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Risk of Seizure Recurrence Due to Autoimmune Encephalitis With NMDAR, LGI1, CASPR2, and GABABR Antibodies: Implications for Return to Driving

Rada, Anna
Autor Rada, Anna ORCID From the Department of Epileptology (Krankenhaus Mara) (A.R., C.G.B., U.S.), Medical School, Bielefeld University, Campus Bielefeld-Bethel Society for Epilepsy Research (A.H.), Bielefeld, Germany Department of Neurology (C.A.P., M.B.), Odense University Hospital Department of Clinical Research (M.B.), University of Southern Denmark, Odense, Denmark Department of Epileptology (T. Baumgartner, R.S.), University Hospital Bonn, Germany Department of Immunology and Biotechnology (T. Berki), University of Pécs, Medical School, Hungary Department of Neurology (J.B., Y.C., M.J.T., J.M.V.), Erasmus Medical Center, Rotterdam, Zuid-Holland, the Netherlands Division of Epilepsy (J.W.B., K.M.S.), Department of Neurology, Mayo Clinic, Rochester, MN NYU Comprehensive Epilepsy Center (A.C., C. Steriade), New York French Reference Center on Paraneoplastic Neurological Syndromes and Autoimmune Encephalitis (N.L.C.-P., A.F., J. Honnorat, S.M.-C.), Hospices Civils de Lyon, Hôpital Neurologique, UMR MELIS Inserm 1314 / CNRS 5284, Université Claude Bernard Lyon1, France Department of Neurology (M.E., P.M.), Second Faculty of Medicine, Charles University, Motol University Hospital, Prague, Czech Republic Department of Neurology (A.R.F., J. Hébert), Columbia University Irving Medical Center (CUIMC)/New York Presbyterian Hospital, New York Department of Neurology (Z. Hayden), Medical School, University of Pécs, Pécs, Hungary Division of Neurology (J. Hébert), University of Toronto, Ontario, Canada Epilepsy-Center Berlin-Brandenburg (M.H., M.I.-F.), Department of Neurology, Charité - Universitätsmedizin Berlin, Germany Department of Neurology (Z. Hong), West China Hospital, Sichuan University, Chengdu, China Oxford Autoimmune Neurology Group (S.R.I., S.R., C.E.U.), Nuffield Department of Clinical Neurosciences, Oxford, United Kingdom Department of Neurology and Neurosciences (S.R.I.), Mayo Clinic, Jacksonville, FL Department of Neurology with Institute of Translational Neurology (S.K., C. Strippel), University Hospital Münster, Germany Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead Faculty of Medicine and Health, University of Sydney Department of Neurology, Concord Hospital, Sydney, Australia Division of Neurology (C.E.U.), Department of Medicine, University of British Columbia, Vancouver, Canada and Laboratory Krone (C.G.B.), Bad Salzuflen, Germany
Hagemann, Anne
Autor Hagemann, Anne ORCID From the Department of Epileptology (Krankenhaus Mara) (A.R., C.G.B., U.S.), Medical School, Bielefeld University, Campus Bielefeld-Bethel Society for Epilepsy Research (A.H.), Bielefeld, Germany Department of Neurology (C.A.P., M.B.), Odense University Hospital Department of Clinical Research (M.B.), University of Southern Denmark, Odense, Denmark Department of Epileptology (T. Baumgartner, R.S.), University Hospital Bonn, Germany Department of Immunology and Biotechnology (T. Berki), University of Pécs, Medical School, Hungary Department of Neurology (J.B., Y.C., M.J.T., J.M.V.), Erasmus Medical Center, Rotterdam, Zuid-Holland, the Netherlands Division of Epilepsy (J.W.B., K.M.S.), Department of Neurology, Mayo Clinic, Rochester, MN NYU Comprehensive Epilepsy Center (A.C., C. Steriade), New York French Reference Center on Paraneoplastic Neurological Syndromes and Autoimmune Encephalitis (N.L.C.-P., A.F., J. Honnorat, S.M.-C.), Hospices Civils de Lyon, Hôpital Neurologique, UMR MELIS Inserm 1314 / CNRS 5284, Université Claude Bernard Lyon1, France Department of Neurology (M.E., P.M.), Second Faculty of Medicine, Charles University, Motol University Hospital, Prague, Czech Republic Department of Neurology (A.R.F., J. Hébert), Columbia University Irving Medical Center (CUIMC)/New York Presbyterian Hospital, New York Department of Neurology (Z. Hayden), Medical School, University of Pécs, Pécs, Hungary Division of Neurology (J. Hébert), University of Toronto, Ontario, Canada Epilepsy-Center Berlin-Brandenburg (M.H., M.I.-F.), Department of Neurology, Charité - Universitätsmedizin Berlin, Germany Department of Neurology (Z. Hong), West China Hospital, Sichuan University, Chengdu, China Oxford Autoimmune Neurology Group (S.R.I., S.R., C.E.U.), Nuffield Department of Clinical Neurosciences, Oxford, United Kingdom Department of Neurology and Neurosciences (S.R.I.), Mayo Clinic, Jacksonville, FL Department of Neurology with Institute of Translational Neurology (S.K., C. Strippel), University Hospital Münster, Germany Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead Faculty of Medicine and Health, University of Sydney Department of Neurology, Concord Hospital, Sydney, Australia Division of Neurology (C.E.U.), Department of Medicine, University of British Columbia, Vancouver, Canada and Laboratory Krone (C.G.B.), Bad Salzuflen, Germany
Aaberg Poulsen, Charlotte
Autor Aaberg Poulsen, Charlotte From the Department of Epileptology (Krankenhaus Mara) (A.R., C.G.B., U.S.), Medical School, Bielefeld University, Campus Bielefeld-Bethel Society for Epilepsy Research (A.H.), Bielefeld, Germany Department of Neurology (C.A.P., M.B.), Odense University Hospital Department of Clinical Research (M.B.), University of Southern Denmark, Odense, Denmark Department of Epileptology (T. Baumgartner, R.S.), University Hospital Bonn, Germany Department of Immunology and Biotechnology (T. Berki), University of Pécs, Medical School, Hungary Department of Neurology (J.B., Y.C., M.J.T., J.M.V.), Erasmus Medical Center, Rotterdam, Zuid-Holland, the Netherlands Division of Epilepsy (J.W.B., K.M.S.), Department of Neurology, Mayo Clinic, Rochester, MN NYU Comprehensive Epilepsy Center (A.C., C. Steriade), New York French Reference Center on Paraneoplastic Neurological Syndromes and Autoimmune Encephalitis (N.L.C.-P., A.F., J. Honnorat, S.M.