Neuronal correlates of gastric pain induced by fundus distension: a 3T-fMRI study
Neuronal correlates of gastric pain induced by fundus distension: a 3T-fMRI study
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DOI：
10.1111/j.1365-2982.2004.00562.x
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发表时间：
2004-10-01
影响因子：
3.5
通讯作者：
Hsieh, JC
中科院分区：
文献类型：
--
作者：
Lu, CL;Wu, YT;Hsieh, JC
胃底内脏过敏是功能性消化不良的可能发病机制。胃底的皮质表征仍不清楚。越来越多的证据表明，岛叶，而不是初级或次级体感区域（SI 或 SII），可能是内脏疼痛的皮质目标。动物研究还表明，杏仁核在处理内脏疼痛中发挥着重要作用。我们使用功能磁共振成像来研究眼底球囊扩张引起的胃痛的中心投射。我们还测试了这样的假设：眼底扩张时既不会有 S1 也不会有 S2 激活，而是杏仁核激活。对 10 名健康受试者在基线、身高 (12.7 +/- 0.6 mmHg) 和中度胃痛 (17.0 +/- 0.8 mmHg) 期间进行了 3T-fMRI。通过对预定的心理物理反应进行卷积来对功能磁共振成像信号进行建模。在组水平上的条件之间进行统计比较。胃痛激活了广泛的皮质和皮质下结构，包括丘脑和岛叶、前扣带皮层和后扣带皮层、基底神经节、尾状核、杏仁核、脑干、小脑和前额皮质（P < 0.001）。这些神经元基质的一个子集参与饱腹感的中央处理。 SI和SII在眼底刺激期间没有被激活。总之，除了没有 SI 或 SII 激活之外，由眼底扩张激活的神经元结构群与引起肌肉皮肤疼痛的疼痛矩阵重叠。这可以解释内脏感觉/疼痛的模糊性质。我们的数据还证实，岛叶和杏仁核可能在内脏感觉/疼痛以及所提出的疼痛学习和记忆的感觉边缘模型中发挥核心作用。
Visceral hypersensitivity in gastric fundus is a possible pathogenesis for functional dyspepsia. The cortical representation of gastric fundus is still unclear. Growing evidence shows that the insula, but not the primary or secondary somatosensory region (SI or SII), may be the cortical target for visceral pain. Animal studies have also demonstrated that amygdala plays an important role in processing visceral pain. We used fMRI to study central projection of stomach pain from fundus balloon distension. We also tested the hypothesis that there will be neither S1 nor S2 activation, but amygdala activation with the fundus distension. A 3T-fMRI was performed on 10 healthy subjects during baseline, tallness (12.7 +/- 0.6 mmHg) and moderate gastric pain (17.0 +/- 0.8 mmHg). fMRI signal was modelled by convolving the predetermined psychophysical response. Statistical comparisons were performed between conditions on a group level. Gastric pain activated a wide range of cortical and subcortical structures, including thalamus and insula, anterior and posterior cingulate cortices, basal ganglia, caudate nuclei, amygdala, brain stem, cerebellum and prefrontal cortex (P < 0.001). A subset of these neuronal substrates was engaged in the central processing of fullness sensation. SI and SII were not activated during the fundus stimulation. in conclusion, the constellation of neuronal structures activated by fundus distension overlaps the pain matrices induced musculocutaneous pain, with the exception of the absence of SI or SII activation. This may account for the vague nature of visceral sensation/ pain. Our data also confirms that the insula and amygdala may act as the central role in visceral sensation/pain, as well as in the proposed sensory-limbic model of learning and memory of pain.