Abstract

Significant recent advances in basic and clinical science have improved our understanding of irritable bowel syndrome (IBS). Sensory abnormalities, particularly visceral hypersensitivity after sensitizing stimulation, indicate neural dysfunction in patients with IBS. This dysfunction could be mediated by N-methyl-D-aspartate or calcium gene-related peptide receptors in the spinal cord. The stress response in the gut is augmented in IBS, which may be related to hypothalamic release of corticotropin-releasing factor. Postinfectious IBS may be related to psychologic factors that allow persistent inflammation. Finally, functional brain imaging has shown augmented central nervous system responses to visceral pain in IBS, particularly in the prefrontal cortex. Low-dose tricyclic antidepressants are useful to control symptoms, and the new serotonin type 3 (5-HT3) receptor antagonists show promise for symptom control.

Full Text
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