New Developments in the Medical Treatment of Spasticity

Abstract

The medical treatment of established spasticity is principally of symptomatic nature, since spasticity is generally a consequence of irreversible central nervous system damage. This damage is not amenable to causative treatment. As spasticity presents with polymorphic clinical pictures resulting in various types and degrees of discomfort and dysfunction, the aim of the symptomatic treatment also varies. In general, it includes relief of subjective discomfort, facilitation of patient care, improvement of functional capacity, and protection of the long-term consequences of unevenly distributed excessive muscle tone. Theoretically, the main aim of an antispastic agent is to reduce increased muscle tone, given the definition of spasticity in strictly physiologic terms as a “velocity-dependent increase in tonic stretch reflexes (muscle tone)” (Lance 1980). However, spasticity is associated with other symptoms including brisk tendon reflexes, clonus, flexor, extensor, or adductor spasms which can be painful, loss of dexterity, and paresis, all of which constitute the upper motor neuron or spastic syndrome. Indeed, spasticity is sometimes used as a synonym for the upper motor neuron syndrome (Young and Delwaide 1981). The other positive signs of this syndrome, such as clonus and release phenomena (flexor reflex, spasms), are also amenable to medical treatment, whereas negative signs such as loss of dexterity and paresis are not.