Spasticity is commonly defined as excessive motor activity characterized by a velocity-dependent increase in tonic stretch reflexes. It is often associated with exaggerated tendon jerks, and is often accompanied by abnormal cutaneous and autonomic reflexes, muscle weakness, lack of dexterity, fatigability, and co-contraction of agonist and antagonist muscles (Young, 1987; Young, 2002; Sanger et al., 2003). It is a common complication of central nervous system disorders, including stroke, traumatic brain injury, cerebral palsy, multiple sclerosis, anoxic brain injury, spinal cord injury, primary lateral sclerosis, and hereditary spastic paraparesis (Young, 2002).

In many individuals, the presence of spasticity has negative consequences, interfering with mobility and activities of daily living. Disability may result from spasticity-related impairment of posture, abnormal quality of movement, painful spasms, and poor hygiene. In these patients treatment of spasticity is often considered. This chapter will review the pathophysiology of spasticity, outline the rationale for treatment and the development of treatment goals. In addition, pharmacologic and surgical management strategies will be discussed.

Physiology

Muscle tone, defined as the resistance to externally imposed muscle movement, is modulated by central nervous system influences on the alpha motor neuron in the spinal cord (Rossi, 1994). The pathways that regulate tone are similar to those that regulate voluntary and involuntary motor movements and, as a final common pathway, involve the spinal reflex arc. Alpha motor neurons that innervate muscle fibers are located in the ventral horns of the spinal cord, and comprise the efferent limb of this reflex arc. Afferent sensory impulses from muscle spindles are relayed to the spinal cord via Ia fibers. Some of these fibers synapse directly on alpha motor neurons that innervate agonist muscles.