Calcium channel antibodies in patients with absence epilepsy. (1st July 2014)

• Record Type: Journal Article
• Authors: Tektürk, Pınar; Baykan, Betül; Ekizoğlu, Esme; Ulusoy, Canan; Aydin-Özemir, Zeynep; İçöz, Sema; Kınay, Demet; Tüzün, Erdem
• Is Part Of: International journal of neuroscience. Volume 124:Number 7(2014:Jul.)
• Page Start: 486
• Page End: 490
• Publication Date: 2014-07-01
• Subjects: Nervous system -- Periodicals; 612.805
• DOI: 10.3109/00207454.2013.858337
• Languages: English
• ISSNs: 0020-7454

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <p>Autoimmunity has aroused interest in the last years as a contributory mechanism of epilepsy, especially in epilepsies with unknown cause or therapy resistance. Since the relationship of absence epilepsy (AE) with calcium channels is well established, we aimed to investigate related antibodies in patients diagnosed with AE. Consecutive patients with typical absence seizures having either childhood absence epilepsy (CAE) or juvenile absence epilepsy (JAE) with generalized spike and wave discharges on electroencephalography (EEG) were included after their consent. The patients were diagnosed according to the International League Against Epilepsy (ILAE) 2010 criteria. Antibodies against P-Q type voltage gated calcium channels (VGCC) and T-type VGCC subunit Cav3.2 (encoded by the CACNA1H gene) were investigated by RIA and ELISA, respectively. We searched for these antibodies in 32 patients with AE and 53 patients with focal epilepsy of unknown cause (FEOUC) as the disease control group; furthermore, 30 healthy persons served as the healthy controls. Eleven patients (34.3%) with AE had CAE and the remaining patients had JAE. Only a 47-year-old female FEOUC patient, who also had systemic lupus erythematosus with normal MRI scans showed antibodies against P-Q type VGCC, whereas no antibody positivity could be found in other FEOUC and AE patients and healthy controls. Our results might suggest that calcium channel antibodies do not play an important role in the pathophysiology of AE. Further studies with larger groups of other epileptic syndromes are needed to confirm our results.</p> </abstract>