Deficit in intersegmental torques drives post-stroke stiff-knee gait.

Walking, a seemingly simple task for many, becomes a challenge for people after a stroke. Typically, the swinging leg kinematics is fine-tuned to provide toe clearance, but reduced knee flexion after stroke requires adaptive gait strategies, such as hip hiking and circumduction, to prevent stumbling. The cause of reduced knee flexion in a dynamic system is unintuitive and often obscured by muscle weakness, hyperactivity, or abnormal joint coordination. Using physical models, we predicted that intersegmental forces may be largely responsible for the deficits. Leveraging subject-specific inverse modeling of body dynamics, we compared force generation in post-stroke and neurotypical participants in overground walking. We tested if the contribution of active muscle-generated and passive intersegmental torques from neighboring segments may be responsible for the observed reduced knee flexion. The similar levels of active knee torque across both study groups at the onset of swing indicated that knee interaction torque is the main cause; the component of this torque generated at the hip was decreased (more than that at the ankle) in the post-stroke group. Identified deficit in hip flexion torque at swing onset unveils a key biomechanical mechanism underlying reduced knee flexion post-stroke, providing a physics-informed target for post-stroke gait rehabilitation.