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Published on: January 21, 2015
Differences in brain responses to visceral pain between patients with irritable bowel syndrome and ulcerative colitis
Emeran A Mayer1, Steven Berman, Brandall Suyenobu
1Center for Neurovisceral Sciences and Women's Health, David Geffen School of Medicine, University of California, Los Angeles, CA, USA Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, CA, USA Brain Research Institute, David Geffen School of Medicine, University of California, Los Angeles, CA, USA Division of Mental Health, VA GLA Healthcare System, Los Angeles, CA, USA Division of Nuclear Medicine, VA GLA Healthcare System, Los Angeles, CA, USA Department of Biomathematics & Biostatistics, University of California, Irvine, CA, USA Departments of Physics, University of California, Irvine, CA, USA.
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.
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