Esophageal Achalasia: Causes, Symptoms, Diagnosis, and Treatment

What is Esophageal Achalasia?

Esophageal achalasia is a rare but significant disorder of the esophagus, the hollow muscular tube that carries food and liquids from the throat down to the stomach. Although it is not widely known to the general public, achalasia can profoundly affect quality of life, making even the most basic act of eating or drinking a painful and distressing experience.

The condition is characterized by the failure of the lower esophageal sphincter (LES) to relax properly during swallowing, combined with a loss of normal, coordinated muscle contractions (peristalsis) along the length of the esophagus. The result is that food and liquids become stuck in the esophagus, unable to pass freely into the stomach.

Understanding achalasia, including its underlying mechanisms, risk factors, clinical presentation, and treatment options, is essential for patients living with this condition, their families, and anyone who wishes to be informed about digestive health. This article provides a thorough, evidence-based overview of esophageal achalasia, drawing on authoritative medical sources to help you navigate this complex condition with clarity and confidence.

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What Is Esophageal Achalasia?

The word “achalasia” comes from the Greek language and literally means “failure to relax”. This name succinctly captures the core problem: the esophageal muscles and the lower esophageal sphincter lose their ability to relax in a coordinated, timely manner in response to swallowing.

The Normal Swallowing Mechanism

To fully appreciate what goes wrong in achalasia, it helps to understand how the healthy esophagus works:

1. Initiation of swallowing: When you swallow, a complex reflex sequence is triggered, coordinated by the nervous system.
2. Peristalsis: Waves of coordinated muscular contractions propel food and liquid from the upper esophagus downward toward the stomach. These are called peristaltic waves, and they move in a carefully timed, organized fashion.
3. Lower esophageal sphincter (LES) relaxation: As the food bolus approaches the stomach, the LES, a ring of muscle at the junction between the esophagus and the stomach, relaxes to allow the contents through. Once the food has passed, the sphincter contracts again to prevent stomach acid from flowing back up.

What Goes Wrong in Achalasia

In patients with achalasia, two fundamental problems occur simultaneously:

• Loss of peristalsis: The normal wave-like muscular contractions of the esophagus are absent or severely impaired, so food cannot be propelled effectively toward the stomach.
• Failure of LES relaxation: The lower esophageal sphincter remains abnormally tight and fails to open adequately (or may not open at all), creating a functional obstruction at the bottom of the esophagus.

Together, these abnormalities cause food, liquids, and even saliva to accumulate in the esophagus, leading to regurgitation, aspiration into the lungs, recurrent chest infections, and progressive malnutrition. Over time, the esophagus may dilate significantly as it stretches under the pressure of retained contents.

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How Common Is Achalasia?

Esophageal achalasia is classified as a rare disease. Its estimated incidence is approximately 1 in 100,000 people per year, with a prevalence of around 10 per 100,000 individuals in the general population. While it can theoretically occur at any age, the peak incidence is observed between the ages of 30 and 50 years. Notably, achalasia affects men and women in roughly equal proportions, and there does not appear to be a significant difference in prevalence between the sexes.

Although rare, achalasia is one of the most studied and well-characterized esophageal motility disorders. Advances in diagnostic technology, particularly high-resolution esophageal manometry, have improved the accuracy and speed with which it is identified.

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Causes

Despite decades of research, the precise cause of esophageal achalasia remains incompletely understood in most patients. What is clear, however, is that the condition results from damage to or degeneration of the myenteric (Auerbach’s) plexus, a network of nerve cells (neurons) embedded within the walls of the esophagus that normally coordinates muscle activity.

Neuronal Degeneration

Pathological examination of esophageal tissue from patients with achalasia consistently reveals a loss of inhibitory neurons in the myenteric plexus. This particularly affects neurons that produce vasoactive intestinal peptide (VIP) and nitric oxide (NO), two key chemical messengers responsible for signaling the LES to relax. Without these signals, the sphincter remains in a state of persistent contraction.

Possible Causes and Contributing Factors

Several mechanisms have been proposed to explain why this neuronal degeneration occurs:

1. Autoimmune Mechanisms

A growing body of evidence suggests that achalasia may be, at least in part, an autoimmune disease. In autoimmune conditions, the body’s own immune system mistakenly attacks its own tissues. In achalasia, the immune system may target the neurons of the myenteric plexus, leading to progressive loss of function. This hypothesis is supported by the finding of inflammatory infiltrates (particularly T lymphocytes) around the surviving neurons in esophageal specimens from achalasia patients.

