Evidence map›Paper›PMID 31356292›Full record

ReviewContinuum (Minneapolis, Minn.)2019

Ataxia.

Sheng-Han Kuo

Open access · greenAbstract readCase ReportsReview
In one paragraph

Review in Continuum (Minneapolis, Minn.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 5 pooled it
1.3field-weighted citation impact, top 22% 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

35 citing papers in PubMed, 5 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Article
  8. Article
  9. Article
  10. Review
  11. Classifying neurogenic dysphagia as a movement disorder.Brain : a journal of neurology · 2025
    Review
  12. Review
  13. Hereditary Ataxias in Argentina.Cerebellum (London, England) · 2025
    Review
  14. Scorpionism in Pará, Brazil: Clinical assessment of neuromuscular manifestations.Revista da Sociedade Brasileira de Medicina Tropical · 2025
    Observational
  15. Review
  16. Review
  17. Genetic aspects of ataxias in a cohort of Turkish patients.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Article
  18. Article
  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

1 author.

Sheng-Han Kuo

Funding

True Metal fac coreP30ES009089 · NIEHS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MATTHEW S PERZANOWSKI · 1998 to 2026
$44.7M
Cerebellar Circuitry in the Pathophysiology of TremorR01NS104423 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI KUO, SHENG-HAN · 2018 to 2022
$2.0M
Clinical Research Consortium for Spinocerebellar AtaxiasRC1NS068897 · NINDS · UNIVERSITY OF FLORIDA · PI ASHIZAWA, TETSUO · 2009 to 2010
$1.0M
The role of glucocerebrosidase and chaperone_mediated autophagy in Parkinsons disK08NS083738 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI KUO, SHENG-HAN · 2013 to 2017
$940k
Dietary Contribution in Cerebellar AtaxiaR03NS114871 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI KUO, SHENG-HAN · 2019 to 2020
$162k
NIEHS NIH HHS P30 ES009089NINDS NIH HHS K08 NS083738NINDS NIH HHS R01 NS104423NINDS NIH HHS R03 NS114871NINDS NIH HHS RC1 NS068897
6 · The paper itself

Abstract

purpose of reviewThis article reviews the symptoms, laboratory and neuroimaging diagnostic tests, genetics, and management of cerebellar ataxia. RECENT

findingsRecent advances in genetics have led to the identification of novel genetic causes for ataxia and a more comprehensive understanding of the biological pathways critical for normal cerebellar function. When these molecular pathways become dysfunctional, patients develop cerebellar ataxia. In addition, several ongoing clinical trials for Friedreich ataxia and spinocerebellar ataxia will likely result in novel symptomatic and disease-modifying therapies for ataxia. Antisense oligonucleotides for spinocerebellar ataxias associated with CAG repeat expansions might be a promising therapeutic strategy. SUMMARY: Cerebellar ataxias include heterogeneous disorders affecting cerebellar function, leading to ataxic symptoms. Step-by-step diagnostic workups with genetic investigations are likely to reveal the underlying causes of ataxia. Some disease-specific therapies for ataxia exist, such as vitamin E for ataxia with vitamin E deficiency and thiamine for Wernicke encephalopathy, highlighting the importance of recognizing these forms of ataxia. Finally, genetic diagnosis for patients with ataxia will accelerate clinical trials for disease-modifying therapy and will have prognostic value and implications for family planning for these patients.

Indexed as

AtaxiaCerebellar AtaxiaDopamine AgentsFemaleFriedreich AtaxiaHumansMaleMiddle AgedPhysical Therapy ModalitiesDopamine Agents

Identifiers

PMID31356292
PMCPMC7339377
OpenAlexW4238040070

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.