Achalasia of the cardia is a rare swallowing disorder where the valve at the bottom of your esophagus fails to open properly, trapping food and liquid above your stomach. It affects roughly 7 to 32 people per 100,000, and while it can develop at any age, most cases are diagnosed between ages 25 and 60. The condition is chronic and progressive, but several effective treatments can restore the ability to eat and drink normally.
What Happens Inside the Esophagus
Your esophagus is lined with a network of nerve cells called the myenteric plexus, which coordinates the wave-like muscle contractions that push food downward. At the bottom of the esophagus sits a ring of muscle called the lower esophageal sphincter (LES), sometimes referred to as the cardia. In a healthy swallow, these nerve cells signal the LES to relax and open as food arrives, then close again to prevent stomach acid from flowing back up.
In achalasia, those nerve cells progressively degenerate and die. Without them, two things go wrong simultaneously: the LES stays clenched shut, and the esophagus loses its ability to contract in coordinated waves. Food has no muscular push behind it and nowhere to go, so it collects in the esophagus, which gradually stretches and widens over years. The exact trigger for this nerve cell loss isn’t fully understood, though it likely involves an autoimmune process in genetically susceptible people. In Central and South America, a parasitic infection called Chagas disease can cause an identical pattern of nerve destruction.
Symptoms and How They Progress
The hallmark symptom is difficulty swallowing both solids and liquids. Unlike conditions that block the esophagus physically (such as a tumor or stricture), achalasia typically causes trouble with liquids from the start, not just solids. Many people describe a sensation of food “sticking” behind the breastbone and learn to eat slowly, take small bites, or drink water between mouthfuls to push food down.
Regurgitation of undigested food is common, sometimes hours after eating. Because the food never reached the stomach, it doesn’t taste acidic the way reflux does. Nighttime regurgitation can lead to coughing, choking, or even aspiration of food into the lungs. Chest pain, weight loss, and heartburn-like discomfort round out the typical picture. Symptoms usually develop gradually over months to years, which is why diagnosis is often delayed.
Three Subtypes of Achalasia
Doctors classify achalasia into three types based on how the esophageal muscles behave on pressure testing. The distinction matters because it predicts how well each treatment works.
- Type I: The esophagus has completely lost its ability to contract. No peristalsis, no pressure buildup. The esophagus essentially becomes a floppy, dilated tube.
- Type II: The esophagus also can’t produce normal contractions, but the entire organ pressurizes uniformly during at least 20% of swallows, almost like a compression squeeze. This is the most common subtype and tends to respond best to treatment.
- Type III: Instead of normal waves, the esophagus produces poorly timed, spastic contractions. This subtype can be the most challenging to treat and is sometimes called spastic achalasia.
How Achalasia Is Diagnosed
If your doctor suspects achalasia, the workup typically involves three tests, each providing different information.
Barium Swallow
You drink a chalky liquid while X-rays are taken. In achalasia, the barium pools in a widened esophagus and tapers to a narrow point at the LES, creating a characteristic “bird’s beak” appearance. A timed version of this test measures how much barium remains at 1, 2, and 5 minutes. In healthy people, barium clears completely within 1 minute for most and within 5 minutes for all. In achalasia, the barium column can still measure 15 centimeters or more in height at the 5-minute mark.
High-Resolution Manometry
This is the gold standard. A thin catheter threaded through the nose into the esophagus measures pressure at dozens of points simultaneously while you swallow small sips of water. The test confirms that the LES isn’t relaxing properly (measured as an elevated “integrated relaxation pressure”) and that the esophagus has lost all normal peristalsis. It also determines which of the three subtypes you have.
Upper Endoscopy
A camera passed down the throat rules out other causes of obstruction, particularly cancer at the junction of the esophagus and stomach. This step is essential because a tumor mimicking achalasia (called pseudoachalasia) requires completely different treatment.
Treatment Options
There is no way to restore the lost nerve cells, so all treatments focus on the same goal: reducing the pressure of the clenched LES so food can pass through by gravity and whatever residual muscle function remains.
Endoscopic Myotomy (POEM)
Per-oral endoscopic myotomy is a newer technique performed entirely through the mouth with an endoscope. The doctor tunnels beneath the inner lining of the esophagus and cuts the muscle fibers of the LES from the inside. No external incisions are involved. A large randomized trial found a clinical success rate of 75% at five years. Recovery is typically fast, with most people eating soft foods within a day or two and returning to normal activity within a week.
The main trade-off is acid reflux. Because the LES is cut without adding any anti-reflux barrier, about 41% of patients show signs of reflux on endoscopy at five years, with 14% having more significant inflammation. That said, actual reflux symptoms are mild for most people, and reflux is manageable with acid-reducing medication.
Laparoscopic Heller Myotomy
This surgical approach has been the standard for decades. A surgeon makes small incisions in the abdomen and cuts the LES muscle fibers from the outside, then wraps part of the stomach around the lower esophagus (a partial fundoplication) to create a valve that limits reflux. Five-year success rates are around 71%, similar to POEM. The added anti-reflux wrap means lower rates of post-procedure reflux: about 31% show esophageal inflammation at five years, with only 7% in the more significant category.
Recovery takes slightly longer than POEM, typically one to two weeks before returning to normal activities, but the reduced reflux burden can be an advantage for younger patients facing decades of follow-up.
Pneumatic Dilation
For patients who prefer a less invasive option or aren’t good candidates for surgery, a balloon can be inflated inside the LES to forcibly stretch and partially tear the muscle fibers. Balloons come in 30, 35, and 40 millimeter sizes, and doctors often start with the smallest, moving to larger sizes in repeat sessions if symptoms return. Pneumatic dilation is effective in the short term but has lower long-term durability than myotomy, meaning many people need repeat procedures over the years.
Botox Injections
Injecting a muscle-relaxing toxin directly into the LES during endoscopy can temporarily ease symptoms, but the effect typically wears off within 6 to 12 months. This option is generally reserved for people who can’t tolerate more definitive treatment, such as elderly or frail patients.
Long-Term Outlook and Cancer Risk
Most people with achalasia achieve good symptom control with treatment, but the esophagus never returns to normal function. Follow-up with periodic barium swallows or endoscopy helps detect treatment failure early, before the esophagus stretches further.
One concern that deserves attention is esophageal cancer. People with achalasia face roughly a ninefold increase in the risk of squamous cell carcinoma of the esophagus compared to the general population. In those who have undergone myotomy or dilation, the risk is even higher, around 16 times the baseline, likely because even treated achalasia still causes chronic food stasis and irritation. The absolute risk remains low because esophageal cancer itself is uncommon, but it’s the reason many specialists recommend periodic surveillance endoscopy, particularly after 10 to 15 years of disease.
Achalasia also carries a moderate association with esophageal adenocarcinoma, the type linked to chronic acid reflux, though much of that connection appears to be driven by post-treatment reflux rather than achalasia itself.