Gastroenterology clinics of North America
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Gastroenterol. Clin. North Am. · Jun 2005
ReviewThe role of food intolerance in irritable bowel syndrome.
Irritable bowel syndrome patients frequently believe that food intolerances are to blame for many of their symptoms, although not uncommonly this is caused by the nonspecific increase in gut motility that occurs with food ingestion. Nevertheless, dietary manipulation may result in substantial improvement in IBS symptomatology provided it is individualized to the particular patient. By further understanding the mechanisms involved in dietary intolerance, it should be possible to optimize the benefits of this approach to treatment.
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Gastroenterol. Clin. North Am. · Jun 2005
ReviewBrain responses to visceral and somatic stimuli in irritable bowel syndrome: a central nervous system disorder?
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. ⋯ 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.