Preswing Knee Flexion Assistance Is Coupled With Hip Abduction in People With Stiff-Knee Gait After Stroke

So? What's the solution? No solution you don't belong in stroke. But you do ask for further studies.

Preswing Knee Flexion Assistance Is Coupled With Hip Abduction in People With Stiff-Knee Gait After Stroke

 

James S. Sulzer

,

Keith E. Gordon

,

Yasin Y. Dhaher

,

Michael A. Peshkin

, and

James L. Patton

Originally published24 Jun 2010https://doi.org/10.1161/STROKEAHA.110.586917Stroke. 2010;41:1709–1714

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Abstract

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.

Stiff-knee gait (SKG), defined as reduced and delayed knee flexion during the swing phase,¹ is a common disability in people with stroke. Individuals with SKG often exhibit exaggerated frontal plane movements such as hip circumduction and hip hiking.² These frontal plane movements are energetically demanding³ and may lead to chronic joint pain.⁴ There is believed to be a cause-and-effect relationship between these two sets of movements.¹ Reduced knee flexion decreases an individual’s ability to clear the foot during the swing phase. In turn, subjects make compensatory frontal plane movements that facilitate toe clearance. Although this compensatory theory is commonly accepted, there are no quantitative in vivo studies examining the interaction between the swing phase knee flexion angle and proximal frontal plane kinematic behaviors in individuals with poststroke hemiparesis. If a kinematic connectivity indeed exists, it would indicate that the observed frontal plane behaviors may in part be a response to mechanical constraints imposed at the knee.

Alternatively, exaggerated frontal plane motions may be due to abnormal motor control. Recent studies in patients with stroke have found abnormal across-joint torque activation coupling, or synergies, between hip and knee activation. For example, several studies have found evidence of abnormal coupling of knee flexion/extension and hip abduction/adduction activity in both reflex⁵ and voluntary^6,7 muscle activity. These findings suggest that improving swing phase knee flexion angle may not resolve exaggerated frontal plane movements.

Accordingly, we sought to examine the effect of assistive knee flexion torque during preswing on frontal plane gait compensations. To achieve this goal, we developed a lightweight, backdrivable actuator capable of selectively applying knee flexion torque during the preswing phase of gait without imposing any significant mechanical constraints on the subject.⁸ To assess if the observed frontal plane behaviors during the assisted steps were a result of a mechanically coupled response to the “perturbation” or due to motor control compensation to the assistance, catch trials (no assist) were introduced at random.⁹ If kinematic changes persist during the no assist trials, it would suggest the presence of an acute motor adaptation induced by knee flexion assistance.¹⁰ Thus, to examine the potential effect of anticipatory motor commands to the repeated assistance, kinematic comparisons between the assisted and unanticipated steps with no assistance (catch trials) were conducted. Quantitative metrics of gait stability¹¹ were used to evaluate the potential effect that the knee flexion assistance may have had on locomotor stability in both the stroke and healthy participants. Knowledge gleaned from this study will improve our understanding of the relationship between knee impairments and the proximal 3-dimensional movements in people with SKG poststroke. Specifically, this study will help identify whether abnormal frontal plane behaviors are a response to local knee impairment or a manifestation of an abnormal multisegmental motor program. We argue that identifying these aberrant biomechanical interactions will help guide future clinical investigations and the development of assistive technology for individuals with stroke.