Background and Purpose— Stiff-knee gait is defined as reduced knee flexion during the swing phase. It is accompanied by frontal plane compensatory movements (eg, circumduction and hip hiking) typically thought to result from reduced toe clearance. As such, we examined if knee flexion assistance before foot-off would reduce exaggerated frontal plane movements in people with stiff-knee gait after stroke. Methods— We used a robotic knee orthosis to assist knee flexion torque during the preswing phase in 9 chronic stroke subjects with stiff-knee gait on a treadmill and compared peak knee flexion, hip abduction, and pelvic obliquity angles with 5 nondisabled control subjects. Results— Maximum knee flexion angle significantly increased in both groups, but instead of reducing gait compensations, hip abduction significantly increased during assistance in stroke subjects by 2.5°, whereas no change was observed in nondisabled control subjects. No change in pelvic obliquity was observed in either group. Conclusions— Hip abduction increased when stroke subjects received assistive knee flexion torque at foot-off. These findings are in direct contrast to the traditional belief that pelvic obliquity combined with hip abduction is a compensatory mechanism to facilitate foot clearance during swing. Because no evidence suggested a voluntary mechanism for this behavior, we argue that these results were most likely a reflection of an altered motor template occurring after stroke.

Background and Purpose— Although stroke survivors often display abnormal joint torque patterns, studies of torque-coupling in the lower limb are lacking, despite their potential impact on gait abnormalities. Methods— Twenty-two chronic ambulating stroke subjects and 11 age-matched control subjects produced isometric hip torques in the frontal and sagittal planes with the hemiparetic leg (or randomly selected leg for the control group) in postures that resemble stages of gait. The involuntary knee torques were also recorded although no feedback or instructions were given. Results— In the toe-off and midswing postures, the stroke group had a significant torque bias toward extension and adduction, whereas the control group had a symmetric torque space. The stroke group also produced significantly smaller torques than the control group in the flexion and abduction/flexion directions. Finally, the stroke group displayed abnormal coupling of knee extension with hip adduction, unique to the toe-off position. Conclusions— Whereas gait abnormalities after stroke have been attributed to a number of factors, including sagittal plane strength impairments at the hip, knee, and ankle, our findings indicate that neuromechanical changes after stroke may play a significant role in determining the nature of the movement abnormality. Specifically, abnormal hip adduction and knee extension torque coupling was observed, in addition to direction-specific hip torque weakness. Future studies are needed to delineate the differential contributions of each potential factor to gait abnormalities. Understanding the underlying neuromechanical changes after stroke may aid the development of rehabilitation strategies.

Clinical outcomes after robotic training are often not superior to conventional therapy. One key factor responsible for this is the use of control strategies that provide substantial guidance. This strategy not only leads to a reduction in volitional physical effort, but also interferes with motor relearning.