-C.), Hospices Civils de Lyon, Hôpital Neurologique, UMR MELIS Inserm 1314 / CNRS 5284, Université Claude Bernard Lyon1, France Department of Neurology (M.E., P.M.), Second Faculty of Medicine, Charles University, Motol University Hospital, Prague, Czech Republic Department of Neurology (A.R.F., J. Hébert), Columbia University Irving Medical Center (CUIMC)/New York Presbyterian Hospital, New York Department of Neurology (Z. Hayden), Medical School, University of Pécs, Pécs, Hungary Division of Neurology (J. Hébert), University of Toronto, Ontario, Canada Epilepsy-Center Berlin-Brandenburg (M.H., M.I.-F.), Department of Neurology, Charité - Universitätsmedizin Berlin, Germany Department of Neurology (Z. Hong), West China Hospital, Sichuan University, Chengdu, China Oxford Autoimmune Neurology Group (S.R.I., S.R., C.E.U.), Nuffield Department of Clinical Neurosciences, Oxford, United Kingdom Department of Neurology and Neurosciences (S.R.I.), Mayo Clinic, Jacksonville, FL Department of Neurology with Institute of Translational Neurology (S.K., C. Strippel), University Hospital Münster, Germany Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead Faculty of Medicine and Health, University of Sydney Department of Neurology, Concord Hospital, Sydney, Australia Division of Neurology (C.E.U.), Department of Medicine, University of British Columbia, Vancouver, Canada and Laboratory Krone (C.G.B.), Bad Salzuflen, Germany
Baumgartner, Tobias
Autor Baumgartner, Tobias From the Department of Epileptology (Krankenhaus Mara) (A.R., C.G.B., U.S.), Medical School, Bielefeld University, Campus Bielefeld-Bethel Society for Epilepsy Research (A.H.), Bielefeld, Germany Department of Neurology (C.A.P., M.B.), Odense University Hospital Department of Clinical Research (M.B.), University of Southern Denmark, Odense, Denmark Department of Epileptology (T. Baumgartner, R.S.), University Hospital Bonn, Germany Department of Immunology and Biotechnology (T. Berki), University of Pécs, Medical School, Hungary Department of Neurology (J.B., Y.C., M.J.T., J.M.V.), Erasmus Medical Center, Rotterdam, Zuid-Holland, the Netherlands Division of Epilepsy (J.W.B., K.M.S.), Department of Neurology, Mayo Clinic, Rochester, MN NYU Comprehensive Epilepsy Center (A.C., C. Steriade), New York French Reference Center on Paraneoplastic Neurological Syndromes and Autoimmune Encephalitis (N.L.C.-P., A.F., J. Honnorat, S.M.-C.), Hospices Civils de Lyon, Hôpital Neurologique, UMR MELIS Inserm 1314 / CNRS 5284, Université Claude Bernard Lyon1, France Department of Neurology (M.E., P.M.), Second Faculty of Medicine, Charles University, Motol University Hospital, Prague, Czech Republic Department of Neurology (A.R.F., J. Hébert), Columbia University Irving Medical Center (CUIMC)/New York Presbyterian Hospital, New York Department of Neurology (Z. Hayden), Medical School, University of Pécs, Pécs, Hungary Division of Neurology (J. Hébert), University of Toronto, Ontario, Canada Epilepsy-Center Berlin-Brandenburg (M.H., M.I.-F.), Department of Neurology, Charité - Universitätsmedizin Berlin, Germany Department of Neurology (Z. Hong), West China Hospital, Sichuan University, Chengdu, China Oxford Autoimmune Neurology Group (S.R.I., S.R., C.E.U.), Nuffield Department of Clinical Neurosciences, Oxford, United Kingdom Department of Neurology and Neurosciences (S.R.I.), Mayo Clinic, Jacksonville, FL Department of Neurology with Institute of Translational Neurology (S.K., C. Strippel), University Hospital Münster, Germany Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead Faculty of Medicine and Health, University of Sydney Department of Neurology, Concord Hospital, Sydney, Australia Division of Neurology (C.E.U.), Department of Medicine, University of British Columbia, Vancouver, Canada and Laboratory Krone (C.G.B.), Bad Salzuflen, Germany
Berki, Timea
Autor Berki, Timea From the Department of Epileptology (Krankenhaus Mara) (A.R., C.G.B., U.S.), Medical School, Bielefeld University, Campus Bielefeld-Bethel Society for Epilepsy Research (A.H.), Bielefeld, Germany Department of Neurology (C.A.P., M.B.), Odense University Hospital Department of Clinical Research (M.B.), University of Southern Denmark, Odense, Denmark Department of Epileptology (T. Baumgartner, R.S.), University Hospital Bonn, Germany Department of Immunology and Biotechnology (T. Berki), University of Pécs, Medical School, Hungary Department of Neurology (J.B., Y.C., M.J.T., J.M.V.), Erasmus Medical Center, Rotterdam, Zuid-Holland, the Netherlands Division of Epilepsy (J.W.B., K.M.S.), Department of Neurology, Mayo Clinic, Rochester, MN NYU Comprehensive Epilepsy Center (A.C., C. Steriade), New York French Reference Center on Paraneoplastic Neurological Syndromes and Autoimmune Encephalitis (N.L.C.-P., A.F., J. Honnorat, S.M.-C.), Hospices Civils de Lyon, Hôpital Neurologique, UMR MELIS Inserm 1314 / CNRS 5284, Université Claude Bernard Lyon1, France Department of Neurology (M.E., P.M.), Second Faculty of Medicine, Charles University, Motol University Hospital, Prague, Czech Republic Department of Neurology (A.R.F., J. Hébert), Columbia University Irving Medical Center (CUIMC)/New York Presbyterian Hospital, New York Department of Neurology (Z. Hayden), Medical School, University of Pécs, Pécs, Hungary Division of Neurology (J. Hébert), University of Toronto, Ontario, Canada Epilepsy-Center Berlin-Brandenburg (M.H., M.I.-F.), Department of Neurology, Charité - Universitätsmedizin Berlin, Germany Department of Neurology (Z. Hong), West China Hospital, Sichuan University, Chengdu, China Oxford Autoimmune Neurology Group (S.R.I., S.R., C.E.U.), Nuffield Department of Clinical Neurosciences, Oxford, United Kingdom Department of Neurology and Neurosciences (S.R.I.), Mayo Clinic, Jacksonville, FL Department of Neurology with Institute of Translational Neurology (S.K., C. Strippel), University Hospital Münster, Germany Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead Faculty of Medicine and Health, University of Sydney Department of Neurology, Concord Hospital, Sydney, Australia Division of Neurology (C.E.U.), Department of Medicine, University of British Columbia, Vancouver, Canada and Laboratory Krone (C.G.B.), Bad Salzuflen, Germany
