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Regional effects of lamotrigine on cerebral glucose metabolism in idiopathic generalized epilepsy

Regional effects of lamotrigine on cerebral glucose metabolism in idiopathic generalized epilepsy
Eun Y.J.Woo S.T.Seung B.H.
Ewha Authors
Issue Date
Journal Title
Archives of Neurology
0003-9942JCR Link
vol. 63, no. 9, pp. 1282 - 1286
Background: Antiepileptic drugs have been reported to affect cerebral metabolism. We performed 18F-fluorodeoxyglucose positron emission tomography (PET) before and after lamotrigine administration to investigate its effects on cerebral glucose metabolism in patients with drug-naïve idiopathic generalized epilepsy. Design: We included patients who were newly diagnosed as having idiopathic generalized epilepsy or who had not taken an antiepileptic drug after the diagnosis was made. Antiepileptic drug 18F-fluorodeoxyglucose PETs were obtained before and after lamotrigine administration in 21 subjects (male-female ratio, 10:11; mean±SD age, 24.3±2.8 years). The mean lamotrigine dosage was 211.9 mg/d (range, 175.0-275.0 mg/d). For statistical parametric mapping analysis, all PET images were spatially normalized to the standard PET template and then smoothed using a 14-mm full width at half-maximum gaussian kernel. The paired t test was used to compare premedication and postmedication 18F-fluorodeoxyglucoae PET images. Results: After lamotrigine administration, cerebral metabolism was decreased in bilateral thalami, bilateral caudate nuclei, the left side of the putamen, the left entorhinal area, bilateral parahippocampal gyri, the right inferior temporal gyrus, the left rectosubcallosal gyrus, bilateral superior frontal gyri, the left middle frontal gyrus, the right precentral gyrus, left pericentral gyri, the right superior parietal lobule, and bilateral substantia nigra at P<.05 corrected for multiple comparisons using the false discovery rate approach. No brain region showed increased metabolism after lamotrigine administration. Conclusion: This study revealed that lamotrigine treatment reduces glucose metabolism in the thalamus, basal ganglia, and multiple regions of the cerebral cortex in drug-naïve patients with idiopathic generalized epilepsy. © 2006 American Medical Association. All rights reserved.
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