Determinants of muscle function in the spastic lower extremity

Abstract

The upper motor neuron lesion that causes hemiplegia impairs the patient's selective control and exposes primitive modes of muscle activation. Significant inconsistency between the clinical findings and the patient's gait may result. Dynamic electromyography revealed the primitive mechanisms leading to these inconsistencies. The rate of stretch does not differentiate spasticity from contracture, since either a quick or slow stretch frequently causes a sustained muscle response. Using knee flexion to differentiate gastrocnemius and soleus spasticity is not reliable, since the change in neurologic input with flexion may inhibit the extensor muscle's response to stretch so that the soleus is also relaxed. The change in body position from lying supine to sitting can double the intensity of soleus spasticity, and standing further increases the tone. Primitive patterns of mass extension and flexion, while voluntary, inhibit normal progression during walking. Simultaneous activation of the soleus and gastrocnemius with the knee's quadriceps causes premature ankle plantar flexion as the limb is loaded in stance. The primitive flexion synergy between the hip, knee, and ankle (dorsiflexion) inhibits terminal swing knee extension while the hip remains flexed. Consequently, surgical planning for the hemiparetic limb must rely heavily on gait analysis findings (systematic observation or by instrumentation).