Significance of visceral hypersensitivity in IBS
IBS patients have lower pain thresholds to balloon-distention volumes specific to the GI tract (i.e., rectosigmoid, descending colon, small intestine, stomach, and esophagus) in comparison with healthy individuals.
The cause of visceral hypersensitivity in IBS is not completely understood. However, researchers now believe that noxious stimuli can change the synaptic efficiency of peripheral and central neurons. This may occur through altered release of serotonin (5-HT) from the enteroenteric cells in the myenteric plexus or release of inflammatory cytokines from activated immune or inflammatory cells in response to infection or injury. Through a process known as the wind-up, neurons can develop a pain memory that can persist long after the noxious stimulus is removed. IBS patients may also be prone to developing sensitization. Repetitive sigmoid contractions, such as those that may occur during intense stress, could induce sensitization in a person predisposed to developing IBS, thereby causing rectosigmoid hypersensitivity.
Although 95% of IBS patients have rectal sensory abnormalities, rectal sensitivity testing is not currently widely used in the diagnosis or management of IBS, partly because of the lack of standardization in balloon-distention protocols, the limited correlation between symptom severity or response to therapy, and the significant overlap with other GI diseases. Therefore, its clinical utility in making a definitive diagnosis of IBS is limited.