Dimcevski Georg, Schipper Klaus P, Tage-Jensen Ulrik, Funch-Jensen Peter, Krarup Anne L, Toft Egon, Thorsgaard Niels, Arendt-Nielsen Lars, Drewes Asbjørn M
Centre for Visceral Biomechanics and Pain, Department of Gastroenterology, Aalborg University Hospital, Aalborg, Denmark.
Eur J Gastroenterol Hepatol. 2006 Jul;18(7):755-64. doi: 10.1097/01.meg.0000223903.70492.c5.
To gain more information of the pain mechanisms in chronic pancreatitis we applied standardized experimental pain stimulation of the duodenum, oesophagus and the skin in 12 healthy controls and 13 patients with chronic pancreatitis and typical pain attacks.
Using endoscopy a guide wire was positioned into the horizontal part of the duodenum, and a probe with a distal balloon was introduced over the guide wire. Mechanical stimuli were given as tonic (38 ml/min) or phasic (increasing volume steps of 5 ml delivered for 60 s) distensions of the balloon. After stimulation of the duodenum, the distal oesophagus was stimulated with the same protocol. Finally, the skin was stimulated with 'single and repeated burst' electrical stimuli reflecting activation of peripheral and central pain mechanisms.
The stimuli reliably evoked both painful and non-painful local and referred sensations. The patients had hyposensitivity to both tonic and phasic mechanical stimuli of the duodenum and the oesophagus (P=0.001). Hypoalgesia was also observed to single and repeated electrical skin stimuli in the patients, most evident for repeated stimuli (P=0.001). The evoked referred pain did not differ between the groups, but the patients used on average more words from the McGill Pain Questionnaire to describe the pain evoked in the duodenum (P=0.02).
Generalized hypoalgesia to experimental visceral and somatic stimulations was found in chronic pancreatitis. The findings suggest that the activation and modulation of central mechanisms is fundamental in pancreatic pain, and future studies should address the effect of analgesics with central effects in the treatment of these patients.
为了获取更多关于慢性胰腺炎疼痛机制的信息，我们对12名健康对照者和13名患有慢性胰腺炎且有典型疼痛发作的患者进行了十二指肠、食管和皮肤的标准化实验性疼痛刺激。
通过内镜将导丝置于十二指肠水平部，然后将带有远端球囊的探头经导丝插入。机械刺激通过球囊的持续性（38毫升/分钟）或阶段性（以5毫升的增量递增，持续60秒）扩张来进行。在刺激十二指肠后，以相同方案刺激食管远端。最后，用反映外周和中枢疼痛机制激活的“单次和重复脉冲”电刺激来刺激皮肤。
刺激可靠地诱发了疼痛和非疼痛的局部及牵涉性感觉。患者对十二指肠和食管的持续性及阶段性机械刺激均存在感觉减退（P = 0.001）。在患者中还观察到对单次和重复的皮肤电刺激存在痛觉减退，重复刺激时最为明显（P = 0.001）。两组之间诱发的牵涉痛没有差异，但患者平均使用更多的麦吉尔疼痛问卷中的词汇来描述十二指肠诱发的疼痛（P = 0.02）。
在慢性胰腺炎中发现对实验性内脏和躯体刺激存在全身性痛觉减退。这些发现表明，中枢机制的激活和调节在胰腺疼痛中至关重要，未来的研究应探讨具有中枢作用的镇痛药对这些患者治疗的效果。
