Rectus femoris hyperreflexia contributes to Stiff-Knee gait after stroke

So what? What is the solution?

Rectus femoris hyperreflexia contributes to Stiff-Knee gait after stroke

• Tunc Akbas,
• Kyoungsoon Kim,
• Kathleen Doyle,
• Kathleen Manella,
• Robert Lee,
• Patrick Spicer,
• Maria Knikou &
• James Sulzer 

Journal of NeuroEngineering and Rehabilitation volume 17, Article number: 117 (2020) Cite this article

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Abstract

Background

Stiff-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 hyperreflexia plays a role in this activation. The goal of this study was to establish the relationship between quadriceps hyperreflexia and knee flexion angle during walking in post-stroke SKG.

Methods

The rectus femoris (RF) H-reflex was recorded in 10 participants with post-stroke SKG and 10 healthy controls during standing and walking at the pre-swing phase. In order to attribute the pathological neuromodulation to quadriceps muscle hyperreflexia and activation, healthy individuals voluntarily increased quadriceps activity using electromyographic (EMG) feedback during standing and pre-swing upon RF H-reflex elicitation.

Results

We observed a negative correlation (R = − 0.92, p = 0.001) between knee flexion angle and RF H-reflex amplitude 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 muscle activity was not correlated with knee flexion angle. We observed a body position-dependent RF H-reflex modulation between standing and walking in healthy individuals with voluntarily increased RF activity (d = 2.86, p = 0.007), but such modulation was absent post-stroke (d = 0.73, p = 0.296).

Conclusions

RF reflex modulation is impaired in post-stroke SKG. The strong correlation between RF hyperreflexia and knee flexion angle indicates a possible regulatory role of spinal reflex excitability in post-stroke SKG. Interventions targeting quadriceps hyperreflexia could help elucidate the causal role of hyperreflexia on knee joint function in post-stroke SKG.

Introduction

Stiff-Knee gait (SKG) is one of the most common gait disabilities following stroke. SKG is defined as reduced knee flexion [30] during the swing phase. Those with SKG have joint pain [16], energy inefficiency due to compensatory motions [9, 36, 38] and increased risk of falls [3]. Post-stroke SKG has been attributed to overactivity of rectus femoris (RF) muscle [2, 13, 14] and decreased activity of ankle plantar flexors and iliopsoas that generate knee flexion moment [23, 29]. Quadriceps muscle overactivity is the most widely accepted cause of SKG [18, 33, 42]. To this end, Botulinum toxin (Botox) injections that block acetylcholine release in the femoral nerve show modest improvements in knee flexion [34, 35, 39], suggesting that rectus femoris (RF) reflex excitability contributes to SKG. However, the cause of excessive RF muscle activity is unclear. One hypothesis is that increased quadriceps activation could be achieved voluntarily to improve stability during the stance phase, but then fails to relax during the pre-swing phase [18, 33]. RF overactivity could additionally be explained as spasticity in the form of reflex hyperexcitability and lack of reciprocal inhibition.

Accumulating evidence suggests that reduced knee flexion in post-stroke SKG depends on pathological modulation of spinal reflex loops. For example, Lewek et al. [27] found increased quadriceps short-latency reflex excitability following hip extension perturbations in post-stroke individuals. The degree of hyperexcitability was correlated to knee flexion angle, suggesting that altered involuntary responses could play a role in diminished knee flexion during the swing phase of post-stroke SKG. Others found that hip abduction perturbations elicited abnormally coordinated RF activation, suggesting a role of abnormal reflex-mediated coordination in post-stroke gait [12]. Using a custom robotic actuator [41] to perturb knee flexion during pre-swing in individuals with post-stroke SKG [40], we observed a sharp knee extension velocity following initial increased knee flexion angle during swing. However, no such reaction was found during steps where the assistance was temporarily removed, or in a baseline period before the assistance was applied, indicating that the knee extension was induced by the robotic assistance. The knee extension was preceded by increased RF electromyographic (EMG) activity within a short latency following the perturbation, and further musculoskeletal modeling analysis showed a correlation between RF fiber stretch velocity and RF activity [1]. Taken together, this evidence points to RF reflex hyperexcitability influencing knee flexion in post-stroke SKG. Representative altered reflex pathways in post-stroke include reduced gait phase-dependent modulation [8, 21] and changes in presynaptic inhibition [11]. However, their relation to SKG has yet to be determined.

The objective of this study(wrong objective, nothing here helps survivors recover) was to characterize the relation of hyperreflexia to knee flexion in post-stroke SKG. We investigated reflex excitability via the monosynaptic H-reflex with well-established neuronal pathways [20]. H-reflexes are a reliable and consistent probe in identifying the altered neuronal pathways [28]. We examined the modulation of monosynaptic RF H-reflexes during standing and walking in people post-stroke compared to healthy control subjects in order to establish the extent to which reflex modulation is related to the knee flexion angle after stroke. In order to determine the possibility that hyperreflexia is a byproduct of improper timing of RF activity, we compared our results to healthy controls with volitionally up-regulated RF activity during pre-swing. We hypothesized that RF H-reflex hyperexcitability during standing and walking in pre-swing phase in people with post-stroke is associated with decreased knee flexion during swing phase in SKG compared to healthy controls. Characterization of the role of hyperreflexia in SKG and other neuromuscular disorders could help to design targeted treatments for hyperreflexia including but not limited to operant H-reflex conditioning training [43].