Motility, heartburn and dyspepsia
Disordered motility has been considered fundamental to the pathophysiology of gastro-oesophageal reflux disease and a number of dyspeptic syndromes. Motor activity is certainly essential for the homeostasis of the oesophagus and stomach - in the oesophagus, the lower oesophageal sphincter and peristalsis are fundamental components of the 'normal' anti-reflux defence mechanism, whereas, in the stomach, contractile activity regulates the orderly emptying of the various components of a meal. Recent. studies have clarified considerably the role of the lower oesophageal sphincter in permitting reflux to occur under both physiological and pathological situations, and transient relaxation of the lower oesophageal sphincter is now regarded as the most important mechanism of reflux. Interest has also been renewed in the role of hiatus hernia in the pathogenesis of reflux disease. By moving tile lower oesophageal sphincter into the thorax, a hiatus hernia deprives this sphincter of the beneficial effects of intra-abdominal pressure and crural augmentation. Altered anatomical relationships also predispose the patient with a non-reducing hiatus hernia to impaired clearance of acid, thus exacerbating reflux. Relationships between disordered peristalsis and reflux are complex. Primary disorders of peristalsis, such as scleroderma, are associated with severe and often complicated reflux disease. It is also evident that reflux may itself result in impaired peristalsis, particularly in the distal oesophagus. Whether aggressive treatment of reflux disease by either medical or surgical means can restore peristaltic function remains uncertain. The importance of co-ordinated function of the antrum, pylorus and duodenum in the regulation of gastric emptying is being increasingly recognized. Foregut motor dysfunction is implicated in dyspepsia. Abnormalities in patients with dyspepsia include gastroparesis, antral hypomotility, gastric dysrhythmias, duodenal dysmotility, and duodeno-gastric reflux. The true prevalence of these disorders is uncertain, and the reported relationship between these abnormalities and symptoms has often been inconsistent. The specificity of the abnormalities for dyspepsia is also open to question. In many instances, it remains unclear whether the motor abnormality is truly primary or rather an epi-phenomenon. It seems reasonable to conclude that while considerable advances have been made in our understanding of both foregut motor physiology and the role of motor dysfunction in patients with reflux disease, the role of dysmotility in dyspeptic patients remains uncertain.