ArticleMuscle & nerve2018
In vivo assessment of muscle membrane properties in the sodium channel myotonias.
Article in Muscle & nerve, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 23 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
- 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
- Excitability properties of mouse and human skeletal muscle fibres compared by muscle velocity recovery cycles.Neuromuscular disorders : NMD · 2022Article
- 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
- Myotonia in a patient with a mutation in an S4 arginine residue associated with hypokalaemic periodic paralysis and a concomitant synonymous CLCN1 mutation.Scientific reports · 2019Article
- Ageing contributes to phenotype transition in a mouse model of periodic paralysis.JCSM rapid communicationsArticle
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
introductionThe gain-of-function mutations that underlie sodium channel myotonia (SCM) and paramyotonia congenital (PMC) produce differing clinical phenotypes. We used muscle velocity recovery cycles (MVRCs) to investigate membrane properties.
methodsMVRCs and responses to trains of stimuli were compared in patients with SCM (n = 9), PMC (n = 8), and normal controls (n = 26).
resultsThe muscle relative refractory period was reduced in SCM, consistent with faster recovery of the mutant sodium channels from inactivation. Both SCM and PMC showed an increased early supernormality and increased mean supernormality following multiple conditioning stimuli, consistent with slowed sodium channel inactivation. Trains of fast impulses caused a loss of amplitude in PMC, after which only half of the muscle fibers recovered, suggesting that the remainder stayed depolarized by persistent sodium currents. DISCUSSION: The differing effects of mutations on sodium channel function can be demonstrated in human subjects in vivo using this technique. Muscle Nerve 57: 586-594, 2018.
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Registered trials
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