Bothersome postprandial fullness
Early satiation
Epigastric pain
Epigastric burning
No evidence of structural disease (including at upper gastrointestinal endoscopy) that is likely to explain the symptoms; and
No evidence that dyspepsia is exclusively relieved by defecation or associated with the onset of a change in stool frequency or stool form (i.e. not irritable bowel syndrome)
Dyspepsia subgroups
Ulcer-like dyspepsia: pain centered in the upper abdomen is the predominant (most bothersome) symptom
Dysmotility-like dyspepsia: an unpleasant or troublesome nonpainful sensation (discomfort) centered in the upper abdomen is the predominant symptom; characterized by or associated with fullness, early satiety, bloating, or nausea
Unspecified dyspepsia: symptoms do not fulfill the criteria for ulcer-like or dysmotility-like dyspepsia
A diagnosis of functional dyspepsia can be further categorized into several disorders: altered gastric motor function, abnormal gastrointestinal sensory function, and infection or inflammation. In addition, psychological factors must be considered in order to understand the severity of symptoms and impact on quality of life.
Disturbed gastric motor function
Approximately 40% of patients with functional dyspepsia exhibit postprandial antral hypomotility or delayed gastric emptying; however, symptoms and delays in gastric emptying are weakly linked at best. Some patients with functional dyspepsia have an impaired gastric fundus accommodation reflex, which may underlie postprandial discomfort or fullness. Additional rhythm disturbances of the gastric slow wave have been reported with functional dyspepsia.
Disturbed gastric sensory function
Many patients with functional dyspepsia exhibit reduced tolerance to balloon distension of the stomach and duodenum, which is not accompanied by changes in wall compliance. This finding suggests that functional dyspepsia in these individuals stems from exaggerated responsiveness of visceral afferent nerve pathways. The pathogenesis of visceral hypersensitivity in functional dyspepsia is poorly understood. The prevalence of back pain and headache in functional dyspepsia suggests possible abnormalities in cerebral cortical processing of pain information.
Gastric acid, duodenitis, and postinfectious dyspepsia
Acid secretion is normal in most patients with functional dyspepsia. Histological duodenitis is present in 14–83% of individuals with functional dyspepsia and many of these ultimately develop duodenal ulcers. However, erosive duodenitis is more appropriately considered within the spectrum of peptic ulcer disease, rather than functional dyspepsia. Helicobacter pylori infection is found in 40% of patients with functional dyspepsia but similar rates are found in matched asymptomatic populations. Furthermore, eradication of H. pylori clearly alleviates symptoms in only a subset of patients with functional dyspepsia.
Finally, a small subgroup of patients with functional dyspepsia develops symptoms after a clearly defined acute attack of infectious gastroenteritis.
Psychological factors
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