Blaabjerg, Morten
Autor Blaabjerg, Morten From the Department of Epileptology (Krankenhaus Mara) (A.R., C.G.B., U.S.), Medical School, Bielefeld University, Campus Bielefeld-Bethel Society for Epilepsy Research (A.H.), Bielefeld, Germany Department of Neurology (C.A.P., M.B.), Odense University Hospital Department of Clinical Research (M.B.), University of Southern Denmark, Odense, Denmark Department of Epileptology (T. Baumgartner, R.S.), University Hospital Bonn, Germany Department of Immunology and Biotechnology (T. Berki), University of Pécs, Medical School, Hungary Department of Neurology (J.B., Y.C., M.J.T., J.M.V.), Erasmus Medical Center, Rotterdam, Zuid-Holland, the Netherlands Division of Epilepsy (J.W.B., K.M.S.), Department of Neurology, Mayo Clinic, Rochester, MN NYU Comprehensive Epilepsy Center (A.C., C. Steriade), New York French Reference Center on Paraneoplastic Neurological Syndromes and Autoimmune Encephalitis (N.L.C.-P., A.F., J. Honnorat, S.M.-C.), Hospices Civils de Lyon, Hôpital Neurologique, UMR MELIS Inserm 1314 / CNRS 5284, Université Claude Bernard Lyon1, France Department of Neurology (M.E., P.M.), Second Faculty of Medicine, Charles University, Motol University Hospital, Prague, Czech Republic Department of Neurology (A.R.F., J. Hébert), Columbia University Irving Medical Center (CUIMC)/New York Presbyterian Hospital, New York Department of Neurology (Z. Hayden), Medical School, University of Pécs, Pécs, Hungary Division of Neurology (J. Hébert), University of Toronto, Ontario, Canada Epilepsy-Center Berlin-Brandenburg (M.H., M.I.-F.), Department of Neurology, Charité - Universitätsmedizin Berlin, Germany Department of Neurology (Z. Hong), West China Hospital, Sichuan University, Chengdu, China Oxford Autoimmune Neurology Group (S.R.I., S.R., C.E.U.), Nuffield Department of Clinical Neurosciences, Oxford, United Kingdom Department of Neurology and Neurosciences (S.R.I.), Mayo Clinic, Jacksonville, FL Department of Neurology with Institute of Translational Neurology (S.K., C. Strippel), University Hospital Münster, Germany Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead Faculty of Medicine and Health, University of Sydney Department of Neurology, Concord Hospital, Sydney, Australia Division of Neurology (C.E.U.), Department of Medicine, University of British Columbia, Vancouver, Canada and Laboratory Krone (C.G.B.), Bad Salzuflen, Germany
Brenner, Juliette
Autor Brenner, Juliette ORCID From the Department of Epileptology (Krankenhaus Mara) (A.R., C.G.B., U.S.), Medical School, Bielefeld University, Campus Bielefeld-Bethel Society for Epilepsy Research (A.H.), Bielefeld, Germany Department of Neurology (C.A.P., M.B.), Odense University Hospital Department of Clinical Research (M.B.), University of Southern Denmark, Odense, Denmark Department of Epileptology (T. Baumgartner, R.S.), University Hospital Bonn, Germany Department of Immunology and Biotechnology (T. Berki), University of Pécs, Medical School, Hungary Department of Neurology (J.B., Y.C., M.J.T., J.M.V.), Erasmus Medical Center, Rotterdam, Zuid-Holland, the Netherlands Division of Epilepsy (J.W.B., K.M.S.), Department of Neurology, Mayo Clinic, Rochester, MN NYU Comprehensive Epilepsy Center (A.C., C. Steriade), New York French Reference Center on Paraneoplastic Neurological Syndromes and Autoimmune Encephalitis (N.L.C.-P., A.F., J. Honnorat, S.M.-C.), Hospices Civils de Lyon, Hôpital Neurologique, UMR MELIS Inserm 1314 / CNRS 5284, Université Claude Bernard Lyon1, France Department of Neurology (M.E., P.M.), Second Faculty of Medicine, Charles University, Motol University Hospital, Prague, Czech Republic Department of Neurology (A.R.F., J. Hébert), Columbia University Irving Medical Center (CUIMC)/New York Presbyterian Hospital, New York Department of Neurology (Z. Hayden), Medical School, University of Pécs, Pécs, Hungary Division of Neurology (J. Hébert), University of Toronto, Ontario, Canada Epilepsy-Center Berlin-Brandenburg (M.H., M.I.-F.), Department of Neurology, Charité - Universitätsmedizin Berlin, Germany Department of Neurology (Z. Hong), West China Hospital, Sichuan University, Chengdu, China Oxford Autoimmune Neurology Group (S.R.I., S.R., C.E.U.), Nuffield Department of Clinical Neurosciences, Oxford, United Kingdom Department of Neurology and Neurosciences (S.R.I.), Mayo Clinic, Jacksonville, FL Department of Neurology with Institute of Translational Neurology (S.K., C. Strippel), University Hospital Münster, Germany Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead Faculty of Medicine and Health, University of Sydney Department of Neurology, Concord Hospital, Sydney, Australia Division of Neurology (C.E.U.), Department of Medicine, University of British Columbia, Vancouver, Canada and Laboratory Krone (C.G.B.), Bad Salzuflen, Germany
Britton, Jeffrey W
Autor Britton, Jeffrey W ORCID From the Department of Epileptology (Krankenhaus Mara) (A.R., C.G.B., U.S.), Medical School, Bielefeld University, Campus Bielefeld-Bethel Society for Epilepsy Research (A.H.), Bielefeld, Germany Department of Neurology (C.A.P., M.B.), Odense University Hospital Department of Clinical Research (M.B.), University of Southern Denmark, Odense, Denmark Department of Epileptology (T. Baumgartner, R.S.), University Hospital Bonn, Germany Department of Immunology and Biotechnology (T. Berki), University of Pécs, Medical School, Hungary Department of Neurology (J.B., Y.C., M.J.T., J.M.V.), Erasmus Medical Center, Rotterdam, Zuid-Holland, the Netherlands Division of Epilepsy (J.W.B., K.M.S.), Department of Neurology, Mayo Clinic, Rochester, MN NYU Comprehensive Epilepsy Center (A.C., C. Steriade), New York French Reference Center on Paraneoplastic Neurological Syndromes and Autoimmune Encephalitis (N.L.C.-P., A.F., J. Honnorat, S.M.