Achalasia has also been associated with other autoimmune conditions. Certain genetic variants in the human leukocyte antigen (HLA) system, which plays a key role in immune regulation, have been linked to an increased risk of developing achalasia.

2. Viral Infection

Some researchers hypothesize that an initial viral infection may trigger an autoimmune response that subsequently damages the esophageal neurons. Several viruses have been implicated as potential triggers, including herpes simplex virus (HSV), varicella-zoster virus (VZV), and measles virus, though definitive proof of causation has not yet been established.

3. Infectious Causes: Chagas Disease

In certain geographic regions, particularly Latin America, achalasia can develop as a direct consequence of infection with Trypanosoma cruzi, the parasitic organism responsible for Chagas disease. This neurotropic pathogen destroys the ganglion cells of the enteric nervous system throughout the gastrointestinal tract, and the resulting esophageal dysfunction is clinically indistinguishable from idiopathic achalasia. In endemic regions, Chagas disease is an important consideration in the differential diagnosis.

4. Genetic Factors

Although the vast majority of achalasia cases are sporadic (occurring without a family history), rare familial cases have been described. These suggest that genetic predisposition may play a role in a small subset of patients, though the specific genes involved have not been conclusively identified.

5. Secondary (Pseudoachalasia)

A condition known as pseudoachalasia can mimic true achalasia but has a distinct cause, typically a tumor at the gastroesophageal junction (most commonly gastric carcinoma) or, rarely, other structural abnormalities. It is critical to distinguish pseudoachalasia from idiopathic achalasia, particularly in older patients with rapid weight loss, as the treatment approach differs entirely.

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Symptoms

The clinical presentation of esophageal achalasia is variable. In some patients, the condition remains asymptomatic for extended periods, particularly in its early stages. However, as the disease progresses, one or more characteristic symptoms typically emerge and gradually worsen over time.

Dysphagia: The Cardinal Symptom

The hallmark symptom of achalasia is dysphagia, difficulty swallowing. This symptom is present in virtually all patients with achalasia and tends to be both progressive and persistent. What distinguishes achalasia-related dysphagia from dysphagia caused by other conditions is an important clinical clue:

In the early stages, patients with achalasia often describe paradoxical dysphagia, that is, they initially find it more difficult to swallow liquids than solids. This counterintuitive finding occurs because solid food, by virtue of its greater weight and mass, can generate enough gravitational force to push past the tight lower esophageal sphincter, whereas thin liquids may be more easily held up. As the disease advances, dysphagia typically affects both solids and liquids equally, and eventually swallowing may become extremely painful or nearly impossible.

Regurgitation

As food and liquid accumulate in the dilated esophagus, regurgitation becomes a prominent symptom. Unlike vomiting, which is an active process driven by stomach contractions, regurgitation in achalasia is passive. Undigested food and saliva simply flow back up from the esophagus without warning, particularly when the patient bends forward or lies down. This can occur minutes or even hours after eating and is often described as bringing up food that has no taste of stomach acid (unlike the acidic regurgitation typical of reflux disease).

Chest Pain

Many patients with achalasia experience chest pain or discomfort, which can be severe and may mimic cardiac pain (angina). This pain likely results from the forceful, uncoordinated muscular contractions of the esophagus (sometimes called “tertiary contractions”) and from the distension of the esophageal wall. Chest pain may occur independently of meals or be provoked by eating and drinking.

Heartburn and Retrosternal Burning

Paradoxically, many achalasia patients report heartburn: a burning sensation in the chest. This can lead to misdiagnosis as gastroesophageal reflux disease (GERD), delaying the correct identification of achalasia. In achalasia, the burning sensation is thought to result from the fermentation of retained food in the esophagus and the production of lactic acid, rather than from reflux of stomach acid.

Chronic Cough and Risk of Aspiration

The regurgitation of esophageal contents can lead to aspiration, which is the accidental inhalation of food or liquid into the airways. Chronic cough is therefore common, particularly at night when the patient is lying flat, and recurrent aspiration pneumonia (polmonite ab ingestis) is one of the most serious potential complications of uncontrolled achalasia.

Weight Loss

Because eating becomes increasingly difficult and painful, many patients with achalasia progressively reduce their food intake, leading to unintentional weight loss. This can range from mild to severe depending on the stage and duration of the disease, and in advanced cases, malnutrition may become a significant clinical concern.

