Home > Neurology > EAN 2020 > Epilepsy > Prevalence of autoantibodies in epilepsy almost 10%

Prevalence of autoantibodies in epilepsy almost 10%

Presented by
Dr Ronan McGinty, University of Oxford, UK
Conference
EAN 2020
Doi
https://doi.org/10.55788/e158c1a0
At clinics in the UK, 9.3% of epilepsy outpatients had potentially pathogenic autoantibodies. The proportion of antibody-positive patients was similar across patients with new-onset focal epilepsy, drug-resistant epilepsy, and seizure-free epilepsy.

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 “striking” absence of GAD65 antibodies in new-onset focal epilepsy also warrants explanation.

 

  1. McGinty RN, et al. Abstract O3008, EAN 2020.

 



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