Incomplete relaxation of the lower oesophageal sphincter (LOS) following deglutition and absence of oesophageal peristalsis, in most cases accompanied by an increased resting tone of the LOS, are the manometric hallmarks of idiopathic achalasia.^1–3 The net result of these motor abnormalities is stasis of saliva and food in the oesophagus leading to the typical symptoms of achalasia: dysphagia for both solids and liquids, regurgitation of undigested food, respiratory complications (nocturnal cough and aspiration), chest pain, and weight loss.⁴ The treatment of this relatively rare disorder (incidence of approximately 1/100 000 per year) mainly aims at reducing the resistance to flow at the oesophagogastric junction. This can be achieved by reduction of LOS pressure by pharmacological drugs (nitrates, Ca²⁺ channel blockers, botulinum toxin), by forceful dilation using endoscopic techniques, or by surgical myotomy.⁵ With the introduction of minimally invasive techniques, the surgical approach in particular has recently gained a significant increase in interest and has become the method of choice in several centres.⁶ Large prospective randomised studies comparing the two most widely used therapies—that is, endoscopic pneumatic dilation and laparoscopic Heller myotomy combined with an antireflux procedure—are required to determine the most optimal treatment for patients with achalasia.

Although achalasia is the best characterised oesophageal motor disorder, its pathogenesis is still incompletely understood.^7,8 Histological examination reveals a significant decrease in the number of myenteric neurones, especially inhibitory nitric oxide releasing neurones, in the distal oesophagus and at the level of the LOS,⁹ but the underlying mechanism leading to neuronal loss remains unknown. Familial, neurodegenerative, genetic, …