Developmental Remodelling of the Motor Cortex in Hemiparetic Children With Perinatal Stroke.


Journal

Pediatric neurology
ISSN: 1873-5150
Titre abrégé: Pediatr Neurol
Pays: United States
ID NLM: 8508183

Informations de publication

Date de publication:
11 2020
Historique:
received: 13 03 2020
revised: 28 07 2020
accepted: 01 08 2020
pubmed: 11 9 2020
medline: 24 8 2021
entrez: 10 9 2020
Statut: ppublish

Résumé

Perinatal stroke often leads to lifelong motor impairment. Two common subtypes differ in timing, location, and mechanism of injury: periventricular venous infarcts (PVI) are fetal white matter lesions while most arterial ischemic strokes (AIS) are cortical injuries acquired near term birth. Both alter motor system development and primary motor cortex (M1) plasticity, often with retained ipsilateral corticospinal fibers from the non-lesioned motor cortex (M1'). Task-based functional magnetic resonance imaging was used to define patterns of motor cortex activity during paretic and unaffected hand movement. Peak coordinates of M1, M1', and the supplementary motor area in the lesioned and intact hemispheres were compared to age-matched controls. Correlations between displacements and clinical motor function were explored. Forty-nine participants included 14 PVI (12.59 ± 3.7 years), 13 AIS (14.91 ± 3.9 years), and 22 controls (13.91 ± 3.4 years). AIS displayed the greatest M1 displacement from controls in the lesioned hemisphere while PVI locations approximated controls. Peak M1' activations were displaced from the canonical hand knob in both PVI and AIS. Extent of M1 and M1' displacement were correlated (r = 0.50, P = 0.025) but were not associated with motor function. Supplementary motor area activity elicited by paretic tapping was displaced in AIS compared to controls (P = 0.003). Motor network components may be displaced in both hemispheres after perinatal stroke, particularly in AIS and those with ipsilateral control of the affected limb. Modest correlations with clinical function may support that more complex models of developmental plasticity are needed to inform targets for individualized neuromodulatory therapies in children with perinatal stroke.

Sections du résumé

BACKGROUND
Perinatal stroke often leads to lifelong motor impairment. Two common subtypes differ in timing, location, and mechanism of injury: periventricular venous infarcts (PVI) are fetal white matter lesions while most arterial ischemic strokes (AIS) are cortical injuries acquired near term birth. Both alter motor system development and primary motor cortex (M1) plasticity, often with retained ipsilateral corticospinal fibers from the non-lesioned motor cortex (M1').
METHODS
Task-based functional magnetic resonance imaging was used to define patterns of motor cortex activity during paretic and unaffected hand movement. Peak coordinates of M1, M1', and the supplementary motor area in the lesioned and intact hemispheres were compared to age-matched controls. Correlations between displacements and clinical motor function were explored.
RESULTS
Forty-nine participants included 14 PVI (12.59 ± 3.7 years), 13 AIS (14.91 ± 3.9 years), and 22 controls (13.91 ± 3.4 years). AIS displayed the greatest M1 displacement from controls in the lesioned hemisphere while PVI locations approximated controls. Peak M1' activations were displaced from the canonical hand knob in both PVI and AIS. Extent of M1 and M1' displacement were correlated (r = 0.50, P = 0.025) but were not associated with motor function. Supplementary motor area activity elicited by paretic tapping was displaced in AIS compared to controls (P = 0.003).
CONCLUSION
Motor network components may be displaced in both hemispheres after perinatal stroke, particularly in AIS and those with ipsilateral control of the affected limb. Modest correlations with clinical function may support that more complex models of developmental plasticity are needed to inform targets for individualized neuromodulatory therapies in children with perinatal stroke.

Identifiants

pubmed: 32911261
pii: S0887-8994(20)30277-0
doi: 10.1016/j.pediatrneurol.2020.08.004
pii:
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

34-43

Subventions

Organisme : CIHR
Pays : Canada

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Auteurs

Kayla Baker (K)

Calgary Pediatric Stroke Program, Alberta Children's Hospital, Calgary, Alberta, Canada; Alberta Children's Hospital Research Institute (ACHRI), Calgary, Alberta, Canada; Department of Pediatrics, University of Calgary, Calgary, Alberta, Canada; Department of Neurosciences, University of Calgary, Calgary, Alberta, Canada.

Helen L Carlson (HL)

Calgary Pediatric Stroke Program, Alberta Children's Hospital, Calgary, Alberta, Canada; Alberta Children's Hospital Research Institute (ACHRI), Calgary, Alberta, Canada; Department of Pediatrics, University of Calgary, Calgary, Alberta, Canada.

Ephrem Zewdie (E)

Calgary Pediatric Stroke Program, Alberta Children's Hospital, Calgary, Alberta, Canada; Alberta Children's Hospital Research Institute (ACHRI), Calgary, Alberta, Canada; Department of Pediatrics, University of Calgary, Calgary, Alberta, Canada.

Adam Kirton (A)

Calgary Pediatric Stroke Program, Alberta Children's Hospital, Calgary, Alberta, Canada; Alberta Children's Hospital Research Institute (ACHRI), Calgary, Alberta, Canada; Department of Pediatrics, University of Calgary, Calgary, Alberta, Canada; Department of Neurosciences, University of Calgary, Calgary, Alberta, Canada. Electronic address: Adam.Kirton@albertahealthservices.ca.

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