Auerbach plexus
Summary
The Auerbach (myenteric) plexus is the enteric nervous system plexus located between the inner circular and outer longitudinal layers of the muscularis externa. It primarily controls GI motility (peristalsis), whereas the Meissner (submucosal) plexus controls secretion and blood flow. Its absence in the distal bowel causes Hirschsprung disease (aganglionic megacolon) and its destruction in the esophagus causes achalasia.
Detail
**Location:** Between the inner circular and outer longitudinal smooth muscle layers of the muscularis externa, extending along the entire GI tract from esophagus to anus. (Meissner/submucosal plexus lies in the submucosa and is found mainly in the small and large intestine.)
**Function:** Part of the enteric nervous system ("little brain of the gut"). It regulates motility: coordinates peristalsis, segmentation, and tone of the gut wall. Excitatory neurons release ACh and substance P (contraction); inhibitory neurons release VIP and NO (relaxation, e.g., lower esophageal sphincter and internal anal sphincter). It receives parasympathetic (vagus, pelvic splanchnic) input, which is stimulatory, and sympathetic input, which is inhibitory. It can also function independently of the CNS.
**Embryology:** Derived from neural crest cells that migrate in a craniocaudal direction (vagal neural crest) to colonize the gut. RET (receptor tyrosine kinase) signaling is essential for this migration.
**Clinical correlates:** - **Hirschsprung disease:** Failure of neural crest migration leads to absence of ganglion cells in both Auerbach and Meissner plexuses, starting at the internal anal sphincter and extending proximally for a variable distance (rectosigmoid most commonly). The aganglionic segment stays tonically contracted, so the proximal bowel dilates (megacolon). Presents with failure to pass meconium in the first 48 h, chronic constipation, and a "squirt sign" on rectal exam. Associated with RET mutations and Down syndrome. Diagnosis is by rectal suction biopsy showing absent ganglion cells and hypertrophied nerve trunks, with increased acetylcholinesterase staining. Treatment is surgical resection of the aganglionic segment. - **Achalasia:** Degeneration of inhibitory (NO/VIP) myenteric neurons in the esophagus leads to failure of LES relaxation and absent peristalsis. Presents with dysphagia to both solids and liquids. Barium swallow shows a "bird's beak." Manometry is the gold standard (incomplete LES relaxation, high LES pressure, aperistalsis). Secondary achalasia occurs in Chagas disease (*Trypanosoma cruzi* destroys the myenteric plexus), which causes megaesophagus and megacolon. Achalasia carries an increased risk of squamous cell carcinoma of the esophagus. - **Other:** Diabetic gastroparesis and autonomic neuropathy, and paraneoplastic (anti-Hu) dysmotility in small cell lung cancer, can also involve myenteric dysfunction.
**High-yield mnemonic:** Auerbach = "Between" the muscle layers = motility. Meissner = "Mucosa side" (submucosa) = secretion.
**Board pearl:** Both plexuses are absent in Hirschsprung disease, but the clinical consequence (obstruction) arises mainly from loss of inhibitory myenteric innervation.
Sources
- First Aid for the USMLE Step 1 (Gastrointestinal: Anatomy/Embryology)
- Robbins & Cotran Pathologic Basis of Disease (Hirschsprung disease, achalasia)
- Costanzo Physiology (GI regulation, enteric nervous system)
- Sketchy Medical / Pathoma (GI motility disorders)
- Guyton and Hall Textbook of Medical Physiology (Enteric Nervous System)
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