Pathophysiologic factors that may contribute to stiff knee gait in persons with brain injury are muscle hypertonicity of the quadriceps muscles, hip flexor weakness, and over activity of the gastrocsoleus muscles in terminal stance(1). Kerrigan et al (2) reported that hyperactivity of the Rectus Femoris (RF) during swing phase was a key contributor to this dynamic swing phase deficit in adults with spastic paresis. Overactivity of the RF muscle during early swing phase has also been identified as a major contributor to stiff knee gait dysfunction in children with cerebral palsy (3). Recognition of the role of RF over-activity in stiff knee gait in the cerebral palsy population has led to surgical and medical interventions aimed to minimize this constraint on swing phase mechanics, such as RF transfers, RF release, and Botulinum toxin injections (BTX-A)(4,5). Research in the cerebral palsy population supports the application of these interventions to improve knee flexion during swing phase and improve overall gait function and efficiency (6).