Achalasia: A vagus nerve disorder and its connection to the neck

Ross Hauser, MD.

We are going to talk about it interesting disease called Achalasia. It is a condition whereby the lower esophagus motility is lost. Most of us are familiar with gastroparesis. Gastroparesis is the condition where the motility (the ability to move food out) of the stomach is lost, but, esophageal dysmotility, and gastrointestinal dysmotility, are conditions where the contraction of the digestive tract, more than just the stomach, is abnormal.

There can be many causes for these esophageal and digestive disorders. In this article, we will explore one possible cause, cervical spine instability. When someone has issues of nausea, the sensation of stuck food, difficulty swallowing, many tests, diet rotations, and medications may be tried first before a cervical spine structural cause is examined, if examined at all. What I am suggesting and will demonstrate in the video, explanatory notes, and the research presented throughout this article is that many of these problems of motility and associated conditions are caused by vagus nerve degeneration.

For more discussion on gastroparesis, please see my companion article: How neck pain and cervical spine instability cause nausea, gastroparesis, and other digestive problems.

Why you haven’t heard the term achalasia in your many diagnoses?

Why you haven’t heard the term achalasia is because many times people actually have achalasia but it’s diagnosed as gastroesophageal reflux. Typically in the past, these conditions would be diagnosed as a problem of excessive stomach acid and treated with antacids. What I am hoping to demonstrate in the video and explanatory notes and research presented throughout this article is that many of these problems of motility and associated conditions are caused by vagus nerve degeneration from vagus nerve compression in the neck.

In the image above we see an illustration of the problem of Achalasia. On the left side image, we see that the lower esophageal sphincter fails to relax. Food and liquid get stuck in the esophagus. On the right side, we see a catheter stretching the restriction with balloon dilation.

The diagnosis of Achalasia

For most people, a diagnosis of Achalasia means you have been told that you have a rare swallowing disorder caused by degenerative damage to the nerves, or more specifically the vagus nerves,  that control muscle contracture in the esophagus. (For further discussion of swallowing difficulties please see my article Cervical disc disease and difficulty swallowing – cervicogenic dysphagia )It may have not started out as an esophageal disorder. You may have visited the doctor with acid reflux, a sensation that food gets caught, chronic heartburn, and chest pain. You may also have frequent hiccupping. (Please see my article Hiccups, Cough, Neck Pain, and Vagus and Phrenic Nerve Injury). You may have also been diagnosed with vomiting or regurgitation disorder. As time passes you may also experience significant weight loss.

As the symptoms worsened you may have been sent for diagnostic testing including:

The treatment of Achalasia

In February 2022 surgeons writing in the World Journal of Surgery (2) discussed the challenges of treating achalasia.

“Esophageal achalasia is a primary esophageal motility disorder of unknown origin. Treatment is palliative and its goal is to decrease the resistance posed by a non-relaxing and often hypertensive lower esophageal sphincter. This goal can be accomplished by different treatment modalities such as pneumatic dilatation, laparoscopic myotomy, or peroral endoscopic myotomy. In some patients, however, symptoms tend to recur over time.”

In the illustration above we see that Achalasia treatment may include Pneumatic dilation or balloon dilation to stretch open the lower esophageal sphincter so food may pass through into the digestive tract.

Heller myotomy and peroral endoscopic myotomy

GERD after Peroral endoscopic myotomy

A May 2022 paper in the journal Surgical Endoscopy (5) wrote about the increasing popularity of Peroral endoscopic myotomy (POEM), this is a somewhat new procedure where an endoscope is inserted down the throat into the esophagus. A series of small incisions are then made esophagus to help relax the esophageal muscles and the esophagus. The paper from the National University Health System of Singapore writes: “Peroral endoscopic myotomy (POEM) is gaining traction as a minimally invasive treatment of achalasia. Increased reflux is reported after (the procedure) but the incidence, type, and severity of reflux are not fully understood.  The researchers found Peroral endoscopic myotomy (POEM) was an effective treatment for achalasia. However, GERD was common after the procedure with the incidence of 43% on symptom score, 60% on endoscopy, and 56% on the pH-impedance test (the evaluation of acid reflux in the patient).”

Achalasia: a vagal disease

Ross Hauser, MD discusses achalasia and other common digestive disorders and their connection to the vagus nerve, as well as the patient cases that we’ve seen which have these disorders due to compression and degeneration of the vagus nerve from cervical dysstructure.

Vagus neuropathy

At 1:38 of the video, Dr. Hauser discusses 2004 research on the death of vagus cells that cause esophagus dysfunction. Data in this and other research suggests that achalasia or a loss of contractility of the lower esophagus is because of vagal nerve cells dying and that these nerve cell die-offs are causing various nerve plexuses (an intersection where nerves meet) in the esophagus. The suggestion is then that achalasia can be caused by damage or death of the vagal neuron cells, a type of neuropathy, “vagus neuropathy.” It is my documented opinion that vagal neuropathy can be caused by cervical dysstructure or breakdown of the natural structure of the neck causing stretch compression of the vagus nerve.

