Evidence map›Paper›PMID 24578548›Full record

Observational studyBrain : a journal of neurology2014

Episodic ataxia type 1: clinical characterization, quality of life and genotype-phenotype correlation.

Tracey D Graves, Yoon-Hee Cha, Angelika F Hahn, Richard Barohn, Mohammed K Salajegheh, Robert C Griggs, Brian N Bundy, Joanna C Jen, Robert W Baloh, Michael G Hanna and 1 more

Registry-linked trialOpen access · bronzeAbstract readMulticenter StudyObservational Study
In one paragraph

Observational study in Brain : a journal of neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00266760 (Episodic Ataxia Syndrome), which is not on this map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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.

NCT00266760 completednot on this map

Episodic Ataxia Syndrome: Genotype-phenotype Correlation and Longitudinal Study

TypeobservationalSponsorUniversity of California, Los AngelesRan2006 to 2011Enrolled39ConditionsEpisodic Ataxia Syndrome, Cerebellar Diseases
3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Episodic Ataxias: Primary and Secondary Etiologies, Treatment, and Classification Approaches.Tremor and other hyperkinetic movements (New York, N.Y.) · 2023
    Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Hereditary kidney diseases associated with hypomagnesemia.Kidney research and clinical practice · 2021
    Article
  12. Review
  13. Review
  14. Article
  15. A NovelJournal of clinical neurology (Seoul, Korea) · 2021
    Article
  16. Article
  17. Paroxysmal Movement Disorders.Frontiers in neurology · 2021
    Review
  18. Review
  19. 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

11 authors at 8 institutions in 3 countries.

Tracey D Graves1 MRC Centre for Neuromuscular Disease, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK.
Yoon-Hee Cha
Angelika F Hahn
Richard Barohn
Mohammed K Salajegheh
Robert C Griggs
Brian N Bundy
Joanna C Jen
Robert W Baloh
Michael G Hanna
CINCH Investigators
National Hospital for Neurology and Neurosurgery · GBUCLA Medical Center · USBrigham and Women's Hospital · USFlorida College · USLaureate Institute for Brain Research · USLondon Health Sciences Centre · CAUniversity of Kansas Medical Center · USUniversity of Rochester · US

Funding

UNIVERSITY OF ROCHESTER'S RESEARCH ASSOCIATE ORGANIZATIONUL1RR024160 · NCRR · UNIVERSITY OF ROCHESTER · PI PEARSON, THOMAS ARTHUR · 2006 to 2011
$38.7M
The University of Rochester's Clinical and Translational Science InstituteUL1TR000042 · NCATS · UNIVERSITY OF ROCHESTER · PI BENNETT, NANCY M, KIEBURTZ, KARL D. · 2012 to 2015
$14.4M
Heartland Institute for Clinical and Translational ResearchUL1TR000001 · NCATS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BAROHN, RICHARD J. · 2012 to 2015
$13.0M
Nervous System Channelopathies: Pathogenesis & TreatmentU54NS059065 · NINDS · UNIVERSITY OF ROCHESTER · PI GRIGGS, ROBERT C · 2006 to 2010
$5.9M
Medical Research Council G0601943Medical Research Council MR/K000608/1NCATS NIH HHS UL1TR000001NCATS NIH HHS UL1 TR000042NCRR NIH HHS UL1 RR 024160NINDS NIH HHS 2U54NS059065
6 · The paper itself

Abstract

Episodic ataxia type 1 is considered a rare neuronal ion channel disorder characterized by brief attacks of unsteadiness and dizziness with persistent myokymia. To characterize the natural history, develop outcome measures for future clinical trials, and correlate genotype with phenotype, we undertook an international, prospective, cross-sectional study. Thirty-nine individuals (51% male) were enrolled: median age 37 years (range 15-65 years). We identified 10 different pathogenic point mutations in KCNA1 that accounted for the genetic basis of 85% of the cohort. Participants with KCNA1 mutations were more likely to have a positive family history. Analysis of the total cohort showed that the first episode of ataxia occurred before age 20 in all but one patient, with an average age of onset of 7.9 years. Physical exertion, emotional stress and environmental temperature were the most common triggers for attacks. Attack frequency ranged from daily to monthly, even with the same KCNA1 genotype. Average attack duration was in the order of minutes. Ten participants (26%) developed permanent cerebellar signs, which were related to disease duration. The average Scale for the Assessment and Rating of Ataxia score (SARA, a standardized measure of cerebellar dysfunction on clinical examination, scores range from 0-40) was an average of 3.15 for all participants (range 0-14), but was only 2 in those with isolated episodic ataxia compared with 7.7 in those with progressive cerebellar ataxia in addition to episodic ataxia. Thirty-seven participants completed the SF-36, a quality of life survey; all eight domain norm-based average scores (mean=50) were below normal with mental health being the lowest (41.3) in those with mutation positive episodic ataxia type 1. Scores on SF-36 correlated negatively with attack frequency. Of the 39 participants in the study, 33 harboured mutations in KCNA1 whereas the remaining six had no mutation identified. Episodic ataxia type 1 phenocopies have not been described previously and we report their clinical features, which appear to be different to those with a KCNA1 mutation. This large prospective study of both genetically confirmed episodic ataxia type 1 and episodic ataxia type 1 phenocopies provides detailed baseline characteristics of these disorders and their impact on participants. We found that attacks had a significant effect on quality of life. Unlike previous studies, we found that a significant number of individuals with genetically confirmed episodic ataxia type 1 (21%) had accumulated persistent cerebellar symptoms and signs. These data will enable the development of outcome measures for clinical trials of treatment.

Indexed as

Genetic Association StudiesQuality of LifeAdolescentAdultAgedAge of OnsetAtaxiaCross-Sectional StudiesFemaleHumansKv1.1 Potassium ChannelMaleMiddle AgedMyokymiaPoint MutationYoung AdultKCNA1 protein, humanKv1.1 Potassium Channelepisodic ataxia type 1 (EA1)KCNA1quality of life

Identifiers

PMID24578548
PMCPMC3959554
OpenAlexW2167182675

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.