Evidence map›Paper›PMID 19425168›Full record

ArticleThe Journal of clinical investigation2009

Inactivation of sodium channels underlies reversible neuropathy during critical illness in rats.

Kevin R Novak, Paul Nardelli, Tim C Cope, Gregory Filatov, Jonathan D Glass, Jaffar Khan, Mark M Rich

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.2field-weighted citation impact, top 9% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 112 citations in OpenAlex.

  1. Review
  2. Review
  3. Vitamin D Serum Levels and the Development of Intensive Care Unit-Acquired Weakness: Insights from a COVID-19 Intensive Care Cohort.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
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  6. Review
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  8. Imbalanced Subthreshold Currents Following Sepsis and Chemotherapy: A Shared Mechanism Offering a New Therapeutic Target?The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022
    Article
  9. Screening Power of Short Tau Inversion Recovery Muscle Magnetic Resonance Imaging in Critical Illness Myoneuropathy and Guillain-Barre Syndrome in the Intensive Care Unit.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2022
    Article
  10. Molecular mechanisms of postintensive care syndrome.Intensive care medicine experimental · 2021
    Review
  11. Article
  12. MitoTEMPOL, a mitochondrial targeted antioxidant, prevents sepsis-induced diaphragm dysfunction.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  13. Observational
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. [Critical illness myopathy and polyneuropathy].Medizinische Klinik, Intensivmedizin und Notfallmedizin · 2017
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Kevin R NovakDepartment of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, Ohio 45435, USA.
Paul Nardelli
Tim C Cope
Gregory Filatov
Jonathan D Glass
Jaffar Khan
Mark M Rich
Wright State University · USEmory University · US

Funding

Loss of muscle excitability in acute quadriplegic myopathyR01NS040826 · NINDS · WRIGHT STATE UNIVERSITY · PI RICH, MARK M · 2001 to 2009
$2.4M
NINDS NIH HHS NS040826NINDS NIH HHS R01 NS040826
6 · The paper itself

Abstract

Neuropathy and myopathy can cause weakness during critical illness. To determine whether reduced excitability of peripheral nerves, rather than degeneration, is the mechanism underlying acute neuropathy in critically ill patients, we prospectively followed patients during the acute phase of critical illness and early recovery and assessed nerve conduction. During the period of early recovery from critical illness, patients recovered from neuropathy within days. This rapidly reversible neuropathy has not to our knowledge been previously described in critically ill patients and may be a novel type of neuropathy. In vivo intracellular recordings from dorsal root axons in septic rats revealed reduced action potential amplitude, demonstrating that reduced excitability of nerve was the mechanism underlying neuropathy. When action potentials were triggered by hyperpolarizing pulses, their amplitudes largely recovered, indicating that inactivation of sodium channels was an important contributor to reduced excitability. There was no depolarization of axon resting potential in septic rats, which ruled out a contribution of resting potential to the increased inactivation of sodium channels. Our data suggest that a hyperpolarized shift in the voltage dependence of sodium channel inactivation causes increased sodium inactivation and reduced excitability. Acquired sodium channelopathy may be the mechanism underlying acute neuropathy in critically ill patients.

Indexed as

Critical IllnessAction PotentialsAnimalsCell MembraneChannelopathiesElectric ImpedanceElectrolytesElectromyographyFemaleHumansMembrane PotentialsMotor NeuronsMuscle WeaknessMuscular DiseasesNeural ConductionPeripheral Nervous System DiseasesElectrolytesSodium Channels

Identifiers

PMID19425168
PMCPMC2673869
OpenAlexW1972670391

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.