-C.), Hospices Civils de Lyon, Hôpital Neurologique, UMR MELIS Inserm 1314 / CNRS 5284, Université Claude Bernard Lyon1, France Department of Neurology (M.E., P.M.), Second Faculty of Medicine, Charles University, Motol University Hospital, Prague, Czech Republic Department of Neurology (A.R.F., J. Hébert), Columbia University Irving Medical Center (CUIMC)/New York Presbyterian Hospital, New York Department of Neurology (Z. Hayden), Medical School, University of Pécs, Pécs, Hungary Division of Neurology (J. Hébert), University of Toronto, Ontario, Canada Epilepsy-Center Berlin-Brandenburg (M.H., M.I.-F.), Department of Neurology, Charité - Universitätsmedizin Berlin, Germany Department of Neurology (Z. Hong), West China Hospital, Sichuan University, Chengdu, China Oxford Autoimmune Neurology Group (S.R.I., S.R., C.E.U.), Nuffield Department of Clinical Neurosciences, Oxford, United Kingdom Department of Neurology and Neurosciences (S.R.I.), Mayo Clinic, Jacksonville, FL Department of Neurology with Institute of Translational Neurology (S.K., C. Strippel), University Hospital Münster, Germany Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead Faculty of Medicine and Health, University of Sydney Department of Neurology, Concord Hospital, Sydney, Australia Division of Neurology (C.E.U.), Department of Medicine, University of British Columbia, Vancouver, Canada and Laboratory Krone (C.G.B.), Bad Salzuflen, Germany
Christiana, Andrew
Autor Christiana, Andrew ORCID From the Department of Epileptology (Krankenhaus Mara) (A.R., C.G.B., U.S.), Medical School, Bielefeld University, Campus Bielefeld-Bethel Society for Epilepsy Research (A.H.), Bielefeld, Germany Department of Neurology (C.A.P., M.B.), Odense University Hospital Department of Clinical Research (M.B.), University of Southern Denmark, Odense, Denmark Department of Epileptology (T. Baumgartner, R.S.), University Hospital Bonn, Germany Department of Immunology and Biotechnology (T. Berki), University of Pécs, Medical School, Hungary Department of Neurology (J.B., Y.C., M.J.T., J.M.V.), Erasmus Medical Center, Rotterdam, Zuid-Holland, the Netherlands Division of Epilepsy (J.W.B., K.M.S.), Department of Neurology, Mayo Clinic, Rochester, MN NYU Comprehensive Epilepsy Center (A.C., C. Steriade), New York French Reference Center on Paraneoplastic Neurological Syndromes and Autoimmune Encephalitis (N.L.C.-P., A.F., J. Honnorat, S.M.-C.), Hospices Civils de Lyon, Hôpital Neurologique, UMR MELIS Inserm 1314 / CNRS 5284, Université Claude Bernard Lyon1, France Department of Neurology (M.E., P.M.), Second Faculty of Medicine, Charles University, Motol University Hospital, Prague, Czech Republic Department of Neurology (A.R.F., J. Hébert), Columbia University Irving Medical Center (CUIMC)/New York Presbyterian Hospital, New York Department of Neurology (Z. Hayden), Medical School, University of Pécs, Pécs, Hungary Division of Neurology (J. Hébert), University of Toronto, Ontario, Canada Epilepsy-Center Berlin-Brandenburg (M.H., M.I.-F.), Department of Neurology, Charité - Universitätsmedizin Berlin, Germany Department of Neurology (Z. Hong), West China Hospital, Sichuan University, Chengdu, China Oxford Autoimmune Neurology Group (S.R.I., S.R., C.E.U.), Nuffield Department of Clinical Neurosciences, Oxford, United Kingdom Department of Neurology and Neurosciences (S.R.I.), Mayo Clinic, Jacksonville, FL Department of Neurology with Institute of Translational Neurology (S.K., C. Strippel), University Hospital Münster, Germany Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead Faculty of Medicine and Health, University of Sydney Department of Neurology, Concord Hospital, Sydney, Australia Division of Neurology (C.E.U.), Department of Medicine, University of British Columbia, Vancouver, Canada and Laboratory Krone (C.G.B.), Bad Salzuflen, Germany
Ciano-Petersen, Nicolás L
Autor Ciano-Petersen, Nicolás L ORCID From the Department of Epileptology (Krankenhaus Mara) (A.R., C.G.B., U.S.), Medical School, Bielefeld University, Campus Bielefeld-Bethel Society for Epilepsy Research (A.H.), Bielefeld, Germany Department of Neurology (C.A.P., M.B.), Odense University Hospital Department of Clinical Research (M.B.), University of Southern Denmark, Odense, Denmark Department of Epileptology (T. Baumgartner, R.S.), University Hospital Bonn, Germany Department of Immunology and Biotechnology (T. Berki), University of Pécs, Medical School, Hungary Department of Neurology (J.B., Y.C., M.J.T., J.M.V.), Erasmus Medical Center, Rotterdam, Zuid-Holland, the Netherlands Division of Epilepsy (J.W.B., K.M.S.), Department of Neurology, Mayo Clinic, Rochester, MN NYU Comprehensive Epilepsy Center (A.C., C. Steriade), New York French Reference Center on Paraneoplastic Neurological Syndromes and Autoimmune Encephalitis (N.L.C.-P., A.F., J. Honnorat, S.M.-C.), Hospices Civils de Lyon, Hôpital Neurologique, UMR MELIS Inserm 1314 / CNRS 5284, Université Claude Bernard Lyon1, France Department of Neurology (M.E., P.M.), Second Faculty of Medicine, Charles University, Motol University Hospital, Prague, Czech Republic Department of Neurology (A.R.F., J. Hébert), Columbia University Irving Medical Center (CUIMC)/New York Presbyterian Hospital, New York Department of Neurology (Z. Hayden), Medical School, University of Pécs, Pécs, Hungary Division of Neurology (J. Hébert), University of Toronto, Ontario, Canada Epilepsy-Center Berlin-Brandenburg (M.H., M.I.-F.), Department of Neurology, Charité - Universitätsmedizin Berlin, Germany Department of Neurology (Z. Hong), West China Hospital, Sichuan University, Chengdu, China Oxford Autoimmune Neurology Group (S.R.I., S.R., C.E.U.), Nuffield Department of Clinical Neurosciences, Oxford, United Kingdom Department of Neurology and Neurosciences (S.R.I.), Mayo Clinic, Jacksonville, FL Department of Neurology with Institute of Translational Neurology (S.K., C. Strippel), University Hospital Münster, Germany Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead Faculty of Medicine and Health, University of Sydney Department of Neurology, Concord Hospital, Sydney, Australia Division of Neurology (C.E.U.), Department of Medicine, University of British Columbia, Vancouver, Canada and Laboratory Krone (C.G.B.), Bad Salzuflen, Germany

