The Effects of Botulinum Toxin (Btx-A) on Spasticity of the Lower Limb and on Gait in Cerebral Palsy

Spasticity in cerebral palsy stems from a net disinhibition of spinal reflexes because of a primary non-progressive cerebral lesion. The resulting hyperactive reflexes and increased muscle tone create a dynamic, shortening deformity which is exacerbated by longitudinal skeletal growth in the growing child. This makes the management of dynamic deformities such as an equinus gait by physiotherapy and orthoses, particularly difficult during growth spurts. The objectives of management in spasticity are to optimise functional movement and prevent fixed deformity such as joint contracture and bony torsion. Botulinum toxin (BTX-A) has been used since the early nineties in the management of focal spasticity in cerebral palsy. 1 It is a clostridial neurotoxin which achieves a reduction in tone and spasticity in a targeted muscle by temporary disruption of acetylcholine exocytosis at the motor endplate. The resulting reduction of overactivity seen in an injected muscle facilitates the function of its antagonists, allowing a change in muscle balance which may make joint movement easier. Of the seven serotypes (A-G) of botulinum toxin, serotypes A, B and F have been used in clinical practice. BTX-A has the longest duration of action, the greatest potency and is the most relevant serotype. There are significant differences between Botox (Ipsen Ltd, Slough, Berkshire, UK) and Dysport (Allergan Inc, Irvine, California), the two commercially available preparations of type-A botulinum toxin, in terms of potency and therefore dosage, total protein load and antigenicity. 2