Functional Dyspepsia: Motor Abnormalities, Sensory Dysfunction
Functional Dyspepsia: Motor Abnormalities, Sensory Dysfunction
Functional dyspepsia is a common condition, but as yet, the underlying etiology is unclear. In this article, upper gastrointestinal motor and sensory physiology are reviewed and the current evidence for motor and/or sensory functional abnormalities causing dyspeptic symptoms is presented. The complex interrelationship between abnormal motor activity and sensation is explored, as well as the potential roles for autonomic dysfunction and psychological state in modulating gastrointestinal sensation and motor function. Finally, based on clinical trial evidence, a treatment pathway for functional dyspepsia is suggested.
Dyspepsia is defined as episodic or persistent symptoms of abdominal pain or discomfort referable to the upper gastrointestinal tract. However, actual mucosal lesions, such as erosions or ulcers, are found in as few as 20% of dyspeptic patients. In patients without mucosal changes, the dyspepsia is thought to be secondary to a disorder of function, rather than structure, hence the name "functional dyspepsia" (FD). Typical symptoms of FD include postprandial epigastric pain, early satiety, belching, bloating, and nausea. The current Rome II criteria for FD are symptoms for at least a 12-wk duration, which need not be consecutive, within the preceding year of (a) persistent or recurrent dyspepsia, (b) no evidence of organic disease (including at upper gastrointestinal endoscopy) that is likely to explain the symptoms, (c) 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).
Symptoms in functional dyspepsia may fit into the descriptive patterns of reflux-like dyspepsia, ulcer-like dyspepsia, and dysmotility-like and idiopathic dyspepsia, as shown in Table 1 , but these descriptive labels do not indicate pathophysiological mechanisms and as such are not very useful in practice. The subgroup "reflux-like dyspepsia" is particularly controversial, due to the overlap with endoscopy-negative gastroesophageal reflux, NERD (nonerosive or negative-endoscopy reflux disease). Despite much ongoing research in FD, the causes of the symptom production remain unclear. The role of Helicobacter pylori in symptom production in the absence of mucosal lesions is controversial and the symptomatic benefit of treating H. pylori is disputed. Nevertheless, the Second Maastricht Consensus Report recommends H. pylori eradication in patients with functional dyspepsia in whom no other cause of symptoms has been identified.
This article will review the two principal abnormalities that have been described and studied in FD, namely upper gut motor abnormalities and visceral sensory dysfunction. In both cases, a brief overview of normal upper gut physiology will be followed by the abnormalities in function that have been described to date. Finally, the evidence for success of various treatment modalities in FD will be reviewed and a possible treatment pathway suggested.
Functional dyspepsia is a common condition, but as yet, the underlying etiology is unclear. In this article, upper gastrointestinal motor and sensory physiology are reviewed and the current evidence for motor and/or sensory functional abnormalities causing dyspeptic symptoms is presented. The complex interrelationship between abnormal motor activity and sensation is explored, as well as the potential roles for autonomic dysfunction and psychological state in modulating gastrointestinal sensation and motor function. Finally, based on clinical trial evidence, a treatment pathway for functional dyspepsia is suggested.
Dyspepsia is defined as episodic or persistent symptoms of abdominal pain or discomfort referable to the upper gastrointestinal tract. However, actual mucosal lesions, such as erosions or ulcers, are found in as few as 20% of dyspeptic patients. In patients without mucosal changes, the dyspepsia is thought to be secondary to a disorder of function, rather than structure, hence the name "functional dyspepsia" (FD). Typical symptoms of FD include postprandial epigastric pain, early satiety, belching, bloating, and nausea. The current Rome II criteria for FD are symptoms for at least a 12-wk duration, which need not be consecutive, within the preceding year of (a) persistent or recurrent dyspepsia, (b) no evidence of organic disease (including at upper gastrointestinal endoscopy) that is likely to explain the symptoms, (c) 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).
Symptoms in functional dyspepsia may fit into the descriptive patterns of reflux-like dyspepsia, ulcer-like dyspepsia, and dysmotility-like and idiopathic dyspepsia, as shown in Table 1 , but these descriptive labels do not indicate pathophysiological mechanisms and as such are not very useful in practice. The subgroup "reflux-like dyspepsia" is particularly controversial, due to the overlap with endoscopy-negative gastroesophageal reflux, NERD (nonerosive or negative-endoscopy reflux disease). Despite much ongoing research in FD, the causes of the symptom production remain unclear. The role of Helicobacter pylori in symptom production in the absence of mucosal lesions is controversial and the symptomatic benefit of treating H. pylori is disputed. Nevertheless, the Second Maastricht Consensus Report recommends H. pylori eradication in patients with functional dyspepsia in whom no other cause of symptoms has been identified.
This article will review the two principal abnormalities that have been described and studied in FD, namely upper gut motor abnormalities and visceral sensory dysfunction. In both cases, a brief overview of normal upper gut physiology will be followed by the abnormalities in function that have been described to date. Finally, the evidence for success of various treatment modalities in FD will be reviewed and a possible treatment pathway suggested.
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