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Esophageal peristalsis consists of initial inhibition followed by excitation, for which there may be parallel pathways from the central pattern generator, traveling via the vagus nerve to communicate with the inhibitory and excitatory neurons of the myenteric plexus. Primary and secondary esophageal peristalsis are associated with concurrent contraction and relaxation of the circular and longitudinal muscle layers. The longitudinal muscle contraction in the contracted segment exerts mechanical stretch on the segment ahead of it, which likely activates the mechanosensitive inhibitory motor neurons in the myenteric plexus to induce descending relaxation, a peripheral mechanism of the peristaltic reflex. In achalasia esophagus, there is inflammation and fibrosis in the muscularis propria and myenteric plexus, resulting in loss of inhibitory nerves in the myenteric plexus. It also results in replacement of muscle with fibrous tissue in the muscularis propria of the lower esophageal sphincter (LES), impaired LES relaxation, and low distensibility of the esophagogastric junction in achalasia esophagus. The esophageal hiatus contains a pad of fat that is replaced with fibrosis in patients with achalasia esophagus. Whether hiatal fibrosis leads to impaired LES relaxation\/low distensibility of the esophagogastric junction and changes in esophageal peristalsis are secondary to obstruction requires further study. Esophageal hypersensitivity is currently the favored mechanism of \u201cangina-like\u201d esophageal pain and refractory heartburn. 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