Differences in brain responses to visceral pain between patients with irritable bowel syndrome and ulcerative colitis - PubMed (original) (raw)

Comparative Study

. 2005 Jun;115(3):398-409.

doi: 10.1016/j.pain.2005.03.023.

Affiliations

Comparative Study

Differences in brain responses to visceral pain between patients with irritable bowel syndrome and ulcerative colitis

Emeran A Mayer et al. Pain. 2005 Jun.

Abstract

Patients with mild chronic inflammation of the rectum or ileum have reduced perceptual responses to rectosigmoid distension compared to patients with irritable bowel syndrome (IBS). The current study sought to identify differences in regional cerebral blood flow (rCBF) during rectal distension, which might correspond to these perceptual differences. In 8 male ulcerative colitis (UC) patients with quiescent disease, 7 male IBS patients and 7 healthy male controls, rCBF was assessed using 15O-water positron emission tomography at baseline and during actual and anticipated but undelivered rectal distensions. No group differences were seen in anterior insula and dorsal anterior cingulate cortex (dACC), two regions consistently activated by painful intestinal stimuli. However, IBS patients showed greater activation of the amygdala, rostroventral ACC, and dorsomedial frontal cortical regions. In contrast, no significant differences were observed between UC and controls. When these two non-IBS groups were combined, functional connectivity analyses showed that right lateral frontal cortex (RLFC) activation positively correlated with activation of the dorsal pons/periaqueductal gray, a key region involved in endogenous pain inhibition. According to the connectivity analysis, this effect was mediated by inhibition of medial frontal cortex by the RLFC. Chronic colonic inflammation is not necessarily associated with increased visceral afferent input to the brain during rectal distension. In the sample studied, the primary difference between functional and quiescent inflammatory disease of the colon was in terms of greater activation of limbic/paralimbic circuits in IBS, and inhibition of these circuits in UC and controls by the RLFC.

PubMed Disclaimer

Comment in

Similar articles

Cited by

References

    1. Augustine JR. Circuitry and functional aspects of the insular lobe in primates including humans. Brain Res Rev. 1996;22:229-244.
    1. Baron RM, Kenny DA. The moderator-mediator variable distinction in social psychological research: conceptual, strategic, and statistical considerations. J Pers Soc Psychol. 1986;51:1173-1182.
    1. Basbaum AI, Fields HL. Endogenous pain control systems: brainstem spinal pathways and endorphin circuitry. Annu Rev Neurosci. 1984;7:309-338.
    1. Berman S, Munakata J, Naliboff B, Chang L, Mandelkern M, Silverman DH, Kovalik E, Mayer EA. Gender differences in regional brain response to visceral pressure in IBS patients. Eur J Pain. 2000;4:157-172.
    1. Berman SM, Chang L, Suyenobu B, Derbyshire SW, Stains J, FitzGerald L, Mandelkern M, Hamm L, Vogt B, Naliboff BD, Mayer EA. Condition-specific deactivation of brain regions by 5-HT3 receptor antagonist alosetron. Gastroenterology. 2002;123:969-977.

Publication types

MeSH terms

LinkOut - more resources