Inability to Burp or Belch

Inability to burp or belch occurs when the upper esophageal sphincter (cricopharyngeus muscle) cannot relax in order to release the “bubble” of air. The sphincter is a muscular valve that encircles the upper end of the esophagus just below the lower end of the throat passage. If looking from the front at a person’s neck, it is just below the “Adam’s / Eve’s apple,” directly behind the cricoid cartilage.

If you care to see this on a model, look at the photos below. That sphincter muscle relaxes for about a second every time we swallow saliva, food, or drink. All of the rest of the time it is contracted. Whenever a person belches, the same sphincter needs to let go for a split second in order for the excess air to escape upwards. In other words, just as it is necessary that the sphincter “let go” to admit food and drink downwards in the normal act swallowing, it is also necessary that the sphincter be able to “let go” to release air upwards for belching. The formal name for this disorder is retrograde cricopharyngeus dysfunction (R-CPD).

People who cannot release air upwards are miserable. They can feel the “bubble” sitting at the mid to low neck with nowhere to go. Or they experience gurgling when air comes up the esophagus only to find that the way of escape is blocked by a non-relaxing sphincter. It is as though the muscle of the esophagus continually churns and squeezes without success.

The person so wants and needs to burp, but continues to experience this inability to burp. Sometimes this can even be painful. Such people often experience chest pressure or abdominal bloating, and even abdominal distention. Flatulence is also severe in most persons with R-CPD. Other less universal symptoms are nausea after eating, painful hiccups, hypersalivation, or a feeling of difficulty breathing with exertion when “full of air.” Many persons with R-CPD have undergone extensive testing and treatment trials without benefit. R-CPD reduces quality of life, and is often socially disruptive and anxiety-provoking. Common (incorrect) diagnoses are “acid reflux” and “irritable bowel syndrome,” and therefore treatments for these conditions do not relieve symptoms significantly.

Approaches for treating the inability to burp:

For people who match the syndrome of:
1) Inability to belch
2) Gurgling noises
3) Chest/abdominal pressure and bloating
4) Flatulence

Here is the most efficient way forward: First, a consultation to determine whether or not the criteria for diagnosing R-CPD are met. Next, a simple office-based videoendoscopic swallow study which incorporates a neurological examination of tongue, pharynx (throat) and larynx muscles and often includes a mini-esophagoscopy. This establishes that the sphincter works normally in a forward (antegrade) swallowing direction, but not in a reverse (retrograde) burping or regurgitating fashion. Along with the symptoms described above, this straightforward office consultation and swallowing evaluation establishes the diagnosis of retrograde cricopharyngeus dysfunction (non-relaxation).

The second step is to place Botox into the malfunctioning sphincter muscle. The desired effect of Botox in muscle is to weaken it for at least several months. The person thus has many weeks to verify that the problem is solved or at least minimized.

The Botox injection could potentially be done in an office setting, but we recommend the first time (at least) placing it during a very brief general anesthetic in an outpatient operating room. That’s because the first time, it is important to answer the question definitively, that is, that the sphincter’s inability to relax when presented with a bubble of air from below, is the problem. Furthermore, based upon an experience with more than 190 patients as of August 2019, a single injection appears to “train” the patient how to burp. Approximately 80% of patients have maintained the ability to burp long after the effect of the Botox has dissipated. That is, long past 6 months from the time of injection.

Patients treated for R-CPD as just described should experience dramatic relief of their symptoms. And to repeat, our experience in treating more than 190 patients (and counting) suggests that this single Botox injection allows the system to “reset” and the person may never lose his or her ability to burp. Of course, if the problem returns, the individual could elect to pursue additional Botox treatments, or might even elect to undergo endoscopic laser cricopharyngeus myotomy. To learn more about this condition, see Dr. Bastian’s description of his experience with the first 51 of his much larger caseload at

Photos of the cricopharyngeus muscle:

1. The highlighted oval represents the location of the cricopharyngeus muscle.
2. The cricopharyngeus muscle in the open position.
3. The cricopharyngeus muscle in the contracted position.
Cross section of the head and neck showing the location of the cricopharyngeus muscleCross section of the head and neck showing the cricopharyngeus muscle in the open positionCross section of the head and neck showing the cricopharyngeus muscle in the contracted position

Where have patients traveled from?

Map of the world showing the countries of origin for patients we treated.










Marfan syndrome

A genetic connective tissue disorder caused by a defect in gene FBN1, which codes for abnormal structure of fibrillin-1, a protein crucial for formation of normal connective tissue. Most critical is Marfan syndrome’s effect on heart and blood vessels, which tend to dilate and be at risk of rupture. Connective tissue in bones, ligaments, and other parts of the body is also affected.

Laryngologists may encounter Marfan syndrome because parts or all of the aorta may need to be replaced over time, due to abnormal dilation of the weakened arterial wall, with risk of rupture. When such surgery is done, the left recurrent nerve is at risk of injury, and this would lead to left vocal cord paralysis. With Marfan syndrome, it is rare to live to age 70.



