Evidence map›Paper›PMID 21303695›Full record

ReviewNeurobiology of disease2011

The functional neuroanatomy of dystonia.

Vladimir K Neychev, Robert E Gross, Stephane Lehéricy, Ellen J Hess, H A Jinnah

Open access · greenAbstract readReview
In one paragraph

Review in Neurobiology of disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed, 6 pooled it
20.4field-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

242 citing papers in PubMed, 6 syntheses or guidelines pooled it, 466 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. The anatomical basis of upper limb dystonia: lesson from secondary cases.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2016
    Pooled it
  6. Pooled it
  7. Trial
  8. Trial
  9. Article
  10. Predictors of cognitive performance in idiopathic adult-onset dystonia.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Stuttering and Dystonia: Is There a Possible Overlap?Movement disorders clinical practice · 2026
    Article
  16. Movement Disorders in Antibody-Associated Neurologic Diseases: A Nationwide Study.Neurology(R) neuroimmunology & neuroinflammation · 2026
    Observational
  17. Article
  18. Mapping the Neuroanatomy of Dystonia Using Causal Brain Lesions.medRxiv : the preprint server for health sciences · 2025
    Article
  19. Article
  20. Somato-Cognitive Action Network in Focal Dystonia.Movement disorders : official journal of the Movement Disorder Society · 2025
    Article

182 more citing papers are in PubMed but not listed here.

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 2 countries.

Vladimir K NeychevDepartment of Surgery, Danbury Hospital, CT, USA.
Robert E Gross
Stephane Lehéricy
Ellen J Hess
H A Jinnah
Emory University · USDanbury Hospital · USSorbonne Université · FR

Funding

Dystonia CoalitionU54NS065701 · NINDS · EMORY UNIVERSITY · PI JINNAH, HYDER A · 2009 to 2014
$7.0M
Pathophysiology of dystonia: animal modelsR01NS033592 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HESS, ELLEN J. · 2001 to 2010
$3.5M
Dystonia CoalitionU54TR001456 · NCATS · EMORY UNIVERSITY · PI JINNAH, HYDER A · 2015 to 2016
$2.5M
NEUROBIOLOGY OF DYSTONIAR01NS040470 · NINDS · JOHNS HOPKINS UNIVERSITY · PI JINNAH, HYDER A · 2000 to 2008
$2.5M
MOLECULAR BASIS OF THE TOTTERING PHENOTYPER29NS033592 · NINDS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI HESS, ELLEN J. · 1995 to 1999
–
NCATS NIH HHS U54 TR001456NINDS NIH HHS NS033592NINDS NIH HHS NS040470NINDS NIH HHS NS967501NINDS NIH HHS R01 NS033592NINDS NIH HHS R01 NS040470NINDS NIH HHS R29 NS033592NINDS NIH HHS U54 NS065701
6 · The paper itself

Abstract

Dystonia is a neurological disorder characterized by involuntary twisting movements and postures. There are many different clinical manifestations, and many different causes. The neuroanatomical substrates for dystonia are only partly understood. Although the traditional view localizes dystonia to basal ganglia circuits, there is increasing recognition that this view is inadequate for accommodating a substantial portion of available clinical and experimental evidence. A model in which several brain regions play a role in a network better accommodates the evidence. This network model accommodates neuropathological and neuroimaging evidence that dystonia may be associated with abnormalities in multiple different brain regions. It also accommodates animal studies showing that dystonic movements arise with manipulations of different brain regions. It is consistent with neurophysiological evidence suggesting defects in neural inhibitory processes, sensorimotor integration, and maladaptive plasticity. Finally, it may explain neurosurgical experience showing that targeting the basal ganglia is effective only for certain subpopulations of dystonia. Most importantly, the network model provides many new and testable hypotheses with direct relevance for new treatment strategies that go beyond the basal ganglia. This article is part of a Special Issue entitled "Advances in dystonia".

Indexed as

AnimalsBrainDystoniaDystonic DisordersHumans

Identifiers

PMID21303695
PMCPMC3478782
OpenAlexW2030471788

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.