Evidence map›Paper›PMID 35977840›Full record

SynthesisNeurology2022

Clinical and Structural Findings in Patients With Lesion-Induced Dystonia: Descriptive and Quantitative Analysis of Published Cases.

Daniel T Corp, Christopher J Greenwood, Jordan Morrison-Ham, Jaakko Pullinen, Georgia M McDowall, Ellen F P Younger, Hyder A Jinnah, Michael D Fox, Juho Joutsa

Open access · greenAbstract readSystematic Review
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. An Exploratory, Randomized, Double-Blind Clinical Trial of Dipraglurant for Blepharospasm.Movement disorders : official journal of the Movement Disorder Society · 2024
    Trial
  2. Article
  3. Article
  4. Article
  5. Mapping the Neuroanatomy of Dystonia Using Causal Brain Lesions.medRxiv : the preprint server for health sciences · 2025
    Article
  6. MRI evidence of cerebellar vermian hypoplasia in a patient with cervical dystonia.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  7. Article
  8. Article
  9. Definition and Classification of Dystonia.Movement disorders : official journal of the Movement Disorder Society · 2025
    Review
  10. Article
  11. Thalamic deep brain stimulation improves movement in a cerebellar model of lesion-based status dystonicus.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  12. Engaging dystonia networks with subthalamic stimulation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Article
  14. Is Routine Neuroimaging Needed in Adult-Onset Isolated Cervical Dystonia?Tremor and other hyperkinetic movements (New York, N.Y.) · 2025
    Article
  15. Lesion-Induced Blepharospasm: Epidemiology and Clinical Characteristics.Tremor and other hyperkinetic movements (New York, N.Y.) · 2025
    Article
  16. Article
  17. Brain network pathophysiology in dystonia.Dystonia (Lausanne, Switzerland) · 2025
    Article
  18. Engaging dystonia networks with subthalamic stimulation.medRxiv : the preprint server for health sciences · 2024
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 3 countries.

