Evidence map›Paper›PMID 16389314›Full record

ReviewNeuroRx : the journal of the American Society for Experimental NeuroTherapeutics2005

Animal models of generalized dystonia.

Robert S Raike, H A Jinnah, Ellen J Hess

Open access · bronzeAbstract readReview
In one paragraph

Review in NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.1field-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

31 citing papers in PubMed, 79 citations in OpenAlex.

  1. The Second Hit Hypothesis in Animal and Human Dystonia: The Role of Peripheral Nerve Trauma and Spinal Cord Injury.Movement disorders : official journal of the Movement Disorder Society · 2026
    Review
  2. Article
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  6. Acute Dystonia Following a Switch in Treatment from Atomoxetine to Low-dose Aripiprazole.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2016
    Article
  7. Review
  8. Article
  9. Review
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  11. Abnormal high-frequency burst firing of cerebellar neurons in rapid-onset dystonia-parkinsonism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  12. Engineering animal models of dystonia.Movement disorders : official journal of the Movement Disorder Society · 2013
    Review
  13. Article
  14. Article
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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

3 authors at 2 institutions in 1 country.

Robert S RaikeDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
H A Jinnah
Ellen J Hess
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Pathophysiology of dystonia: animal modelsR01NS033592 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HESS, ELLEN J. · 2001 to 2010
$3.5M
NEUROBIOLOGY OF DYSTONIAR01NS040470 · NINDS · JOHNS HOPKINS UNIVERSITY · PI JINNAH, HYDER A · 2000 to 2008
$2.5M
NINDS NIH HHS R01 NS033592NINDS NIH HHS R01 NS040470NINDS NIH HHS R01 NS33592NINDS NIH HHS R01 NS40470
6 · The paper itself

Abstract

Dystonia is a prevalent neurological disorder characterized by abnormal co-contractions of antagonistic muscle groups that produce twisting movements and abnormal postures. The disorder may be inherited, arise sporadically, or result from brain insult. Dystonia is a heterogeneous disorder because patients may exhibit focal or generalized symptoms associated with abnormalities in many brain regions including basal ganglia and cerebellum. Elucidating the pathogenic mechanisms underlying dystonia has therefore been challenging. Animal models of dystonia exhibit similar heterogeneity and are useful for understanding pathogenesis. The neurochemical and neurophysiological abnormalities in rodents with idiopathic generalized dystonia suggest that dysfunctional output from basal ganglia, cerebellum, or from multiple systems is the cause of motor dysfunction. Findings from drug- or toxin-induced dystonia in rodents and nonhuman primates mirror the genetic models. The parallels between dystonia in humans and animals suggest that the models will continue to prove useful in determining pathogenesis. Furthermore, detailed characterization of the existing models of dystonia and the development of new models hold promise for the identification of novel therapeutics.

Indexed as

AnimalsBasal Ganglia DiseasesCerebellar DiseasesCricetinaeDisease Models, AnimalDystoniaHumansMiceMice, Neurologic MutantsRats

Identifiers

PMID16389314
PMCPMC1144494
OpenAlexW2082346091

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.