Martin Elisak1, David Krysl2, Jitka Hanzalova3, Kamila Volna4, Christian G Bien5, Frank Leypoldt6, Petr Marusic4. 1. Department of Neurology, Second Faculty of Medicine, Charles University, Motol University Hospital, Czech Republic. Electronic address: martin.elisak@fnmotol.cz. 2. Institute of Neuroscience and Physiology, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden. 3. Department of Neurology, Second Faculty of Medicine, Charles University, Motol University Hospital, Czech Republic; Department of Immunology, Second Faculty of Medicine, Charles University, Motol University Hospital, Czech Republic. 4. Department of Neurology, Second Faculty of Medicine, Charles University, Motol University Hospital, Czech Republic. 5. Epilepsy Centre Bethel, Krankenhaus Mara, Bielefeld, Germany. 6. Neuroimmunology, Inst. of Clinical Chemistry and Dep. of Neurology, UKSH, Kiel, Germany.
Abstract
PURPOSE: Epileptic seizures are a common manifestation of autoimmune encephalitis, but the role of neural antibodies in long-term epilepsy remains unclear. The aim of this study was to assess the prevalence of neural-surface antibodies (NSAbs) and antibodies against glutamic acid decarboxylase (GAD) in patients with chronic temporal lobe epilepsy (TLE). METHOD: Patients with an electro-clinical diagnosis of TLE and a disease duration longer than one year were included. NSAbs (LGI1, CASPR2, AMPAR1/2, NMDAR, GABABR) and antibodies against GAD were detected. Only patients with significant antibody levels in serum, and/or positivity in CSF (according to antibody subtype), were enrolled in the seropositive group. Cohorts of seropositive and seronegative patients were compared regarding clinical and imaging data. RESULTS: Significant serum levels of antibodies were detected in eight out of 163 (5%) TLE patients (CASPR2 n = 2, GAD n = 3, LGI1 n = 2, and GABABR n = 1). In four of them, antibodies were detected in the CSF as well (CASPR2 in one, GAD in three). Five seropositive patients had uni- or bilateral temporal lobe lesions on MRI and three patients were non-lesional. All seropositive patients had TLE of unknown cause. Seropositive patients had higher age at epilepsy onset and autoimmune comorbidity, but did not differ in other clinical, EEG or neuroimaging characteristics. Response to immunotherapy (seizure reduction >50%) was observed in three of the six patients treated. CONCLUSIONS: Besides older age at epilepsy onset and autoimmune comorbidity, seropositive patients cannot be distinguished from seronegative patients on the basis of clinical, EEG or neuroimaging data.
PURPOSE:Epileptic seizures are a common manifestation of autoimmune encephalitis, but the role of neural antibodies in long-term epilepsy remains unclear. The aim of this study was to assess the prevalence of neural-surface antibodies (NSAbs) and antibodies against glutamic acid decarboxylase (GAD) in patients with chronic temporal lobe epilepsy (TLE). METHOD:Patients with an electro-clinical diagnosis of TLE and a disease duration longer than one year were included. NSAbs (LGI1, CASPR2, AMPAR1/2, NMDAR, GABABR) and antibodies against GAD were detected. Only patients with significant antibody levels in serum, and/or positivity in CSF (according to antibody subtype), were enrolled in the seropositive group. Cohorts of seropositive and seronegative patients were compared regarding clinical and imaging data. RESULTS: Significant serum levels of antibodies were detected in eight out of 163 (5%) TLEpatients (CASPR2 n = 2, GAD n = 3, LGI1 n = 2, and GABABR n = 1). In four of them, antibodies were detected in the CSF as well (CASPR2 in one, GAD in three). Five seropositive patients had uni- or bilateral temporal lobe lesions on MRI and three patients were non-lesional. All seropositive patients had TLE of unknown cause. Seropositive patients had higher age at epilepsy onset and autoimmune comorbidity, but did not differ in other clinical, EEG or neuroimaging characteristics. Response to immunotherapy (seizure reduction >50%) was observed in three of the six patients treated. CONCLUSIONS: Besides older age at epilepsy onset and autoimmune comorbidity, seropositive patients cannot be distinguished from seronegative patients on the basis of clinical, EEG or neuroimaging data.
Authors: Anna E M Bastiaansen; Hana Mojzisova; Marienke A A M de Bruijn; Agnes van Sonderen; Roland D Thijs; Marian J M Majoie; Rob P W Rouhl; Marleen H van Coevorden-Hameete; Juna M de Vries; Amaia Muñoz Lopetegi; Bob Roozenbeek; Marco W J Schreurs; Peter A E Sillevis Smitt; Maarten J Titulaer Journal: Ann Neurol Date: 2021-01-27 Impact factor: 10.422
Authors: Gabriela Dumitrita Stanciu; Veronica Bild; Daniela Carmen Ababei; Razvan Nicolae Rusu; Sorin Ioan Beschea Chiriac; Elena Rezuş; Andrei Luca Journal: Int J Mol Sci Date: 2019-09-13 Impact factor: 5.923