Abstract
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 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.
