Literature DB >> 20090435

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

Steve Heymen1, William Maixner, William E Whitehead, Rebecca R Klatzkin, Beth Mechlin, Kathleen C Light.   

Abstract

OBJECTIVE: 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.
METHODS: 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.
RESULTS: 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. DISCUSSION: 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.

Entities:  

Mesh:

Year:  2010        PMID: 20090435      PMCID: PMC4321817          DOI: 10.1097/AJP.0b013e3181bff800

Source DB:  PubMed          Journal:  Clin J Pain        ISSN: 0749-8047            Impact factor:   3.442


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