Evidence map›Paper›PMID 33119692›Full record

Trial reportPloS one2020

Adult-onset temporal lobe epilepsy suspicious for autoimmune pathogenesis: Autoantibody prevalence and clinical correlates.

Julia C Kuehn, Carolin Meschede, Christoph Helmstaedter, Rainer Surges, Randi von Wrede, Elke Hattingen, Hartmut Vatter, Christian E Elger, Susanne Schoch, Albert J Becker and 1 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  6. Review
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  10. Review
  11. Increased expression of GABABrain communications · 2021
    Article
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

11 authors at 2 institutions in 1 country.

Julia C KuehnSection for Translational Epilepsy Research, Dept. of Neuropathology, University Hospital Bonn, Bonn, Germany.
Carolin MeschedeDept. of Epileptology, University Hospital Bonn, Bonn, Germany.
Christoph HelmstaedterDept. of Epileptology, University Hospital Bonn, Bonn, Germany.
Rainer SurgesDept. of Epileptology, University Hospital Bonn, Bonn, Germany.
Randi von WredeDept. of Epileptology, University Hospital Bonn, Bonn, Germany.ORCID 0000-0002-9430-5037
Elke HattingenDept. of Neuroradiology, University Clinic of Frankfurt, Frankfurt, Germany.
Hartmut VatterClinic for Neurosurgery, University Hospital Bonn, Bonn, Germany.
Christian E ElgerDept. of Epileptology, University Hospital Bonn, Bonn, Germany.
Susanne SchochSection for Translational Epilepsy Research, Dept. of Neuropathology, University Hospital Bonn, Bonn, Germany.
Albert J BeckerSection for Translational Epilepsy Research, Dept. of Neuropathology, University Hospital Bonn, Bonn, Germany.
Julika PitschSection for Translational Epilepsy Research, Dept. of Neuropathology, University Hospital Bonn, Bonn, Germany.ORCID 0000-0002-6688-4916
University Hospital Bonn · DEGoethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Temporal lobe adult-onset seizures (TAOS) related to autoimmunity represent an increasingly recognized disease syndrome within the spectrum of epilepsies. In this context, certain autoantibodies (autoABs) were often associated with limbic encephalitis (LE). Here, we aimed to gain insights into (a) the distribution of 'neurological' autoABs (neuroABs, defined as autoABs targeting neuronal surface structures or 'onconeuronal' ABs or anti-glutamate acid decarboxylase 65 (GAD65) autoABs) in a large consecutive TAOS patient cohort, to characterize (b) clinical profiles of seropositive versus seronegative individuals and to find (c) potential evidence for other autoABs. Blood sera/cerebrospinal fluid (CSF) of TAOS patients (n = 800) and healthy donors (n = 27) were analyzed for neuroABs and screened for other autoABs by indirect immunofluorescence on hippocampal/cerebellar sections and immunoblots of whole brain and synaptosome lysates. Serological results were correlated with clinico-neuropsychological features. 13% of TAOS patients (n = 105) were neuroAB+, with anti-GAD65 and anti-N-methyl-D-aspartate receptors (NMDAR) as most frequent autoABs in this group. In our screening tests 25% of neuroAB- patients (n = 199) were positive (screening+), whereas all control samples were negative (n = 27). Intriguingly, key clinico-neuropsychological characteristics including magnetic resonance imaging (MRI) findings, epileptiform electroencephalographic (EEG) activity, and inflammatory cellular infiltrates in CSF were shared to a greater extent by neuroAB+ with neuroAB-/screening+ patients than with neuroAB-/screening- patients. Serological testing in a large consecutive TAOS patient series revealed seropositivity for anti-GAD65 autoABs as the most frequent neuroAB. Intriguingly, neuroAB+ individuals were virtually indistinguishable from neuroAB-/screening+ patients in several major clinical features. In contrast, neuroAB-/screening- TAOS patients differed in many parameters. These data support the potential presence of so far unrecognized autoABs in patients with TAOS.

Indexed as

Antibody SpecificityAutoantibodiesAutoimmune DiseasesEpilepsy, Temporal LobeAdultFemaleHumansMaleMiddle AgedPrevalenceAutoantibodies

Identifiers

PMID33119692
PMCPMC7595292
OpenAlexW3097548998

What OpenQuestion holds

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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.