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Gastroenterol Clin North Am. 2005 Jun;34(2):271-9.

Brain responses to visceral and somatic stimuli in irritable bowel syndrome: a central nervous system disorder?

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Center for Neurovisceral Sciences & Women's Health, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA 90024, USA.


In healthy subjects, the brain regions most consistently activated in visceral and somatic pain are the key regions in the central pain matrix,including the mid/anterior insula, subregions of the ACC, PFC, thalamus,and in some cases, pontine regions such as the dorsal pons and PAG. Functional neuroimaging studies have demonstrated evidence of altered regional brain activation responses during visceral and somatic stimuli in IBS that have been associated with perceptual differences. Although perceptual studies have shown increased sensitivity to rectosigmoid distension in IBS, most somatic pain studies have demonstrated normal or decreased sensitivity compared with controls; however, a recent study showed increased sensitivity to thermal heat. Altered brain responses in IBS,particularly to visceral stimuli, include activation of regions concerned with attentional processes and response selection, corticolimbic regions concerned with emotional and autonomic responses to stimuli, and subcortical regions receiving cortical projections from the latter and afferent input from the soma and viscera. Altered activations of these regions also may be present in the absence of a noxious visceral stimulus. Changes in rCBF of some of these regions have been associated with treatment response in IBS. With regard to differences in cortical processing of visceral versus somatic stimuli in IBS, there have been only two studies. Greater activations of the dorsal ACC, thalamus, and PFC have been shown with visceral stimuli compared with somatic stimuli in IBS. A plausible hypothesis for the observations from brain imaging studies is that IBS patients demonstrate a compromised activation of pain inhibition circuits including those of the cortico-pontine circuit but increased activation of limbic and paralimbic circuits that may be related to pain facilitation.

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