Rectus femoris hyperreflexia contributes to Stiff-Knee gait after stroke
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(2020) 17:117
RESEARCH
Open Access
Rectus femoris hyperreflexia contributes to Stiff-Knee gait after stroke Tunc Akbas1, Kyoungsoon Kim2, Kathleen Doyle2, Kathleen Manella3, Robert Lee4, Patrick Spicer5, Maria Knikou6 and James Sulzer2*
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 poststroke SKG. Keywords: Post-stroke gait, Stiff-knee gait, Spasticity, Hyperreflexia, H-reflex
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 * Correspondence: [email protected] 2 Walker Department of Mechanical Engineering, The University of Texas at Austin, Austin, TX, USA Full list of author information is available at the end of the article
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
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