ReviewDegenerative neurological and neuromuscular disease2019
Lambert-Eaton Myasthenic syndrome: early diagnosis is key.
Review in Degenerative neurological and neuromuscular disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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.
Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Anti-VGCC negative and Anti-SOX1 positive Lambert-Eaton myasthenic syndrome as the initial presentation of small cell lung cancer: a case report.Frontiers in oncology · 2026Article
- Article
- Marked under-diagnosis of Lambert-Eaton myasthenic syndrome in small cell lung cancer: an analysis of real-world claims data.Frontiers in oncology · 2025Article
- Understanding Autoimmunity: Mechanisms, Predisposing Factors, and Cytokine Therapies.International journal of molecular sciences · 2024Review
- Independence in activities of daily living was achieved using aerobic exercise without overwork weakness during rehabilitation: a case report of Lambert-Eaton myasthenic syndrome.Journal of physical therapy science · 2024Article
- Article
- SOX-1 antibodies positive Lambert-Eaton myasthenic syndrome with occult small cell lung cancer: A case report.The clinical respiratory journal · 2024Article
- Clinical presentations, electrophysiologic features, and long-term follow-up in Lambert-Eaton myasthenic syndrome: a series of six patients.Frontiers in neurology · 2024Article
- Spontaneous regression of small cell lung cancer associated with Lambert-Eaton Myasthenic Syndrome: Case report.Radiology case reports · 2023Article
- Paraneoplastic Lambert-Eaton myasthenic syndrome: a diagnostic challenge.BMJ case reports · 2023Article
- The European Lambert-Eaton Myasthenic Syndrome Registry: Long-Term Outcomes Following Symptomatic Treatment.Neurology and therapy · 2022Article
- Paraneoplastic neurological syndrome: an evolving story.Neuro-oncology practice · 2021Review
- Combination therapy: Future directions of immunotherapy in small cell lung cancer.Translational oncology · 2021Review
- Epidemiological analysis of Lambert-Eaton myasthenic syndrome in Türkiye: insights from a nationwide electronic health database.Frontiers in neurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lambert-Eaton myasthenic syndrome (LEMS) is an uncommon disorder of neuromuscular transmission with distinctive pathophysiological, clinical, electrophysiological and laboratory features. There are two forms of LEMS. The paraneoplastic (P-LEMS) form is associated with a malignant tumor that is most frequently a small cell lung carcinoma (SCLC), and the autoimmune (A-LEMS) form is often related to other dysimmune diseases. Approximately 90% of LEMS patients present antibodies against presynaptic membrane P/Q-type voltage-gated calcium channels (VGCC). These antibodies are directly implicated in the pathophysiology of the disorder, provoke reduced acetylcholine (ACh) at the nerve terminal and consequently lead to muscle weakness. LEMS is clinically characterized by proximal muscle weakness, autonomic dysfunction and areflexia. In clinically suspected cases, diagnoses are confirmed by serological and electrodiagnostic tests. The detection of P/Q-type VGCC antibodies is supportive when there is clinical suspicion but should be carefully interpreted in the absence of characteristic clinical or electrodiagnostic features. Typical electrodiagnostic findings (ie, reduced compound motor action potentials (CMAPs), significant decrements in the responses to low frequency stimulation and incremental responses after brief exercise or high-frequency stimulation) reflect the existence of a presynaptic transmission defect and are key confirmatory criteria. Diagnosis requires a high level of awareness and necessitates the initiation of a prompt screening and surveillance process to detect and treat malignant tumors. In clinically affected patients without cancer and after cancer treatment, symptomatic treatment with 3,4-diaminopyridine or immunosuppressive agents can significantly improve neurologic symptoms and the quality of life. We present a detailed review of LEMS with special emphasis on the pathophysiological mechanisms, clinical manifestation and diagnostic procedure.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.