ArticleMuscle & nerve2016
In vivo assessment of muscle membrane properties in myotonic dystrophy.
Article in Muscle & nerve, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 20 citations in OpenAlex.
- Muscle velocity recovery cycles as pharmacodynamic biomarker: Effects of mexiletine in a randomized double-blind placebo-controlled cross-over study.Clinical and translational science · 2022Trial
- Myotonia: Recognition, Evaluation, and Differential Diagnosis.Muscle & nerve · 2026Review
- Emergent technologies in clinical neurophysiology to study the neuromuscular system: IFCN handbook chapter.Clinical neurophysiology practice · 2026Review
- Muscle excitability testing: Age and sex dependency of normative data.Clinical neurophysiology practice · 2025Article
- Leg pain in neuropathic postural tachycardia syndrome is associated with altered muscle membrane properties.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2021Article
- In vivo assessment of muscle membrane properties in the sodium channel myotonias.Muscle & nerve · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
Abstract
introductionMyotonia in myotonic dystrophy types 1 (DM1) and 2 (DM2) is generally attributed to reduced chloride-channel conductance. We used muscle velocity recovery cycles (MVRCs) to investigate muscle membrane properties in DM1 and DM2, using comparisons with myotonia congenita (MC).
methodsMVRCs and responses to repetitive stimulation were compared between patients with DM1 (n = 18), DM2 (n = 5), MC (n = 18), and normal controls (n = 20).
resultsBoth DM1 and DM2 showed enhanced late supernormality after multiple conditioning stimuli, indicating delayed repolarization as in MC. Contrary to MC, however, DM1 showed reduced early supernormality after multiple conditioning stimuli, and weak DM1 patients also showed abnormally slow latency recovery after repetitive stimulation.
conclusionsThese findings support the presence of impaired chloride conductance in both DM1 and DM2. The early supernormality changes indicate that sodium currents were reduced in DM1, whereas the weakness-associated slow recovery after repetitive stimulation may provide an indication of reduced Na(+) /K(+) -ATPase activation. Muscle Nerve 54: 249-257, 2016.
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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.