Gastroparesis: Autonomic nervous system and vagus nerve (Part Six)

Gastric emptying is facilitated by neurologic signals through the autonomic nervous system.  The autonomic nervous system controls many of the involuntary functions of the body, such as digestion.  The autonomic nervous system has two components: the parasympathetic nervous system, which manages activities pertaining to digestion, among other things; and the sympathetic nervous system, which mediates the fight-or-flight response.  Normally, upper GI function receives parasympathetic neurologic signals from the vagus nerve.  Sympathetic control is maintained by nerves originating at spinal T5-T10.

The vagus nerve sends signals the enteric neurons, nerve cells in the GI tract, to increase gastric motility.  The vagus nerve does not directly stimulate smooth muscle in the GI tract.  Signals from the vagus nerve help to relax the stomach to allow room for food, contract to move the food to the pyloric sphincter, and relax the pyloric sphincter to pass stomach contents to the small intestine.  These actions occur by coordinating the signals among the enteric neurons (GI nerve cells), interstitial cells of Cajal (which control smooth muscle contraction) and smooth muscle cells.

Normally, food passes through the esophagus and into the portion of the stomach closest to the esophagus.  The pressure of the food in this area causes other parts of the stomach to relax and allow food.  The stomach then contracts to break up food and push it towards the small intestine.

At any part of this process, dysfunction of the autonomic nervous system can inhibit proper digestion and gastric emptying.  Gastroparesis is a frequent complication of conditions affecting autonomic function, like orthostatic intolerance.  In some cases, treatment of the orthostatic intolerance can improve gastroparesis symptoms.

Vagotomy, an outmoded surgical treatment for ulcers that severs the vagus nerve, prevents the stomach from being able to relax to accept food.  It can trigger rapid movement of liquids through the stomach, while not allowing solids to be emptied.   Unintentional damage to the vagus nerve can be occur for a number of other reasons, including surgery or persistent high blood sugar, as in some diabetics.

The tone of the stomach and how much food can fit is controlled by enteric nerve cells that release nitric oxide (NO.)  NO keeps the stomach relaxed.  Interfering with cholinergic signaling can also keep the stomach relaxed, to fit more food.  Medications like opiates and anticholinergics have this effect.

In GP patients, stomach biopsies show that the enteric neurons are not shaped correctly. There are far fewer interstitial cells of Cajal than normal, and those that remain look damaged.  There are less nerve fibers than normal.  83% of GP patients have abnormalities in their stomach biopsies.

References:

Sarosiek, Irene, et al. Surgical approaches to treatment of gastroparesis: Gastric electrical stimulation, pyloroplasty, total gastrectomy and enteral feeding tubes.  Gastroenterol Clin N Am 44 (2015) 151-167.

Pasricha, Pankaj Jay, Parkman, Henry P. Gastroparesis: Definitions and Diagnosis. Gastroenterol Clin N Am 44 (2015) 1-7.

Parkman, H. P. Idiopathic Gastroparesis. Gastroenterol Clin N Am 44 (2015) 59-68.

Nguyen, Linda Anh, Snape Jr., William J. Clinical presentation and pathophysiology of gastroparesis.  Gastroenterol Clin N Am 44 (2015) 21-30.

Bharucha, Adil E. Epidemiology and natural history of gastroparesis. Gastroenterol Clin N Am 44 (2015) 9-19.

Camilleri, Michael, et al. Clinical guideline: Management of gastroparesis. Am J Gastroenterol 2013; 108: 18-37.