Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (874 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A disorder of neuromuscular transmission characterized by fatigable weakness of cranial and skeletal muscles with elevated titers of acetylcholine receptors or muscle-specific receptor tyrosine kinase (MuSK) autoantibodies. Clinical manifestations may include ocular muscle weakness (fluctuating, asymmetric, external ophthalmoplegia; diplopia; ptosis; and weakness of eye closure) and extraocular fatigable weakness of facial, bulbar, respiratory, and proximal limb muscles. The disease may remain limited to the ocular muscles (ocular myasthenia). thymoma is commonly associated with this condition.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Myasthenia Gravis, Generalized; Generalized Myasthenia Gravis; Myasthenia Gravis, Ocular; Ocular Myasthenia Gravis; Muscle-Specific Receptor Tyrosine Kinase Myasthenia Gravis; Muscle Specific Receptor Tyrosine Kinase Myasthenia Gravis; MuSK Myasthenia Gravis; Myasthenia Gravis, MuSK.
Where it fits in the MeSH classification
- Broader topics
- Paraneoplastic Syndromes, Nervous System; Autoimmune Diseases of the Nervous System; Neuromuscular Junction Diseases
- Narrower topics
- Lambert-Eaton Myasthenic Syndrome; Myasthenia Gravis, Autoimmune, Experimental; Myasthenia Gravis, Neonatal
- See also
- Thymus Hyperplasia
Related concepts
- Acetylcholine Receptors
- Thymoma
Research landscape
PubMed indexes 18,511 records tagged with the MeSH heading “Myasthenia Gravis” (counts retrieved 2026-10-29). 3,062 of them (16.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 9,462 records.
Reviews account for 2,483 records (13.4%) and meta-analyses for 102. Randomized controlled trials number 185 (1.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 9,462 |
| 2000-2009 | 2,766 |
| 2010-2019 | 3,221 |
| 2020 onward | 3,062 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,483 | 13.4% |
| Meta-analyses | 102 | 0.6% |
| Randomized controlled trials | 185 | 1.0% |
Method: PubMed query "Myasthenia Gravis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cancer and oncology
Cancer research spans very different kinds of evidence. Laboratory studies in cell lines and animal models reveal mechanisms but often do not translate to patients. Early-phase trials mainly test safety and dosing, while phase 3 randomized trials and their meta-analyses are the usual basis for treatment conclusions. Outcomes also differ in meaning: tumour shrinkage, progression-free survival and overall survival are not interchangeable, and screening studies can be distorted by lead-time and overdiagnosis. When reading a result, check the cancer type and stage studied, the comparison treatment, and which outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Management of immune-related myocarditis, myositis and myasthenia gravis (MMM) overlap syndrome: a single institution case series and literature review [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundImmune checkpoint inhibitors (ICIs) have revolutionized the treatment of various malignancies, particularly melanoma.
- Closing excerpt
- Further research is needed to refine diagnostic criteria, identify predictive biomarkers, and establish standardized treatment protocols.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (250 words)
BackgroundImmune checkpoint inhibitors (ICIs) have revolutionized the treatment of various malignancies, particularly melanoma. However, immune-related adverse events (irAEs) pose significant challenges, particularly in cases of severe toxicity syndromes. One such life-threatening irAE is the myocarditis, myositis, and myasthenia gravis (MMM) overlap syndrome, which occurs in less than 1% of patients but has in-hospital mortality rates ranging from 40 to 60%. Due to its rarity and complexity, early recognition and a multidisciplinary approach are critical to improving outcomes.MethodsWe present a single-institution case series of four patients diagnosed with MMM overlap syndrome following ICI therapy. Clinical presentation, laboratory findings, imaging, and electrophysiological tests were analyzed to confirm the diagnosis. Therapeutic interventions-including corticosteroids, intravenous immunoglobulins (IVIG), plasma exchange (PLEX), tocilizumab, and rituximab- were evaluated in terms of efficacy and clinical outcomes.ResultsThe onset of MMM syndrome varied from 2 to 4 weeks after initiating ICI therapy. Patients presented with rapidly progressive symptoms, including ptosis, bulbar dysfunction, respiratory distress, myopathy, and cardiac conduction abnormalities. Immunosuppressive therapy with high-dose corticosteroids was initiated in all cases. Additional immunomodulatory treatments (IVIG, tocilizumab, PLEX, and rituximab) were administered based on clinical deterioration and autoimmune profile. Two patients achieved complete recovery, one remains on maintenance immunosuppression, and one died due to respiratory failure despite aggressive treatment.ConclusionMMM overlap syndrome is a severe and often fatal irAE associated with ICI therapy. Early identification, aggressive immunosuppressive treatment, and individualized therapeutic strategies are essential to optimize patient outcomes. Further research is needed to refine diagnostic criteria, identify predictive biomarkers, and establish standardized treatment protocols.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40406130 · DOI · PMC12095175
Durability of Response to B-Cell Maturation Antigen-Directed mRNA Cell Therapy in Myasthenia Gravis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- ObjectiveWe report the 12-month follow-up outcomes from a Phase 2 clinical trial (NCT04146051) evaluating Descartes-08, a BCMA-directed RNA chimeric antigen receptor T-cell (rCAR-T) therapy for refractory generalized myasthenia gravis (MG).
