The etiology of this disease is still unknown. It is generally believed to be a neurogenic disease. The lesion is seen as a reduction or even complete absence of ganglion cells in the vagus nerve, its dorsal nucleus and the intermuscular plexus in the esophageal wall. This shows that the innervation of the vagus nerve only ends at the upper part of the esophagus, while the function of the lower part of the esophagus is innervated by the intermuscular plexus of the esophageal wall. The neurotransmitters are purine nucleotides and vasoactive intestinal peptide (VIP). 28.6 mol/g) VIP has the effect of inhibiting the tension of LES in resting state, and the significant decrease of VIP in LES causes the loss of inhibition and increase of tension of LES, which causes achalasia. Some chronic animal models of esophageal achalasia are produced by bilateral cervical vagotomy or by toxin destruction of ganglion cells in the dorsal nucleus of the vagus nerve or the intermuscular plexus of the esophageal wall. In some cases of esophageal cardia, dysphagia often occurs suddenly and is associated with degenerative changes in the vagus nerve and myenteric plexus of the esophageal wall, so it has been suggested that the disease may be caused by a neurotoxic virus, but this has not been confirmed.