Debunking the pathophysiological puzzle of dystonia--with special reference to botulinum toxin therapy

Abstract

New neurophysiological insights into the natural behaviour of dystonia, obtained during the successful botulinum toxin A (BoNT) treatment of the disorder, have urged the inclusion of sensory (and particularly somatosensory) mechanisms into the pathophysiological background of dystonia. Muscle spindles play a pivotal role in the generation of dystonic movements. Abnormal behaviour in the muscle spindles that generates an irregular proprioceptive input via the group-IA afferents may result in abnormal cortical excitability and intracortical inhibition in dystonia. The aim of this article is to support our hypothesis that dystonic movement is at the end of an impaired function of somatosensory pathways and analysers, which, in turn, may be hinged on the abnormality of sensorimotor integration, that is, brain plasticity. BoNT treatment can potentially modulate this plasticity mechanism and is probably the seminal cause of the sustained effect of the subsequent BoNT-treatment sessions and the long-term alleviation of symptoms of dystonia.