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

My conclusion is that this was totally useless since nothing here was created to fix the problems cited.

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

 

• Lydia G. Brough,
• Steven A. Kautz &
• Richard R. Neptune 

Journal of NeuroEngineering and Rehabilitation volume 19, Article number: 55 (2022) Cite this article

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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.

(My problem is that most of my pre-motor cortex is dead and nothing here addresses that. Do you people ever consider that you're supposed to be solving stroke problems for everyone?)

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.

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 post-stroke [4, 5] and may influence swing phase knee flexion [2, 6,7,8].

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 pre-swing 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 [22,23,24]. 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 propulsion, but rather greater braking [26] likely due to co-activation of the plantarflexors and vasti muscles, which are primary contributors to braking [9]. Knee flexion velocity at toe-off may be diminished by late braking forces because muscles such as the vasti and rectus femoris that contribute to braking also contribute to knee extension and oppose leg swing initiation in late-stance [9]. In addition, late stance braking forces in individuals post-stroke predict less knee flexion during swing [6]. However, it is unknown if the relationships between braking, propulsion and swing phase kinematics are causal or correlative. Due to the characteristically high variability between individuals post-stroke, there are a number of mechanisms that can cause both propulsion and knee flexion deficits.(So you're justifying your failure to solve this because it is hard. Well, fuck you then. Hope you're OK with this when you're the 1 in 4 per WHO that has a stroke.)

Previous work has established the importance of pre-swing conditions to achieving adequate swing phase knee flexion. However, actual muscle contributions to propulsion, knee velocity and leg-swing initiation in individuals post-stroke and their relationship to swing-phase knee flexion has not been established. Thus, the objectives of this study were to determine the underlying causes of propulsion and braking deficits and identify muscle contributors to pre-swing knee flexion acceleration and leg swing initiation in individuals post-stroke with and without stiff knee gait. We hypothesized that (1) braking and propulsion asymmetries would be caused by both low plantarflexor contributions to propulsion and high vasti contributions to braking, (2) vasti and plantarflexor contributions to propulsion and braking in pre-swing would predict swing phase knee flexion, (3) the rectus femoris would be a major contributor to knee extension in pre-swing in individuals with stiff knee gait, and (4) total musculotendon power delivered to the leg in pre-swing would predict knee flexion during swing. The outcomes of this work will highlight specific deficits in propulsion and leg swing initiation post-stroke and their implications for swing phase knee flexion, which will provide a basis for developing targeted rehabilitation strategies.