安慰剂镇痛机制:前扣带回皮层招募皮层下抗伤害感受网络。

Mechanisms of placebo analgesia: rACC recruitment of a subcortical antinociceptive network.

作者信息

Bingel U, Lorenz J, Schoell E, Weiller C, Büchel C

机构信息

NeuroImage Nord, Institute for Systems Neuroscience, University Medical Center Hamburg Eppendorf, Germany NeuroImage Nord, Department of Neurology, University Medical Center Hamburg Eppendorf, Germany Department of Physiology, University Medical Center Hamburg Eppendorf, Germany Department of Neurology, University of Freiburg, Germany.

出版信息

Pain. 2006 Jan;120(1-2):8-15. doi: 10.1016/j.pain.2005.08.027. Epub 2005 Dec 20.

Abstract

Placebo analgesia is one of the most striking examples of the cognitive modulation of pain perception and the underlying mechanisms are finally 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) represents a crucial cortical area 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. Nineteen healthy subjects received and rated painful 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 confirmed placebo related activity in the rACC, a connectivity analysis identified placebo dependent contributions 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.

摘要

安慰剂镇痛是疼痛感知认知调节最显著的例子之一,其潜在机制终于开始被理解。根据药理学研究,内源性阿片系统对安慰剂镇痛至关重要。最近的功能成像数据表明,喙前扣带回皮质(rACC)是这种内源性疼痛控制的关键皮质区域。因此,我们假设安慰剂镇痛会激活rACC以外的其他脑区,并且rACC与这些脑区的相互作用介导了阿片类药物依赖的内源性抗伤害感受,这是一种自上而下机制的一部分。19名健康受试者接受并对双手背部的疼痛激光刺激进行评分,其中一只手用假镇痛乳膏(安慰剂)治疗。在疼痛刺激之前有一个听觉提示,指示下一次激光刺激的部位。使用事件相关功能磁共振成像(fMRI)评估在安慰剂和无安慰剂条件下对疼痛激光刺激的血氧水平依赖(BOLD)反应。在确认rACC中存在安慰剂相关活动后,连通性分析确定了rACC活动对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一种观点,即安慰剂镇痛取决于rACC与对条件学习和伤害感受下行抑制至关重要的皮质下脑结构之间增强的功能连通性。

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