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The exact cause of Irritable Bowel Syndrome is not known, but altered bowel motility, visceral hypersensitivity, psychosocial factors, an imbalance in neurotransmitters and infection have all be proposed to contribute to the development of irritable bowel syndrome.
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Alterations in the contractility of the bowel have been described in patients with IBS. Psychological, physical stress and ingestion of food can alter the motility of the colon. Motility patterns among patients with IBS are qualitatively similar to healthy individuals, but are exaggerated in response to certain stimuli.
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Heightened sensitivity to visceral distension has been described in several studies. Balloon distension studies of the rectosigmoid and ileum have shown that patients with IBS experience pain and bloating at balloon volumes and pressures that are significantly lower than those that induce pain in control subjects. Some have suggested that hypervigilance rather than true visceral hypersensitivity is responsible. Anecdotally, IBS patients are more sensitive to manipulation and air insufflation during colonoscopy.
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Psychological stress can alter motor function in the small bowel and colon, both in normal subjects and in patients with the irritable bowel syndrome. In addition, any chronic illness has psychological consequences on one’s general well-being, sense of control over symptoms and daily function status. Raising awareness of this can help the patient cope better with the symptoms. Coping better can help reduce stress and break the vicious cycle.
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Five percent of serotonin (5-hydroxtryptamine, 5-HT) is located in the central nervous system, and the remaining 95 percent is in the gastrointestinal tract, within enterochromaffin cells, neurons, mast cells and smooth-muscle cells. When released by enterochromaffin cells, serotonin stimulates extrinsic vagal afferent nerve fibres and intrinsic enteric afferent nerve fires, resulting in physiological responses such as intestinal secretion and peristaltic reflex and in symptoms such as nausea, vomiting, abdominal pain and bloating. Other neurotransmitters may also be implicated in IBS.
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There is evidence that inflammation of the enteric mucosa or neural plexuses initiates or contributes to symptoms associated with irritable bowel syndrome. Mucosal inflammatory cytokines may activate peripheral sensitization or hyper motility. 30 percent of patients with IBS report their symptoms began after an episode of gastroenteritis and similarly, 30 percent of patients develop IBS symptoms after the infection has resolved.
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