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The role of neuroinflammation in initiating or maintaining epileptic activity has been establishe.
This study aimed to evaluate the clinical characteristics, epilepsy semiotics, paraclinical findings, and treatment options of epilepsy patients with secondary AEs in a large retrospective multicenter cohor.
A ten-year (2010 to 2020) retrospective observational cohort study was conducte.
Antibody type
All paired serum and cerebrospinal fluid samples were analyzed for anti-neural antibodies using commercial kits (Euroimmon, Germany) or in-house assay.
Overall, 263 patients (138 women; median age 55 years, range 4-86) were followed for 30 months (range 12-120.
Immunotherapy for responders
Anti-neural antibodies were detected in 167 patients (650%), of which 133 (765%) had antibodies against neuronal cell surface antigens: LGI1 (n=64), NMDAR (n=48), Caspr2 (n=14) , GABAAR (n=3), GABABR (n=2), GlyR (n=1.
The recognition of seizures secondary to AEs represents a rare opportunity for etiology-driven seizure managemen.