Neurology® neuroimmunology & neuroinflammation. 2024 ; 11 (4) : e200225. [pub] 20240604

Neurol Neuroimmunol Neuroinflamm
ISSN 2332-7812
Medvik
Zdroj

BACKGROUND AND OBJECTIVES: Patients with ongoing seizures are usually not allowed to drive. The prognosis for seizure freedom is favorable in patients with autoimmune encephalitis (AIE) with antibodies against NMDA receptor (NMDAR), leucine-rich glioma-inactivated 1 (LGI1), contactin-associated protein-like 2 (CASPR2), and the gamma-aminobutyric-acid B receptor (GABABR). We hypothesized that after a seizure-free period of 3 months, patients with AIE have a seizure recurrence risk of <20% during the subsequent 12 months. This would render them eligible for noncommercial driving according to driving regulations in several countries. METHODS: This retrospective multicenter cohort study analyzed follow-up data from patients aged 15 years or older with seizures resulting from NMDAR-, LGI1-, CASPR2-, or GABABR-AIE, who had been seizure-free for ≥3 months. We used Kaplan-Meier (KM) estimates for the seizure recurrence risk at 12 months for each antibody group and tested for the effects of potential covariates with regression models. RESULTS: We included 383 patients with NMDAR-, 440 with LGI1-, 114 with CASPR2-, and 44 with GABABR-AIE from 14 international centers. After being seizure-free for 3 months after an initial seizure period, we calculated the probability of remaining seizure-free for another 12 months (KM estimate) as 0.89 (95% confidence interval [CI] 0.85-0.92) for NMDAR, 0.84 (CI 0.80-0.88) for LGI1, 0.82 (CI 0.75-0.90) for CASPR2, and 0.76 (CI 0.62-0.93) for GABABR. DISCUSSION: Taking a <20% recurrence risk within 12 months as sufficient, patients with NMDAR-AIE and LGI1-AIE could be considered eligible for noncommercial driving after having been seizure-free for 3 months.

MeSH
autoprotilátky * krev MeSH
dospělí MeSH
encefalitida * imunologie MeSH
Hashimotova nemoc imunologie krev MeSH
intracelulární signální peptidy a proteiny * imunologie MeSH
kohortové studie MeSH
lidé středního věku MeSH
lidé MeSH
membránové proteiny * imunologie MeSH
mladiství MeSH
mladý dospělý MeSH
následné studie MeSH
proteiny nervové tkáně * imunologie MeSH
proteiny imunologie MeSH
receptory GABA-B * imunologie MeSH
receptory N-methyl-D-aspartátu imunologie MeSH
recidiva * MeSH
retrospektivní studie MeSH
senioři MeSH
záchvaty etiologie imunologie MeSH
Check Tag
dospělí MeSH
lidé středního věku MeSH
lidé MeSH
mladiství MeSH
mladý dospělý MeSH
mužské pohlaví MeSH
senioři MeSH
ženské pohlaví MeSH
Publikační typ
časopisecké články MeSH
multicentrická studie MeSH

