[Clinical treatment of spasticity--spastic movement disorders]

Spasticity develops as a consequence of damage to the central nervous system (CNS). Clinically, spasticity is characterized by muscle hypertension and exaggerated reflexes and is associated with varying degrees of paresis. Together this results in the syndrome of spastic paresis. Patients suffer from impeded and retarded movement ability. Electrophysiological investigations of functional arm and leg movements (e.g. in walking) show a reduced activation of arm and leg muscles which can be explained by the loss of activating signals from motor brain centers and functional reflex systems. This effect predominates over the increased tendon-reflex activity. The reduced muscle activation caused by paresis is partially compensated by structural alterations of the muscle fibers (e.g. loss of sarcomeres). For this reason a functional improvement mostly cannot be achieved by antispastic medication which targets the deactivation of tendon-reflexes. However, they are useful in immobilized patients. In mobile patients functional improvement can be achieved by functional training which is accompanied by an adapted, i.e. reduced, spastic muscle tone.