Atkinson M, Ogilvie A L, Robertson C S, Smart H L
Department of Surgery, University of Nottingham, University Hospital, Queen's Medical Centre.
Q J Med. 1987 Apr;63(240):297-303.
Autonomic nervous function in achalasia of the cardia was assessed by measuring the response of the lower oesophageal sphincter to abdominal compression, the gastric secretory response to insulin-induced hypoglycaemia and the pulse rate variability with deep respiration. Twenty-eight patients with symptomatic achalasia and 24 age and sex-matched control subjects were studied. Rise in intra-abdominal pressure normally causes a rise in lower oesophageal pressure through a vagally-mediated mechanism. Before treatment this response was unimpaired in eight of 10 patients with achalasia. A sub-normal response was found in eight of 10 patients who had previously had pneumatic dilatation of the cardia and in three of four who had had a cardiomyotomy. These abnormalities reflected the effect of treatment in disrupting the sphincter rather than impairment of its innervation. The gastric acid secretory response to insulin-induced hypoglycaemia, expressed as a ratio of that to pentagastrin, was normal in each of the nine patients studied. Pulse rate variability with deep respiration, a test of cardiac vagal function, was normal in 22 of 25 patients studied. It is concluded that in achalasia the vagal trunks appear functionally intact and that the myenteric plexus lesion rarely affects the responsiveness of the lower oesophageal sphincter to increase in intra-abdominal pressure.