Článek

Preassembly of specific Gβγ subunits at GABAB receptors through auxiliary KCTD proteins accelerates channel gating

Biochemical pharmacology. 2024 ; 228 (-) : 116176. [pub] 20240328

Biochem Pharmacol
ISSN 1873-2968
Medvik
Zdroj

GABAB receptors (GBRs) are G protein-coupled receptors for GABA, the main inhibitory neurotransmitter in the brain. GBRs regulate fast synaptic transmission by gating Ca2+ and K+ channels via the Gβγ subunits of the activated G protein. It has been demonstrated that auxiliary GBR subunits, the KCTD proteins, shorten onset and rise time and increase desensitization of receptor-induced K+ currents. KCTD proteins increase desensitization of K+ currents by scavenging Gβγ from the channel, yet the mechanism responsible for the rapid activation of K+ currents has remained elusive. In this study, we demonstrate that KCTD proteins preassemble Gβγ at GBRs. The preassembly obviates the need for diffusion-limited G protein recruitment to the receptor, thereby accelerating G protein activation and, as a result, K+ channel activation. Preassembly of Gβγ at the receptor relies on the interaction of KCTD proteins with a loop protruding from the seven-bladed propeller of Gβ subunits. The binding site is shared between Gβ1 and Gβ2, limiting the interaction of KCTD proteins to these particular Gβ isoforms. Substituting residues in the KCTD binding site of Gβ1 with those from Gβ3 hinders the preassembly of Gβγ with GBRs, delays onset and prolongs rise time of receptor-activated K+ currents. The KCTD-Gβ interface, therefore, represents a target for pharmacological modulation of channel gating by GBRs.

MeSH
draslíkové kanály metabolismus genetika MeSH
gating iontového kanálu * fyziologie MeSH
HEK293 buňky MeSH
lidé MeSH
proteiny vázající GTP - beta-podjednotky * metabolismus genetika MeSH
proteiny vázající GTP - gama-podjednotky * metabolismus genetika MeSH
receptory GABA-B * metabolismus genetika MeSH
Xenopus laevis MeSH
zvířata MeSH
Check Tag
lidé MeSH
zvířata MeSH
Publikační typ
časopisecké články MeSH

Článek

Corticosteroids as Selective and Effective Modulators of Glycine Receptors

ACS chemical neuroscience. 2023 ; 14 (17) : 3132-3142. [pub] 20230816

ACS Chem Neurosci
ISSN 1948-7193
Medvik
Zdroj

The mechanism of the negative impact of corticosteroids on the induction and progress of mental illness remains unclear. In this work, we studied the effects of corticosteroids on the activity of neuronal glycine receptors (GlyR) and GABA-A receptors (GABAAR) by measuring the chloride current induced by the application of GABA (2 or 5 μM) to isolated cerebellar Purkinje cells (IGABA) and by the application of glycine (100 μM) to pyramidal neurons of the rat hippocampus (IGly). It was found that corticosterone, 5α-dihydrodeoxycorticosterone, allotetrahydrocorticosterone, cortisol, and 17α,21-dihydroxypregnenolone were able to accelerate the desensitization of the IGly at physiological concentrations (IC50 values varying from 0.39 to 0.72 μM). Next, cortisone, 11-deoxycortisol, 11-deoxycorticosterone, 5β-dihydrodeoxycorticosterone, and tetrahydrocorticosterone accelerated the desensitization of IGly with IC50 values varying from 10.3 to 15.2 μM. Allotetrahydrocorticosterone and tetrahydrocorticosterone potentiated the IGABA albeit with high EC50 values (18-23 μM). The rest of the steroids had no effect on IGABA in the range of concentrations of 1-100 μM. Finally, our study has suggested a structural relationship of the 3β-hydroxyl group/3-oxo group with the selective modulatory activity on GlyRs in contrast to the 3α-hydroxyl group that is pivotal for GABAARs. In summary, our results suggest that increased GlyR desensitization by corticosteroids may contribute to brain dysfunction under chronic stress and identify corticosteroids for further development as selective modulators of GlyRs.

MeSH
GABA farmakologie MeSH
glycin * farmakologie MeSH
hormony kůry nadledvin farmakologie MeSH
krysa rodu rattus MeSH
neurony MeSH
receptory GABA-A MeSH
receptory glycinu * fyziologie MeSH
zvířata MeSH
Check Tag
krysa rodu rattus MeSH
zvířata MeSH
Publikační typ
časopisecké články MeSH
práce podpořená grantem MeSH

Článek

The role of GABAB receptors in the subcortical pathways of the mammalian auditory system

Frontiers in endocrinology. 2023 ; 14 (-) : 1195038. [pub] 20230811

Front. endocrinol.
ISSN 1664-2392
Medvik
Zdroj

GABAB receptors are G-protein coupled receptors for the inhibitory neurotransmitter GABA. Functional GABAB receptors are formed as heteromers of GABAB1 and GABAB2 subunits, which further associate with various regulatory and signaling proteins to provide receptor complexes with distinct pharmacological and physiological properties. GABAB receptors are widely distributed in nervous tissue, where they are involved in a number of processes and in turn are subject to a number of regulatory mechanisms. In this review, we summarize current knowledge of the cellular distribution and function of the receptors in the inner ear and auditory pathway of the mammalian brainstem and midbrain. The findings suggest that in these regions, GABAB receptors are involved in processes essential for proper auditory function, such as cochlear amplifier modulation, regulation of spontaneous activity, binaural and temporal information processing, and predictive coding. Since impaired GABAergic inhibition has been found to be associated with various forms of hearing loss, GABAB dysfunction could also play a role in some pathologies of the auditory system.

Článek

Léčba insomnie

Vimmerová Lattová, Zuzana
Autor Autorita Ústav patlogické fyziologie 3. LF UK, Praha Spánková ambulance FN KV, Praha

Profi medicína. 2023 ; 8 (1-2) : 9-11.

