Prevalence, Related Factors, and Gait-Related Mechanisms of Knee Pain in Ambulatory Chronic Stroke Survivors

Knee pain is a clinically important but under-recognized problem in ambulatory stroke survivors. It may limit walking ability, reduce participation in rehabilitation, and impair quality of life. Knee pain after stroke may result from multiple interacting factors, including pre-existing knee osteoarthritis, muscle weakness, spasticity, abnormal limb loading, and gait deviations. Among these gait deviations, knee hyperextension during stance may increase abnormal mechanical stress on the knee joint. However, the prevalence, related factors, and gait-related mechanisms of knee pain in ambulatory chronic stroke survivors remain insufficiently understood.

This dissertation aimed to investigate the prevalence, related factors, and gait-related mechanisms of knee pain in ambulatory chronic stroke survivors. Two related studies were conducted. First study was a multicenter cross-sectional study examining the prevalence of knee pain and associated clinical and gait-related factors. Second study was a crossover randomized controlled trial examining whether adding botulinum toxin type A injection into the rectus femoris could modify knee hyperextension and other gait parameters in stroke survivors with rectus femoris spasticity and reduced knee flexion during swing.

In first study, knee pain was present in 19.8% of ambulatory chronic stroke survivors. Knee pain was associated with clinical factors, including older age, stroke-related characteristics, and prior knee osteoarthritis. Gait analysis showed that greater knee hyperextension during stance was associated with ipsilateral knee pain, suggesting that abnormal knee mechanics may contribute to knee symptoms in some stroke survivors.

In second study, rectus femoris injection significantly reduced knee-extensor spasticity when assessed using the pendulum test, although no significant effect was detected using the Modified Ashworth Scale. Rectus femoris injection was associated with a small, nonsignificant improvement in minimal knee angle during stance, indicating less knee hyperextension. In contrast, maximal knee flexion during swing improved significantly by 6.2°. No significant effects were observed for maximal walking speed or stride length.

Overall, this dissertation demonstrates that knee pain is a clinically relevant problem in ambulatory chronic stroke survivors and that knee hyperextension is a gait-related factor associated with knee pain. However, rectus femoris overactivity may contribute more clearly to reduced knee flexion during swing than to stance-phase knee hyperextension. These findings support mechanism-based assessment of knee pain and gait abnormalities after stroke.