Many children with cerebral palsy walk with a stiff knee gait, or a reduction and delay in swing phase knee flexion, which causes tripping or energy-inefficient compensatory movements. Since over-activity of the rectus femoris muscle is frequently implicated as the cause, a common treatment is transfer of the distal end of the rectus femoris from its insertion on the patella to a location behind the knee. Outcomes, though positive on average, vary among individuals, with some patients demonstrating unimproved or worsened knee flexion postoperatively. This variability is due in part to insufficient understanding of the biomechanical causes of stiff-knee gait and the functional effects of surgical treatment. The goal of this dissertation was to clarify the causes of stiff-knee gait and examine the biomechanical mechanism of improvement following rectus femoris transfer surgery.

Swing-phase rectus femoris activity is commonly thought to cause of stiff-knee gait, despite evidence that many patients have excessive knee extension moments in preswing rather than swing phase. We compared the effects of preswing to swing phase activity of the rectus femoris on peak knee flexion in swing by creating and analyzing musculoskeletal simulations of subjects with stiff-knee gait. We found that in six out of ten subjects preswing rectus femoris activity had at least a 90% higher effect on peak knee flexion than swing phase rectus femoris activity, suggesting that preswing rectus femoris activity is an important factor limiting knee flexion in some subjects and should be examined to better determine the factors leading to stiff-knee gait.

To understand how other muscles, besides rectus femoris, may limit knee flexion in stiff-knee gait, it is first necessary to understand how muscles coordinate successful swing phase knee flexion in unimpaired gait and how muscle contributions change with walking speed, since many stiff-knee subjects walk slowly. We analyzed simulations of unimpaired subjects walking at different speeds to determine the muscles that accelerated and decelerated knee flexion prior to swing. We found that preswing knee flexion acceleration was achieved primarily by the hip flexor muscles with help from biceps femoris short head, suggesting that weakness in these muscles may contribute to stiff-knee gait. Vasti and soleus decelerated knee flexion, suggesting over-activity in these muscles may contribute to stiff-knee gait.

We also investigated the mechanism of improvement following rectus femoris transfer surgery. We altered the geometry of rectus femoris and simulated the dynamics of the swing phase of subjects with stiff-knee gait after different surgical procedures. Analysis of the simulations demonstrated that knee flexion may be improved with a reduction of the knee extension moment generated by the rectus femoris, even if the muscle is not converted to a knee flexor.

This dissertation clarifies preswing rectus femoris activity as a cause of stiff-knee gait, demonstrates the functional mechanism of improvement following transfer surgery, and informs future research investigating other potential contributors to stiff-knee gait.