ISSN 2571-2527
Medvik
Zdroj

MeSH
antidepresiva farmakologie terapeutické užití MeSH
behaviorální terapie MeSH
lidé MeSH
poruchy iniciace a udržování spánku * terapie MeSH
receptory GABA terapeutické užití MeSH
Check Tag
lidé MeSH

Článek

Effects of Pregnanolone Glutamate and Its Metabolites on GABAA and NMDA Receptors and Zebrafish Behavior

ACS chemical neuroscience. 2023 ; 14 (10) : 1870-1883. [pub] 20230501

ACS Chem Neurosci
ISSN 1948-7193
Medvik
Zdroj

Multiple molecular targets have been identified to mediate membrane-delimited and nongenomic effects of natural and synthetic steroids, but the influence of steroid metabolism on neuroactive steroid signaling is not well understood. To begin to address this question, we set out to identify major metabolites of a neuroprotective synthetic steroid 20-oxo-5β-pregnan-3α-yl l-glutamyl 1-ester (pregnanolone glutamate, PAG) and characterize their effects on GABAA and NMDA receptors (GABARs, NMDARs) and their influence on zebrafish behavior. Gas chromatography-mass spectrometry was used to assess concentrations of PAG and its metabolites in the hippocampal tissue of juvenile rats following intraperitoneal PAG injection. PAG is metabolized in the peripheral organs and nervous tissue to 20-oxo-17α-hydroxy-5β-pregnan-3α-yl l-glutamyl 1-ester (17-hydroxypregnanolone glutamate, 17-OH-PAG), 3α-hydroxy-5β-pregnan-20-one (pregnanolone, PA), and 3α,17α-dihydroxy-5β-pregnan-20-one (17-hydroxypregnanolone, 17-OH-PA). Patch-clamp electrophysiology experiments in cultured hippocampal neurons demonstrate that PA and 17-OH-PA are potent positive modulators of GABARs, while PAG and 17-OH-PA have a moderate inhibitory effect at NMDARs. PAG, 17-OH-PA, and PA diminished the locomotor activity of zebrafish larvae in a dose-dependent manner. Our results show that PAG and its metabolites are potent modulators of neurotransmitter receptors with behavioral consequences and indicate that neurosteroid-based ligands may have therapeutic potential.

Článek

Ablation of Gabra5 Influences Corticosterone Levels and Anxiety-like Behavior in Mice

Genes. 2023 ; 14 (2) : . [pub] 20230121

ISSN 2073-4425
Medvik
Zdroj

Stress responses are activated by the hypothalamic-pituitary-adrenal axis (HPA axis), culminating in the release of glucocorticoids. During prolonged periods of secretion of glucocorticoids or inappropriate behavioral responses to a stressor, pathologic conditions may occur. Increased glucocorticoid concentration is linked to generalized anxiety, and there are knowledge gaps regarding its regulation. It is known that the HPA axis is under GABAergic control, but the contribution of the individual subunits of the GABA receptor is largely unknown. In this study, we investigated the relationship between the α5 subunit and corticosterone levels in a new mouse model deficient for Gabra5, which is known to be linked to anxiety disorders in humans and phenologs observed in mice. We observed decreased rearing behavior, suggesting lower anxiety in the Gabra5-/- animals; however, such a phenotype was absent in the open field and elevated plus maze tests. In addition to decreased rearing behavior, we also found decreased levels of fecal corticosterone metabolites in Gabra5-/- mice indicating a lowered stress response. Moreover, based on the electrophysiological recordings where we observed a hyperpolarized state of hippocampal neurons, we hypothesize that the constitutive ablation of the Gabra5 gene leads to functional compensation with other channels or GABA receptor subunits in this model.

MeSH
glukokortikoidy * MeSH
kortikosteron * MeSH
lidé MeSH
myši MeSH
receptory GABA-A genetika metabolismus MeSH
receptory GABA metabolismus MeSH
systém hypofýza - nadledviny metabolismus MeSH
systém hypotalamus-hypofýza metabolismus MeSH
úzkost MeSH
zvířata MeSH
Check Tag
lidé MeSH
myši MeSH
zvířata MeSH
Publikační typ
časopisecké články MeSH
práce podpořená grantem MeSH

Článek

Promising anticonvulsant N-[(2,4-dichlorophenyl) methyl]-2-(2,4-dioxo-1H-quinazolin-3-yl) acetamide: dose-dependent study and evaluation of anticonvulsant action spectrum in vivo and in silico [Slibné antikonvulzivum N-[(2,4-dichlorfenyl) methyl]-2-(2,4-dioxo-1H-chinazolin-3-yl) acetamid: studium působení v závislosti na dávce a hodnocení spektra antikonvulzivního účinku in vivo a in silico]

Česká a slovenská farmacie. 2022 ; 71 (5) : 224-233.

ISSN 1210-7816
Medvik
Zdroj

Bylo studováno antikonvulzivní spektrum původního slibného antikonvulziva N-[(2,4-dichlorfenyl) methyl]-2-(2,4-dioxo-1H-chinazolin-3-yl) acetamidu. Sloučenina vykazovala výrazný antikonvulzivní účinek a významně snižovala mortalitu myší na modelech záchvatů vyvolaných pentylenetetrazolem, pikrotoxinem, strychninem a kofeinem. Na modelu záchvatů vyvolaných thiosemikarbazidem testovaná sloučenina mortalitu nesnížila. Získané výsledky naznačily, že mechanismus antikonvulzivního účinku zahrnuje GABA-ergní (účinnost v modelech záchvatů vyvolaných pentylenetetrazolem a pikrotoxinem), glycinergní (účinnost v modelu paroxyzmů vyvolaných strychninem) a adenosynergní (účinnost v modelu záchvatů vyvolaných kofeinem). Molekulární dokování slibného antikonvulziva k antikonvulzivním biologickým cílům bylo v souladu s mechanismy chemoindukovaných záchvatů, konkrétně GABA, glycinu a adenosinových receptorů typu A2A, GABAAT a enzymů BCAT. Byla zjištěna shoda mezi výsledky studií in vivo a in silico.

