Department of Medicine, Division of Gastroenterology, UNC Center for Functional Gastroenterology and Motility Disorders, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7080, USA.
Clin J Pain. 2010 Feb;26(2):104-9. doi: 10.1097/AJP.0b013e3181bff800.
To compare a central analgesic mechanism known as diffuse noxious inhibitory controls (DNIC) using somatic test stimuli and somatic conditioning stimuli, (CS) in irritable bowel syndrome (IBS) patients and healthy controls.
Participants were 48 premenopausal females (27 with IBS), mean age of 29 years. The phasic heat test stimulus (peak temperature, 50 degrees C) was applied to the left palm. The DNIC effect, which measured reductions in average pain ratings (APR) during counter irritation (submersion of the participant's right hand in painful 12 degrees C circulating water) compared with baseline, was compared between groups. In addition, a second, counterbalanced, CS protocol (right hand submerged in nonpainful 32 degrees C circulating water) was performed. Differences in APR between the 2 counterirritation protocols were compared between groups to control for nonspecific effects known to influence DNIC. Psychologic measures and cardiovascular reactivity were also assessed.
IBS patients demonstrated smaller DNIC than controls (P=0.011, repeated measures analysis of variance), and greater state-anxiety, depression, catastrophizing, and anger-out expression (P<0.05). Group differences in DNIC were enhanced after controlling for nonspecific effects occurring during the nonpainful CS, and for psychologic measures (P=0.001, repeated measures analysis of covariance). There were no group differences in age, cardiovascular reactivity, APR, or pain ratings for the 12 degrees C CS.
These data demonstrate deficient DNIC in IBS. This is the first study to adequately control for alternative explanations of pain reduction during counterirritation. Only by controlling for nonspecific effects can evidence of deficient DNIC be attributed to dysregulation in endogenous analgesic mechanisms.
比较躯体刺激和躯体条件刺激引起的弥散性伤害性抑制控制（DNIC）这一已知的中枢镇痛机制，在肠易激综合征（IBS）患者和健康对照者中。
参与者为 48 名绝经前女性（27 名 IBS 患者），平均年龄 29 岁。将阶段性热刺激（峰值温度 50°C）施加于左手掌。通过比较对照刺激（将参与者右手浸入疼痛的 12°C 循环水中）与基础值时的平均疼痛评分（APR）的降低，来评估 DNIC 效应。此外，还进行了第二个、平衡的对照 CS 方案（右手浸入无痛的 32°C 循环水中）。比较两组之间 2 种对照刺激方案 APR 的差异，以控制已知影响 DNIC 的非特异性效应。还评估了心理测量和心血管反应性。
IBS 患者的 DNIC 小于对照组（P=0.011，重复测量方差分析），且状态焦虑、抑郁、灾难化和愤怒表达较高（P<0.05）。在控制非特异性效应（发生在无痛 CS 期间）和心理测量指标后，DNIC 的组间差异增强（P=0.001，重复测量协方差分析）。两组之间年龄、心血管反应性、APR 或 12°C CS 的疼痛评分均无差异。
这些数据表明 IBS 中存在 DNIC 缺陷。这是第一项充分控制对照刺激时疼痛减轻的替代解释的研究。只有通过控制非特异性效应，才能将 DNIC 缺陷归因于内源性镇痛机制的失调。
