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Causes of achalasia of the cardia
Last reviewed: 06.07.2025
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The causes of achalasia of the cardia have not yet been clarified.
In the etiology of achalasia of the cardia, two factors are currently of primary interest:
- Histologically, degenerative changes of the intramural nerve plexuses of the esophagus are almost always found. (Similar changes have been described in Chagas disease and therefore trypanosomiasis has been recognized as one of the possible causes of megaesophagus, as in megacolon.) But the question remains whether these changes are not consequences of, for example, pressure necrosis due to congestion in the dilated esophagus.
- Psychogenesis is evident in the majority of patients.
Psycho-emotional stressful situations and the consumption of very cold food play a certain role.
In the initial stages of achalasia of the cardia, no organic changes are detected during esophagoscopy and in biopsies of the mucous membrane. However, a number of studies devoted to a detailed histological study of the esophageal wall have established persistent changes in the intramural nervous apparatus. At present, it has been established that this disorder is based on a deficiency of a specific neurotransmitter - nitrogen oxide (NO), formed from L-arginine with the participation of the enzyme NO synthetase. The effects of NO are realized through cyclic guanosine monophosphate. NO leads to relaxation of the smooth muscle cell. In recent years, a significant decrease in the content of the enzyme NO synthetase in the tissue of the lower esophageal sphincter has been revealed in patients with achalasia of the cardia. This leads to a decrease in NO formation and a loss of the ability to relax the lower esophageal sphincter. As the disease progresses, changes in the muscle fibers of the esophagus are observed (proliferation of collagen fibers between myofiobrils). Electron microscopy also revealed degenerative changes in the branches of the vagus nerve.
Probably, disturbances of the innervation of the esophagus are the main mechanism of development of achalasia of the cardia. Along with the disturbance of relaxation of the lower esophageal sphincter, the contractility of the thoracic esophagus also decreases due to the presence of an obstacle to the passage of food in the form of a non-relaxing lower esophageal sphincter.
[ Pathogenesis of achalasia of the cardia
The pathogenesis of achalasia of the cardia is associated with congenital or acquired damage to the intramural nerve plexus of the esophagus (intermuscular - Auerbach's) with a decrease in the number of ganglion cells. As a result, the consistent peristaltic activity of the esophageal wall is disrupted and there is no relaxation of the lower esophageal sphincter in response to swallowing (which served as the basis for introducing the term "achalasia": Greek a - absence, chalasis- relaxation). Most likely, this is due to a deficiency of inhibitory neurotransmitters, primarily nitric oxide (N0). Thus, an obstacle in the form of an unrelaxed sphincter appears on the path of the food bolus and the entry of food into the stomach is difficult: for example, it can only occur with additional filling of the esophagus with liquid, when the mass of its column exerts a mechanical effect on the cardiac sphincter.