# Functional GI Disorders IBS at a Glance Nosology-Epidemiology-Pathophysiology



## Jeffrey Roberts (Apr 15, 1987)

Originally from: http://www.gastro.org/adhf/gi_ibs.html CME Monograph I: Functional GI Disorders IBS at a Glance Nosology- Epidemiology-Pathophysiology Inflammation Intestinal inflammation can cause neurological changes with effects on GI motility and visceral perception. Structural changes to the enteric nervous system are not restricted to areas of active inflammation. Functional abnormalities can persist long after resolution of the inflammation. Many patients with acute gastroenteritis develop chronic functional GI symptoms. Brain Physiology Stress reproducibly alters gastrointestinal motility and sensation. The release of corticotropin releasing factor from the hypothalamus may mediate the stress response. Brain centers important in mediating visceral pain include the thalamus (general sensory), insular cortex (visceral sensory), anterior cingulate cortex (general pain awareness), and prefrontal cortex (general pain processing). Visceral pain in IBS is associated with increased prefrontal cortex activation. The normal correlation between subjective pain intensity and activation of the anterior cingulate and insula cortices is lost in IBS. The limbic system is involved in emotion, mood, and visceral autonomic control. Limbic abnormalities are seen in depression and IBS. Thus, this system is a possible site of convergence where emotional disturbance provokes intestinal dysfunction. Psychosocial Factors It is no longer reasonable to discriminate between physiological and psychological factors; both are operative in IBS. It is likely that dysregulation of the ï¿½brain-gutï¿½ neuroenteric systems, rather than the presence of structural disease, promotes the development and persistence of IBS. While psychosocial factors are not part of the diagnosis of IBS, they have a significant effect on gut motility, symptom experience, and health outcome. To legitimize the condition, it is essential to continue research-based efforts to challenge the myths associated with IBS. Nosology Functional GI disorders are sub-classified according to the regions involved. There are no biologic or pathophysiologic markers by which to define IBS. IBS is characterized by a cluster of certain symptoms; diagnosis is augmented by prudent exclusion of structural disorders. Epidemiology IBS is common, affecting 10%-20% of adults. IBS overlaps with other functional disorders and symptoms fluctuate over time. The prevalence of IBS is significantly greater in women than in men. A history of physical or sexual abuse is associated with increased severity of disease and greater healthcare utilization. The disorder is common in all ages and ethnic groups. IBS accounts for significant healthcare utilization and indirect costs. Motility and Electrophysiology In IBS, diarrhea is characterized by decreased segmenting sigmoid contractions and an increased frequency in long spike bursts. Constipation and abdominal pain are characterized by increased segmenting sigmoid contractions and an increased frequency in short spike bursts. IBS patients may have diffuse motility abnormalities in the esophagus, stomach, and small intestine. Measured abnormalities in GI motor function do not define IBS. VisCeral Sensitivity and Perception Altered visceral perception via changes in reflex responses and viscerosomatic referral areas is common in IBS. Both hyperalgesia (lower pain threshold) and allodynia (pain perceived in non-nociceptive pathways) are involved in the development of visceral hypersensitivity. Visceral perception can be modulated by the CNS (e.g., stress, anxiety, and distraction). It is believed that, as a result of central sensitization, a nociceptive memory response is created, which exaggerates and prolongs subsequent stimulation. The pathophysiology of visceral hyperalgesia is incompletely understood and appears to be multifactorial.


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## JeanG (Oct 20, 1999)

Thanks, Jeff!







JeanG


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