Spasticity affects subjects with cerebral palsy, stroke, multiple sclerosis, and traumatic brain injury. The need to develop a deeper understanding of spasticity is driven by the existing limited understanding and the lack of satisfactory interventions for this disabling phenomenon.

An inverse model is implemented to describe the motion in the pendulum knee drop test. Inverse kinematic modeling is implemented to investigate the pathophysiology of spasticity.

Using the equilibrium point hypothesis as a conceptual framework to explain disabled and non-disabled neuromuscular control, it has been demonstrated that the equilibrium point of the passive knee is dynamic and exhibits a pseudo-exponential trajectory in spasticity that is different from the non-spastic case. In non-spastic subjects, this research has shown that there is nonlinearity at the highest velocity of the pendulum knee drop test due to muscle activation. In spastic subjects, this research has also demonstrated that the passive linear stiffness is increased. This work now allows biomechanical variants to be linked with two important clinical concepts associated with spasticity. Increases in passive linear stiffness can be equated with increased tone in spasticity. The dynamic equilibrium point trajectory can be used to explain the hyperactive stretch reflex.