Irritable bowel syndrome (IBS), a functional gastrointestinal disorder long considered a diagnosis of exclusion, has chronic symptoms that vary over time and overlap with those of non-IBS disorders. Traditional symptom-based criteria effectively identify IBS patients but are not easily applied in clinical practice, leaving over 40% of patients to experience symptoms up to 5 years before diagnosis.
The myoelectric activity of the colon is composed of background slow waves with superimposed spike potentials. Colonic dysmotility in irritable bowel syndrome manifests as variations in slow-wave frequency and a blunted, late-peaking, postprandial response of spike potentials. Patients who are prone to diarrhea demonstrate this disparity to a greater degree than patients who are prone to constipation.
Small bowel dysmotility manifests in delayed meal transit in patients prone to constipation and in accelerated meal transit in patients prone to diarrhea. In addition, patients exhibit shorter intervals between migratory motor complexes (the predominant interdigestive small bowel motor patterns).
Current theories integrate these widespread motility aberrations and hypothesize a generalized smooth muscle hyperresponsiveness. They describe increased urinary symptoms, including frequency, urgency, nocturia, and hyperresponsiveness to methacholine challenge.
Visceral hypersensitivity (the experience of pain in internal organs at an increased level than what is normally expected) may also play a role in irritable bowel syndrome (IBS). This pain sensitivity is usually studied using some variation of balloon distention in the rectum, and as an overall research trend people who suffer from IBS experience discomfort and pain in the rectal area at lower levels of pressure than individuals who do not suffer from IBS. But the issue is not a simple one; it appears likely that the visceral hypersensitivity seen in some IBS patients is a result of changes in nervous system functioning on both the level of the intestines and the brain. At the level of the gut, it seems as if nerve pathways in the gastrointestinal tract become sensitized to stimulation, resulting in over-reactivity and resulting in pain amplification. Brain imaging studies provide more clues; in individuals who do not have IBS, rectal distension triggers a response in parts of the brain that are associated with modulating pain. In IBS patients, this same rectal stimulation triggers a response in the parts of the brain associated with vigilance and anxiety -- parts of the brain that serve to amplify the sensation of pain.
Certain types of psychotherapy have been shown to be effective in reducing IBS symptoms. Although it is not known precisely why therapy is beneficial, it is thought to be related to the effect of the therapy on the close interconnections between the brain and the intestinal system.