SECONDARY ESOPHAGEAL PERISTALSIS IN PATIENTS WITH NONOBSTRUCTIVE DYSPHAGIA

Secondary peristalsis was investigated in 30 patients with non-obstruc tive dysphagia and 20 age matched controls. Oesophageal motility was r ecorded at 3 cm intervals along the oesophageal body. Primary peristal sis was tested with 5 mi water swallows. Secondary peristalsis was sti mulated with 10 mi boluses of air and water injected in the mid-oesoph agus and by distensions (5 seconds duration) with a 3 cm balloon at th e same level. Primary peristalsis was normal in 19 of the 20 control s ubjects and in nine of the 30 patients with dysphagia; 11 patients had diffuse spasm and 10 had non-specific abnormalities of primary perist alsis. Secondary peristalsis was triggered significantly less frequent ly by air and water distension in dysphagia patients (median success r ate of 10% for the air boluses and 0% for the water boluses) than in c ontrol subjects (50% and 30% respectively, p<0.005), and was abnormal in six of nine patients with normal primary peristalsis, nine of 11 pa tients with diffuse spasm and eight of 10 patients with non-specific m otor abnormalities. The median frequency of balloon induced secondary peristalsis, however, was not significantly different in the two group s (0% controls, 40% nonobstructive dysphagia, p=0.22). For each stimul us, there were no significant differences in the response rate in the three subgroups of patients. The major pattern of failure of secondary peristalsis in response to the air and water boluses was the complete absence of any oesophageal response. The amplitude of complete second ary peristalsis triggered by the water boluses and the balloon was gre ater in the patients with dysphagia (p=0.03) than in normal subjects, while the amplitude of the secondary peristaltic responses triggered b y the air boluses was similar in the two groups. Secondary peristaltic velocity was also similar in normal subjects and patients with nonobs tructive dysphagia. Patients with non-obstructive dysphagia show a not iceable defect in the triggering of secondary peristalsis which may ma ke an important contribution to the delayed oesophageal bolus transit and dysphagia seen in this condition.