In contrast to the conscious perception of all sensory stimuli affecting our external body surface, the great majority of events within the gastrointestinal tract such as the chemical breakdown of food, the absorption of nutrients or the involuntary peristaltic action of the gut are not consciously perceived in the healthy state. However, an alteration in perception of sensations arising from the gut has been implicated in the generation of symptoms in patients with Irritable Bowel Syndrome (IBS). Even though studies investigating gastrointestinal sensitivity date back to the early 1900’s and reports describing sensory disturbances of the gut in patients with IBS first appeared in the 1970’s, it is not until recently that well-controlled studies using controlled experimental distension of the gut have begun to characterize the mechanisms underlying IBS symptom generation. The most commonly reported perceptual abnormality in IBS patients has been a lowered discomfort threshold to rectosigmoid balloon distension. However, only a subset of IBS patients shows this perceptual alteration during baseline conditions and recent evidence suggests that the abnormality is more related to hypervigilance rather than increased pain perception.

In a recent study published in Gastroenterology, investigators from the UCLA Neuroenteric Disease Section tested the hypothesis that IBS patients show an altered perceptual response to irritation of the gastrointestinal tract by repetitive distension. They found that even though IBS patients may have normal pain thresholds during rectal balloon distension under control conditions, repetitive colonic distension results in an enhanced perception of intestinal stimuli in nearly 100% of IBS patients. In contrast, in healthy control subjects, no such sensitization was observed, while some patients with inflammatory bowel disease even developed intestinal hyposensitivity.

The findings by the UCLA researchers are consistent with several clinical observations that suggest a compromised ability of IBS patients to activate the body’s own pain inhibition systems in response to irritation of the digestive tract. For example, the fact that healthy subjects do not perceive even the most intense sigmoid contractions during stress and following food intake, in IBS patients such prolonged high intensity sigmoid motor activity may result in sensitization of the colon, manifesting as pain and discomfort. Similarly, the fact that certain individuals with documented enteric infections and associated colonic inflammation will develop a prolonged IBS-like syndrome, while the majority of people will become asymptomatic once the infection is cleared, is consistent with a model by which a compromised ability of the nervous system to counter regulate sensitization of sensory nerve pathways during inflammation. Several studies are underway at UCLA to identify the cause for this abnormality, and to identify the regions and receptors within the nervous system that could be involved.

These findings not only have significant implications for our understanding of mechanisms underlying IBS symptom generation, but they also form the basis for a series of new studies testing the efficacy of several promising new drug therapies for IBS. Without having to evaluate symptom responses in hundreds of patients, the colorectal sensitization study makes it possible to determine quickly if a newly developed IBS drug can prevent the development of sensitization.

Should you be interested in more information about these exciting research studies, or should you consider to participate, please call at (310) 268-3432.