The pathogenesis of functional dyspepsia remains poorly understood. There i
s increasing evidence pointing to a predominant role of gastroduodenal visc
eral hypersensitivity in the pathogenesis, where patients have abnormally r
educed gastric and small intestinal sensory thresholds. Motor abnormalities
observed in subgroups of patients include delayed gastric emptying, antral
hypomotility, gastric dysrhythmias, abnormal gastrointestinal reflexes and
small intestinal dysmotility, but these may be secondary pheno nena. The c
entral nervous system modifies peripheral visceral afferent pathways and, h
ente, psychological factors may possibly alter symptom status. Other putati
ve mechanisms include Helicobacter pylori gastritis and gastric acid hypers
ecretion or sensitivity, but the role of these remain controversial.