Secondary oesophageal peristalsis in patients with non-obstructive dysphagia.

Secondary peristalsis was investigated in 30 patients with non-obstructive dysphagia and 20 age matched controls. Oesophageal motility was recorded at 3 cm intervals along the oesophageal body. Primary peristalsis was tested with 5 ml water swallows. Secondary peristalsis was stimulated with 10 ml boluses of air and water injected in the mid-oesophagus and by distensions (5 seconds duration) with a 3 cm balloon at the same level. Primary peristalsis was normal in 19 of the 20 control subjects and in nine of the 30 patients with dysphagia; 11 patients had diffuse spasm and 10 had non-specific abnormalities of primary peristalsis. Secondary peristalsis was triggered significantly less frequently by air and water distension in dysphagia patients (median success rate of 10% for the air boluses and 0% for the water boluses) than in control subjects (50% and 30% respectively, p < 0.005), and was abnormal in six of nine patients with normal primary peristalsis, nine of 11 patients with diffuse spasm and eight of 10 patients with non-specific motor abnormalities. The median frequency of balloon induced secondary peristalsis, however, was not significantly different in the two groups (0% controls, 40% non-obstructive dysphagia, p = 0.22). For each stimulus, 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 secondary peristalsis triggered by the water boluses and the balloon was greater in the patients with dysphagia (p = 0.03) than in normal subjects, while the amplitude of the secondary peristaltic responses triggered by the air boluses was similar in the two groups. Secondary peristaltic velocity was also similar in normal subjects and patients with non-obstructive dysphagia. Patients with non-obstructive dysphagia show a noticeable defect in the triggering of secondary peristalsis which may make an important contribution to the delayed oesophageal bolus transit and dysphagia seen in this condition.