Sensory-motor network functional connectivity in children with unilateral cerebral palsy secondary to perinatal stroke.


Journal

NeuroImage. Clinical
ISSN: 2213-1582
Titre abrégé: Neuroimage Clin
Pays: Netherlands
ID NLM: 101597070

Informations de publication

Date de publication:
2019
Historique:
received: 06 07 2018
revised: 23 12 2018
accepted: 07 01 2019
pubmed: 16 1 2019
medline: 4 1 2020
entrez: 16 1 2019
Statut: ppublish

Résumé

Perinatal stroke is the most common cause of unilateral cerebral palsy. Mechanisms of post-stroke developmental plasticity in children are poorly understood. To better understand the relationship between functional connectivity and disability, we used resting-state fMRI to compare sensorimotor connectivity with clinical dysfunction. School-aged children with periventricular venous infarction (PVI) and unilateral cerebral palsy were compared to controls. Resting-state BOLD signal was acquired on 3 T MRI and analyzed using CONN in SPM12. Functional connectivity was computed between S1, M1, supplementary motor area (SMA), and thalamus of the left/non-lesioned and right/lesioned hemisphere. Primary outcome was connectivity expressed as a Fisher-transformed correlation coefficient. Motor function was measured using the Assisting Hand Assessment (AHA), and Melbourne Assessment (MA). Proprioceptive function was measured using a robotic position matching task (VarXY). Participants included 15 PVI and 21 controls. AHA and MA in stroke patients were negatively correlated with connectivity (increased connectivity = poorer performance). Position sense was inversely correlated with connectivity (increased connectivity = improved performance) between the non-lesioned S1 and thalamus/SMA. In controls, VarXY was positively correlated with connectivity between the thalamus and bilateral sensorimotor regions. Resting state fMRI measures of sensorimotor connectivity are associated with clinical sensorimotor function in children with unilateral cerebral palsy secondary to PVI. Greater insight into understanding reorganization of brain networks following perinatal stroke may facilitate personalized rehabilitation.

Sections du résumé

BACKGROUND
Perinatal stroke is the most common cause of unilateral cerebral palsy. Mechanisms of post-stroke developmental plasticity in children are poorly understood. To better understand the relationship between functional connectivity and disability, we used resting-state fMRI to compare sensorimotor connectivity with clinical dysfunction.
METHODS
School-aged children with periventricular venous infarction (PVI) and unilateral cerebral palsy were compared to controls. Resting-state BOLD signal was acquired on 3 T MRI and analyzed using CONN in SPM12. Functional connectivity was computed between S1, M1, supplementary motor area (SMA), and thalamus of the left/non-lesioned and right/lesioned hemisphere. Primary outcome was connectivity expressed as a Fisher-transformed correlation coefficient. Motor function was measured using the Assisting Hand Assessment (AHA), and Melbourne Assessment (MA). Proprioceptive function was measured using a robotic position matching task (VarXY).
RESULTS
Participants included 15 PVI and 21 controls. AHA and MA in stroke patients were negatively correlated with connectivity (increased connectivity = poorer performance). Position sense was inversely correlated with connectivity (increased connectivity = improved performance) between the non-lesioned S1 and thalamus/SMA. In controls, VarXY was positively correlated with connectivity between the thalamus and bilateral sensorimotor regions.
CONCLUSIONS
Resting state fMRI measures of sensorimotor connectivity are associated with clinical sensorimotor function in children with unilateral cerebral palsy secondary to PVI. Greater insight into understanding reorganization of brain networks following perinatal stroke may facilitate personalized rehabilitation.

Identifiants

pubmed: 30642756
pii: S2213-1582(19)30020-8
doi: 10.1016/j.nicl.2019.101670
pmc: PMC6412078
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

101670

Subventions

Organisme : CIHR
Pays : Canada

Informations de copyright

Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.

Auteurs

K E Woodward (KE)

Department of Clinical Neurosciences, Cumming School of Medicine, Alberta Children's Hospital Research Institute, University of Calgary, 2888 Shaganappi Trial NW, Calgary, AB T3B6A8, Canada. Electronic address: kristine.woodward@ahs.ca.

H L Carlson (HL)

Department of Clinical Neurosciences, Cumming School of Medicine, Alberta Children's Hospital Research Institute, University of Calgary, 2888 Shaganappi Trial NW, Calgary, AB T3B6A8, Canada. Electronic address: helen.carlson@ahs.ca.

A Kuczynski (A)

Department of Neurosciences and Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, 3330 Hospital Dr NW, Calgary, AB T2N4N1, Canada. Electronic address: andrea.kuczynski@ahs.ca.

J Saunders (J)

Calgary Pediatric Stroke Program, Alberta Children's Hospital, University of Calgary, 2888 Shaganappi Trial NW, Calgary, AB T3B6A8, Canada. Electronic address: jenny.saunders@ahs.ca.

J Hodge (J)

Calgary Pediatric Stroke Program, Alberta Children's Hospital, University of Calgary, 2888 Shaganappi Trial NW, Calgary, AB T3B6A8, Canada. Electronic address: Jacquie.hodge@ahs.ca.

A Kirton (A)

Calgary Pediatric Stroke Program, Alberta Children's Hospital, University of Calgary, 2888 Shaganappi Trial NW, Calgary, AB T3B6A8, Canada; Department of Clinical Neurosciences, Cumming School of Medicine, Alberta Children's Hospital Research Institute, University of Calgary, 2888 Shaganappi Trial NW, Calgary, AB T3B6A8, Canada; Department of Neurosciences and Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, 3330 Hospital Dr NW, Calgary, AB T2N4N1, Canada. Electronic address: adam.kirton@ahs.ca.

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