Department of Neurology, Fixel Institute for Neurological Diseases, University of Florida, 3009 Williston Road, Gainesville, 32608, Florida, United States.
Toxicon. 2024 Jan;237:107251. doi: 10.1016/j.toxicon.2023.107251. Epub 2023 Aug 11.
Dystonia is a network disorder involving multiple brain regions, such as the motor cortex, sensory cortex, basal ganglia, and cerebellum. Botulinum toxin (BoNT) is the first-line therapy for treating focal dystonia and is a potent molecule that blocks the release of acetylcholine at the peripheral neuromuscular junction. However, the clinical benefits of BoNT are not solely related to peripheral muscle relaxation or modulation of afferent input from the muscle spindle. An increasing body of evidence, albeit in smaller cohorts, has shown that BoNT leads to distant modulation of the pathological brain substrates implicated in dystonia. A single treatment session of BoNT has been observed to reduce excessive motor excitability and improve sensory processing. Furthermore, owing to plasticity effects that are induced by botulinum, neural reorganization of pathological networks occurs, presumably leading to defective motor programs of dystonia replaced with normal movement patterns. However, longitudinal studies investigating the effects of multiple treatment sessions in large, well-characterized homogenous cohorts of dystonia will provide further compelling evidence supporting central botulinum mechanisms.
肌张力障碍是一种涉及多个脑区的网络紊乱，如运动皮层、感觉皮层、基底节和小脑。肉毒毒素（BoNT）是治疗局灶性肌张力障碍的一线治疗方法，是一种能在周围神经肌肉接头阻断乙酰胆碱释放的有效分子。然而，BoNT 的临床疗效不仅与外周肌肉松弛或肌梭传入输入的调制有关。越来越多的证据（尽管在较小的队列中）表明，BoNT 导致与肌张力障碍相关的病理大脑基质的远距离调制。单次 BoNT 治疗已被观察到可降低过度运动兴奋性并改善感觉处理。此外，由于肉毒毒素诱导的可塑性效应，病理网络的神经重组发生，可能导致肌张力障碍的缺陷运动程序被正常运动模式取代。然而，对大而特征明确的同质肌张力障碍队列进行多次治疗的纵向研究将提供进一步的有力证据，支持中枢 BoNT 机制。
