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      Muscle contributions to pre-swing biomechanical tasks influence swing leg mechanics in individuals post-stroke during walking

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          Abstract

          Background

          Successful walking requires the execution of the pre-swing biomechanical tasks of body propulsion and leg swing initiation, which are often impaired post-stroke. While excess rectus femoris activity during swing is often associated with low knee flexion, previous work has suggested that deficits in propulsion and leg swing initiation may also contribute. The purpose of this study was to determine underlying causes of propulsion, leg swing initiation and knee flexion deficits in pre-swing and their link to stiff knee gait in individuals post-stroke.

          Methods

          Musculoskeletal models and forward dynamic simulations were developed for individuals post-stroke (n = 15) and healthy participants (n = 5). Linear regressions were used to evaluate the relationships between peak knee flexion, braking and propulsion symmetry, and individual muscle contributions to braking, propulsion, knee flexion in pre-swing, and leg swing initiation.

          Results

          Four out of fifteen of individuals post-stroke had higher plantarflexor contributions to propulsion and seven out of fifteen had higher vasti contributions to braking on their paretic leg relative to their nonparetic leg. Higher gastrocnemius contributions to propulsion predicted paretic propulsion symmetry (p = 0.005) while soleus contributions did not. Higher vasti contributions to braking in pre-swing predicted lower knee flexion (p = 0.022). The rectus femoris had minimal contributions to lower knee flexion acceleration in pre-swing compared to contributions from the vasti. However, for some individuals with low knee flexion, during pre-swing the rectus femoris absorbed more power and the iliopsoas contributed less power to the paretic leg. Total musculotendon work done on the paretic leg in pre-swing did not predict knee flexion during swing.

          Conclusions

          These results emphasize the multiple causes of propulsion asymmetry in individuals post-stroke, including low plantarflexor contributions to propulsion, increased vasti contributions to braking and reliance on compensatory mechanisms. The results also show that the rectus femoris is not a major contributor to knee flexion in pre-swing, but absorbs more power from the paretic leg in pre-swing in some individuals with stiff knee gait. These results highlight the need to identify individual causes of propulsion and knee flexion deficits to design more effective rehabilitation strategies.

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s12984-022-01029-z.

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          Most cited references48

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          Heart Disease and Stroke Statistics—2020 Update

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            OpenSim: open-source software to create and analyze dynamic simulations of movement.

            Dynamic simulations of movement allow one to study neuromuscular coordination, analyze athletic performance, and estimate internal loading of the musculoskeletal system. Simulations can also be used to identify the sources of pathological movement and establish a scientific basis for treatment planning. We have developed a freely available, open-source software system (OpenSim) that lets users develop models of musculoskeletal structures and create dynamic simulations of a wide variety of movements. We are using this system to simulate the dynamics of individuals with pathological gait and to explore the biomechanical effects of treatments. OpenSim provides a platform on which the biomechanics community can build a library of simulations that can be exchanged, tested, analyzed, and improved through a multi-institutional collaboration. Developing software that enables a concerted effort from many investigators poses technical and sociological challenges. Meeting those challenges will accelerate the discovery of principles that govern movement control and improve treatments for individuals with movement pathologies.
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              Merging of healthy motor modules predicts reduced locomotor performance and muscle coordination complexity post-stroke.

              Evidence suggests that the nervous system controls motor tasks using a low-dimensional modular organization of muscle activation. However, it is not clear if such an organization applies to coordination of human walking, nor how nervous system injury may alter the organization of motor modules and their biomechanical outputs. We first tested the hypothesis that muscle activation patterns during walking are produced through the variable activation of a small set of motor modules. In 20 healthy control subjects, EMG signals from eight leg muscles were measured across a range of walking speeds. Four motor modules identified through nonnegative matrix factorization were sufficient to account for variability of muscle activation from step to step and across speeds. Next, consistent with the clinical notion of abnormal limb flexion-extension synergies post-stroke, we tested the hypothesis that subjects with post-stroke hemiparesis would have altered motor modules, leading to impaired walking performance. In post-stroke subjects (n = 55), a less complex coordination pattern was shown. Fewer modules were needed to account for muscle activation during walking at preferred speed compared with controls. Fewer modules resulted from merging of the modules observed in healthy controls, suggesting reduced independence of neural control signals. The number of modules was correlated to preferred walking speed, speed modulation, step length asymmetry, and propulsive asymmetry. Our results suggest a common modular organization of muscle coordination underlying walking in both healthy and post-stroke subjects. Identification of motor modules may lead to new insight into impaired locomotor coordination and the underlying neural systems.
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                Author and article information

                Contributors
                rneptune@mail.utexas.edu
                Journal
                J Neuroeng Rehabil
                J Neuroeng Rehabil
                Journal of NeuroEngineering and Rehabilitation
                BioMed Central (London )
                1743-0003
                3 June 2022
                3 June 2022
                2022
                : 19
                : 55
                Affiliations
                [1 ]GRID grid.89336.37, ISNI 0000 0004 1936 9924, Walker Department of Mechanical Engineering, , The University of Texas at Austin, ; Austin, TX USA
                [2 ]GRID grid.280644.c, ISNI 0000 0000 8950 3536, Ralph H Johnson VA Medical Center, ; Charleston, SC USA
                [3 ]GRID grid.259828.c, ISNI 0000 0001 2189 3475, Department of Health Sciences & Research and Division of Physical Therapy, , Medical University of South Carolina, ; Charleston, SC USA
                [4 ]GRID grid.89336.37, ISNI 0000 0004 1936 9924, Walker Department of Mechanical Engineering, , The University of Texas at Austin, ; 204 E. Dean Keeton Street, Stop C2200, Austin, TX 78712-1591 USA
                Author information
                http://orcid.org/0000-0003-3151-8235
                http://orcid.org/0000-0003-2425-004X
                Article
                1029
                10.1186/s12984-022-01029-z
                9166530
                190c5d65-c87f-42d8-ba50-da414f9886ac
                © The Author(s) 2022

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 1 November 2021
                : 18 May 2022
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: P20HD109040
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000738, U.S. Department of Veterans Affairs;
                Award ID: 1I01RX001935
                Award Recipient :
                Categories
                Research
                Custom metadata
                © The Author(s) 2022

                Neurosciences
                stiff knee gait,modeling,gait,compensation,biomechanics
                Neurosciences
                stiff knee gait, modeling, gait, compensation, biomechanics

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