Department of Neurology, Palacky University Medical School, Olomouc, Czech Republic.
Parkinsonism Relat Disord. 2011 Nov;17 Suppl 1:S11-4. doi: 10.1016/j.parkreldis.2011.06.018.
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.
新的神经生理学见解表明，在成功的肉毒毒素 A（BoNT）治疗该疾病的过程中，获得了局灶性肌张力障碍的自然行为，促使将感觉（特别是躯体感觉）机制纳入肌张力障碍的病理生理背景中。肌梭在产生肌张力障碍运动中起着关键作用。通过 Ia 传入纤维产生不规则本体感觉输入的肌梭异常行为可能导致肌张力障碍的皮质兴奋性和皮质内抑制异常。本文的目的是支持我们的假设，即肌张力障碍运动是感觉通路和分析器功能障碍的结果，而这反过来又可能取决于感觉运动整合的异常，也就是大脑的可塑性。BoNT 治疗可能会调节这种可塑性机制，并且可能是随后 BoNT 治疗效果持续和肌张力障碍症状长期缓解的主要原因。