A review of the Achalasia research

In the 2004 paper (6) from the Department of Medicine at Malmö University Hospital, Sweden, doctors wrote: “Achalasia is considered to be a primary motor disorder of the esophagus. However, there is increasing evidence to suggest extra-esophageal involvement in this disease. (The esophagus is the “victim” of a problem from outside the esophagus causing motor disorder.) Vagal disturbances at different levels and extra-esophageal dysmotility have been reported in several studies.”

In this study, the aim was to examine cardiovascular reflexes in patients with achalasia and further evaluate the involvement of the autonomic nervous system outside the esophagus in this disorder.

Phrenic and Vagus nerve innervation of the esophagus

What are we seeing in the image below? The caption of the illustration reads: Phrenic and vagus nerve innervation of the diaphragm and esophagus (and lower esophageal sphincter, respectively. A broken neck structure (cervical dysstructure) can significantly affect breathing through the phrenic nerve, which innervates the diaphragm. In addition, swallowing can be negatively impacted because of vagus nerve stretch and compression as it innervates the esophagus and lower esophageal sphincter.

The vagus nerve influences intestinal permeability. What are we seeing in this image?

For proper digestion and absorption of nutrients through the intestinal wall, normal, healthy function of the vagus nerve is needed to cause “tight junctions” of the gut’s epithelial cells. When there is vagus nerve degeneration, intestinal permeability increases, leading to a leaky gut.

“Vagal sensory neurons mediate the vago-vagal reflex which, in turn, regulates a wide array of gastrointestinal functions including esophageal motility, gastric accommodation, and pancreatic enzyme secretion.”

In 2017, doctors at the Division of Gastroenterology, Department of Internal Medicine, University of Michigan wrote in the medical journal Medicina (7): “Vagal sensory neurons mediate the vago-vagal reflex which, in turn, regulates a wide array of gastrointestinal functions including esophageal motility, gastric accommodation, and pancreatic enzyme secretion. These neurons also transmit sensory information from the gut to the central nervous system, which then mediates the sensations of nausea, fullness, and satiety. Recent research indicates that vagal afferent neurons process non-uniform properties and a significant degree of plasticity (the nervous system has rerouted or changed its ability to send messages back and forth. In many cases these alterations cause distorted messages which contribute to esophageal and gastric problems). These properties are important to ensure that vagally regulated gastrointestinal functions respond rapidly and appropriately to various intrinsic and extrinsic factors. Similar plastic changes in the vagus also occur in pathophysiological conditions, such as obesity and diabetes, resulting in abnormal gastrointestinal functions. A clear understanding of the mechanisms which mediate these events may provide novel therapeutic targets for the treatment of gastrointestinal disorders due to vago-vagal pathway malfunctions.”

Even though the vagus nerve pathway remains intact, something is causing the impairment of the vagal afferents.

In a February 2021 paper in the journal Neural regeneration research (8) looked at patients’ neurotrauma, traumatic brain injury, and spinal cord injury and their gastrointestinal dysfunctions. Specifically, they looked at the vagus nerve, the primary parasympathetic control of the gastrointestinal tract, which in many of these injuries, remains intact. The researchers noted that “individuals with traumatic brain injury or spinal cord injury are highly susceptible to gastrointestinal dysfunctions. Such gastrointestinal dysfunctions attribute to higher morbidity and mortality following traumatic brain injury and spinal cord injury. While the vagal efferent output remains capable of eliciting motor responses following injury, evidence suggests impairment of the vagal afferents.”

The suggestion is that even though the vagus nerve pathway remains intact, something is causing the impairment of the vagal afferents. In this research, a possible culprit is “systemic inflammation contributes to multi-organ compromise, including the gastrointestinal tract. Whether this systemic inflammation causes vagal afferent plasticity or the plasticity of the vagal afferents contributes to systemic inflammation has yet to be determined. This dysregulation may exist in concert with, or independent of, alterations in the gut microbiome.”

This may be the vicious cycle. People with neck injuries including degenerative disc disease of the neck can have digestive disorders and an altered gut microbiome by way of vagus nerve compression or impairment. The vagus nerve messages are compromised, not correct. These messages are causing digestive problems, the vagus nerve also senses that digestive problems are occurring and sends further incorrect messages.

Ineffective esophageal motility is characterized by low to very low amplitude (nerve signals) propulsive contractions in the distal esophagus, hence primarily affecting the smooth muscle part of the esophagus.

