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许多文献资料报道了安慰剂对疼痛的镇痛效果。人体大脑功能影像技术可以在无创伤条件下研究安慰剂镇痛的大脑功能解剖结构及其神经生物学机制。功能磁共振成像和正电子发射断层扫描(PET)的脑血流测定表明大脑前扣带回喙部(rACC)、脑岛、丘脑和脑干的中脑导水管周围灰质(PAG)及延髓头端腹侧部的神经兴奋性降低与安慰剂镇痛调节有关。内源性吗啡肽系统及激活吗啡肽μ受体参与安慰剂的镇痛作用。吗啡肽μ受体标记的PET影像研究提示安慰剂镇痛伴随着疼痛相关大脑部位(如rACC、前额叶皮层、脑岛、丘脑、杏仁核、伏隔核、PAG等)中内源性吗啡肽活性的降低。此外,标记多巴胺D2/D3受体的PET实验证明基底核包括伏隔核的多巴胺活性与安慰剂镇痛相关。安慰剂镇痛引起的伏隔核的多巴胺释放与安慰剂期待相关。以上结果提示上述大脑区域和内源性吗啡肽及多巴胺在安慰剂镇痛方面有重要作用。
Many articles report the analgesic effect of placebo on pain. Human Brain Functional Imaging studies the functional anatomy of the brain and its neurobiological mechanisms of placebo-analgesia under noninvasive conditions. Cerebral blood flow measurements by functional magnetic resonance imaging and positron emission tomography (PET) showed that the periaqueductal gray (PAG) and the rostral medulla oblongata in the anterior cingulate gyrus (rACC), insula, thalamus and brainstem, Decreased neuronal excitability in the ventral part is associated with a placebo-controlled analgesia. The endogenous morphine system and the activation of morphine receptor μ are involved in the analgesic effect of placebo. Morphine peptide mu receptor-labeled PET imaging studies suggest that placebo analgesia is associated with endogenous morphine peptides in pain-associated brain regions such as rACC, prefrontal cortex, insula, thalamus, amygdala, nucleus accumbens, PAG, Decreased activity. In addition, PET experiments labeling dopamine D2 / D3 receptors demonstrated that dopamine activity in the basal ganglia, including the nucleus accumbens, correlates with placebo analgesia. Placebo analgesia-induced dopamine release from the nucleus accumbens correlates with placebo expectation. The above results suggest that these brain regions and endogenous morphine peptides and dopamine play an important role in the placebo analgesia.