Introduction

Spasticity is part of the upper motor neuron syndrome produced by conditions such as stroke, multiple sclerosis, traumatic brain injury, spinal cord injury, or cerebral palsy that affect upper motor neurons or their efferent pathways in the brain or spinal cord. It is characterized by increased muscle tone, exaggerated tendon reflexes, repetitive stretch reflex discharges (clonus), and released flexor reflexes (great toe extension; flexion at the ankle, knee, and hip) (Lance, 1981). Late sequelae may include contracture, pain, fibrosis, and muscle atrophy. Chemodenervation by intramuscular injection of botulinum toxin can reduce spastic muscle tone, normalize limb posture, ameliorate pain, and may improve motor function and prevent contractures.

Reduction of muscle tone, as measured by the Ashworth scale and by changes in range of motion after treatment with botulinum toxin, is best documented in the upper limbs (Brashear et al., 2002; Childers et al., 2004; Suputtitada & Suwanwela, 2005). In the lower limbs, muscle tone improvements are modest, with best results achieved from treatment below the knee.

Improvement of motor function has been noted in some studies, using measures such as the Barthel index, dressing, analyses of gait parameters such as walking speed, and the performance of other standardized tasks (Sheean, 2001; Brashear et al., 2002). In summary, motor function may be improved in a select subgroup of patients who retain selective motor control and some degree of dexterity in important distal muscles, require injection of relatively few target muscles, and especially if combined with other interventions such as physical therapy (Bhakta et al., 2000; Sheean, 2001).