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 neurotoxin (BoNT) can reduce spastic muscle tone (usually measured by the Ashworth Scale or Modified Ashworth Scale), normalize limb posture, ameliorate pain, modestly improve motor function (measured by performance of standardized motor tasks or activities of daily living) and prevent contractures. Such efficacy is best documented for the upper limbs (Bhakta et al., 2000; Sheean, 2001; Brashear et al., 2002; Childers et al., 2004; Suputtitada and Suwanwela, 2005; Bergfeldt et al., 2006; Kaňovský et al., 2009; Barnes et al., 2010; Ryuji et al., 2010a; Shaw et al., 2011). In the lower limbs, efficacy is more limited, although rectification of plantar-flexed foot posture is documented (Baricich et al., 2008), and there is a modicum of evidence for amelioration of gait (Bleyenheuft et al., 2009; Ryuji et al., 2010b). In 2008, a large evidence-based review concluded that BoNT should be offered for treatment of spasticity in adults, with level A evidence for improvement of muscle tone and level B for improvement of motor function (Simpson et al., 2008; Elia et al., 2009).