Achalasia: A vagus nerve disorder linked to cervical instability?

Ross Hauser, MD.

Achalasia 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, are 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, or 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.

Article outline:

Part 1: Diagnosis, conservative care and surgery for Achalasia

  • Why you haven’t heard the term achalasia in your many diagnoses?
  • The diagnosis of Achalasia.
  • Medications for Achalasia.
  • Botulinum Toxin A injections.
  • The surgical treatment of Achalasia.
  • Heller myotomy and peroral endoscopic myotomy have some complications.
  • GERD after Peroral endoscopic myotomy.

Part 2 Achalasia: a vagal disease

  • Vagus neuropathy.
  • A review of the Achalasia research and vagus nerve dysfunction.
  • Phrenic and Vagus nerve innervation of the esophagus.
  • The vagus nerve influences intestinal permeability. What are we seeing in this image?
  • “Vagal sensory neurons mediate the vago-vagal reflex which, in turn, regulates a wide array of gastrointestinal functions including esophageal motility”
  • Even though the vagus nerve pathway remains intact, something is causing the impairment of the vagal afferents.
  • Ineffective esophageal motility is characterized by low to very low amplitude (nerve signals) propulsive contractions in the distal esophagus.
  • Anxiety for no reason.
  • Tachycardia
  • Achalasia, Eosinophilic Esophagitis, and Mast Cells – An allergy connection?

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:

  • Esophageal high-resolution manometry
    • A May 2022 paper in the journal Gastroenterology (1) wrote: “High-resolution esophageal manometry has improved the sensitivity for detecting achalasia and has also enhanced (the) understanding of spastic and hypomotility disorders of the esophageal body.”
  • Chest X-ray.
  • Barium esophagogram.
  • Upper endoscopy.

Medications for Achalasia

Your doctor may, or has prescribed calcium channel blockers or nitrates for you in an effort to relax or “unclench” the lower esophageal sphincter muscles to get food and liquids into the stomach. These medications are typically taken before meals.

A June 2022 paper in the journal Frontiers in Medicine (2) by Dr. Francisco Tustumi, acknowledges that “few published articles address (the) medical treatment for achalasia . . . Drugs acting in the esophagus are usually seen only as adverse events for other disease treatments and not as therapeutic choices for achalasia. (The calcium channel blockers are primarily given as a blood pressure medication to relax the arteries and the nitrates are given for chest pain. Nitrates also relax the arteries.) Theoretically, patients with mild dysphagia due to achalasia not desiring to be submitted to invasive procedures could benefit from medications before meals. However, oral intake drugs may not be absorbable in esophageal stasis, and erratic absorption could prone achalasia patients to a significant risk for complications.”

Botulinum Toxin A injections

Many patients find good success with Botulinum Toxin A injections, however, an April 2023 paper in the journal Gastroenterology and Hepatology (3) did list some drawbacks. The authors noted: “Although Botulinum Toxin A is safe and minimally invasive, it has several drawbacks. Although initial response can be excellent (better than 75% of patients), only two-thirds of patients have sustained response at 6 months, with 60% of patients having recurrent dysphagia at one year and 80% at 2 years. . . Patients older than 50 years have higher response rates to Botulinum Toxin A injections compared with younger patients for unclear reasons (82% vs 43%, respectively).” The researchers also cited research in elderly patients with achalasia (ages 81-94 years), 78% of patients were responders at 1 year, and 54% were considered responders at 2 years.

A November 2021 paper in the Journal of Clinical Medicine (4) discusses the openness of doctors to move away from these injections to surgery: “Botulinum toxin injection has been used for achalasia treatment since 1994 and is traditionally considered the preferred treatment for fragile elder patients. However, recently more evidence has become available regarding the safety and effectiveness of pneumatic balloon dilation (BD), laparoscopic Heller myotomy (LHM), and per-oral endoscopic myotomy (POEM) in elderly patients with achalasia.”

The surgical treatment of Achalasia

The surgical treatment of Achalasia

An October 2023 paper from doctors at the Scientific Institute San Raffaele in Milan Italy, published in the medical journal Life (5) explored outcomes of peroral endoscopic myotomies (POEMs – the surgical treatment of muscles to alleviate swallowing disorders) in the upper gastrointestinal tract. The researchers discuss the successes and challenges of surgeries with the message of looking at minimizing the surgery and identifying the patients who would most benefit from it. They write:

“In recent years, peroral endoscopic myotomies (POEMs) have brought about a revolution in the treatment of upper gastrointestinal tract motility disorders. Esophageal POEM, the first to be introduced, has now been validated as the primary treatment for achalasia.