Daniel T CorpFrom the Cognitive Neuroscience Unit (D.T.C., J.M.-H., G.M., E.Y.), School of Psychology, Deakin University, Geelong, Australia; Center for Brain Circuit Therapeutics (D.T.C., M.D.F., J.J.), Brigham and Women's Hospital, Boston, MA; Deakin University (C.G.), Centre for Social and Early Emotional Development, School of Psychology, Faculty of Health, Geelong, Australia; Murdoch Children's Research Institute (C.G.), Centre for Adolescent Health, Melbourne, Australia; Turku Brain and Mind Center (J.P., J.J.), Clinical Neurosciences, University of Turku, Finland; Departments of Neurology and Human Genetics (H.J.), Emory University, School of Medicine, Atlanta, GA; Department of Neurology (M.D.F.), Harvard Medical School, Boston, MA; and Turku PET Centre (J.J.), Neurocenter, Turku University Hospital, Finland. daniel.corp@deakin.edu.au.
Christopher J GreenwoodFrom the Cognitive Neuroscience Unit (D.T.C., J.M.-H., G.M., E.Y.), School of Psychology, Deakin University, Geelong, Australia; Center for Brain Circuit Therapeutics (D.T.C., M.D.F., J.J.), Brigham and Women's Hospital, Boston, MA; Deakin University (C.G.), Centre for Social and Early Emotional Development, School of Psychology, Faculty of Health, Geelong, Australia; Murdoch Children's Research Institute (C.G.), Centre for Adolescent Health, Melbourne, Australia; Turku Brain and Mind Center (J.P., J.J.), Clinical Neurosciences, University of Turku, Finland; Departments of Neurology and Human Genetics (H.J.), Emory University, School of Medicine, Atlanta, GA; Department of Neurology (M.D.F.), Harvard Medical School, Boston, MA; and Turku PET Centre (J.J.), Neurocenter, Turku University Hospital, Finland.ORCID 0000-0002-9211-6312
Jordan Morrison-HamFrom the Cognitive Neuroscience Unit (D.T.C., J.M.-H., G.M., E.Y.), School of Psychology, Deakin University, Geelong, Australia; Center for Brain Circuit Therapeutics (D.T.C., M.D.F., J.J.), Brigham and Women's Hospital, Boston, MA; Deakin University (C.G.), Centre for Social and Early Emotional Development, School of Psychology, Faculty of Health, Geelong, Australia; Murdoch Children's Research Institute (C.G.), Centre for Adolescent Health, Melbourne, Australia; Turku Brain and Mind Center (J.P., J.J.), Clinical Neurosciences, University of Turku, Finland; Departments of Neurology and Human Genetics (H.J.), Emory University, School of Medicine, Atlanta, GA; Department of Neurology (M.D.F.), Harvard Medical School, Boston, MA; and Turku PET Centre (J.J.), Neurocenter, Turku University Hospital, Finland.
Jaakko PullinenFrom the Cognitive Neuroscience Unit (D.T.C., J.M.-H., G.M., E.Y.), School of Psychology, Deakin University, Geelong, Australia; Center for Brain Circuit Therapeutics (D.T.C., M.D.F., J.J.), Brigham and Women's Hospital, Boston, MA; Deakin University (C.G.), Centre for Social and Early Emotional Development, School of Psychology, Faculty of Health, Geelong, Australia; Murdoch Children's Research Institute (C.G.), Centre for Adolescent Health, Melbourne, Australia; Turku Brain and Mind Center (J.P., J.J.), Clinical Neurosciences, University of Turku, Finland; Departments of Neurology and Human Genetics (H.J.), Emory University, School of Medicine, Atlanta, GA; Department of Neurology (M.D.F.), Harvard Medical School, Boston, MA; and Turku PET Centre (J.J.), Neurocenter, Turku University Hospital, Finland.ORCID 0000-0002-5081-047X
Georgia M McDowallFrom the Cognitive Neuroscience Unit (D.T.C., J.M.-H., G.M., E.Y.), School of Psychology, Deakin University, Geelong, Australia; Center for Brain Circuit Therapeutics (D.T.C., M.D.F., J.J.), Brigham and Women's Hospital, Boston, MA; Deakin University (C.G.), Centre for Social and Early Emotional Development, School of Psychology, Faculty of Health, Geelong, Australia; Murdoch Children's Research Institute (C.G.), Centre for Adolescent Health, Melbourne, Australia; Turku Brain and Mind Center (J.P., J.J.), Clinical Neurosciences, University of Turku, Finland; Departments of Neurology and Human Genetics (H.J.), Emory University, School of Medicine, Atlanta, GA; Department of Neurology (M.D.F.), Harvard Medical School, Boston, MA; and Turku PET Centre (J.J.), Neurocenter, Turku University Hospital, Finland.
Ellen F P YoungerFrom the Cognitive Neuroscience Unit (D.T.C., J.M.-H., G.M., E.Y.), School of Psychology, Deakin University, Geelong, Australia; Center for Brain Circuit Therapeutics (D.T.C., M.D.F., J.J.), Brigham and Women's Hospital, Boston, MA; Deakin University (C.G.), Centre for Social and Early Emotional Development, School of Psychology, Faculty of Health, Geelong, Australia; Murdoch Children's Research Institute (C.G.), Centre for Adolescent Health, Melbourne, Australia; Turku Brain and Mind Center (J.P., J.J.), Clinical Neurosciences, University of Turku, Finland; Departments of Neurology and Human Genetics (H.J.), Emory University, School of Medicine, Atlanta, GA; Department of Neurology (M.D.F.), Harvard Medical School, Boston, MA; and Turku PET Centre (J.J.), Neurocenter, Turku University Hospital, Finland.
Hyder A JinnahFrom the Cognitive Neuroscience Unit (D.T.C., J.M.-H., G.M., E.Y.), School of Psychology, Deakin University, Geelong, Australia; Center for Brain Circuit Therapeutics (D.T.C., M.D.F., J.J.), Brigham and Women's Hospital, Boston, MA; Deakin University (C.G.), Centre for Social and Early Emotional Development, School of Psychology, Faculty of Health, Geelong, Australia; Murdoch Children's Research Institute (C.G.), Centre for Adolescent Health, Melbourne, Australia; Turku Brain and Mind Center (J.P., J.J.), Clinical Neurosciences, University of Turku, Finland; Departments of Neurology and Human Genetics (H.J.), Emory University, School of Medicine, Atlanta, GA; Department of Neurology (M.D.F.), Harvard Medical School, Boston, MA; and Turku PET Centre (J.J.), Neurocenter, Turku University Hospital, Finland.
Michael D FoxFrom the Cognitive Neuroscience Unit (D.T.C., J.M.-H., G.M., E.Y.), School of Psychology, Deakin University, Geelong, Australia; Center for Brain Circuit Therapeutics (D.T.C., M.D.F., J.J.), Brigham and Women's Hospital, Boston, MA; Deakin University (C.G.), Centre for Social and Early Emotional Development, School of Psychology, Faculty of Health, Geelong, Australia; Murdoch Children's Research Institute (C.G.), Centre for Adolescent Health, Melbourne, Australia; Turku Brain and Mind Center (J.P., J.J.), Clinical Neurosciences, University of Turku, Finland; Departments of Neurology and Human Genetics (H.J.), Emory University, School of Medicine, Atlanta, GA; Department of Neurology (M.D.F.), Harvard Medical School, Boston, MA; and Turku PET Centre (J.J.), Neurocenter, Turku University Hospital, Finland.ORCID 0000-0001-8848-6399
Juho JoutsaFrom the Cognitive Neuroscience Unit (D.T.C., J.M.-H., G.M., E.Y.), School of Psychology, Deakin University, Geelong, Australia; Center for Brain Circuit Therapeutics (D.T.C., M.D.F., J.J.), Brigham and Women's Hospital, Boston, MA; Deakin University (C.G.), Centre for Social and Early Emotional Development, School of Psychology, Faculty of Health, Geelong, Australia; Murdoch Children's Research Institute (C.G.), Centre for Adolescent Health, Melbourne, Australia; Turku Brain and Mind Center (J.P., J.J.), Clinical Neurosciences, University of Turku, Finland; Departments of Neurology and Human Genetics (H.J.), Emory University, School of Medicine, Atlanta, GA; Department of Neurology (M.D.F.), Harvard Medical School, Boston, MA; and Turku PET Centre (J.J.), Neurocenter, Turku University Hospital, Finland.
Brigham and Women's Hospital · US

