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 abnormal spastic posturing. Late sequelae may include contracture, pain, fibrosis and muscle atrophy. The most common pattern of spasticity in the upper limb involves flexion of the fingers, wrist and elbow, adduction with internal rotation at the shoulder and sometimes thumb curling across the palm or fist. The most common pattern of spasticity in the lower limb involves extension at the knee, plantarflexion at the ankle and sometimes inversion of the foot.

Chemodenervation by intramuscular injection of botulinum toxin can reduce spastic muscle tone, normalize limb posture, ameliorate pain, modestly improve motor function and prevent contractures. This chapter uses anatomical illustrations to depict the muscles involved in common patterns of spastic posturing, using a “clinician’s eye” view to demonstrate approaches to injection points, discusses guidance techniques such as electromyography and tabulates dose ranges of the common toxin preparations for specific muscles.

In the upper motor neuron syndrome, there are abnormalities of spinal reflexes. The disordered monosynaptic muscle stretch reflex is manifest by a velocity dependent increase in muscle tone and exaggerated tendon jerks. The cutaneous reflex to plantar stimulation is abnormal in that plantar flexion of the great toe is lost. Disinhibition of the polysynaptic spinal flexion reflex is responsible for the Babinski sign and the clasp-knife phenomenon.