ReviewPostgraduate medical journal1999
Lambert-Eaton myasthenic syndrome.
Review in Postgraduate medical journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 31 citations in OpenAlex.
- Presynaptic Paraneoplastic Disorders of the Neuromuscular Junction: An Update.Brain sciences · 2021Review
- Autoimmune Channelopathies at Neuromuscular Junction.Frontiers in neurology · 2019Review
- Five years experience on 3,4-diaminopyridine phosphate in Lambert-Eaton syndrome: Case reports.Medicine · 2017Article
- The European LEMS Registry: Baseline Demographics and Treatment Approaches.Neurology and therapy · 2015Article
- Lambert-Eaton myasthenic syndrome and solitary cerebellar metastasis in a patient with occult small-cell lung cancer: a rare experience.BMJ case reports · 2012Article
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
The Lambert-Eaton myasthenic syndrome is a neuromuscular disorder characterised by defective neurotransmitter release at autonomic neurones and presynaptic terminals of the neuromuscular junction. It is caused by an IgG autoantibody formed against especially the P/Q type of voltage-gated calcium channels (VGCC) which is an essential component of the mechanism of neurotransmitter release. Many patients have an associated small cell carcinoma of the lung which appears to provide the antigenic stimulus for antibody production, although there is another group with no underlying malignancy. Both groups show an association with immunological disorders. Assay of VGCC antibody titres and electrophysiological tests help to differentiate Lambert-Eaton myasthenic syndrome from other disorders of the neuromuscular junction. Several drugs and therapeutic interventions capable of producing significant clinical improvement are currently available. Patients should also be investigated for underlying tumours, the specific treatment of which can result in remission or amelioration of symptoms.
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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.