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Epilepsy Res. 2013 Jul;105(1-2):229-33. doi: 10.1016/j.eplepsyres.2012.11.004. Epub 2013 Jan 8.

The role of SLC2A1 in early onset and childhood absence epilepsies.

Author information

1
Department of Neuropediatrics, University Medical Center Schleswig-Holstein, Christian-Albrechts University, Kiel, Germany. Muhle@pedneuro.uni-kiel.de

Abstract

Early Onset Absence Epilepsy constitutes an Idiopathic Generalized Epilepsy with absences starting before the age of four years. Mutations in SLC2A1, encoding the glucose transporter, account for approximately 10% of EOAE cases. The role of SLC2A1 mutations in absence epilepsies with a later onset has not been assessed. We found two mutation carriers in 26 EOAE patients, while no mutations were found in 124 probands affected by CAE or JAE.

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