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.

8 Responses

  1. cheryl brakespear September 3, 2015 / 5:22 am

    Another really helpful bit of information, thanks. I’ve seen in the literature that MCA can cause diminished GIT motility, was aware that it’s thought to be the cause of post op ileus…my son and I have a long history of assorted gut issues which have been shown to respond to H1 and H2 antagonists but because we present with constipation more than hypermotility our rather inadequate consultant is thrown into confusion. Dysphagia has been problematic since childhood, meds especially sticking and needing to be shoved down with a bit of cheese or whatever. We are known to get severe oesophageal spasm, reflux at times, nausea and sudden vomiting, along with abdo pain, bloating and post prandial pooling in the splanchnic bed, so severe in my son he gets severe hypotension and cardiac arrhythmias after most meals, having to lay with legs elevated…I have GU pain which switches off with antihistamines, I get probable cornary artery spasm, we both get histamine storms when our skin turns red, tense, hyperaemic and prickly and I have pigmented hives on my fore arms, which came on in midwinter…but, because my tryptase was 5 on one occasion he thinks that’s investigation enough and he can’t be sure this is MCA!

    • Lisa Klimas September 3, 2015 / 9:57 am

      Post-operative ileus is probably from a combination of things, but one of those things is absolutely mast cell degranulation. This has been demonstrated a number of times and is the reason GI surgery requires careful management for us. My life is one long story about my GI tract not working well, so you are in good company for sure. I have struggled with very severe constipation, and studies have shown that while diarrhea is more often assigned as a mast cell symptom, an awful lot of patients are actually constipated or have both.

      Where do you live? I can reach out and see if there is a good mast cell doctor in your area.

      • cheryl brakespear September 5, 2015 / 4:43 am

        Hello. Thanks for replying, my son and I are feeling very ‘us against the world’. We live in the UK (Cheltenham), I assume you’re in the USA… I asked a UK blogger about MCA literate consultants and was told Dr Grattan at Guy’s (London). We’d already been referred to that unit, the national dermatology unit, for possible late stage Lyme. Acrodermatitis Chronica Atrophicans, late stage skin Lyme, is I understand a European thing, not endemic in the US. Anyway, I saw an old bloke, semi retired, who clearly knew nothing about Lyme, had a lot of misconceptions about ACA, but since the unit deals with MCAD I laid that on him. Got all excited that I had found someone… sadly, on the second visit I found that he thought a random tryptase being normal was investigation enough. I took abstracts to enlighten him that MCAD can cause constipation, he couldn’t get his head around the lack of diarrhoea. It turned into yet another seminar with me teaching him his subject. He was OK about it, a nice man, but I was supposed to be consulting him, not him me. He’s agreed to ask Grattan to see us, but I already feel like I’m asking for things I have no right to ask. We have severe symptoms, potentially life threatening, my son is especially at risk from cardiovascular instability with a marked orthostatic/exercise element. We’ve both had actual anaphylactic episodes, mine to anti-tetanus serum, years ago, Nick to routine eye-drops, phenylephrine and an atropine analogue prior to examination. We have almost the full list of possible MCAD symptoms. I have pigmented hives on my forearms, which the old geezer didn’t intend to biopsy…VERY frustrated. Sorry to rant.

        • Lisa Klimas September 5, 2015 / 12:02 pm

          That sounds very frustrating. I have some contacts in the UK, I will see if there have been any new developments regarding care for MCAD patients who don’t have SM. It is the worst when you don’t feel heard by the people who are supposed to be helping you.

        • Jess Hobart September 10, 2015 / 3:36 am

          Hi Cheryl, Your name doesn’t look familiar to me, so forgive me if you’ve joined us and I missed it! Please do consider joining the UK Mastocytosis Support Group. We have an increasing number of MCAS patients (most still undiagnosed because of the challenges associated with that) and though we don’t have all the answers, by joining forces we are hoping to improve the quality of care for people with MCAS in the UK. More voices gives us more influence. We do have a few new doctors who are expressing some interest in MCAS– and are holding a seminar in October with Dr. Lawrence Afrin while he is visiting Europe. Best regards, Jess Hobart (jess@ukmasto.org)

          • Lisa Klimas September 11, 2015 / 12:32 am

            Thanks, Jess! Cheryl, Jess is a great resource and advocate for mast cell patients in the UK.

  2. kathy September 3, 2015 / 8:29 am

    very interesting- thanks!!! We’re about to embark on testing/eval for MCAD for my daughter (28 yo). Pretty nervous about not hitting the mark on doctor/testing/treatment.
    Any input would be greatly appreciated!

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