Other Symptoms

Additional symptoms that may occur in patients with achalasia include:

• Halitosis (bad breath): Caused by the fermentation and decomposition of food retained in the esophagus.
• Excessive salivation (sialorrhea): The body may produce more saliva in response to the retained esophageal contents.
• Nausea and vomiting: Less common, but may occur.
• Nocturnal symptoms: Regurgitation, coughing, and choking episodes are often worse at night due to the horizontal body position, which allows retained contents to flow more easily toward the throat.

The Progressive Nature of Achalasia Symptoms

It is important to emphasize that the symptoms of achalasia typically evolve slowly and insidiously over months to years. Many patients adapt to the progressive difficulty swallowing by modifying their eating habits. They may chew more thoroughly, eat more slowly, consume mostly soft or liquid foods, or drink large amounts of water during meals to help push food down. These compensatory strategies may mask the severity of the condition and delay the diagnosis by years.

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Complications

When achalasia is not adequately treated, or when diagnosis is significantly delayed, several serious complications can develop:

Aspiration Pneumonia

The aspiration of food particles or regurgitated material into the lungs can cause recurrent aspiration pneumonia. These bacterial lung infections, if repeated, may lead to chronic lung damage, pulmonary fibrosis, and in severe cases, life-threatening respiratory compromise.

Esophageal Dilation (Megaesophagus)

Over time, the persistent retention of food and the increased intraesophageal pressure can cause the esophagus to dilate dramatically, a condition known as megaesophagus or sigmoid esophagus. A markedly dilated, tortuous esophagus is both a consequence of longstanding achalasia and a complication that makes treatment more technically challenging.

Malnutrition and Dehydration

The inability to eat and drink adequately can result in significant malnutrition and dehydration, with associated deficiencies in essential vitamins and minerals. This is particularly concerning in elderly patients or those with other underlying health conditions.

Esophageal Cancer

One of the most clinically significant long-term complications of untreated achalasia is an increased risk of esophageal carcinoma, specifically squamous cell carcinoma of the esophagus. The risk is estimated to be approximately 30 times higher in patients with achalasia compared to the general population, though the absolute risk remains relatively low given the rarity of the disease. The mechanism is thought to involve chronic irritation of the esophageal mucosa from retained, fermenting food. This risk underscores the importance of initiating treatment promptly after diagnosis and of maintaining long-term follow-up even after successful symptom relief.

Esophageal Candidiasis

The stagnation of food and saliva in the esophagus creates a favorable environment for fungal overgrowth, particularly Candida species. Esophageal candidiasis can cause additional pain and discomfort and may complicate the overall management of achalasia.

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Diagnosis

Because many symptoms of achalasia, particularly dysphagia and heartburn, overlap with those of more common conditions like gastroesophageal reflux disease (GERD), the diagnosis is often delayed. On average, patients wait several years from the onset of symptoms before receiving a correct diagnosis. A high index of clinical suspicion and the appropriate use of diagnostic tests are essential.

Clinical Evaluation

The diagnostic process begins with a thorough medical history and physical examination. Key features that should raise suspicion for achalasia include:

• Progressive dysphagia for both solids and liquids
• Regurgitation of undigested food
• Absence of improvement with proton pump inhibitors (PPIs), which are effective for GERD but not achalasia
• Unexplained weight loss
• Nocturnal cough or aspiration episodes

Esophageal Manometry

Esophageal manometry is currently considered the gold standard for diagnosing achalasia. In this procedure, a thin, flexible pressure-sensing catheter is passed through the nose or mouth into the esophagus. As the patient swallows small sips of water, the catheter measures the pressure at multiple points along the length of the esophagus and at the lower esophageal sphincter.

The classic manometric findings in achalasia include:

• Absence or significant impairment of peristalsis in the body of the esophagus
• Incomplete or absent relaxation of the LES upon swallowing
• Elevated resting LES pressure (in some subtypes)

The advent of high-resolution manometry (HRM) with esophageal pressure topography has significantly refined the diagnosis of achalasia and allowed for the identification of three distinct subtypes (Chicago Classification):

• Type I (Classic Achalasia): Absent peristalsis with minimal esophageal pressurization
• Type II: Absent peristalsis with intermittent pan-esophageal pressurization (the most common and best-prognosis subtype)
• Type III (Spastic Achalasia): Premature or spastic contractions without normal peristalsis

Identifying the subtype is clinically relevant because it influences the choice of treatment and predicts outcomes.

