ReviewCurrent treatment options in neurology2016
Myotonic Dystrophy Type 1 Management and Therapeutics.
Review in Current treatment options in neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled 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.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Health-Related Quality of Life in Patients with Adult-Onset Myotonic Dystrophy Type 1: A Systematic Review.The patient · 2019Pooled it
- A mouse model of myotonic dystrophy type 1 exhibits pain-like behavior and peripheral nociceptor hyperexcitability.bioRxiv : the preprint server for biology · 2026Article
- Characterization ofNAR molecular medicine · 2025Article
- Multisystem Symptoms in Myotonic Dystrophy Type 1: A Management and Therapeutic Perspective.International journal of molecular sciences · 2025Review
- Use of HSALab animal · 2025Article
- Therapeutic potential of oleic acid supplementation in myotonic dystrophy muscle cell models.Biological research · 2024Article
- Gastrointestinal and nutritional care in pediatric neuromuscular disorders.World journal of clinical pediatrics · 2023Review
- Calcitriol increases MBNL1 expression and alleviates myotonic dystrophy phenotypes in HSAJournal of translational medicine · 2022Article
- Condensation properties of stress granules and processing bodies are compromised in myotonic dystrophy type 1.Disease models & mechanisms · 2022Article
- [Rare diseases in the differential diagnosis of myalgia].Schmerz (Berlin, Germany) · 2022Article
- Targeting Myotonic Dystrophy Type 1 with Metformin.International journal of molecular sciences · 2022Review
- Healthcare resource utilization, total costs, and comorbidities among patients with myotonic dystrophy using U.S. insurance claims data from 2012 to 2019.Orphanet journal of rare diseases · 2022Article
- Cellular Senescence and Aging in Myotonic Dystrophy.International journal of molecular sciences · 2022Review
- RNA-binding proteins and post-transcriptional regulation in lens biology and cataract: Mediating spatiotemporal expression of key factors that control the cell cycle, transcription, cytoskeleton and transparency.Experimental eye research · 2022Review
- Article
- Preclinical characterization of antagomiR-218 as a potential treatment for myotonic dystrophy.Molecular therapy. Nucleic acids · 2021Article
- Genetic burden linked to founder effects in Saguenay-Lac-Saint-Jean illustrates the importance of genetic screening test availability.Journal of medical genetics · 2021Review
- Musashi-2 contributes to myotonic dystrophy muscle dysfunction by promoting excessive autophagy throughMolecular therapy. Nucleic acids · 2021Article
- miR-322/miR-503 clusters regulate defective myoblast differentiation in myotonic dystrophy RNA-toxic by targeting Celf1.Toxicology research · 2021Article
- Variant repeats within theNeurology. Genetics · 2020Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
opinion statementMyotonic dystrophy (DM1) is the most common form of adult muscular dystrophy. It is a multisystem disorder with a complex pathophysiology. Although inheritance is autosomal dominant, disease variability is attributed to anticipation, a maternal expansion bias, variable penetrance, somatic mosaicism, and a multitude of aberrant pre-mRNA splicing events. Patient presentations range from asymptomatic or mild late onset adult to severe congenital forms. Multiple organ systems may be affected. Patients may experience early cataracts, myotonia, muscle weakness/atrophy, fatigue, excessive daytime sleepiness, central/obstructive apnea, respiratory failure, cardiac arrhythmia, insulin resistance, dysphagia, GI dysmotility, cognitive impairment, Cluster C personality traits, and/or mood disorders. At present, there is no curative or disease-modifying treatment, although clinical treatment trials have become more promising. Management focuses on genetic counseling, preserving function and independence, preventing cardiopulmonary complications, and symptomatic treatment (e.g., pain, myotonia, hypersomnolence, etc.). Currently, there is an increasing international consensus on monitoring and treatment options for these patients which necessitates a multidisciplinary team to provide comprehensive, coordinated clinical care.
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.