Giamberardino Maria Adele, Affaitati Giannapia, Lerza Rosanna, Lapenna Domenico, Costantini Raffaele, Vecchiet Leonardo
Ce.S.I., G. D'Annunzio Foundation, G. D'Annunzio University of Chieti, Pescara, Italy.
Pain. 2005 Mar;114(1-2):239-49. doi: 10.1016/j.pain.2004.12.024. Epub 2005 Jan 26.
The relationship was investigated between algogenic potential of gallbladder pathology and occurrence/extent of sensory and trophic changes in the referred area. Five groups of subjects were studied, with: symptomatic gallbladder calculosis (3-20 colics); asymptomatic calculosis; symptomatic gallbladder shape abnormality (8-18 colics); asymptomatic shape abnormality; normal gallbladder/no symptoms. At the cystic point (CP) and contralaterally, all underwent measurement of: pain thresholds to electrical stimulation of skin, subcutis and muscle; thickness of subcutis and muscle via ultrasounds. Contralaterally to CP, all thresholds were not significantly different in the five groups. At CP, subcutis and muscle thresholds were significantly lower in symptomatic vs asymptomatic patients and/or normals (0.0001<P< 0.05). In symptomatic cases, at CP compared to contralaterally, subcutis and muscle thresholds were significantly lower (0.0001<P<0.02), subcutis thickness was significantly higher and muscle thickness significantly lower (0.006<P<0.02). Subcutis and muscle thresholds at CP in symptomatic patients were significantly and inversely correlated linearly to the number of colics (P<0.0004; P<0.0001). Patients with symptomatic calculosis were re-evaluated after 6 months; those not presenting further colics showed a significant increase in subcutis and muscle thresholds at CP, while those who continued presenting colics showed a further significant threshold decrease (0.01<P<0.05); tissue thickness did not vary. Referred hyperalgesia and altered trophism from the gallbladder only occur in painful pathology, their extent being modulated by the amount of perceived pain. The results suggest different mechanisms by which visceral nociceptive inputs trigger sensory vs trophic changes in the referred area.
研究了胆囊病变的致痛潜能与牵涉区感觉和营养变化的发生/程度之间的关系。对五组受试者进行了研究，分别为：有症状的胆囊结石病（3 - 20次绞痛）；无症状结石病；有症状的胆囊形态异常（8 - 18次绞痛）；无症状形态异常；胆囊正常/无症状。在胆囊点（CP）及其对侧，所有受试者均接受了以下测量：皮肤、皮下组织和肌肉电刺激的疼痛阈值；通过超声测量皮下组织和肌肉的厚度。在CP对侧，五组之间所有阈值均无显著差异。在CP处，有症状的患者与无症状患者和/或正常受试者相比，皮下组织和肌肉阈值显著更低（0.0001 < P < 0.05）。在有症状的病例中，与对侧相比，CP处的皮下组织和肌肉阈值显著更低（0.0001 < P < 0.02），皮下组织厚度显著更高，肌肉厚度显著更低（0.006 < P < 0.02）。有症状患者CP处的皮下组织和肌肉阈值与绞痛次数呈显著负线性相关（P < 0.0004；P < 0.0001）。有症状的结石病患者在6个月后重新进行评估；那些未再出现绞痛的患者CP处的皮下组织和肌肉阈值显著增加，而那些继续出现绞痛的患者阈值则进一步显著降低（0.01 < P < 0.05）；组织厚度没有变化。牵涉性痛觉过敏和来自胆囊的营养改变仅发生在疼痛性病变中，其程度受感知疼痛量的调节。结果提示了内脏伤害性传入触发牵涉区感觉和营养变化的不同机制。
