One of the commonest problems presenting in gastrointestinal practice is the patient with chronic or recurrent epigastric pain or discomfort where routine diagnostic testing has failed to identify a definite structural cause for the symptoms.1 Empiric antisecretory and prokinetic agents remain the mainstay of treatment for patients with a diagnosis of functional (or non-ulcer) dyspepsia, but only a minority experience complete symptom relief with these agents.2 Rational medical treatment for patients with functional dyspepsia remains an elusive goal partly because functional dyspepsia seems to comprise a heterogeneous syndrome.1 For example, approximately 50% of patients have Helicobacter pylori gastritis, up to 50% have delayed gastric emptying and perhaps 50% of patients have visceral hypersensitivity to mechanical distension of the stomach or duodenum1; clearly, these pathophysiological subsets overlap, although visceral hypersensitivity is currently postulated to be of central importance.3 ,4In addition to being sensitive to mechanical distension, patients with functional dyspepsia as a group may be more sensitive to other stimuli such as pentagastrin injection or intragastric infusions of acid, saline and pancreatic or biliary secretions.1 Although there is heightened visceral nocioception, somatic pain sensation is normal3 suggesting that the sensory defect is localised to the gastrointestinal tract, although these observations may also be explained by aberrant processing of signals at the spinal cord or central nervous system level.

Patients with the irritable bowel syndrome (IBS) have well documented visceral hypersensitivity to mechanical distension of the colon and small bowel.4 ,5 Furthermore, rectal hypersensitivity seems to be inducible in patients with IBS following mechanical stimulation of …