Funding

Dystonia Coalition- Pilot ProjectU54NS116025 · NINDS · EMORY UNIVERSITY · PI JINNAH, HYDER A · 2019 to 2023
$7.1M
Dystonia CoalitionU54NS065701 · NINDS · EMORY UNIVERSITY · PI JINNAH, HYDER A · 2009 to 2014
$7.0M
Using human brain connectivity to identify the causal neuroanatomical substrate of depression symptomsR01MH113929 · NIMH · BRIGHAM AND WOMEN'S HOSPITAL · PI MICHAEL D FOX · 2017 to 2026
$6.9M
Repetitive TMS-induced modulation of cortical excitability in ADR01MH115949 · NIMH · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SHAFI, MOUHSIN · 2018 to 2022
$3.2M
Treating hyperexcitability in Alzheimer’s disease with levetiracetam to improve brain function and cognitionR01AG060987 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SHAFI, MOUHSIN · 2019 to 2023
$3.0M
Dystonia CoalitionU54TR001456 · NCATS · EMORY UNIVERSITY · PI JINNAH, HYDER A · 2015 to 2016
$2.5M
Deep phenotyping in blepharospasmR01NS119831 · NINDS · EMORY UNIVERSITY · PI JINNAH, HYDER A, YEO, WOON-HONG · 2021 to 2024
$1.5M
Transdiagnostic memory, mood and motor circuits in Alzheimer's and neurodegenerative diseaseR56AG069086 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI FOX, MICHAEL D · 2021 to 2021
$873k
Targeted modulation of symptom-specific brain circuits with transcranial magnetic stimulationR21MH126271 · NIMH · BRIGHAM AND WOMEN'S HOSPITAL · PI FOX, MICHAEL D · 2021 to 2022
$492k
NCATS NIH HHS U54 TR001456NIA NIH HHS R01 AG060987NIA NIH HHS R56 AG069086NIMH NIH HHS R01 MH113929NIMH NIH HHS R01 MH115949NIMH NIH HHS R21 MH126271NINDS NIH HHS R01 NS119831NINDS NIH HHS U54 NS065701NINDS NIH HHS U54 NS116025
6 · The paper itself

Abstract

BACKGROUND AND

objectivesBrain lesions are a well-recognized etiology of dystonia. These cases are especially valuable because they offer causal insight into the neuroanatomical substrates of dystonia. To date, knowledge of lesion-induced dystonia comes mainly from isolated case reports or small case series, restricting broader description and analysis.

methodsCases of lesion-induced dystonia were first identified from a systematic review of published literature. Latent class analysis then investigated whether patients could be classified into subgroups based on lesion location and body regions affected by dystonia. Regression analyses subsequently investigated whether subgroup membership predicted clinical characteristics of dystonia.

resultsThree hundred fifty-nine published cases were included. Lesions causing dystonia occurred in heterogeneous locations, most commonly in the basal ganglia (46.2%), followed by the thalamus (28.1%), brainstem (22.6%), and white matter (21.2%). The most common form of lesion-induced dystonia was focal dystonia (53.2%), with the hand (49.9%) and arm (44.3%) most commonly affected. Of all cases, 86.6% reported co-occurring neurologic manifestations and 26.1% reported other movement disorders. Latent class analysis identified 3 distinct subgroups of patients: those with predominantly limb dystonias, which were associated with basal ganglia lesions; those with hand dystonia, associated with thalamic lesions; and those with predominantly cervical dystonia, associated with brainstem and cerebellar lesions. Regression demonstrated significant differences between these subgroups on a range of dystonia symptoms, including dystonic tremor, symptom latency, other movement disorders, and dystonia variability. DISCUSSION: Although dystonia can be induced by lesions to numerous brain regions, there are distinct relationships between lesion locations and dystonic body parts. This suggests that the affected brain networks are different between types of dystonia.

Indexed as

Dystonic DisordersMovement DisordersTorticollisBasal GangliaBrainHumans

Identifiers

PMID35977840
PMCPMC9651464
OpenAlexW4292148543

What OpenQuestion holds

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Registered trials

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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.