A 2016 paper published in the journal Clinical and Experimental Gastroenterology (9) wrote: “Ineffective esophageal motility is characterized by low to very low amplitude (nerve signals) propulsive contractions in the distal esophagus, hence primarily affecting the smooth muscle part of the esophagus. (Low or no signaling is preventing the smooth muscles of the esophagus from moving food down the line). Ineffective esophageal motility is often found in patients with dysphagia (difficulty swallowing) or heartburn and is commonly associated with gastroesophageal reflux disease.”

This paper also discussed the problem of accurate diagnosis – “Ineffective esophageal motility is assumed to be associated with ineffective bolus (food) transport; however, this can be verified using impedance measurements or evaluation of a barium coated marshmallow swallow. Furthermore, water swallows may not assess accurately the motor capabilities of the esophagus, since contraction amplitude is strongly determined by the size and consistency of the (food) bolus. The “peristaltic reserve” (abnormalities in the ability to clear food out of the esophagus) can be evaluated by multiple rapid swallows that, after a period of diglutative inhibition (swallowing inhibition), normally give a powerful peristaltic contraction suggestive of the integrity of neural orchestration and smooth muscle action. . . This is strongly influenced by vagal efferent motor neurons and this, in turn, is influenced by vagal afferent neurons that send bolus information to the solitary nucleus. (The solitary nucleus receives messages from the vagus nerve about among other things, are messages about what is going on in the abdomen) where programmed activation of the vagal motor neurons to the smooth muscle esophagus is initiated. (This is part of the interaction that allows) swallowing activities and respiratory and cardiac activities and allows the influence of acute and chronic emotional states on swallowing behavior.”

There are lots of different clues that a person would have Achalasia from a vagus nerve injury

In the image below, right side vagopathy (dysfunction of the vagus nerve) is demonstrated by the lack of palatal elevation on the right side when saying “Ahhh.” This is caused by weakness in this patient’s right levantor veli palatini muscle which is innervated by the right vagus nerve.

Anxiety for no reason

Tachycardia

One of the more common problems we see as it relates to these cardiovascular-like attacks, heart palpitations, and blood pressure problems is Postural Orthostatic Tachycardia Syndrome POTS. POTS is the most common form of dysautonomia –  problems of dysfunction of the autonomic nervous system. I discuss these subjects at length in my article: Postural Orthostatic Tachycardia Syndrome (POTS), the Vagus Nerve, and Cervical Spine instability.

A Case history at 4:20 of this video

What is happening in this photo? Stuck food in the esophagus

The video picks up here at 7:24 where the image above is discussed. The patient is taking a barium swallow test. You can see the patient’s problem. The food is struggling to get out of the esophagus and into the stomach.

 


1 Patel DA, Yadlapati R, Vaezi MF. Esophageal Motility Disorders: Current Approach to Diagnostics and Therapeutics. Gastroenterology. 2022 Feb 25. [Google Scholar]
2 Patti MG, Schlottmann F, Herbella FA. Esophageal Achalasia: Evaluation and Treatment of Recurrent Symptoms. World Journal of Surgery. 2022 Feb 15:1-6. [Google Scholar]
3 Krause AJ, Triggs JR, Carlson DA, Campagana RA, Jain A, Kahrilas PJ, Hungness E, Pandolfino JE. 423 Blown out Myotomy (BOM), a Complication Following Laparoscopic Heller Myotomy and Per-Oral Endoscopic Myotomy. Official journal of the American College of Gastroenterology| ACG. 2019 Oct 1;114:S248-9. [Google Scholar]
4 Halder S, Acharya S, Kou W, Campagna RA, Triggs JR, Carlson DA, Aadam AA, Hungness ES, Kahrilas PJ, Pandolfino JE, Patankar NA. Myotomy technique and esophageal contractility impact blown-out myotomy formation in achalasia: an in silico investigation. American Journal of Physiology-Gastrointestinal and Liver Physiology. 2022 May 1;322(5):G500-12. [Google Scholar]
5 Teh JL, Tham HY, Soh AY, Chee C, Kim G, Shabbir A, Wong RK, So JB. Gastro-esophageal reflux disease (GERD) after peroral endoscopic myotomy (POEM). Surgical Endoscopy. 2021 Jul 29:1-9. [Google Scholar]
6 Ohlsson B, Ekberg O, Sundkvist G. Achalasia: a vagal disease. Scandinavian journal of gastroenterology. 2004 Jan 1;39(6):527-30. [Google Scholar]
7 Grabauskas G, Owyang C. Plasticity of vagal afferent signaling in the gut. Medicina. 2017 Apr;53(2):73-84. [Google Scholar]
8 Wang YB, De Lartigue G, Page AJ. Dissecting the role of subtypes of gastrointestinal vagal afferents. Frontiers in Physiology. 2020:643. [Google Scholar]
9 Chen JH. Ineffective esophageal motility and the vagus: current challenges and future prospects. Clinical and Experimental Gastroenterology. 2016;9:291. [Google Scholar]

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