2008.




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Neurology, September 9, 2008; 71(11): 784 - 785.
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