Rectus femoris hyperreflexia contributes to Stiff-Knee gait after stroke

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.

Keywords: H-reflex; Hyperreflexia; Post-stroke gait; Spasticity; Stiff-knee gait.

Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1

Representative H-reflex recruitment curves for each group. Compared to the H-reflex recruitment curve for a healthy baseline representative (left), there exist increased RF H-waves in both the healthy representative with increased voluntary RF contraction (RF↑, middle) and in the participant with post-stroke SKG (right). The RF↑ during recruitment was achieved by providing RF EMG feedback. No substantial change was observed between maximum M-waves (Mmax) between conditions in healthy individuals

Fig. 2

Post-hoc analysis for RF H-reflex magnitude extraction. We modified a previously used method to estimate the H-reflex [24, 25]. EMG response with maximum M-wave (EMGMmax, black) and the current EMG response (EMGcurr, dark blue) with M-wave and H-wave regions (a). An exponential fit (efit, gray) beginning at the peak (Mpeak) of the EMGcurr were subtracted from EMGcurr instead of the previously introduced procedure [24] using hindmost flank of the EMGMmax to reduce selection variability indicated by the light blue region (b). The estimated H-wave (Hest) and the variability of the estimated H-waves resulted from hindmost flank selection (Hvar, light blue area, c)

Fig. 3

Experimental protocol and RF EMG feedback paradigm. The dashed square boxes indicate the four conditions in experimental protocol, Stand (right), during walking at toe-off Walk (right), where no visual feedback is provided. In both the Stand↑ (left) and Walk↑ (middle) conditions, visual feedback of RF EMG is provided for purposes of up-regulation during pre-swing. Participants were instructed to increase RF EMG signal above the threshold value (dashed gray line), 20% of RF maximum voluntary contraction (MVC) following a cue signal in real-time (purple vertical line) with 300 ms and 20 ms offset time prior to stimulation, respectively. For Walk↑, the cue was displayed every gait cycle to account for dynamic adaptation during walking. The trials were considered “successful” if the increased rectified RF EMG exceeded the threshold during stimulation (dashed horizontal line) and considered “fail” otherwise

Fig. 4

Diminished knee flexion is correlated with increased RF H-reflex in post-stroke SKG. Relations between swing-phase knee flexion angle and RF reflex excitability in post-stroke SKG shows a strong negative effect (red triangles) whereas no significant correlation was observed in healthy Walk (green triangles) and healthy Walk↑ (blue triangles). The lines and shaded areas indicate the linear regression fits and 95% confidence interval respectively for the corresponding groups

Fig. 5

Elevated RF H-reflex in post-stroke SKG is higher than increased voluntary RF contraction. During standing, RF H-reflex response was significantly increased in post-stroke SKG and in healthy individuals with increased voluntary RF contraction compared to healthy baseline. During walking however, RF H-reflex response was increased in post-stroke SKG compared to both healthy baseline and with increased voluntary contraction

Fig. 6

RF H-reflex modulation during walking is absent in post-stroke SKG. RF H-reflex magnitudes were decreased in healthy controls between Stand and Walk, and Stand↑ and Walk↑ conditions. There was no significant difference in participants with post-stroke SKG. Triangles represent individual subject data, whereas bars represent mean and 95% confidence intervals of the group