Assessment of experimental pain from skin, muscle, and esophagus in patients with chronic pancreatitis
Assessment of experimental pain from skin, muscle, and esophagus in patients with chronic pancreatitis
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DOI：
10.1097/mpa.0b013e31805c1762
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发表时间：
2007-07-01
期刊：
影响因子：
2.9
通讯作者：
Drewes, Asbjorn Mohr
中科院分区：
文献类型：
--
作者：
Dimcevski, Georg;Staahl, Camilla;Drewes, Asbjorn Mohr
目的：综合实验方法是评估慢性疼痛患者疼痛机制的主要相关方法。慢性胰腺炎被认为涉及其他内脏器官和躯体组织的感觉反应。因此，我们的目的是探索慢性胰腺炎（CP）的疼痛机制，使用多模式和多组织刺激approach.Methods：10例患者（平均年龄，50岁）与CP和13名健康对照（平均年龄，35岁）参加。没有一个病人定期服用止痛药。所有人都暴露于多模式（机械，热和电）实验疼痛的皮肤，肌肉，和esophageal.Results：患者是hyposensitive机械刺激的皮肤（P = 0.001），但没有差异的疼痛，热和电刺激。在肌肉和食管中，没有发现疼痛阈值的差异。反映中枢致敏程度的单次和重复刺激之间的差异在对照组中为17%，在患者中为36%（P = 0.001）。结论：中枢兴奋性、神经可塑性改变和下行痛觉调制通路之间的平衡可以解释CP对实验性多模式刺激的痛觉反应。这也可能反映临床疼痛机制，并可能对治疗选择产生重要影响，应使用对这些机制有潜在影响的药物。
Objectives: Comprehensive experimental methods are of major relevance assessing pain mechanisms in patients with chronic pain. Chronic pancreatitis is thought to involve the sensory response in other visceral organs and somatic tissue. We, therefore, aimed at exploring the pain mechanisms in chronic pancreatitis (CP) using a multimodal and multitissue stimulation approach.Methods: Ten patients (mean age, 50 years) with CP and 13 healthy controls (mean age, 35 years) participated. None of the patients took analgesics regularly. All were exposed to multimodal (mechanical, thermal, and electrical) experimental pain in the skin, Muscles, and esophagus.Results: The patients were hyposensitive to mechanical stimulations of the skin (P = 0.001), but there were no differences in the pain to thermal and electrical stimulations. In the muscle and esophagus, no differences in pain thresholds were found. The difference between single and repeated stimulations reflecting the degree of central sensitization was 17% in controls and 36% in patients (P = 0.001). 2 The referred pain area to electrical stimulation was 30.1 CM in the patients and 7.7 cm(2) for the controls (P = 0.02).Conclusions: The findings suggest that the balance among central hyperexcitability, neuroplastic changes, and descending pain-modulating pathways may explain the pain response to experimental multimodal stimulations in CP. This will likely also reflect the clinical pain mechanisms and may have important impact in selection of treatment, where drugs with potential effects on these mechanisms should be used.