Subsequently, developed, Gastric peroral endoscopic myotomy (G-POEM) displays promising results in addressing refractory gastroparesis. Over time, multiple endoscopic myotomy techniques have emerged. . .

Despite the well-established efficacy outcomes, new challenges arise in the realm of POEMs in the upper gastrointestinal tract. For esophageal POEM, the future scenario lies in customizing the myotomy extent to the minimum necessary, while for G-POEM, it involves identifying patients who can optimally benefit from the treatment.  . . .These challenges align with the concept of precision endoscopy, personalizing the technique for each subject. “

In February 2022 surgeons writing in the World Journal of Surgery (6) 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 have some complications

  • Blown-out myotomy is a common complication of the myotomy procedure in achalasia patients. An April 2019 paper in The American Journal of Gastroenterology (7) suggested that this surgical failure may be caused by “increased esophageal wall strain, whether it be from residual spastic contractility, continued outflow obstruction from fundoplication (surgery for stomach acid reflux), or an incomplete myotomy.”
  • In a May 2022 paper in the American Journal of Physiology Gastrointestinal and Liver Physiology (8) researchers led by Northwestern University observed that the “Longer myotomy was found to be accompanied by a higher bolus volume accumulated at the myotomy site. . . we found that an esophagus with a shorter myotomy performed better at emptying the bolus than that with a longer myotomy” (Food was backing up at the surgical site causing esophageal wall strain). “With respect to esophageal contractions, deformation at the myotomy site was greatest with propagated peristalsis, followed by combined peristalsis and spasm, and pan-esophageal pressurization.” (Simply the contractions to move food had been altered).

A November 2023 study in the Journal of Gastrointestinal Surgery (9) surgical treatment options for Esophagogastric junction outflow obstruction. Here doctors led by the Foregut Division, Surgical Institute, Allegheny Health Network in Pittsburg wrote: “Studies have shown that Heller myotomy with Dor fundoplication (this procedure helps prevent reflux from entering the esophagus from the stomach by repositioning part of the stomach around the esophagus) and per oral endoscopic myotomy (POEM) are effective treatments for Esophagogastric junction outflow obstruction.”

However, the researchers acknowledge there is little by way of data to compare the effectiveness and impact of Heller myotomy with Dor fundoplication and per oral endoscopic myotomy (POEM) and that is what the aim of their study set out to do.

Study summary points:

  • The study consisted of 52 patients. Thirty-five underwent Heller myotomy with Dor fundoplication and seventeen underwent per oral endoscopic myotomy for Esophagogastric junction outflow obstruction.
  • At an average follow-up of 24.6 months, a favorable outcome was achieved by:
    • 30 (85.7%) patients after Heller myotomy with Dor fundoplication and
    • 14 (82.4%) after per oral endoscopic myotomy (POEM)
  • However, when compared to Heller myotomy with Dor fundoplication, oral endoscopic myotomy (POEM) did not perform as well.
    • Patients who had per oral endoscopic myotomy (POEM):
      • saw objective reflux significantly increased
      • increased failed swallows
      • more incomplete bolus clearance

The researchers concluded: “Peroral endoscopic myotomy and Heller myotomy with Dor fundoplication are equally effective at relieving Esophagogastric junction outflow obstruction symptoms. However, POEM causes worse reflux and near complete loss of esophageal body function.”

GERD after Peroral endoscopic myotomy

A May 2022 paper in the journal Surgical Endoscopy (10) 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).”

A December 2023 study published in the Brazilian archives of digestive surgery (11) discussed managing the patient after a failed myotomy.

“To properly manage an achalasia patient with significant symptoms after myotomy, such as dysphagia, regurgitation, thoracic pain, and weight loss, it is necessary to classify symptoms, stratify severity, perform appropriate tests, and define a treatment strategy. . . The treatment options include endoscopic dilation, peroral endoscopic myotomy, redo surgery, and esophagectomy, and the decision should be based on the patient’s individual characteristics.”

