Mechanisms of Placebo Analgesia
Mechanisms of Placebo Analgesia
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安慰剂镇痛机制
DOI：
10.1055/s-2005-919284
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
C. Büchel
中科院分区：
文献类型：
--
作者：
U. Bingel;J. Lorenz;C. Weiller;C. Büchel
认知机制调节疼痛感知是一种日常经验。虽然安慰剂镇痛是疼痛感知认知调节的最突出的例子之一，但其神经机制才刚刚开始被理解。根据药理学研究，内源性阿片系统是安慰剂镇痛所必需的。最近的功能成像数据提供的证据表明，喙前扣带皮层（rACC）可能是这种类型的内源性疼痛控制的关键控制中心。因此，我们假设安慰剂镇痛招募rACC外的其他脑区，rACC与这些脑区的相互作用介导阿片依赖性内源性抗伤害感受，作为自上而下机制的一部分。19名健康受试者接受并评定双手背部的疼痛Tm-YAG激光刺激，其中一人用假止痛膏（安慰剂）治疗。疼痛刺激之前的听觉提示，表明下一个激光刺激的一面。在安慰剂和无安慰剂条件下，使用事件相关功能磁共振成像评估对疼痛激光刺激的BOLD反应。在确定了rACC中的安慰剂相关活性后，连接分析确定了rACC活性与双侧杏仁核和导水管周围灰质（PAG）的安慰剂依赖性贡献。这一发现支持了这样的观点，即安慰剂镇痛依赖于rACC与皮质下脑结构的增强的功能连接，这对于条件学习和伤害感受的下行抑制至关重要
It is an everyday experience that cognitive mechanisms modulate pain perception. Although placebo analgesia is one of the most striking examples of cognitive modulation of pain perception, its neural mechanisms are just beginning to be understood. According to pharmacological studies, the endogenous opioid system is essential for placebo analgesia. Recent functional imaging data provides evidence that the rostral anterior cingulate cortex (rACC) may represent a crucial control center for this type of endogenous pain control. We therefore hypothesized that placebo analgesia recruits other brain areas outside the rACC and that interactions of the rACC with these brain areas mediate opioid-dependent endogenous antinociception as part of a top-down mechanism. 19 healthy subjects received and rated painful Tm-YAG-laser stimuli to the dorsum of both hands, one of them treated with a fake analgesic cream (placebo). Painful stimulation was preceded by an auditory cue, indicating the side of the next laser stimulation. BOLD-responses to the painful laser-stimulation during the placebo and no-placebo condition were assessed using event-related fMRI. After having identified placebo related activity in the rACC, a connectivity analysis identified placebo dependent contribution of rACC activity with bilateral amygdalae and the periaqueductal gray (PAG). This finding supports the view that placebo analgesia depends on the enhanced functional connectivity of the rACC with subcortical brain structures that are crucial for conditioned learning and descending inhibition of nociception