Combining muscle morphology and neuromotor symptoms to explain abnormal gait at the ankle joint level in cerebral palsy.


Journal

Gait & posture
ISSN: 1879-2219
Titre abrégé: Gait Posture
Pays: England
ID NLM: 9416830

Informations de publication

Date de publication:
02 2019
Historique:
received: 22 05 2018
revised: 24 10 2018
accepted: 03 12 2018
pubmed: 10 1 2019
medline: 16 4 2019
entrez: 10 1 2019
Statut: ppublish

Résumé

Individuals with spastic cerebral palsy (CP) have neuromotor symptoms contributing towards their gait patterns. However, the role of altered muscle morphology alongside these symptoms is yet to be fully investigated. To what extent can medial gastrocnemius and tibialis anterior volume and echo-intensity, plantar/dorsiflexion strength and selective motor control, plantarflexion spasticity and passive ankle dorsiflexion explain abnormal ankle gait. In thirty children and adolescents with spastic CP (8.6 ± 3.4 y/mo) and ten typically developing peers (9.9 ± 2.4 y/mo), normalised muscle volume and echo-intensity were estimated. Both cohorts also underwent three-dimensional gait analysis, whilst for participants with spastic CP, plantar/dorsi-flexion strength and selective motor control, plantarflexion spasticity and maximum ankle dorsiflexion were also measured. The combined contribution of these parameters towards five clinically meaningful features of gait were evaluated, using backwards multiple regression analyses. With respect to the typically developing cohort, the participants with spastic CP had deficits in normalised medial gastrocnemius and tibialis anterior volume of 40% and 33%, and increased echo-intensity values of 19% and 16%, respectively. The backwards multiple regression analyses revealed that the combination of reduced ankle dorsiflexion, muscle volume, plantarflexion strength and dorsiflexion selective motor control could account for 12-62% of the variance in the chosen features of gait. The combination of altered muscle morphology and neuromotor symptoms partly explained abnormal gait at the ankle in children with spastic CP. Both should be considered as important measures for informed treatment decision-making, but further work is required to better unravel the complex pathophysiology.

Sections du résumé

BACKGROUND
Individuals with spastic cerebral palsy (CP) have neuromotor symptoms contributing towards their gait patterns. However, the role of altered muscle morphology alongside these symptoms is yet to be fully investigated.
RESEARCH QUESTION
To what extent can medial gastrocnemius and tibialis anterior volume and echo-intensity, plantar/dorsiflexion strength and selective motor control, plantarflexion spasticity and passive ankle dorsiflexion explain abnormal ankle gait.
METHOD
In thirty children and adolescents with spastic CP (8.6 ± 3.4 y/mo) and ten typically developing peers (9.9 ± 2.4 y/mo), normalised muscle volume and echo-intensity were estimated. Both cohorts also underwent three-dimensional gait analysis, whilst for participants with spastic CP, plantar/dorsi-flexion strength and selective motor control, plantarflexion spasticity and maximum ankle dorsiflexion were also measured. The combined contribution of these parameters towards five clinically meaningful features of gait were evaluated, using backwards multiple regression analyses.
RESULTS
With respect to the typically developing cohort, the participants with spastic CP had deficits in normalised medial gastrocnemius and tibialis anterior volume of 40% and 33%, and increased echo-intensity values of 19% and 16%, respectively. The backwards multiple regression analyses revealed that the combination of reduced ankle dorsiflexion, muscle volume, plantarflexion strength and dorsiflexion selective motor control could account for 12-62% of the variance in the chosen features of gait.
SIGNIFICANCE
The combination of altered muscle morphology and neuromotor symptoms partly explained abnormal gait at the ankle in children with spastic CP. Both should be considered as important measures for informed treatment decision-making, but further work is required to better unravel the complex pathophysiology.

Identifiants

pubmed: 30623848
pii: S0966-6362(18)30583-6
doi: 10.1016/j.gaitpost.2018.12.002
pii:
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

531-537

Informations de copyright

Copyright © 2018 Elsevier B.V. All rights reserved.

Auteurs

Simon-Henri Schless (SH)

Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium; Clinical Motion Analysis Laboratory, University Hospitals Leuven, Pellenberg, Belgium. Electronic address: simonhenri.schless@kuleuven.be.

Francesco Cenni (F)

Clinical Motion Analysis Laboratory, University Hospitals Leuven, Pellenberg, Belgium; Department of Mechanical Engineering, KU Leuven, Leuven, Belgium.

Lynn Bar-On (L)

Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium; Amsterdam UMC, Vrije Universiteit Amsterdam, Department of Rehabilitation Medicine, Amsterdam Movement Sciences, Amsterdam, Netherlands.

Britta Hanssen (B)

Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium; Clinical Motion Analysis Laboratory, University Hospitals Leuven, Pellenberg, Belgium.

Marije Goudriaan (M)

Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium; Clinical Motion Analysis Laboratory, University Hospitals Leuven, Pellenberg, Belgium.

Eirini Papageorgiou (E)

Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium; Clinical Motion Analysis Laboratory, University Hospitals Leuven, Pellenberg, Belgium.

Erwin Aertbeliën (E)

Department of Mechanical Engineering, KU Leuven, Leuven, Belgium.

Guy Molenaers (G)

Department of Development and Regeneration, KU Leuven, Leuven, Belgium; Orthopaedic section University Hospitals Leuven, Belgium.

Kaat Desloovere (K)

Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium; Clinical Motion Analysis Laboratory, University Hospitals Leuven, Pellenberg, Belgium.

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