Agnesi Filippo, Johnson Matthew D, Vitek Jerrold L
Department of Biomedical Engineering, University of Minnesota, Minneapolis, MN, USA.
Handb Clin Neurol. 2013;116:39-54. doi: 10.1016/B978-0-444-53497-2.00004-8.
Chronic deep brain stimulation (DBS) has become a widely accepted surgical treatment for medication-refractory movement disorders and is under evaluation for a variety of neurological disorders. In order to create opportunities to improve treatment efficacy, streamline parameter selection, and foster new potential applications, it is important to have a clear and comprehensive understanding of how DBS works. Although early hypothesis proposed that high-frequency electrical stimulation inhibited neuronal activity proximal to the active electrode, recent studies have suggested that the output of the stimulated nuclei is paradoxically activated by DBS. Such regular, time-locked output is thought to override the transmission of pathological bursting and oscillatory activity through the stimulated nuclei, as well as inducing synaptic plasticity and network reorganization. This chapter reviews electrophysiological experiments, biochemical analyses, computer modeling and imaging studies positing that, although general principles exist, the therapeutic mechanism(s) of action depend both on the site of stimulation and on the disorder being treated.
慢性深部脑刺激（DBS）已成为治疗药物难治性运动障碍的一种广泛接受的外科治疗方法，并且正在针对多种神经系统疾病进行评估。为了创造提高治疗效果、简化参数选择并促进新的潜在应用的机会，清楚而全面地了解DBS的工作原理很重要。尽管早期假说是高频电刺激抑制了有源电极近端的神经元活动，但最近的研究表明，DBS反而会激活受刺激核团的输出。这种规律的、时间锁定的输出被认为可以抑制病理性爆发和振荡活动通过受刺激核团的传递，同时诱导突触可塑性和网络重组。本章回顾了电生理实验、生化分析、计算机建模和成像研究，这些研究表明，尽管存在一般原则，但治疗作用机制既取决于刺激部位，也取决于所治疗的疾病。
