Evidence map›Paper›PMID 28784298›Full record

ReviewParkinsonism & related disorders2018

Evolving concepts in the pathogenesis of dystonia.

H A Jinnah, Ellen J Hess

Abstract readReview
In one paragraph

Review in Parkinsonism & related disorders, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-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.

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

32 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. A frameshift mutation in the murinebioRxiv : the preprint server for biology · 2024
    Article
  8. Genetic Update and Treatment for Dystonia.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Decoding Dystonia in Autoimmune Disorders: A Scoping Review.Tremor and other hyperkinetic movements (New York, N.Y.) · 2024
    Article
  11. Article
  12. Pathophysiology of Dyt1-Science translational medicine · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. A novel compound heterozygous mutation ofFrontiers in neurology · 2023
    Article
  17. Article
  18. Diphenhydramine induced acute dystonia: a case report.The Pan African medical journal · 2022
    Article
  19. Observational
  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

2 authors at 1 institution in 1 country.

H A JinnahDepartments of Neurology, Human Genetics and Pediatrics, Emory University, Atlanta, GA, USA. Electronic address: hjinnah@emory.edu.
Ellen J HessDepartment of Pharmacology and Neurology, Emory University, Atlanta, GA, USA.
Emory University · US

Funding

Dystonia CoalitionU54NS065701 · NINDS · EMORY UNIVERSITY · PI JINNAH, HYDER A · 2009 to 2014
$7.0M
Dystonia CoalitionU54TR001456 · NCATS · EMORY UNIVERSITY · PI JINNAH, HYDER A · 2015 to 2016
$2.5M
Dopamine neurotransmission in a model of DOPA-responsive dystoniaR01NS088528 · NINDS · EMORY UNIVERSITY · PI HESS, ELLEN J. · 2015 to 2019
$1.9M
NCATS NIH HHS U54 TR001456NINDS NIH HHS R01 NS088528NINDS NIH HHS U54 NS065701
6 · The paper itself

Abstract

introductionThe dystonias are a group of disorders defined by over-contraction of muscles leading to abnormal movements and postures. In recent years, enormous advances have been made in elucidating the neurobiological mechanisms responsible for many types of dystonia.

methodsA literature review was conducted focusing on evolving concepts in dystonia genetics, anatomy and physiology.

resultsThe list of genes related to dystonia has grown from a relatively small number to more than 100. Concepts regarding the neuroanatomical basis for dystonia have evolved from a relatively narrow focus on dysfunction of the basal ganglia to a broader motor network model in which the basal ganglia, cerebellum, cerebral cortex, and other brain regions play a key role. Physiologically, our understanding of the core abnormalities has matured; and numerous changes in neural signaling have been revealed in the basal ganglia, cerebellum and cortex.

conclusionAlthough the dystonias share certain clinical aspects such as over-contraction of muscles leading to abnormal movements and postures, they actually comprise a very clinically and etiologically heterogeneous group of disorders. Understanding their neurobiological basis is important for devising rational therapies appropriately targeted for specific subgroups of patients.

Indexed as

Dystonic DisordersBrainHumansMolecular ChaperonesMolecular ChaperonesTOR1A protein, humanNeuroanatomyNeurobiologyNeurogeneticsNeurophysiologyPathogenesisPathophysiology

Identifiers

PMID28784298
PMCPMC5696051
OpenAlexW2740733621

What OpenQuestion holds

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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.