Barium Swallow (Barium Esophagram)

In a barium swallow (also called a barium esophagram), the patient drinks a liquid containing barium sulfate. This substance acts as a contrast agent, making it visible on X-ray images. Meanwhile, a series of X-ray images are taken. This allows the radiologist to observe the shape of the esophagus, the pattern of any contractions, and how quickly (or slowly) the contrast passes into the stomach.

Classic radiographic findings in achalasia include:

• A dilated esophagus with a characteristic “bird’s beak” tapering at the gastroesophageal junction, reflecting the tight, non-relaxing LES
• Absence of the normal gastric air bubble (because the LES does not open sufficiently to allow air to enter the stomach)
• Slow or absent emptying of contrast into the stomach
• In advanced cases, a massively dilated, sigmoid-shaped esophagus

Upper Endoscopy (Esophagogastroduodenoscopy)

Gastroscopy, also known as upper endoscopy or esophagogastroduodenoscopy (EGD), involves inserting a thin, flexible instrument with a light and camera (called an endoscope) through the mouth or nose. The device then moves down into the esophagus, stomach, and upper small intestine. This allows the physician to directly visualize the mucosal lining of these structures.

In achalasia, endoscopy typically reveals:

• Retained food and liquid in a dilated esophagus
• A tight, closed LES that resists the passage of the endoscope (though the endoscope can usually be advanced through with gentle pressure, a key finding that helps distinguish achalasia from mechanical obstruction by a tumor)
• Signs of esophagitis or esophageal candidiasis due to food stasis

Endoscopy is also critical for excluding structural causes of dysphagia, particularly malignancy at the gastroesophageal junction (pseudoachalasia), which can mimic achalasia both clinically and radiologically.

Endoscopic Ultrasound (EUS)

In cases where pseudoachalasia is suspected, especially in older patients or those with a rapid onset of symptoms and significant weight loss, endoscopic ultrasound (EUS) may be performed. This procedure evaluates the walls of the esophagus and the surrounding structures for evidence of tumor infiltration.

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Treatment and Management

A critical point to understand is that there is currently no cure for esophageal achalasia. The underlying neuronal degeneration that causes the condition cannot be reversed with currently available treatments. The goals of therapy are therefore:

1. To relieve symptoms, particularly dysphagia and regurgitation
2. To reduce intraesophageal pressure and facilitate gastric emptying
3. To prevent complications, especially aspiration and esophageal cancer
4. To improve quality of life

Multiple treatment options are available, ranging from conservative pharmacological measures to minimally invasive endoscopic procedures and open or laparoscopic surgery. The choice of treatment depends on the patient’s age, overall health status, achalasia subtype, and personal preferences.

1. Pharmacological Therapy

Medications are the least invasive treatment option but are also the least effective for long-term management of achalasia. They are generally reserved for patients who are not candidates for more definitive procedures.

Calcium Channel Blockers and Nitrates

Drugs such as nifedipine (a calcium channel blocker) and long-acting nitrates work by relaxing smooth muscle, including the lower esophageal sphincter, thereby reducing LES pressure and facilitating swallowing. These medications are typically taken sublingually (dissolved under the tongue) 15 to 30 minutes before meals.

However, their use is limited by:

• Modest and variable efficacy: only a minority of patients achieve meaningful symptom relief
• Significant side effects, including headache, flushing, hypotension, and dizziness
• Loss of effect over time (tachyphylaxis)

2. Botulinum Toxin Injection (Botox)

Botulinum toxin (commonly known as Botox) is a powerful neurotoxin that, when injected in small, controlled amounts, can temporarily paralyze or weaken muscles by blocking the release of acetylcholine at the neuromuscular junction.

In the treatment of achalasia, botulinum toxin is injected directly into the lower esophageal sphincter during upper endoscopy, using a sclerotherapy needle. By blocking the signals that cause the LES to remain contracted, the injection promotes sphincter relaxation and improves swallowing.

Key points about botulinum toxin injection for achalasia:

• Efficacy: Approximately 70–80% of patients experience symptom improvement in the short term
• Duration: The effects typically last 6 to 12 months, after which the treatment needs to be repeated
• Tolerability: The procedure is well tolerated and is not generally considered painful; it can be performed on an outpatient basis under light sedation
• Limitations: Repeated injections may lead to submucosal fibrosis, which can make subsequent surgical procedures more technically difficult
• Best candidates: Older patients or those with significant comorbidities who are not suitable for more invasive interventions

3. Pneumatic (Balloon) Dilation

Pneumatic dilation is one of the most commonly performed and effective non-surgical treatments for achalasia. Under endoscopic and fluoroscopic guidance, a specialized balloon catheter is passed through the mouth and positioned across the lower esophageal sphincter. The balloon is then inflated to a controlled, high pressure (typically using balloons of 30–40 mm diameter), forcefully stretching and partially tearing the LES muscle fibers to reduce sphincter resistance.

