Validation of forward simulations to predict the effects of bilateral plantarflexor weakness on gait.

Calf muscle weakness Gait compensations Muscle weakness Neuromuscular diseases Plantar flexors Predictive simulations

Journal

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

Informations de publication

Date de publication:
06 2021
Historique:
received: 09 12 2020
revised: 07 04 2021
accepted: 10 04 2021
pubmed: 22 4 2021
medline: 9 10 2021
entrez: 21 4 2021
Statut: ppublish

Résumé

Bilateral plantarflexor muscle weakness is a common impairment in many neuromuscular diseases. However, the way in which severity of plantarflexor weakness affects gait in terms of walking energy cost and speed is not fully understood. Predictive simulations are an attractive alternative to human experiments as simulations allow systematic alterations in muscle weakness. However, simulations of pathological gait have not yet been validated against experimental data, limiting their applicability. Our first aim was to validate a predictive simulation framework for walking with bilateral plantarflexor weakness by comparing predicted gait against experimental gait data of patients with bilateral plantarflexor weakness. Secondly, we aimed to evaluate how incremental levels of bilateral plantarflexor weakness affect gait. We used a planar musculoskeletal model with 9 degrees of freedom and 9 Hill-type muscle-tendon units per leg. A state-dependent reflex-based controller optimized for a function combining energy cost, muscle activation squared and head acceleration was used to simulate gait. For validation, strength of the plantarflexors was reduced by 80 % and simulated gait compared with experimental data of 16 subjects with bilateral plantarflexor weakness. Subsequently, strength of the plantarflexors was reduced stepwise to evaluate its effect on gait kinematics and kinetics, walking energy cost and speed. Simulations with 80 % weakness matched well with experimental hip and ankle kinematics and kinetics (R > 0.64), but less for knee kinetics (R < 0.55). With incremental strength reduction, especially beyond a reduction of 60 %, the maximal ankle moment and power decreased. Walking energy cost and speed showed a strong quadratic relation (R Our simulation framework predicted most gait changes due to bilateral plantarflexor weakness, and indicates that pathological gait features emerge especially when bilateral plantarflexor weakness exceeds 60 %. Our framework may support future research into the effect of pathologies or assistive devices on gait.

Sections du résumé

BACKGROUND
Bilateral plantarflexor muscle weakness is a common impairment in many neuromuscular diseases. However, the way in which severity of plantarflexor weakness affects gait in terms of walking energy cost and speed is not fully understood. Predictive simulations are an attractive alternative to human experiments as simulations allow systematic alterations in muscle weakness. However, simulations of pathological gait have not yet been validated against experimental data, limiting their applicability.
RESEARCH QUESTION
Our first aim was to validate a predictive simulation framework for walking with bilateral plantarflexor weakness by comparing predicted gait against experimental gait data of patients with bilateral plantarflexor weakness. Secondly, we aimed to evaluate how incremental levels of bilateral plantarflexor weakness affect gait.
METHODS
We used a planar musculoskeletal model with 9 degrees of freedom and 9 Hill-type muscle-tendon units per leg. A state-dependent reflex-based controller optimized for a function combining energy cost, muscle activation squared and head acceleration was used to simulate gait. For validation, strength of the plantarflexors was reduced by 80 % and simulated gait compared with experimental data of 16 subjects with bilateral plantarflexor weakness. Subsequently, strength of the plantarflexors was reduced stepwise to evaluate its effect on gait kinematics and kinetics, walking energy cost and speed.
RESULTS
Simulations with 80 % weakness matched well with experimental hip and ankle kinematics and kinetics (R > 0.64), but less for knee kinetics (R < 0.55). With incremental strength reduction, especially beyond a reduction of 60 %, the maximal ankle moment and power decreased. Walking energy cost and speed showed a strong quadratic relation (R
SIGNIFICANCE
Our simulation framework predicted most gait changes due to bilateral plantarflexor weakness, and indicates that pathological gait features emerge especially when bilateral plantarflexor weakness exceeds 60 %. Our framework may support future research into the effect of pathologies or assistive devices on gait.

Identifiants

pubmed: 33882437
pii: S0966-6362(21)00141-7
doi: 10.1016/j.gaitpost.2021.04.020
pii:
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

33-42

Informations de copyright

Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.

Auteurs

N F J Waterval (NFJ)

Amsterdam UMC, Vrije Universiteit Amsterdam, Department of Rehabilitation Medicine, Amsterdam Movement Sciences, de Boelelaan 1117, Amsterdam, the Netherlands; Amsterdam UMC, University of Amsterdam, Department of Rehabilitation Medicine, Amsterdam Movement Sciences, Meibergdreef 9, Amsterdam, the Netherlands. Electronic address: n.f.waterval@amsterdamumc.nl.

K Veerkamp (K)

Amsterdam UMC, Vrije Universiteit Amsterdam, Department of Rehabilitation Medicine, Amsterdam Movement Sciences, de Boelelaan 1117, Amsterdam, the Netherlands; School of Allied Health Sciences, Griffith University, Gold Coast, Australia; Gold Coast Centre for Orthopaedic Research, Engineering and Education (GCORE), Menzies Health Institute Queensland, and Advanced Design and Prototyping Technologies Institute (ADAPT), Griffith University, Gold Coast, Australia.

T Geijtenbeek (T)

Department of Biomechanical Engineering, Delft University of Technology, Delft, the Netherlands.

J Harlaar (J)

Department of Biomechanical Engineering, Delft University of Technology, Delft, the Netherlands; Department of Orthopaedics, Erasmus Medical Center, Rotterdam, the Netherlands.

F Nollet (F)

Amsterdam UMC, University of Amsterdam, Department of Rehabilitation Medicine, Amsterdam Movement Sciences, Meibergdreef 9, Amsterdam, the Netherlands.

M A Brehm (MA)

Amsterdam UMC, University of Amsterdam, Department of Rehabilitation Medicine, Amsterdam Movement Sciences, Meibergdreef 9, Amsterdam, the Netherlands.

M M van der Krogt (MM)

Amsterdam UMC, Vrije Universiteit Amsterdam, Department of Rehabilitation Medicine, Amsterdam Movement Sciences, de Boelelaan 1117, Amsterdam, the Netherlands.

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