Muscle contributions to pre-swing biomechanical tasks influence swing leg mechanics in individuals post-stroke during walking
Brough et al.
Journal of NeuroEngineering and Rehabilitation
https://doi.org/10.1186/s12984-022-01029-z
(2022) 19:55
Open Access
RESEARCH
Muscle contributions to pre‑swing
biomechanical tasks influence swing
leg mechanics in individuals post‑stroke
during walking
Lydia G. Brough1, Steven A. Kautz2,3 and Richard R. Neptune1,4*
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.
Keywords: Stiff knee gait, Modeling, Gait, Compensation, Biomechanics
*Correspondence:
4
Walker Department of Mechanical Engineering, The University of Texas
at Austin, 204 E. Dean Keeton Street, Stop C2200, Austin, TX 78712‑1591, USA
Full list of author information is available at the end of the article
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Brough et al. Journal of NeuroEngineering and Rehabilitation
(2022) 19:55
Background
Over 795,000 people in the United States experience a
stroke each year and over half of individuals post-stroke
over age 65 have reduced mobility [1]. Regaining walking
ability is an important goal of rehabilitation as walking
speed is a critical predictor of long-term health [2] and
individuals post-stroke who achieve limited or full community walking speeds report an overall higher quality
of life than those who remain household ambulators [3].
Successful walking requires the execution of the critical
pre-swing biomechanical subtasks of body propulsion
and leg swing initiation, which are often impaired poststroke [4, 5] and may influence swing phase knee flexion
[2, 6–8].
For example, modeling studies having identified knee
flexion velocity at toe-off as the primary contributor
to peak knee flexion during swing [9] and low push-off
acceleration has also been linked to stiff knee gait [2].
Moreover, impaired knee flexion is often attributed to
rectus femoris activity [10, 11] and a modeling study
showed that eliminating rectus femoris activity in preswing was more effective than eliminating rectus femoris activity in early swing for improving knee flexion [7].
Decreased gastrocnemius activity may also contribute
to stiff knee gait, as increased gastrocnemius contributions to pre-swing knee flexion were observed after
gait retraining [8]. However, a representative individual
post-stroke with a limited community walking speed
had lower iliopsoas contributions to leg swing initiation
in pre-swing but similar contributions from the gastrocnemius compared to a healthy control [12]. Thus, while
the potential of lower extremity muscles to increase or
decrease knee flexion velocity in late stance has been
documented [13], it is unknown which muscles most
affect pre-swing knee flexion velocity in individuals
post-stroke.
Braking and propulsion deficits are also common in
individuals post-stroke [4], and in addition to predicting
slower walking speeds [14, 15], may contribute to stiff
knee gait. The plantarflexors are primary contributors
to propulsion [16, 17]. Decreased plantarflexor contributions to propulsion have been observed in individuals
post-stroke [12, 18, 19], which could occur due to both
muscle activation deficits [20, 21] and altered muscle
and Achilles tendon properties [22–24]. The gastrocnemius is an important contributor to both propulsion and
leg swing initiation [17], and thus low propulsion may
be related to knee flexion deficits. Stimulating the plantarflexors in pre-swing increases peak knee flexion for
individuals post-stroke [25]. However, the total propulsive force did not predict knee flexion [6]. On average,
individuals with impaired plantarflexor coordination do
not have lower p (...truncated)