Deep brain stimulation: how does it work?

Deep brain stimulation: how does it work?
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DOI:
10.1016/b978-0-444-53497-2.00004-8
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发表时间:
2013-01-01
影响因子:
--
通讯作者:
Vitek, Jerrold L
Vitek, Jerrold L
中科院分区:
其他
文献类型:
--
作者:
Agnesi, Filippo;Johnson, Matthew D;Vitek, Jerrold L

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慢性脑深部刺激(DBS)已经成为一种被广泛接受的治疗药物难治性运动障碍的外科治疗方法,目前正在对各种神经疾病进行评估。为了创造机会来提高治疗效果,简化参数选择,并促进新的潜在应用,重要的是对DBS的工作原理有一个清晰和全面的了解。虽然早期的假说认为高频电刺激抑制了活动电极附近的神经元活动,但最近的研究表明,刺激的核团的输出被DBS矛盾地激活。这种规则的、时间锁定的输出被认为超过了病理性爆发和振荡活动通过刺激核的传递,以及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、计算机模拟和成像研究,提出虽然存在一般原理,但作用的治疗机制(S)既取决于刺激的部位,也取决于正在治疗的疾病。
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.