Tissue related ankle hyper-resistance has been reported to contribute to equinus gait in children with spastic cerebral palsy. Hence, ankle plantarflexor stretching programs have been developed in order to restore passive ankle dorsiflexion. Despite high quality evidence on the limited effects of stretching on passive joint mobility, further muscle-tendon adaptations have been reported which may impact gait performance. As such, children with spastic cerebral palsy subject to long-term manual static stretching achieved dorsiflexion gains through the reduction of muscle and fascicle strain whilst preserving tendon strain, and prolonged use of ankle-foot orthoses achieved similar dorsiflexion gains through increased tendon strain whilst preserving muscle and fascicle strain. The latter concurred with normalization of early stance plantarflexor moment yet reductions in push-off plantarflexor moment given the increase in tendon compliance. Therefore, similar limited gains in passive ankle joint mobility in response to stretching may be achieved either by preserving/restoring optimal muscle-tendon function, or at the expense of muscle-tendon function and thus contributing gait impairments. The largest increase in ankle passive joint mobility in children with SCP has been obtained through prolonged plantarflexor stretching through ankle casting combined with botulinum neurotoxin type A. However, to our knowledge, there are no published studies on muscle-tendinous adaptations to ankle casting combined with botulinum toxin type A and its effect on ankle joint gait kinetics. Therefore, we hypothesized that ankle casting elicits muscle-tendon adaptations which concur with altered ankle joint kinetics during the stance phase of gait in children with SCP. More information is needed about the relationships between muscle structure and function, and the effect of specific interventions designed to alter muscle properties and associated functional outcomes in children with spastic cerebral palsy.

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