- Closing excerpt
- InterpretationThese data support continued development of Descartes-08 in myasthenia gravis and other autoantibody-associated autoimmune disorders.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (240 words)
ObjectiveWe report the 12-month follow-up outcomes from a Phase 2 clinical trial (NCT04146051) evaluating Descartes-08, a BCMA-directed RNA chimeric antigen receptor T-cell (rCAR-T) therapy for refractory generalized myasthenia gravis (MG). These findings provide insight into the potential applicability of BCMA-targeted rCAR-T therapy for antibody-mediated autoimmune diseases.MethodsIn the Phase 2a part of the study, Descartes-08 was administered at 52.5 × 106 CAR+ cells/kg per infusion with varying dosing frequencies as an outpatient treatment and without lymphodepletion chemotherapy. A subset of participants received Descartes-08 as six weekly infusions and were followed long term with assessments conducted at 2, 3, 6, 9, and 12 months.ResultsAll seven participants who received six weekly infusions of Descartes-08 exhibited clinically meaningful improvement in common MG severity scales (MG Composite, MG Activities of Daily Living, Quantitative MG scores, and Quality of Life 15-revised) at Month 3 without significant toxicity. At Month 9 follow-up, all participants continued to experience marked clinically meaningful improvements. Five out of seven participants maintained the response at Month 12. A third participant experienced a relapse approximately 6 months after completing on-study follow-up. All three participants who experienced loss of clinical effects were retreated. Two had rapid improvement in clinical scores with minimal symptom expression at Week 8, which was maintained through 12 months of retreatment follow-up. The third participant experienced similar improvement in MG severity scores to their initial treatment.InterpretationThese data support continued development of Descartes-08 in myasthenia gravis and other autoantibody-associated autoimmune disorders.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40856088 · DOI · PMC12623823
Efficacy and Safety of Efgartigimod for Patients With Myasthenia Gravis in a Real-World Cohort of 77 Patients [3]
Abstract reading summary — source excerpts
- Opening excerpt
- AimsEfgartigimod, a first-in-class neonatal Fc receptor antagonist, is approved for generalized myasthenia gravis (gMG).
- Closing excerpt
- These findings support its potential when conventional therapies fail.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (139 words)
AimsEfgartigimod, a first-in-class neonatal Fc receptor antagonist, is approved for generalized myasthenia gravis (gMG). Its safety and efficacy across MG subtypes remain unclear.MethodsThis single-center real-world study (September 2023-July 2024) analyzed patients from an MG registry study in China. The primary efficacy outcome is the mean MG-ADL score changes from baseline at weeks 4, 8, and 12, analyzed via generalized estimating equations. Safety was assessed by adverse events.ResultsAmong 77 patients (mean age 56.1 ± 15.2 years; 59.7% male), 76 completed at least one treatment cycle (20 completed 2 cycles; 1 completed 3 cycles). After efgartigimod treatment, MG-ADL scores decreased significantly by week 4 (mean difference -6.4, 95% CI -7.2 to -5.6, p ConclusionEfgartigimod safely improved MG-ADL scores and reduced steroid use across MG subtypes, with sustained efficacy through multiple treatment cycles. These findings support its potential when conventional therapies fail.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40237260 · DOI · PMC12001068
Inhibition of Classical and Alternative Complement Pathway by Ravulizumab and Eculizumab [4]
Abstract reading summary — source excerpts
- Opening excerpt
- ObjectiveTo explore the feasibility of classical (CH50) and alternative (AH50) complement pathway activity as potential biomarkers for treatment guidance and monitoring during therapy with ravulizumab in patients with generalized myasthenia gravis (gMG) and compare these to therapeutic drug monitoring under eculizumab.
