Mechanism of esophageal peristalsis or sequential contractions of the skeletal and smooth muscle esophagus resides at multiple levels, i.e., brain stem (central pattern generator), neurons within the wall of the esophagus (myenteric plexus) and smooth muscle (myogenic). Esophageal peristalsis consists of initial inhibition followed by excitation, for which there may be parallel pathways from the central program generator, travelling 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 activate the mechanosensitive inhibitory motor neurons in the myenteric plexus to induce descending relaxation, a peripheral mechanism of the peristaltic reflex. In the achalasia esophagus, there is inflammation and fibrosis in the muscularis propria and myenteric plexus, resulting in loss of inhibitory nerves in the myenteric plexus. The above 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 which 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 “angina like” esophageal pain and refractory heartburn. Spastic or long-duration contractions of the longitudinal muscle of esophagus may also play a role in the genesis of non-cardiac esophageal pain and heartburn sensation.
Mittal et al. (Thu,) studied this question.