The anticonvulsant spectrum of the original promising anticonvulsant N-[(2,4-dichlorophenyl) methyl]-2-(2,4-dioxo-1H-quinazolin-3-yl) acetamide was studied. The compound had a pronounced anticonvulsant effect, significantly reducing the mortality of mice in models of seizures induced by pentylenetetrazole, picrotoxin, strychnine, and caffeine. In the thiosemicarbazideinduced seizure model, the test compound did not reduce mortality. The obtained results indicated that the mechanism of anticonvulsant action involved GABA-ergic (effective in models of pentylenetetrazole and picrotoxin-induced seizures), glycinergic (efficiency in the strychnine model of paroxysms), and adenosinergic (effectiveness in the model of caffeine induced seizures). Molecular docking of a promising anticonvulsant to anticonvulsant biotargets follow the mechanisms of chemo-induced seizures, namely GABA, glycine, and adenosine receptors type A2A, GABAAT, and BCAT enzymes. The conformity between in vivo and in silico studies results was revealed.

MeSH
acetamidy farmakologie MeSH
akční spektrum MeSH
antikonvulziva * farmakologie MeSH
kofein MeSH
modely nemocí na zvířatech MeSH
pentylentetrazol MeSH
pikrotoxin MeSH
receptory GABA MeSH
simulace molekulového dockingu MeSH
záchvaty chemicky indukované farmakoterapie MeSH
zvířata MeSH
Check Tag
zvířata MeSH

Článek

GABBR1 monoallelic de novo variants linked to neurodevelopmental delay and epilepsy

American journal of human genetics. 2022 ; 109 (10) : 1885-1893. [pub] 20220913

Am J Hum Genet
ISSN 1537-6605
Medvik
Zdroj

GABAB receptors are obligatory heterodimers responsible for prolonged neuronal inhibition in the central nervous system. The two receptor subunits are encoded by GABBR1 and GABBR2. Variants in GABBR2 have been associated with a Rett-like phenotype (MIM: 617903), epileptic encephalopathy (MIM: 617904), and milder forms of developmental delay with absence epilepsy. To date, however, no phenotypes associated with pathogenic variants of GABBR1 have been established. Through GeneMatcher, we have ascertained four individuals who each have a monoallelic GABBR1 de novo non-synonymous variant; these individuals exhibit motor and/or language delay, ranging from mild to severe, and in one case, epilepsy. Further phenotypic features include varying degrees of intellectual disability, learning difficulties, autism, ADHD, ODD, sleep disorders, and muscular hypotonia. We functionally characterized the four de novo GABBR1 variants, p.Glu368Asp, p.Ala397Val, p.Ala535Thr, and p.Gly673Asp, in transfected HEK293 cells. GABA fails to efficiently activate the variant receptors, most likely leading to an increase in the excitation/inhibition balance in the central nervous system. Variant p.Gly673Asp in transmembrane domain 3 (TMD3) renders the receptor completely inactive, consistent with failure of the receptor to reach the cell surface. p.Glu368Asp is located near the orthosteric binding site and reduces GABA potency and efficacy at the receptor. GABA exhibits normal potency but decreased efficacy at the p.Ala397Val and p.Ala535Thr variants. Functional characterization of GABBR1-related variants provides a rationale for understanding the severity of disease phenotypes and points to possible therapeutic strategies.

Článek

Pregnane neurosteroids exert opposite effects on GABA and glycine-induced chloride current in isolated rat neurons

Hippocampus. 2022 ; 32 (7) : 552-563. [pub] 20220615

ISSN 1098-1063
Medvik
Zdroj

The ability of endogenous neurosteroids (NSs) with pregnane skeleton modified at positions C-3 and C-5 to modulate the functional activity of inhibitory glycine receptors (GlyR) and ionotropic ɣ-aminobutyric acid receptors (GABAA R) was estimated. The glycine and GABA-induced chloride current (IGly and IGABA ) were measured in isolated pyramidal neurons of the rat hippocampus and in isolated rat cerebellar Purkinje cells, respectively. Our experiments demonstrated that pregnane NSs affected IGABA and IGly in a different manner. At low concentrations (up to 5 μM), tested pregnane NSs increased or did not change the peak amplitude of the IGABA , but reduced the IGly by decreasing the peak amplitude and/or accelerating desensitization. Namely, allopregnanolone (ALLO), epipregnanolone (EPI), pregnanolone (PA), pregnanolone sulfate (PAS) and 5β-dihydroprogesterone (5β-DHP) enhanced the IGABA in Purkinje cells. Dose-response curves plotted in the concentration range from 1 nM to 100 μM were smooth for EPI and 5β-DHP, but bell-shaped for ALLO, PA and PAS. The peak amplitude of the IGly was reduced by PA, PAS, and 5α- and 5β-DHP. In contrast, ALLO, ISO and EPI did not modulate it. Dose-response curves for the inhibition of the IGly peak amplitude were smooth for all active compounds. All NSs accelerated desensitization of the IGly . The dose-response relationship for this effect was smooth for ALLO, PA, PAS and 5β-DHP, but it was U-shaped for EPI, 5α-DHP and ISO. These results, together with our previous results on NSs with androstane skeleton, offer comprehensive overview for understanding the mechanisms of effects of NSs on IGly and IGABA .

MeSH
5alfa-dihydroprogesteron farmakologie MeSH
chloridy farmakologie MeSH
GABA MeSH
glycin farmakologie MeSH
krysa rodu rattus MeSH
neurony fyziologie MeSH
neurosteroidy * MeSH
potkani Wistar MeSH
pregnanolon * farmakologie MeSH
pregnany farmakologie MeSH
receptory GABA-A fyziologie MeSH
zvířata MeSH
Check Tag
krysa rodu rattus MeSH
zvířata MeSH
Publikační typ
časopisecké články MeSH
práce podpořená grantem MeSH

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