Evidence map›Paper›PMID 26886206›Full record

ReviewJournal of neurology2016

Clinical features, pathogenesis, and treatment of myasthenia gravis: a supplement to the Guidelines of the German Neurological Society.

Nico Melzer, Tobias Ruck, Peter Fuhr, Ralf Gold, Reinhard Hohlfeld, Alexander Marx, Arthur Melms, Björn Tackenberg, Berthold Schalke, Christiane Schneider-Gold and 3 more

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed, 5 pooled it
12.3field-weighted citation impact, top 1% 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

141 citing papers in PubMed, 5 syntheses or guidelines pooled it, 274 citations in OpenAlex.

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  20. Telitacicept as a New Therapeutic Avenue for Generalized Myasthenia Gravis and Thymoma-Associated Myasthenia Gravis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article

81 more citing papers are in PubMed but not listed here.

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

13 authors at 9 institutions in 3 countries.

Nico MelzerDepartment of Neurology, University of Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Germany. nico.melzer@ukmuenster.de.
Tobias RuckDepartment of Neurology, University of Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Germany.
Peter FuhrDepartment of Neurology, University of Basel, Basel, Switzerland.
Ralf GoldDepartment of Neurology, University of Bochum, Bochum, Germany.
Reinhard HohlfeldInstitute of Clinical Neuroimmunology, Ludwig-Maximilians-University Munich, Munich, Germany.
Alexander MarxInstitute of Pathology, University Medical Centre Mannheim, University of Heidelberg, Mannheim, Germany.
Arthur MelmsDepartment of Neurology, University of Erlangen, Erlangen, Germany.
Björn TackenbergDepartment of Neurology, University of Marburg, Marburg, Germany.
Berthold SchalkeDepartment of Neurology, University of Regensburg, Regensburg, Germany.
Christiane Schneider-GoldDepartment of Neurology, University of Bochum, Bochum, Germany.
Fritz ZimprichDepartment of Neurology, Medical University of Vienna, Vienna, Austria.
Sven G MeuthDepartment of Neurology, University of Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Germany.
Heinz WiendlDepartment of Neurology, University of Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Germany.
University Hospital Münster · DEUniversity of Münster · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEHeidelberg University · DELudwig-Maximilians-Universität München · DEMedical University of Vienna · ATPhilipps University of Marburg · DEUniversity of Basel · CHUniversity of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myasthenia gravis (MG) is an autoimmune antibody-mediated disorder of neuromuscular synaptic transmission. The clinical hallmark of MG consists of fluctuating fatigability and weakness affecting ocular, bulbar and (proximal) limb skeletal muscle groups. MG may either occur as an autoimmune disease with distinct immunogenetic characteristics or as a paraneoplastic syndrome associated with tumors of the thymus. Impairment of central thymic and peripheral self-tolerance mechanisms in both cases is thought to favor an autoimmune CD4(+) T cell-mediated B cell activation and synthesis of pathogenic high-affinity autoantibodies of either the IgG1 and 3 or IgG4 subclass. These autoantibodies bind to the nicotinic acetylcholine receptor (AchR) itself, or muscle-specific tyrosine-kinase (MuSK), lipoprotein receptor-related protein 4 (LRP4) and agrin involved in clustering of AchRs within the postsynaptic membrane and structural maintenance of the neuromuscular synapse. This results in disturbance of neuromuscular transmission and thus clinical manifestation of the disease. Emphasizing evidence from clinical trials, we provide an updated overview on immunopathogenesis, and derived current and future treatment strategies for MG divided into: (a) symptomatic treatments facilitating neuromuscular transmission, (b) antibody-depleting treatments, and

Indexed as

Disease ManagementMyasthenia GravisGermanyHumansSocieties, MedicalMyasthenia gravisPathogenesisTreatment guidelines

Identifiers

PMID26886206
PMCPMC4971048
OpenAlexW2277245749

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.