Background: Stiff knee gait (SKG), a common occurrence after the onset of stroke, is caused by hyperactivity of the rectus femoris during the swing phase. Another cause of SKG is the weakness of push-off in hemiparetic gait. Prior research did not consider the effect of the magnitude of knee extensors in their subjects.
Research question: Does the cause of SKG differ between patients with high and low knee extensor activities during the swing phase?
Methods: We examined 38 patients with chronic stroke hemiplegia who presented with SKG. After placing an inertia sensor and an electromyogram, patients walked 10 m at a comfortable speed. All patients were categorized per the sign of the principal component 2 (PC2) as a component with large factor loadings of knee extensors attained from the electromyographic amplitude during the early swing phase of the paretic limb. Then, the kinematic parameters of knee flexion and other gait parameters in each group were compared, and a correlation analysis was performed.
Results: In the high PC2 group, the timing of peak knee flexion during the swing phase was early, and vastus lateralis activity during the preswing phase negatively correlated with the knee-flexion angle during the swing phase. In the low PC2 group, the angular velocity of ankle plantar flexion at the toe-off was slow, which positively correlated with the knee-flexion angle during the swing phase.
Significance: The cause of SKG could be an inappropriate activity of the vastus lateralis rather than the rectus femoris in patients with high knee extensor activity and slow plantar-flexion velocity at toe-off in patients with low knee extensor activity. Not all causes of SKG in patients with hemiplegia are common, and different treatment strategies are needed per the individuality of spastic knee extensor activity.
Keywords: Botulinum toxin; Electromyography; Gait; Kinematics; Stiff knee; Stroke.
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