https://doi.org/10.55788/e158c1a0
The prevalence of autoantibodies among people with epilepsy is not clear; rates between 5-80% have previously been reported. By determining the prevalence of largely pathogenic antibodies in prospectively recruited outpatients with new-onset focal epilepsy, drug-resistant epilepsy, and seizure-free epilepsy, British researchers aimed to provide a prevalence rate that is generalisable to the broader population of epilepsy patients [1]. They screened collected serum on live cell-based assays for neuronal-surface antibodies (NSAs) to LGI1, CASPR2, contactin-2, DPPX, antibodies to intracellular GAD65, and the GABAA, GABAB, glycine, and NMDA receptors. Overall, autoantibodies were detected in 51/546 (9.3%) epilepsy outpatients:
- new-onset focal epilepsy, 24/232 (10.3%);
- drug-resistant epilepsy, 22/260 (8.5%);
- seizure-free epilepsy, 5/54 (9.3%);
- healthy controls, 0/55 (0%).
New-onset focal epilepsy patients had NSAs only, whereas drug-resistant epilepsy and seizure-free epilepsy cohorts had NSAs and GAD65 antibodies (drug-resistant epilepsy: 11 NSAs, 11 GAD65; seizure-free epilepsy: 2 NSAs, 3 GAD65). In future studies, the pathophysiological role for antibodies in epilepsy should be examined. The authors concluded that the âstrikingâ absence of GAD65 antibodies in new-onset focal epilepsy also warrants explanation.
- McGinty RN, et al. Abstract O3008, EAN 2020.
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Table of Contents: EAN 2020
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How genetic testing can contribute to epilepsy management
Cenobamate effective in focal epilepsy
Sustained seizure reductions with cannabidiol for Lennox-Gastaut syndrome
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Directional DBS superior to omnidirectional DBS
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