Gastric and autonomic responses to stress in functional dyspepsia.
It has been suggested that functional dyspepsia might arise from the effect of stress on upper gut motility in susceptible individuals. The aim of this study was to evaluate posticibal antral motility in the presence and absence of sustained experimental stress by means of a transcutaneous electrical nerve stimulator. Two groups of patients could be recognized from these studies: first, those with postcibal antral hypomotility that was not changed during stress; and second, patients with normal postcibal motility which was normally suppressed by stress. Experimental stress significantly increased skin conductance and plasma beta-endorphin levels. However, in these two groups, there were no differences in clinical presentation and personality traits or in autonomic and humoral variables either before or during stress. Stepwise discriminant analysis of the autonomic or humoral responses to stress was unable to predict the different postcibal antral motor responses among the subsets of patients with functional dyspepsia. These data suggest that there are two subtypes of antral motility in functional dyspepsia: disordered gastric function under basal conditions resulting in antral hypomotility, and normal basal antral motility and autonomic and gastric motor responses to stress. In the latter subgroup, the cause of symptoms is unclear, but it appears not to be a motility disorder.
D000328:Adult; D001341:Autonomic Nervous System / Q000503:physiopathology*; D004415:Dyspepsia / Q000209:etiology / Q000503:physiopathology*; D004723:Endorphins / Q000097:blood; D005260:Female; D005769:Gastrointestinal Motility; D006801:Humans; D008297:Male; D008365:Manometry; D008875:Middle Aged; D013312:Stress, Physiological / Q000150:complications / Q000503:physiopathology*; D004561:Transcutaneous Electric Nerve Stimulation; D001615:beta-Endorphin
D004723:Endorphins; D001615:beta-Endorphin