Evidence map›Paper›PMID 24890646›Full record

ReviewNature reviews. Neurology2014

Cataplexy--clinical aspects, pathophysiology and management strategy.

Yves Dauvilliers, Jerry M Siegel, Regis Lopez, Zoltan A Torontali, John H Peever

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
9.1field-weighted citation impact, top 1% 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

60 citing papers in PubMed, 186 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. Synchrony of neuromodulatory systems during NREM sleep.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Frozen in Addiction: A New Wave of Drug-Induced Movement Disorders?Movement disorders : official journal of the Movement Disorder Society · 2025
    Article
  8. Review
  9. Narcolepsy and rapid eye movement sleep.Journal of sleep research · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Observational
  19. Article
  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

5 authors at 3 institutions in 3 countries.

Yves DauvilliersDepartment of Neurology, INSERM U1061, University of Montpellier, Montpellier 34295, France.
Jerry M SiegelNeurobiology Research 151A3, University College Los Angeles, Veterans Administration Greater Los Angeles Healthcare System, 16111 Plummer Street, North Hills, CA 91343, USA.
Regis LopezDepartment of Neurology, INSERM U1061, University of Montpellier, Montpellier 34295, France.
Zoltan A TorontaliCentre for Brain Sciences, Department of Cell and Systems Biology, University of Toronto, Toronto, ON M4X 1H7, Canada.
John H PeeverCentre for Brain Sciences, Department of Cell and Systems Biology, University of Toronto, Toronto, ON M4X 1H7, Canada.
Inserm · FROntario Brain Institute · CAVA Greater Los Angeles Healthcare System · US

Funding

Role of hypocretin in opiate addiction and withdrawalR01DA034748 · NIDA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SIEGEL, JEROME M · 2014 to 2024
$6.3M
What Causes Human Narcolepsy?I01BX001753 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI SIEGEL, JEROME M · 2013 to 2020
–
BLRD VA I01 BX001753BLRD VA IK6 BX005245NIDA NIH HHS R01 DA034748
6 · The paper itself

Abstract

Cataplexy is the pathognomonic symptom of narcolepsy, and is the sudden uncontrollable onset of skeletal muscle paralysis or weakness during wakefulness. Cataplexy is incapacitating because it leaves the individual awake but temporarily either fully or partially paralyzed. Occurring spontaneously, cataplexy is typically triggered by strong positive emotions such as laughter and is often underdiagnosed owing to a variable disease course in terms of age of onset, presenting symptoms, triggers, frequency and intensity of attacks. This disorder occurs almost exclusively in patients with depletion of hypothalamic orexin neurons. One pathogenetic mechanism that has been hypothesized for cataplexy is the activation, during wakefulness, of brainstem circuitry that normally induces muscle tone suppression in rapid eye movement sleep. Muscle weakness during cataplexy is caused by decreased excitation of noradrenergic neurons and increased inhibition of skeletal motor neurons by γ-aminobutyric acid-releasing or glycinergic neurons. The amygdala and medial prefrontal cortex contain neural pathways through which positive emotions probably trigger cataplectic attacks. Despite major advances in understanding disease mechanisms in cataplexy, therapeutic management is largely symptomatic, with antidepressants and γ-hydroxybutyrate being the most effective treatments. This Review describes the clinical and pathophysiological aspects of cataplexy, and outlines optimal therapeutic management strategies.

Indexed as

CataplexyAnimalsBrainElectroencephalographyHumansMood DisordersMuscle WeaknessNerve DegenerationOcular Motility Disorders

Identifiers

PMID24890646
PMCPMC8788644
OpenAlexW2070509338

What OpenQuestion holds

Textmetadata
LicenceTDM
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.