Restoration of neurological function following injury to the nervous system has long been the aim of neuroscientists and clinicians. The central nervous system (CNS) has proven to be an elusive target for restorative treatment. Although neuroprotective agents show promise, once injury to the brain or spinal cord has extended beyond the acute phase, symptomatic therapies are the focus of treatment.
Spasticity is a common consequence of damage to central motor pathways. The term "spasticity" refers to a disorder of the stretch reflex and muscle tone, 6 although most clinicians use the term in a broader context. Spasticity is but one component of the upper motor neuron syndrome. It is useful to distinguish between the positive symptoms (increased tone, exaggerated tendon, cutaneous and autonomic reflexes, released flexor reflexes) and negative symptoms (weakness, loss of dexterity, fatiguability) of such syndromes. Young has emphasized this distinction with the terms, "spastic paresis" and "spastic dystonia." 13 Superimposed on the physiological changes affecting motor function, there are abnormalities in the physical properties of muscle, tendon, joint, and surrounding soft tissues resulting from chronic positive and negative influences. These rheological changes may lead to contracture, which is difficult to differentiate clinically from severe spasticity. Only those components of joint resistance to passive movement resulting from spasticity are amenable to most pharmacological treatments.
Spasticity may result from diffuse or localized cerebral or spinal pathology, including trauma, anoxic or metabolic encephalopathies, mass lesions, hemorrhage or infarction, multiple sclerosis, and degenerative disease. There are differences in the temporal profile and natural history of these disparate disorders, but the clinical phenomena associated with the upper motor neuron syndrome do not differ markedly in their response to treatment depend-