ReviewCurrent neurology and neuroscience reports2002
Periodic paralysis: understanding channelopathies.
Review in Current neurology and neuroscience reports, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 54 citations in OpenAlex.
- Atypical Electrophysiological Pattern in Hypokalemic Periodic Paralysis With CACNA1S Mutation: A Case Report.Cureus · 2025Article
- Diagnosis, management and outcomes of primary hypokalemic periodic paralysis during pregnancy.Obstetric medicine · 2024Article
- The Role of Nutrition and Physical Activity as Trigger Factors of Paralytic Attacks in Primary Periodic Paralysis.Journal of neuromuscular diseases · 2021Review
- Unusual Clinical Presentation of Periodic Paralysis: Case Report and Literature Review.Cureus · 2020Article
- Overlap of periodic paralysis and paramyotonia congenita caused by SCN4A gene mutations two family reports and literature review.Channels (Austin, Tex.) · 2019Review
- An Up-to-Date Overview of the Complexity of Genotype-Phenotype Relationships in Myotonic Channelopathies.Frontiers in neurology · 2019Review
- Skeletal Muscle Channelopathies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- Symptoms Mimicking Those of Hypokalemic Periodic Paralysis Induced by Soluble Barium Poisoning.Federal practitioner : for the health care professionals of the VA, DoD, and PHS · 2017Article
- Mutational consequences of aberrant ion channels in neurological disorders.The Journal of membrane biology · 2014Review
- Sodium channel blockers for the treatment of neuropathic pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2009Review
- A patient suffering from hypokalemic periodic paralysis is deficient in skeletal muscle ATP-sensitive K channels.Clinical and translational science · 2008Article
- Gating of the HypoPP-1 mutations: I. Mutant-specific effects and cooperativity.Pflugers Archiv : European journal of physiology · 2007Article
- A1152D mutation of the Na+ channel causes paramyotonia congenita and emphasizes the role of DIII/S4-S5 linker in fast inactivation.The Journal of physiology · 2005Article
- Abrupt hypokalemia with paralysis from a clinician's perspective.Journal of molecular medicine (Berlin, Germany) · 2005Article
- Taurine and skeletal muscle disorders.Neurochemical research · 2004Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Familial periodic paralyses are typical channelopathies (i.e., caused by functional disturbances of ion channel proteins). The episodes of flaccid muscle weakness observed in these disorders are due to underexcitability of sarcolemma leading to a silent electromyogram and the lack of action potentials even upon electrical stimulation. Interictally, ion channel malfunction is well compensated, so that special exogenous or endogenous triggers are required to produce symptoms in the patients. An especially obvious trigger is the level of serum potassium (K+), the ion responsible for resting membrane potential and degree of excitability. The clinical symptoms can be caused by mutations in genes coding for ion channels that mediate different functions for maintaining the resting potential or propagating the action potential, the basis of excitability. The phenotype is determined by the type of functional defect brought about by the mutations, rather than the channel effected, because the contrary phenotypes hyperkalemic periodic paralysis (HyperPP) and hypokalemic periodic paralysis (HypoPP) may be caused by point mutations in the same gene. Still, the common mechanism for inexcitability in all known episodic-weakness phenotypes is a long-lasting depolarization that inactivates sodium ion (Na+) channels, initiating the action potential.
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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.