Abstract
Growing evidence suggests that symptoms in patients with irritable bowel syndrome (IBS) may be due to a visceral sensory dysfunction. Specifically, it has been shown that patients with IBS have hypersensitive responses to distension of the rectum, whereas their tolerance to somatic stimuli is normal or even increased. Furthermore, patients with IBS have hypersensitivity of the small bowel, which selectively affects mechanosensitive afferents, with normal perception of electrical stimulation of the gut. Sensory dysfunctions may also be associated with altered reflex activity, which may contribute to the clinical symptoms. Normally, a series of mechanisms at different strata of the nervous system modulate visceral afferent input and determine conscious perception. Conceivably, a dysfunction of these regulatory mechanisms may alter sensitivity in clinical conditions. To date, neither the origin nor the clinical significance of visceral hyperalgesia has been elucidated. However, it seems likely that the sensory and reflex dysfunctions of the gut in IBS may combine to different degrees, and their interaction may explain the clinical pleomorphism of the syndrome.