In October 2023, Japanese researchers wrote in the journal Digestive Endoscopy (12) of the many types of achalasia phenotypes, or the different types of achalasia, that can fall under the same diagnosis but be a different type of disease. Using artificial intelligence or machine learning and high-resolution manometry, the researchers examined 1,778 patients who underwent Peroral endoscopic myotomy (POEM) for achalasia. The artificial intelligence or machine learning identified three achalasia phenotypes:

  • phenotype 1, type I achalasia with a dilated esophagus in 37.0% of the patients.
  • phenotype 2, type II achalasia with a dilated esophagus in 11.1% of the patients.
  • phenotype 3, late-onset type I-III achalasia with a non-dilated esophagus in 33.9% of the patients.

The researchers concluded: “Types I and II achalasia in phenotypes 1 and 2 exhibited different clinical characteristics from those in phenotype 3, implying different pathophysiologies within the same high-resolution manometry diagnosis.”

Part 2 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 and vagus nerve dysfunction

In a 2004 paper (13) 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.

  • In this study, five patients (age range 38-58 years, average age 45 years) diagnosed with achalasia were assessed for the autonomic nerve function by the heart rate reaction to deep breathing, and tilt compared to healthy controls. In the comparison, the researchers found impairment of the vagus nerve. Patients with achalasia have autonomic nerve dysfunction in the vagal nerve outside the esophagus.

A March 2021 study from Mexico’s Instituto de Ciencias Nucleares (Institute of Nuclear Sciences) published in the journal Public Library of Science One (14) furthered this research.

“Achalasia has been associated with extraesophageal dysmotility, suggesting alterations of the autonomic nervous system (ANS) that extend beyond the esophagus.” Here researchers investigated whether achalasia may be interpreted as the esophageal manifestation of a more generalized disturbance of the ANS which includes alterations in heart rate and/or blood pressure.

In their study, “simultaneous non-invasive records of the heart inter-beat intervals (IBI) and beat-to-beat systolic blood pressure (SBP) of 14 patients (9 female, 5 male) with achalasia were compared with the records of 34 rigorously screened healthy control subjects (17 female, 17 male) in three different conditions: supine, standing up, and controlled breathing using a variety of measures in the time and spectral domains.”

The researchers found: “Significant differences in heart rate variability (HRV) and blood pressure variability (BPV) were observed which seem to be due to cardiovagal damage to the heart, i.e., a failure of the ANS, as expected according to our hypothesis.” The researchers suggested that their testing methods “can be employed as an auxiliary clinical protocol to study etiology and evolution of achalasia and other pathologies that damage ANS.”

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 (15): “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.

A February 2021 paper in the journal Neural Regeneration Research (16) 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 contribute 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 a 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, and 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 (17) 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 deglutitive 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

  • Uvula deviation to one side is a sign of vagus nerve degeneration.

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


  • Another clue is bouts of tachycardia. Below I will present a patient case history of a patient who had tachycardia and had seen cardiologists and all kinds of specialists who could not tell her what was causing her problems. Testing ultimately revealed vagus nerve degeneration.

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

  • The patient had complaints of food getting stuck or pressure in the lower esophagus area. She had a barium swallow test.
  • The patient also had complaints of gastroparesis and food getting stuck in her stomach. Her stomach was not digestively working.
  • The patient also had complaints of acid reflux. These problems combined gave evidence that there was vagus nerve dysfunction.
  • The patient had an endoscopy.
  • The patient also had a cervical fusion.

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.

Achalasia, Eosinophilic Esophagitis, and Mast Cells – An allergy connection?

A January 2024 paper (18) led by researchers at Baylor University furthered their previously published research “We proposed an alternative hypothesis that achalasia sometimes might be allergy-driven, caused by a form of eosinophilic esophagitis (EoE) in which activated eosinophils and/or mast cells infiltrating esophageal muscle release products that disrupt motility and damage myenteric neurons”

In their study of  844 patients with achalasia identified (55% female; the average age at diagnosis, was 58 years), 402 (47.6%) had more than one allergic disorder. They concluded: “Achalasia is strongly associated with eosinophilic esophagitis and other allergic disorders. These data support the hypothesis that achalasia sometimes might have an allergic etiology.”

A December 2023 paper in the Ear, Nose, & Throat Journal (19) found in a study of 356,245 participants, a “significant association between chronic rhinosinusitis and premorbid GI tract diseases.” These diseases included gastroesophageal reflux disease (GERD) with/without esophagitis, achalasia, peptic/gastrojejunal ulcer, Crohn’s disease, and ulcerative colitis.

Summary and contact us. Can we help you?

Cervical instability is explained throughout this website: I would like to direct you to these articles to continue your research:

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