Central processing of noxious somatic stimuli in patients with irritable bowel syndrome compared with healthy controls.

Central processing of noxious somatic stimuli in patients with irritable bowel syndrome compared with healthy controls.
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DOI:
10.1097/ajp.0b013e3181bff800
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发表时间:
2010-02
期刊:
The Clinical journal of pain
影响因子:
--
通讯作者:
Light KC
Light KC
中科院分区:
其他
文献类型:
--
作者:
Heymen S;Maixner W;Whitehead WE;Klatzkin RR;Mechlin B;Light KC

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在肠易激综合征(IBS)患者和健康对照者中,使用躯体测试刺激和躯体条件刺激(CS)比较称为弥漫性伤害性抑制对照(DNIC)的中枢镇痛机制。参与者为48名绝经前女性(27名患有IBS),平均年龄29岁。向左手掌施加阶段性热测试刺激(峰值温度,50°C)。DNIC效应,测量在对抗刺激期间(将参与者的右手浸没在疼痛的12°C循环水中)与基线相比的平均疼痛评级(APR)的降低,在两组之间进行比较。此外,进行第二次平衡CS方案(右手浸没在无痛的32°C循环水中)。比较两组之间2种抗刺激方案的APR差异,以控制已知影响DNIC的非特异性效应。心理措施和心血管反应也进行了评估。IBS患者的DNIC低于对照组(P=0.011,重复测量方差分析),而状态焦虑、抑郁、灾难化和愤怒表达高于对照组(P<0.05)。在控制了无痛CS期间发生的非特异性效应和心理测量后,DNIC的组间差异增强(P=0.001,重复测量协方差分析)。对于12°C CS,年龄、心血管反应性、APR或疼痛评级无组间差异。这些数据表明IBS中缺乏DNIC。这是第一项充分控制反刺激期间疼痛减轻的其他解释的研究。只有通过控制非特异性效应,才能将DNIC缺陷的证据归因于内源性镇痛机制的失调。
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°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°C circulating water) compared with baseline, was compared between groups. In addition, a second, counterbalanced, CS protocol (right hand submerged in nonpainful 32°C circulating water) was performed. Differences in APR between the 2 counter-irritation 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°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.