Pathophysiology

IBS is actually a heterogeneous combination of different factors as well as other mechanisms that remain to be elucidated. 

IBS probably represents the common clinical expression of multiple potential pathophysiologic factors. Potential factors that contribute to IBS include a genetic predisposition to the condition, disturbed central nervous system pain processing and visceral hypersensitivity, mucosal inflammation, abnormal colonic motility and emotional stress.

Genetic Predisposition 

It is not uncommon for patients who have suspected IBS to describe similar symptoms, if not the diagnosis, of IBS is family members. This observation gave rise to several studies that evaluated the possible role of a genetic predisposition for IBS, Although these studies do seem to support a genetic contribution for IBS, Although these studies do seem to support a genetic contribution to IBS, the basis of this contribution remains unknown, some investigator hypothesized that differences in inherited patterns of serotonin processing at the neuronal level may play a role, IBS is more common in patients who have first degree relative who has IBS symptoms. Such observational studies, although interesting, do not help us to understand the contribution to "nature versus nurture". The presence of a parent with IBS has been shown to be predictive of the subsequent development of IBS. This finding lends credence to the theory that IS may have a significant learning or behavioral component..

Altered Motility

Numerous motility abnormalities that affect the GI tract have been identified in patients who have IBS. For many years, investigators focused on the role of abnormal motility in the pathogenesis of IBS.

For example, patients whose predominant symptom is diarrhea seem to have accelerated whole gut and colonic transit times. Conversely, Patients who have constipation-predominant IBS demonstrate decreased migrating motor complexes compared with controls who did not have IBS. Whether these motility changes are primary or secondary to another potential etiology of IBS remain to be proven. The degree of variability in observed results and the methodologic limitation of previous trials of colonic motility highlight the need for additional evidence in this area.

Visceral Hypersensitivity and brain-gut interactions

Pain is a central requiremernt of the definition and diagnosis of IBS. The potential roles of heightened visceral sensation, also referred to as "visceral hypersensitivity" and abnormalities in brain=gut interactions have also been implicated in the pathogenesis of IBS. Several Investigators have reported a heightened visceral Sensation in response to rectal balloon distension in patients with IBS and other functional GI Disorder abnormalities have been identified consistently in the activation of the anterior cingulate cortex which probably plays an important role in the development of attention to aa painful stimulus, the unpleasantness associated with a painfull stimulus, and attribution of an emotional response to a painful stimulus. The anterior cingulate cortex also plays an imprtant role in the activation of descending inhibitory pathways that help to gate or control the passage of afferent information from the periphery to the brain.

More on IBS:

• Mucosal Inflamation & Emotional Stress
• Diagnosis
• The role of Diagnostic Testing
• Treatment
• Summary
• Resources