The esophageal musculature is unique in its transition from voluntary striated muscle in the upper esophagus to involuntary smooth muscle in the lower esophagus. Primary peristalsis is triggered by swallowing; secondary peristalsis (autonomous esophageal reflex) clears residual food without conscious swallowing. Achalasia is the paradigm of esophageal motor disorder, absent peristalsis with failed LES relaxation from myenteric plexus degeneration.
| Location | Outer muscle coat of the oesophagus from the pharynx to the stomach |
|---|---|
| Parts |
|
| Nerve Supply | Vagus nerve via the recurrent laryngeal nerves (upper striated part); Vagus nerve via the oesophageal plexus (smooth muscle); Sympathetic trunks |
| Blood Supply | Inferior thyroid artery (neck); Oesophageal branches of the thoracic aorta; Left gastric artery (abdominal part) |
Moves swallowed food to the stomach by waves of peristalsis and keeps the sphincters closed between swallows to prevent reflux.
Esophageal motility disorders are classified by high-resolution manometry: achalasia (absent peristalsis, elevated LES pressure), distal esophageal spasm, hypercontractile esophagus (jackhammer), and ineffective esophageal motility. Achalasia type I (absent peristalsis, dilated esophagus) vs type II (panesophageal pressurisation) vs type III (spastic) guides treatment: pneumatic dilation, Heller myotomy (divides the lower esophageal smooth muscle circular layer), or POEM (per-oral endoscopic myotomy through the submucosal tunnel). The striated muscle of the upper esophagus is innervated by the RLN, explaining the dysphagia in recurrent laryngeal nerve palsy.
Loss of inhibitory myenteric plexus neurons in the distal esophageal smooth muscle produces absent peristalsis and failed LES relaxation, causing progressive dysphagia and esophageal dilation; POEM (peroral endoscopic myotomy) creates a 10-15 cm myotomy of the circular muscle layer through a submucosal tunnel providing durable symptom relief comparable to surgical Heller myotomy.
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