- Closing excerpt
- However, these findings need to be validated in large multicenter studies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (245 words)
ObjectiveTo explore the feasibility of classical (CH50) and alternative (AH50) complement pathway activity as potential biomarkers for treatment guidance and monitoring during therapy with ravulizumab in patients with generalized myasthenia gravis (gMG) and compare these to therapeutic drug monitoring under eculizumab.MethodsIn this prospective, exploratory real-world study CH50 and AH50, eculizumab and ravulizumab blood levels were assessed in patients with acetylcholine-receptor-antibody (AChR-ab) positive gMG. Patients were either pretreated with eculizumab or C5-inhibitor naïve. Samples were collected before the next infusion (end-of-dose). Laboratory data were correlated with patient-reported subjective duration of the ravulizumab effect.ResultsOverall, 61 patients were enrolled. At the end of their respective dosing interval, median AH50 levels were more strongly suppressed with eculizumab than with ravulizumab (1% [0%-2%] versus 5% [3%-9%]; Cohen's d 2.2 [95% CI 1.5-2.8]). Patients who discontinued ravulizumab due to insufficient effects (n = 19; 33%) had higher median AH50 levels than those who continued (7% [4%-13%] versus 5% [3%-8%]; Cohen's d -0.9 [95% CI -1.3 to -0.4]). In 81% (n = 46) of patients, the therapeutic effect of ravulizumab diminished before the subsequent infusion after the standard 8-week interval. Higher AH50 levels were correlated with earlier symptom recurrence.InterpretationOur results indicate potential differences in the ability of eculizumab and ravulizumab to suppress complement pathway activity through their respective dosing intervals. Additionally, higher AH50 levels might be a potential biomarker to predict poor therapy response and faster wearing off of ravulizumab's effect. However, these findings need to be validated in large multicenter studies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41261457 · DOI · PMC13071113
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Epidemiology, diagnostics, and biomarkers of autoimmune neuromuscular junction disorders [5]
- Research article Immune Checkpoint Inhibitor-Induced Myocarditis with Myositis/Myasthenia Gravis Overlap Syndrome: A Systematic Review of Cases [6]
- Research article Efgartigimod: First Approval [7]
- Research article Efficacy and safety of rituximab for myasthenia gravis: a systematic review and meta-analysis [8]
- Research article Autoimmune Pathology in Myasthenia Gravis Disease Subtypes Is Governed by Divergent Mechanisms of Immunopathology [9]
- Research article Myasthenia gravis: the changing treatment landscape in the era of molecular therapies [10]
References
- Sánchez-Camacho A, Torres-Zurita A, Gallego-López L, Hernández-Pacheco R, Silva-Romeiro S, Álamo de la Gala MDC, et al.. Management of immune-related myocarditis, myositis and myasthenia gravis (MMM) overlap syndrome: a single institution case series and literature review. . 2025. PMID 40406130 · DOI · PMC12095175
- Chahin N, Sahagian G, Feinberg MH, Stewart CA, Jewell CM, Kurtoglu M, et al.. Durability of Response to B-Cell Maturation Antigen-Directed mRNA Cell Therapy in Myasthenia Gravis. . 2025. PMID 40856088 · DOI · PMC12623823
- Hao S, Ruan Z, Guo R, Wang Q, Huang X, Sun C, et al.. Efficacy and Safety of Efgartigimod for Patients With Myasthenia Gravis in a Real-World Cohort of 77 Patients. . 2025. PMID 40237260 · DOI · PMC12001068
- Gerischer L, Stascheit F, Mönch M, Doksani P, Dusemund C, Herdick M, et al.. Inhibition of Classical and Alternative Complement Pathway by Ravulizumab and Eculizumab. . 2026. PMID 41261457 · DOI · PMC13071113
- Punga AR, Maddison P, Heckmann JM, Guptill JT, Evoli A. Epidemiology, diagnostics, and biomarkers of autoimmune neuromuscular junction disorders. Lancet Neurol. 2022. PMID 35065040 · DOI
- Pathak R, Katel A, Massarelli E, Villaflor VM, Sun V, Salgia R. Immune Checkpoint Inhibitor-Induced Myocarditis with Myositis/Myasthenia Gravis Overlap Syndrome: A Systematic Review of Cases. Oncologist. 2021. PMID 34378270 · DOI · PMC8649039
- Heo YA. Efgartigimod: First Approval. Drugs. 2022. PMID 35179720 · DOI · PMC8855644
- Iorio R, Damato V, Alboini PE, Evoli A. Efficacy and safety of rituximab for myasthenia gravis: a systematic review and meta-analysis. J Neurol. 2015. PMID 25308632 · DOI
- Fichtner ML, Jiang R, Bourke A, Nowak RJ, O'Connor KC. Autoimmune Pathology in Myasthenia Gravis Disease Subtypes Is Governed by Divergent Mechanisms of Immunopathology. Front Immunol. 2020. PMID 32547535 · DOI · PMC7274207
- Iorio R. Myasthenia gravis: the changing treatment landscape in the era of molecular therapies. Nat Rev Neurol. 2024. PMID 38191918 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.