Prolonged Quadriceps Activity Following Imposed Hip Extension: A Neurophysiological Mechanism for Stiff-Knee Gait?

The biomechanical characteristics of stiff knee gait following neurological injury include decreased knee flexion velocity at toe-off, which may be due to exaggerated quadriceps activity. The neuromuscular mechanism underlying this abnormal activity is unclear, although hyperexcitable heteronymous reflexes may be a source of impaired coordination. The present study examines the contribution of reflex activity from hip flexors on knee extensors following stroke and its association with reduced swing-phase knee flexion during walking. Twelve individuals poststroke and six control subjects were positioned in supine on a Biodex dynamometer with the ankle and knee held in a static position. Isolated hip extension movements were imposed at 60, 90, and 120°/s through a 50° excursion to end-range hip extension. Reflexive responses of the rectus femoris (RF), vastus lateralis (VL), and vastus medialis (VM) were quantified during and after the imposed hip rotation. Gait analysis was also performed for all subjects in the stroke group. In subjects with stroke, imposed hip extension evoked a brief reflexive response in the quadriceps, followed by a heightened level of sustained activity. The initial response was velocity dependent and was larger in the stroke group than in the control group. In contrast, the prolonged response was not velocity dependent, was significantly greater in the VL and RF in subjects with stroke, and, importantly, was correlated to decreased swing-phase knee flexion. Hyperexcitable heteronymous connections from hip flexors to knee extensors appear to elicit prolonged quadriceps activity and may contribute to altered swing-phase knee kinematics following stroke