Key features of pneumatic dilation:

• Efficacy: Approximately 60–90% of patients achieve satisfactory symptom relief following one or more sessions
• Durability: Effects last longer than botulinum toxin injection, but many patients require repeat dilations over time
• Procedure: Performed under general anesthesia or sedation in a hospital setting
• Risk: The most serious complication is esophageal perforation (tearing of the esophageal wall), which occurs in approximately 1–3% of procedures and may require emergency surgical repair
• Achalasia subtype and outcomes: Patients with Type II achalasia tend to respond particularly well to pneumatic dilation

4. Surgical Myotomy: Heller Myotomy

Laparoscopic Heller myotomy (LHM) is a minimally invasive surgical procedure considered the most durable treatment for achalasia, particularly in younger and otherwise healthy patients. During this procedure, the surgeon cuts through the muscle fibers of the lower esophageal sphincter and the lower portion of the esophagus, permanently reducing the pressure in this area and allowing food to pass more easily into the stomach.

To prevent the development of gastroesophageal reflux disease (GERD), which is a common complication of LES division, Heller myotomy is almost always combined with a partial fundoplication. This procedure involves wrapping a portion of the stomach around the lower esophagus to create an anti-reflux barrier.

Key aspects of Heller myotomy:

• Efficacy: Long-term symptom relief in 70–90% of patients
• Approach: Performed laparoscopically (minimally invasive), requiring only small incisions and offering faster recovery compared to open surgery
• Durability: Among the most durable treatments, with many patients maintaining good symptom control for 10 years or more
• Complications: Include GERD (if fundoplication is not performed or is inadequate), esophageal perforation, and, rarely, incomplete myotomy

5. Per-Oral Endoscopic Myotomy (POEM)

Per-oral endoscopic myotomy (POEM) is a revolutionary, minimally invasive endoscopic procedure developed in Japan in 2008 and now widely available in specialized centers around the world. POEM has rapidly gained acceptance as a highly effective treatment for achalasia across all subtypes.

In POEM, the endoscopist uses a flexible endoscope to create a submucosal tunnel within the wall of the esophagus. Through this tunnel, the muscles of the lower esophageal sphincter can be cut under direct vision, and no external incisions are needed.

Key features of POEM:

• Efficacy: Clinical success rates of 90% or higher in most published series
• Advantages over surgery: No external incisions, a shorter hospital stay, faster recovery, and the ability to perform a longer myotomy. This is particularly advantageous in Type III (spastic) achalasia
• Disadvantage: Higher rates of postoperative GERD compared to Heller myotomy (because no anti-reflux procedure is added), requiring long-term monitoring and acid suppression therapy
• Availability: Requires significant endoscopic expertise and specialized equipment; available primarily at tertiary referral centers

6. Esophagectomy

In rare, advanced cases, particularly for patients with a massively dilated, non-functional esophagus (also known as end-stage megaesophagus) or those who have not responded to multiple previous treatments, surgical removal of the esophagus (esophagectomy) may be considered as a last resort. This is a major surgical procedure with significant morbidity and is reserved for exceptional circumstances.

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Living with Achalasia: Diet and Lifestyle Tips

While medical and surgical treatments address the underlying mechanical problem in achalasia, patients can also take several practical steps to manage symptoms and improve daily quality of life.

Dietary Modifications

• Eat slowly and chew thoroughly: Taking extra time to chew food into small pieces reduces the effort required to pass food through the esophagus.
• Choose soft or semi-liquid foods: Foods with a soft consistency, such as yogurt, mashed vegetables, soups, smoothies, scrambled eggs, and well-cooked pasta, are generally easier to swallow than hard, dry, or fibrous foods.
• Avoid problematic foods: Dry bread, tough meats, raw vegetables, and foods that form a sticky bolus (such as peanut butter) are commonly reported as difficult to swallow by patients with achalasia.
• Drink fluids with meals: Sipping water or other liquids between bites can help flush food down through the esophagus.
• Avoid carbonated beverages: While some patients find that carbonated drinks help dislodge food, they can also increase bloating and discomfort.
• Eat smaller, more frequent meals: Smaller portions reduce the volume of food in the esophagus at any one time, making it easier to manage.
• Avoid eating close to bedtime: Eating within 2–3 hours of lying down increases the risk of nocturnal regurgitation and aspiration.

