Abstract
Background & aim: Functional dyspepsia was reclassified into meal-induced dyspepsia as postprandial distress syndrome (PDS) and epigastric pain dyspepsia as epigastric distress syndrome (PDS) in Rome III. Gastric hypersensitivity has been reported to be one of the pathogenetic mechanism of functional dyspepsia, however, it is not known whether subcategories of PDS and EPS demonstrate differencies in gastric hypersensitivity. Therefore we evaluated gastric sensation by the cerebral evoked potential and the water load test in functional dyspepsia patients. Methods: Sixteen FD subjects, fulfilling Rome III criteria for functional dyspepsia, were recruited by ad posters, and were served as functional dyspepsia non-consulters (FD-NC), and 16 healthy subjects (HS) without any dyspeptic symptoms as control participated. All subjects had gastrointestinal endoscopy, urea breath test to rule out any possible pathogenesis, and Gastrointestinal Symptoms Rating-Scale questionnaire (GSRS) for quantitative symptomatic evaluation. Study A): Visceral sensation and evoked cerebral potentials through electrical stimulation of esophageal mucosa at the level of 37cm from nostril were evaluated in 16 subjects with FD-NC and 16HSs. Study B): Water load test was performed to evaluate tolerable volume and subjective symptoms in 16 subjects with FD-NC (8 PDS, 8 EPS) and 15 HSs. Water load test was performed with rapid water drink within 5 minutes at room temperature, and subjective symptoms were evaluated in ordinate scale up to 30 minutes. Results: All subjects had no organic disease in upper GI tract nor Helicobacter pylori infection. FD-NCs showed significantly higher GSRS score than that in HSs. A): FD-NCs had lower pain threshold to the esophageal electrical stimulation than HSs (p=0.076). Latency of N2 and P2 of evoked potential were significantly shorter in FD-NCs than HSs (p<0.05). B): Consumed water volume in WLT were not remarkably different between HSs (mean 853ml), PDS subjects (863ml) and EPS subjects (800ml). However symptom scores of gastric discomfort and fullness were higher and lasted longer in PDS subjects than that in HSs. In EPS subjects, epigastric pain was not induced by WLT. Conclusions: FD-NCs small in intensity but significant symptoms in GSRS scores. Such changes might be correlated with altered brain processing for visceral perception. Subjects with PDS demonstrated significant in intensity and longer duration of symptoms provoked by WLT, which suggest that gastric hypersensitivity and/or impaired gastric accommodation are major candidates for pathogenesis of dyspeptic symptoms in PDS. As WLT did not induce epigastric pain symptom in subjects with EPS, which suggest that mechanical gastric stimulation is not the main factor for the pathogenesis of symptoms of EPS.
