Effectiveness of botulinum toxin in rectus femoris in patients post-stroke with stiff-knee gait

2013 ◽  
Vol 37 ◽  
pp. S1-S2
Author(s):  
M. Bacchini ◽  
C. Rovacchi ◽  
F. Chiampo ◽  
M. Rossi
2009 ◽  
Vol 29 (1) ◽  
pp. 108-112 ◽  
Author(s):  
Johanna V.G. Robertson ◽  
Didier Pradon ◽  
Djamel Bensmail ◽  
Christophe Fermanian ◽  
Bernard Bussel ◽  
...  

2019 ◽  
Author(s):  
Tunc Akbas ◽  
Kyoungsoon Kim ◽  
Kathleen Doyle ◽  
Kathleen Manella ◽  
Robert Lee ◽  
...  

AbstractStiff-knee gait (SKG) after stroke is often accompanied by decreased knee flexion angle during the swing phase. The decreased knee flexion has been hypothesized to originate from excessive quadriceps activation. However, it is unclear whether this activation is due to poor timing or hyperreflexia, both common post-stroke impairments. The goal of this study was to investigate the relation between quadriceps hyperreflexia in post-stroke SKG with knee flexion angle during walking. The rectus femoris (RF) H-reflex was recorded in eleven participants with post-stroke SKG and ten healthy controls during standing and walking during toe-off. In order to separate the effects of poorly timed quadriceps muscle activation from hyperreflexia, healthy individuals voluntarily increased quadriceps activity using RF electromyographic (EMG) biofeedback during standing and pre-swing upon H-reflex stimulation. We observed a negative correlation (R = −0.92, p=0.001) between knee flexion angle and RF H-reflexes in post-stroke SKG. In contrast, H-reflex amplitude in healthy individuals in presence (R = 0.47, p = 0.23) or absence (R = −0.17, p = 0.46) of increased RF activity had no correlation with knee flexion angle. The RF H-reflex amplitude differed between standing and walking in healthy individuals, including when RF activity was increased voluntarily (d = 2.86, p = 0.007), but was not observed post-stroke (d =0.73, p = 0.296). Thus, RF reflex modulation is impaired in post-stroke SKG. Further, RF hyperreflexia, as opposed to overactivity, may play a role in knee flexion kinematics in post-stroke SKG. Interventions targeting self-regulated quadriceps hyperreflexia may be effective in promoting better neural control of the knee joint and thus better quality of walking post-stroke.


2018 ◽  
Author(s):  
Tunc Akbas ◽  
Richard R. Neptune ◽  
James Sulzer

ABSTRACTPost-stroke gait is often accompanied by muscle impairments that result in adaptations such as hip circumduction to compensate for lack of knee flexion. Our previous work robotically enhanced knee flexion in individuals post-stroke with Stiff-Knee Gait (SKG), however, this resulted in greater circumduction, suggesting the existence of abnormal coordination in SKG. The purpose of this work is to investigate two possible mechanisms of the abnormal coordination: 1) an involuntary coupling between stretched quadriceps and abductors, and 2) a coupling between volitionally activated knee flexors and abductors. We used previously collected kinematic, kinetic and EMG measures from nine participants with chronic stroke and five healthy controls during walking with and without the applied knee flexion torque perturbations in the pre-swing phase of gait in the neuromusculoskeletal simulation. The measured muscle activity was supplemented by simulated muscle activations to estimate the muscle states of the quadriceps, hamstrings and hip abductors. We used linear mixed models to investigate two hypotheses: H1) association between quadriceps and abductor activation during an involuntary period (reflex latency) following the perturbation and H2) association between hamstrings and abductor activation after the perturbation was removed. We observed significantly higher rectus femoris (RF) activation in stroke participants compared to healthy controls within the reflex latency period following the perturbation based on both measured (H1, p < 0.001) and simulated (H1, p = 0.022) activity. Simulated RF and gluteus medius (GMed) activations were correlated only in those with SKG, which was significantly higher compared to healthy controls (H1, p = 0.030). There was no evidence of voluntary synergistic coupling between any combination of hamstrings and hip abductors (H2, p > 0.05) when the perturbation was removed. The RF-GMed coupling suggests an underlying abnormal reflex coordination pattern in post-stroke SKG. These results challenge earlier assumptions that hip circumduction in stroke is simply a kinematic adaptation due to reduced toe clearance. Instead, abnormal coordination may underlie circumduction, illustrating the deleterious role of abnormal coordination in post-stroke gait.


2021 ◽  
Author(s):  
Lydia G. Brough ◽  
Steven A. Kautz ◽  
Richard Neptune

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 stroke survivors. Methods Musculoskeletal models and forward dynamic simulations were developed for individuals post-stroke (n=15) and neurotypical 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 27% of individuals post-stroke had higher plantarflexor contributions to propulsion and 47% had higher vasti contributions to braking on their paretic leg relative to their nonparetic leg. Higher gastrocnemius contributions to propulsion were correlated to paretic propulsion symmetry (p=0.005) while soleus contributions were not. Higher vasti contributions to braking in pre-swing predicted lower knee flexion (p=0.022). The rectus femoris and iliopsoas did not directly contribute 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 muscle-tendon work done on the paretic leg in pre-swing was not correlated to 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 further highlight the heterogeneity of the post-stroke population and the need to identify individual causes of propulsion and knee flexion deficits to improve rehabilitation outcomes.


2016 ◽  
Vol 59 ◽  
pp. e142
Author(s):  
Marjorie Kerzoncuf ◽  
Laurent Bensoussan ◽  
Jean Michel Viton ◽  
Alain Delarque ◽  
Christiane Rossi Durand

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