Literally, “old age larynx.” The term presbylarynx is used to signify vocal cord changes (and, by extension, vocal limitations) that accompany aging. Typically, these vocal cord changes include bowing of the cords, atrophy, flaccidity, and sometimes reduced wetness and lubrication of the vocal cords. The symptoms of these changes include foggy or weak voice quality, difficulty being heard in noisy places, and decreased vocal endurance.

Such findings are by no means universal in older individuals, however, and some of these changes may be resisted with vocal conditioning exercises. Moreover, some “presbylarynx” changes can be seen in individuals who are only 40 or 50, due to disuse of the voice or familial predisposition. For these reasons, presbylarynx does not seem to be a very useful term; instead, a precise description of the patient’s vocal cords seems to be more useful.


Bilateral vocal cord fixation

Immobility of both vocal cords due to a scarring rather than paralytic cause. The scarring might manifest as a synechia that tethers the vocal cords to each other and prevents them from separating during breathing. Or it could mean that both cricoarytenoid joints are ankylosed, or “frozen.”

The commonest cause of bilateral vocal cord fixation is prolonged endotracheal intubation, such as in gravely ill or injured persons, who may spend weeks in an intensive care unit and on a ventilator. Vocal cord fixation can rarely be caused by rheumatoid arthritis. It is also seen infrequently as a progressive, late complication of radiation therapy for larynx cancer.



The death of cells or tissue. In laryngology, necrosis is seen most commonly after radiation therapy to the larynx for cancer treatment. Radiation kills the tumor but at the same time damages the blood supply of normal tissue on a permanent basis. Necrosis in this instance is called “radionecrosis.” Or, necrosis could result from trauma (a physical wound) that disrupts blood supply, or occasionally in the context of ulcerative laryngitis, which seems to necrose the superficial layers of the vocal cords. Necrotic tissue typically sloughs off down to viable (living) tissue.


Phonatory insufficiency

When the vocal cords cannot close sufficiently or vibrate adequately to produce a serviceable voice. An inability to close is usually evidenced by air-wasting phenomenology.

This phonatory insufficiency could have one of several causes. It could be due to the loss of part or all of one or both vocal cords, such as after removal of a vocal cord cancer. Or it could follow prolonged intubation and resulting pressure necrosis of the posterior ends of the vocal cords 1. Another possibility might be scarring of the anterior joint capsule of the cricoarytenoid joints, also as a complication of prolonged endotracheal intubation due to grave illness. Yet another cause might be vocal cord paralysis or paresis. The latter problems not only interfere with the cords’ ability to close, but also make the affected cord flaccid, so that it blows out of the way too easily, further wasting the air stream.

When a person with any of these causes of poor vocal cord closure tries to produce voice, maximum phonation time is typically reduced, because only a fraction of the air pushed up from the lungs is converted to sound, with the remainder of the air quickly “wasted.”

The second main category of phonatory insufficiency, in which the vocal cords cannot vibrate adequately, is seen in a person with stiff or scarred vocal cords. Such a person may not waste air, but just be unable to produce other than a harsh whispery sound, because the stiffened vocal cords (now more like thick leather rather than like, as is normal, plastic wrap overlying a thin layer of jello) cannot vibrate as freely or at all.


  1. Bastian RW, Richardson BE. Postintubation phonatory insufficiency: an elusive diagnosis. Otolaryngol Head and Neck Surg. 2001; 124(6): 625-33. 

Arytenoid chondritis / perichondritis

An infectious or inflammatory response with ongoing ulceration or granulation on the superstructure of the arytenoid cartilage. Here we are talking of the arytenoid cartilage and/ or its thin “envelope” of fibrous tissue called perichondrium. The root chondr- refers to cartilage.

A similar and much more common disorder, contact granuloma or contact ulcer, occurs on the medial surface of the arytenoid cartilage, but low and at the level of the vocal process. When arytenoid chondritis or perichondritis occurs, it causes significant chronic pain (in contrast to contact granuloma, which can be pain-free or bring only minor discomfort). We have never diagnosed the underlying cause. Treatment tends to require definitive removal of the area of cartilage involved (not the entire arytenoid, of course), and then typically the area will heal, though often only after a time of re-granulation.


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Flaccidity of the Vocal Cords

Vocal cord flaccidity correlates to some degree with atrophy of the muscle comprising them. Bowing also accompanies flaccidity most of the time. It is possible to have bowed/slender vocal cords that are not particularly flaccid—they still vibrate with good firmness and resilience. Similarly, vocal cords that appear to have good bulk (and are not atrophied) can nevertheless have a flaccid vibratory pattern. Photos below show the visual findings of flaccidity as distinct from bowing and atrophy. Voice manifestations of flaccid vocal cords are similar to bowing in cases such as:

  • Loss of “edge”
  • Reduced ability to be heard in noisy places
  • Reduced vocal endurance (The voice becomes fuzzier or raspier and more air-wasting as the day progresses and the atrophied muscles tire).

Voice Building:

Voice Building (shorter version):

Vocal cord scissoring

Mismatching of the levels of the vocal cords. Vocal cord scissoring may in some cases be asymptomatic, but more often it introduces a rough quality to the voice, because the desired mirror-image bilateral symmetry of oscillation will be lost.