Irritable bowel syndrome patients clearly exhibit disordered motor patterns throughout the gastrointestinal tract, particularly in the small and large intestines. Although past and current research points to an association between irritable bowel syndrome symptoms and abnormal contractility, a causal link has not yet been definitively established. Because abnormal contractility has not yet been clearly linked with symptoms, and because irritable bowel syndrome patients often experience pain during normal motor activity, researchers also have looked at a hyperalgesic (heightened sensitivity to pain) model to explain abdominal pain in irritable bowel syndrome. These two models are discussed in the following sections.
Altered Gastrointestinal Motility
In the large intestine (or colon), three types of myoelectric activity regulate the contraction of smooth muscle. First, slow waves regulate the frequencies of phasic contractions. Second, spike potentials elevate the membrane potential above the threshold needed for contraction. Spike potentials can be either of two types: short spike bursts (SSBs), which last 5-15 seconds in phase with slow waves, or long spike bursts (LSBs), which last up to a minute and are unrelated to slow waves. Both types of spike bursts trigger segmenting contractions, and LSBs also produce some propagating contractions in both the oral and anal directions. The third myoelectric pattern is high-amplitude contraction, called the giant migrating contraction, which occurs once or twice daily and facilitates mass movements of feces and defecation.
Research reveals that, when the colon is unstimulated (i.e., in a fasting state), no clear difference exists between the myoelectric activity in irritable bowel syndrome patients and that in people without irritable bowel syndrome. The stimulated colon normally exhibits spike potential and contractile activity 10 minutes after ingestion of a meal, and such activity usually ceases within 50-60 minutes. In irritable bowel syndrome patients, however, rectosigmoid contractions can continue for up to three hours after a meal. This prolongation is more common in patients with diarrhea-predominant irritable bowel syndrome (D-irritable bowel syndrome), but it is also seen in patients with constipation-predominant irritable bowel syndrome (C-irritable bowel syndrome). Irritable bowel syndrome patients also exhibit myoelectric activity in the colon after a sham feeding (when patients are made to believe they will receive a meal but are denied food at the last moment). This phenomenon suggests that the abnormal contractions may have their origin in the central nervous system control centers.
The role of abnormal myoelectric and motor activity in the small intestine in the pathogenesis of irritable bowel syndrome symptoms is less clear than that of abnormal colonic activity. The small intestine exhibits three motor patterns: (1) migrating motor complexes, which occur cyclically every 90-120 minutes in both the stomach and small intestine, and which clear the gut of undigested debris; (2) discrete clustered contractions, which are bursts of phasic contractions every minute; and (3) prolonged propagating contractions, which are intense ileal contractions that empty the small intestine’s contents, much like the giant migrating contraction in the colon.
Some irritable bowel syndrome patients exhibit postprandial (following a meal) MMC abnormalities. In this subset of patients, migrating motor complexes occur more frequently in D-irritable bowel syndrome patients and are of weaker intensity in C-irritable bowel syndrome patients. Some motility studies have shown that abnormal small intestine contractions correlate with abdominal pain, but such results have not been satisfactorily duplicated.