Positional Strategies

• Sleep with the head of the bed elevated: Using a wedge pillow or raising the head of the bed by 6–8 inches (15–20 cm) can reduce regurgitation during sleep.
• Stay upright after meals: Remaining seated or standing for at least 30–60 minutes after eating helps gravity assist the passage of food into the stomach.
• Raise arms overhead when swallowing: Some patients find that raising both arms above the head while swallowing increases intraesophageal pressure and helps push food through the LES.

Psychological and Emotional Well-Being

Living with a chronic condition that affects eating, one of the most fundamental and social aspects of human life, can take a significant psychological toll. Many patients with achalasia experience anxiety, depression, social isolation, and a significantly reduced quality of life. It is important to:

• Seek support from a mental health professional or counselor familiar with chronic illness
• Connect with patient support groups (several organizations exist for achalasia patients worldwide)
• Communicate openly with healthcare providers about the emotional as well as physical impact of the condition

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Achalasia vs. Gastroesophageal Reflux Disease (GERD)

Because both achalasia and gastroesophageal reflux disease (GERD) can cause heartburn, chest discomfort, and regurgitation, they are frequently confused with each other. In fact, achalasia is often initially misdiagnosed as GERD. This distinction is critically important because the treatments are entirely different, and treating achalasia as GERD (with acid suppressants) will provide no meaningful benefit and may significantly delay appropriate management.

The key difference lies in the origin of the regurgitated material:

Furthermore, in GERD, symptoms are typically worse after meals and when lying down, while in achalasia, symptoms tend to be present throughout the day and night and are not relieved by acid suppression.

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Frequently Asked Questions

Is achalasia hereditary?

In the vast majority of cases, achalasia is not hereditary. It occurs sporadically, without a family history. However, rare familial cases have been reported, and some genetic susceptibility factors related to the immune system (HLA genes) may increase the risk in certain individuals.

Can achalasia be cured?

Currently, there is no definitive cure for achalasia. The underlying nerve damage cannot be repaired. However, treatments such as pneumatic dilation, Heller myotomy, and POEM can provide excellent, long-lasting symptom relief and allow patients to lead near-normal lives.

Does achalasia increase the risk of cancer?

Yes. Patients with achalasia have a statistically significant increased risk of esophageal squamous cell carcinoma compared to the general population, largely due to chronic mucosal irritation from food retention. Regular follow-up and surveillance endoscopy are recommended.

How is achalasia different from other esophageal motility disorders?

Achalasia is characterized by the specific combination of absent peristalsis and impaired LES relaxation. Other esophageal motility disorders (such as diffuse esophageal spasm, jackhammer esophagus, and esophagogastric junction outflow obstruction) have different manometric profiles and may require different treatments.

What is the long-term outlook for patients with achalasia?

With appropriate treatment, most patients with achalasia can achieve significant improvement in symptoms and quality of life. However, achalasia is a chronic condition, and ongoing monitoring is necessary to detect symptom recurrence, complications, or, in rare cases, the development of esophageal cancer.

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Sources and Bibliography

• NHS – Achalasia
• Achalasia – The Lancet (Pandolfino JE, Gawron AJ)
• Vaezi MF, Pandolfino JE, Vela MF. ACG clinical guideline: diagnosis and management of idiopathic achalasia. Am J Gastroenterol. 2013;108(8):1238-1249.
• Boeckxstaens GE, Zaninotto G, Richter JE. Achalasia. Lancet. 2014;383(9911):83-93.
• Inoue H, Minami H, Kobayashi Y, et al. Peroral endoscopic myotomy (POEM) for esophageal achalasia. Endoscopy. 2010;42(4):265-271.
• Kahrilas PJ, Bredenoord AJ, Fox M, et al. The Chicago Classification of esophageal motility disorders, v3.0. Neurogastroenterol Motil. 2015;27(2):160-174.
• Richter JE. Achalasia – an update. J Neurogastroenterol Motil. 2010;16(3):232-242.
• Zaninotto G, Bennett C, Boeckxstaens G, et al. The 2018 ISDE achalasia guidelines. Dis Esophagus. 2018;31(9).