背景:突发脊髓刺激(SCS)技术使用一种新颖的波形,该波形由紧密堆积的高频电脉冲组成,然后是静止期。在不断发展的神经调节领域中,爆发刺激是独一无二的,因为它模仿神经系统的自然爆发,特别是丘脑扣带回的节律性,导致调节疼痛处理的情感和注意力成分(例如,丘脑内侧通路)。
方法:回顾了关于各种慢性疼痛状态的猝发性SCS的临床前和临床研究。
方法:综述了有关爆发刺激技术的现有文献。数据来源包括通过PubMed搜索确定的相关文献,MEDLINE/OVID,Scopus,以及手动搜索已知主要文章和评论文章的参考书目。
方法:主要结果指标是了解与爆发刺激有关的作用机制,并回顾各种慢性疼痛状态下爆发SCS适应症的临床数据。
结果:我们介绍了各种疼痛状态下爆发刺激的作用机制和用途。
结论:爆裂刺激为背部手术失败综合征提供了一种新颖的疼痛减轻工具,没有不舒服的感觉异常,糖尿病性神经性疼痛,和麻醉dolorosa.临床前模型强调,爆发治疗的潜在机制可能与模拟自然神经系统放电模式的神经编码算法有关。导致对内侧和外侧疼痛途径的影响。其他机制包括频率依赖性阿片类药物释放,疼痛门的调制,以及电和化学突触的激活。
BACKGROUND: Burst spinal cord stimulation (SCS) technology uses a novel waveform that consists of closely packed high-frequency electrical impulses followed by a quiescent period. Within the growing field of neuromodulation, burst stimulation is unique in that it mimics the natural burst firing of the nervous system, in particular the thalamo-cingulate rhythmicity, resulting in modulation of the affective and attentional components of pain processing (e.g., medial thalamic pathways).
METHODS: A
review of preclinical and clinical studies regarding burst SCS for various chronic pain states.
METHODS: Available literature was reviewed on burst stimulation technology. Data sources included relevant literature identified through searches of PubMed, MEDLINE/OVID, SCOPUS, and manual searches of the bibliographies of known primary and
review articles.
METHODS: The primary outcome measure was to understand the mechanisms of action with regards to burst stimulation and to
review clinical data on the indications of burst SCS for various chronic pain states.
RESULTS: We present both mechanisms of action and
review uses of burst stimulation for various pain states.
CONCLUSIONS: Burst stimulation offers a novel pain reduction tool with the absence of uncomfortable paresthesia for failed back surgery syndrome, diabetic neuropathic pain, and anesthesia dolorosa. Preclinical models have emphasized that the potential mechanisms for burst therapy could be related to neural coding algorithms that mimic the natural nervous system firing patterns, resulting in effects on both the medial and lateral pain pathways. Other mechanisms include frequency dependent opioid release, modulation of the pain gate, and activation of electrical and chemical synapses.