Botulinum toxin type A in the treatment of spasticity in cerebral palsy: theoretical and practical foundations of effective therapy.

Spasticity is one of the constituent elements of upper motor neuron syndrome. For now, it is also the only symptom which is pharmacologically treatable. The pathophysiology of spasticity is very complex, and many aspects remain unclear. The great majority of commonly used oral drugs modulate the activity of receptors and/or neurotransmitters at different levels of the central nervous system. This is perhaps the main reason for the limited effectiveness of these drugs in many cases. Recently a new strategy - local injections of botulinum toxin type A (BTX-A) - has been introduced for the treatment of spasticity in cerebral palsy and post-stroke patients. BTX-A is a unique drug that acts at the final stage of the common pathway of pathological information mediated through the peripheral nerves to the muscles (at the motor end plates). Its mode of action is known as "chemical denervation", which serves to reduce increased muscle tone, improve the range of motions, positioning, function, and promote muscle growth in children. BTX-A was firstly used in post-stroke spasticity patients by Das and Park in 1989, but the best effects have been achieved in cerebral palsy. Accordingly, since 1997 this method has been approved in many European countries and Australia, and the principles governing this treatment strategy were published in the journal "Gait and Posture" in 2000. In the present paper, the author discusses the mechanism of spasticity, the logical approach to therapy, and many practical problems (injection modality, tolerability).