Article

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.
CI - Copyright (c) 2011 Elsevier Ltd. All rights reserved.

Langue : ANGLAIS

Tiré à part : OUI