**3. Pathophysiology of functional dyspepsia**

Abnormal gastric motility and visceral hypersensitivity are thought to be the phenomena that are most closely related to the manifestation of FD symptoms.

Postprandial gastric motility may involve two possible sites: 1. the proximal stomach (fundus) exhibiting a disordered accommodation reflex after food ingestion, and/or 2. the antrum having abnormal gastric motor contractility. Proximal gastric distention, in fact, correlates very well with dyspeptic symptoms [2, 7]. The accommodation reflex is regarded as an appropriate response by which the stomach provides a reservoir facility for ingested food. In FD, this reflex can be impaired, leading to early satiety [8]. Such impairment occurs in 40 to 50% of FD patients [9]. In addition to impaired accommodation, delayed gastric emptying is also thought to contribute to the pathogenesis of FD. Food that is delayed in leaving the stomach provides the sensation that the stomach feels heavy. Some reports have suggested that delayed gastric emptying may be seen in up to 40% of FD patients [10].

Visceral hypersensitivity is also an important factor contributing to the feeling of dyspepsia. When a balloon is distended in the stomach of an FD patient, the threshold at which pain is perceived is significantly lower in FD patients compared to normal controls [11]. Such gastric hypersensitivity relates to symptoms of postprandial pain, belching and weight loss.
