Evidence map›Paper›PMID 33025119›Full record

ArticleJournal of neurology2021

Seizures associated with antibodies against cell surface antigens are acute symptomatic and not indicative of epilepsy: insights from long-term data.

Anna Rada, Robert Birnbacher, Claudio Gobbi, Martin Kurthen, Albert Ludolph, Markus Naumann, Ulrike Neirich, Tim J von Oertzen, Gerhard Ransmayr, Matthias Riepe and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 44 citations in OpenAlex.

  1. Observational
  2. Autoimmune polyglandular syndrome and GAD65 related-temporal lobe epilepsy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  3. Autoimmune encephalitis.Nature reviews. Disease primers · 2025
    Review
  4. Article
  5. The limbic and extra-limbic encephalitis associated with glutamic acid decarboxylase (GAD)-65 antibodies: an observational study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Observational
  6. Autoimmune encephalitis-associated epilepsy.Nature reviews. Neurology · 2025
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Predictive value of persistent antibodies at 6 months for relapse in neuronal surface antibody-associated autoimmune encephalitis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Do the neurologists recognize autoimmune epilepsy well enough? What is the effect of the pandemic on this matter?Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Article
  18. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 9 institutions in 3 countries.

Anna RadaEpilepsy Center Bethel, Krankenhaus Mara, Epilepsy Centre Bethel, Krankenhaus Mara, Maraweg 17-21, 33617, Bielefeld, Germany.
Robert BirnbacherDepartment of Pediatrics and Adolescent Medicine, Villach General Hospital, Villach, Austria.
Claudio GobbiDepartment of Neurology, Neurocenter of Southern Switzerland (NSI), 6900, Lugano, Switzerland.ORCID http://orcid.org/0000-0002-7554-0664
Martin KurthenSwiss Epilepsy Center, Zürich, Switzerland.
Albert LudolphDepartment of Neurology, University of Ulm, Ulm, Germany.
Markus NaumannDepartment of Neurology and Clinical Neurophysiology, University of Augsburg, Augsburg, Germany.
Ulrike NeirichDepartment of Pediatrics, Neurology, Stiftungskrankenhäuser Frankfurt Am Main, Clementine Kinderhospital, Frankfurt am Main, Germany.
Tim J von OertzenDepartment of Neurology 1, Kepler University Hospital GmbH, Johannes Kepler University Linz, Linz, Austria.ORCID http://orcid.org/0000-0003-2164-7842
Gerhard RansmayrDepartment of Neurology 2, Kepler University Hospital GmbH, Johannes Kepler University Linz, Linz, Austria.
Matthias RiepeDivision of Gerontopsychiatry, Ulm University, Günzburg, Germany.
Mareike SchimmelDepartment of Pediatrics, Section of Neuropediatrics, University of Augsburg, Augsburg, Germany.
Oliver SchwartzDepartment of Pediatric Neurology, Münster University Hospital, Münster, Germany.
Rainer SurgesDepartment of Epileptology, University Hospital of Bonn, Bonn, Germany.ORCID http://orcid.org/0000-0002-3177-8582
Christian G BienEpilepsy Center Bethel, Krankenhaus Mara, Epilepsy Centre Bethel, Krankenhaus Mara, Maraweg 17-21, 33617, Bielefeld, Germany. christian.bien@gmx.de.ORCID http://orcid.org/0000-0003-2225-8654
Universität Ulm · DEUniversity of Augsburg · DEEvangelisches Krankenhaus Bielefeld · DELaboratory for Biomedical Neurosciences · CHLaboratory Krone · DESt. Elisabethen-Krankenhaus Frankfurt · DESwiss Epilepsy Center · CHUniversity Hospital Bonn · DEUniversity Hospital Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClinicians have questioned whether any disorder involving seizures and neural antibodies should be called "(auto)immune epilepsy." The concept of "acute symptomatic seizures" may be more applicable in cases with antibodies against neural cell surface antigens. We aimed at determining the probability of achieving seizure-freedom, the use of anti-seizure medication (ASM), and immunotherapy in patients with either constellation. As a potential pathophysiological correlate, we analyzed antibody titer courses.

methodsRetrospective cohort study of 39 patients with seizures and neural antibodies, follow-up ≥ 3 years.

resultsPatients had surface antibodies against the N-methyl-D-aspartate receptor (NMDAR, n = 6), leucine-rich glioma inactivated protein 1 (LGI1, n = 11), contactin-associated protein-2 (CASPR2, n = 8), or antibodies against the intracellular antigens glutamic acid decarboxylase 65 kDa (GAD65, n = 13) or Ma2 (n = 1). Patients with surface antibodies reached first seizure-freedom (88% vs. 7%, P < 0.001) and terminal seizure-freedom (80% vs. 7%, P < 0.001) more frequently. The time to first and terminal seizure-freedom and the time to freedom from ASM were shorter in the surface antibody group (Kaplan-Meier curves: P < 0.0001 for first seizure-freedom; P < 0.0001 for terminal seizure-freedom; P = 0.0042 for terminal ASM-freedom). Maximum ASM defined daily doses were higher in the groups with intracellular antibodies. Seizure-freedom was achieved after additional immunotherapy, not always accompanied by increased ASM doses. Titers of surface antibodies but not intracellular antibodies decreased over time.

conclusionSeizures with surface antibodies should mostly be considered acute symptomatic and transient and not indicative of epilepsy. This has consequences for ASM prescription and social restrictions. Antibody titers correlate with clinical courses.

Indexed as

Antigens, SurfaceEpilepsyAutoantibodiesHumansReceptors, N-Methyl-D-AspartateRetrospective StudiesSeizuresAntigens, SurfaceAutoantibodiesReceptors, N-Methyl-D-AspartateAcute symptomatic seizuresAutoimmune encephalitisEpilepsyLong-term courseNeural antibodies

Identifiers

PMID33025119
PMCPMC7914192
OpenAlexW3091932761

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.