Post-activation depression of the lower extremities in stroke patients with spasticity and spastic equinovarus deformity Depressão pós-ativação das extremidades inferiores de pacientes com acidente vascular cerebral que apresentam espasticidade e deformidade equinovarus por espasticidade

Spasticity is common in individuals with central nervous system (CNS) disease1. It causes pain and reduces voluntary movement, which can have a disabling effect on patients and negatively affect rehabilitation outcomes. Lance’s widely used definition of spasticity states that spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks caused by stretch reflex hyperexcitability2. A later 1994 definition described “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes that results from abnormal intra-spinal processing of primary afferent input”3. A definition published in 2005 described spasticity as “disordered sensori-motor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles”4. There is general agreement that spasticity is caused by adaptations at the spinal cord level distal to the lesion. Changes in spinal pathways may result in spasticity including altered muscle spindle sensitivity, presynaptic inhibition, recurrent (Renshaw) inhibition, Ib inhibition and facilitation, reciprocal Ia inhibition, group II facilitation, cutaneomuscular pathway changes, and post-activation depression5. The last item has been an invariant finding in spasticity1,6,7, and whether hemiplegic or spinal, this