The Gasping Syndrome

By Dr. Bastian M.D.

A few times a year, distressed patients present from their internists or pulmonologists to see if I can explain their shortness of breath. The patient has already undergone numerous tests: e.g. chest x-ray, pulmonary function tests, EKG, stress test, echocardiogram, CT, blood tests, and even bronchoscopy. Everything has come back normal, or anything even slightly abnormal (the reader can fill in the blank) has been treated maximally without any reduction of the patient’s symptoms.

In short, the patient has complied with every test and treatment recommendation; yet there is still no apparent explanation for this difficulty breathing, and no relief provided by numerous treatment trials.

The patient seems weary of the problem. My “antennae” do not pick up any signals of la belle indifference (a peculiar lack of concern about symptoms that when present suggests that the problem may be non-organic). She tells me that her breathing is never noisy, and that her shortness of breath may or may not be associated with exercise. I apply my subjective but extremely useful “flow-volume loop” by asking her to exhale to “empty” and then rapidly breathe in until completely full, and there is no unusual noise, and no prolongation of the time required to fill.

My initial thought in this scenario? The gasping syndromeWhat is that? A recognizable but to my knowledge previously undescribed disorderHere is my composite description, meaning that individual patients may not fit every element of what follows:

  1. Either with exertion or at rest, the patient has an abrupt* sense of “smothering,” or air hunger. It happens almost from one second to the next. Like the abrupt shooting pain of neuralgia, the abrupt tickle of sensory neuropathic cough / throat clearing, or the abrupt laryngeal closure of laryngospasm. The patient says she can be engrossed in a movie or a book strolling with the dog when suddenly her consciousness is invaded by a need to “get more air.”
  2. She responds by taking a deep breath, but there is no relief and the sensation remains. So, she takes a series of deep breaths, all of them to no avail. The feeling is oppressive, anxiety-provoking, gaspingThis sensation may last for a few seconds, to several hours.* Unfortunately, it can happen again some time later, or maybe just a time or two per day or even per week.

Having seen many people who fit the gasping syndrome across the decades, though not usually more than a handful per year, I have speculated that this is a sensory disturbance. After all, I ponder, if it represents more than a primary neuropathic sensation, why is oxygen saturation measured by oximetry, including during exercise, always normal? Why are all the tests of heart and lung function normal? Why no mitral valve prolapse, or something to explain this? Why nothing on imaging? Why no noisy breathing?

My mind goes to patients who describe a similar sensation at the moment IV contrast is injected for a CT scan. In addition to “warmth,” “a sensation of needing to urinate,” etc., they can have a sensation of abrupt, quite compelling, and thankfully transient smothering.  Or to someone I know who in the middle of an IV infusion of a biologic modifier for cancer, (with prior warning) experienced profound air hunger that started abruptly and was completely gone 20 seconds later. In each of these cases, it seems like a primary sensory phenomenon more than an alerting and protective sensation in response to low oxygen or high carbon dioxide levels.

How would one conceptualize a mechanism? Here is one thought experiment: consider that we are all supplied with pulmonary stretch receptors. They send messages “in the background” several times across the day and night to the respiratory center: Excuse me… Take a deep breath; expand those alveoli; your surfactant is giving you some atelectasis. And so, without being aware of it, we sigh now and then. We roll over in our sleep, mutter, grind our teeth, and take a deep breath. While reading a book we subconsciously shift in our seat and inspire deeply as we turn a page. Again, we are unaware of this, but an observer watching us read or, equipped with night vision goggles and watching us sleep, will see it.

What if the pulmonary stretch receptors send a signal Hey! Time to take a deep breath! and despite our taking a deeper breath outside of conscious awareness, the respiratory center does not receive the return communication, Action completed. Even with normal O2 and CO2 levels, if the brain thinks that deep breath did not happen, would it not intrude on conscious thought to re-command more urgently: Hey! Deep breath please!

Where does one go to help the patient with this thought experiment diagnosis? Just give her this explanation and leave it there? Or, maybe punt back to the primary care or pulmonary or cardiology physician…? But what if the person has already seen 3 of each specialty—one who is local, another at a nearby university center, and a third at a national referral center? What if “every conceivable test” has already been done 3 times?

A follow-on thought experiment: to the patient, and via a summary letter to her doctors, explain the concept of dysesthesia or sensory disturbance. Give her analogies: at the dentist, after anesthesia is in place to allow that root canal or filling, your tongue/lip can feel swollen, but a look in the mirror shows them to be normal. When a leg goes to sleep, it can feel fatter and heavier than the other one, but it is not. When you suffer nerve damage from diabetes, it can feel like bees are stinging your feet, but none are present in the room.

And then explain scenarios where persons have to accommodate to or neglect the feeling of contact lenses. The sound of new tinnitus. The tickling of an indwelling tracheotomy tube. The dramatic sensation a sword swallower must ignore during the show. Or the sensation of air hunger the pearl diver must overcome to stay submerged for 2 minutes while swimming vigorously.

Perhaps point out that it appears there is no danger from this ominous-feeling sensation.  Remind her of the multiplicity of prior “normal” tests. Maybe suggest that she experiment with assuming “control” of her response to the sensation by saying to herself: It is just a feeling! Or, Stupid pulmonary stretch receptors! Maybe gently alter behavior to see if it has any impact. Introduce inspiratory resistance via “straw-breathing.” Or a gentle Valsalva maneuver. Or, exhale slowly through pursed lips whose opening is the size of a coffee-stirrer.

And if nothing else works, suggest trying to mentally shrug and “throw the sensation over the shoulder.” And then keep going. The very worried individual can purchase an oximeter. Or even a stethoscope as a “crutch” to allay anxiety.

All of this can be offered with a physician’s apologies that he or she has nothing better to offer. And also with encouragement that these ideas have “liberated” other patients struggling with the same problem.

A final thought: just as neuromodulators can help persons suffering from neuralgia or sensory neuropathic cough/throat clearing, and laryngospasm, consider a “sensory neuropathic cough” strategy of working one-by-one, from medication to medication such as amitriptyline, gabapentin, etc., hoping to find one that helps.

*Some describe a more continuous, lower-grade background sensation of difficulty breathing with abrupt “peaks”

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Positive/ Negative Practice

This behavioral treatment is prescribed primarily for patients with nonorganic voice disorders. A patient with a nonorganic voice disorder has been diagnosed with aberrant voice production due to the abnormal use of a normal mechanism, often due to stress or some sort of secondary gain. She or he may have been ‘stuck’ with the abnormal voice for months to years, or may lurch between normal and abnormal voice production on an apparently involuntary basis. To help patients first “find” their normal voices, the clinician guides the patient through a variety of vocal elicitations such as: a yell, glissando, siren, or vocal fry. All of this may be with or without clinician digital manipulation of the laryngeal framework.

After preliminarily ‘settling in’ the patient’s reestablished normal voice, the clinician quickly asks the patient to alternate between the re-established normal voice and the old abnormal voice. First, the patient alternates upon clinician cue, again optionally with or without digital manipulation, and then the patient demonstrates the ability to switch between the two kinds of voice production at the sentence level, and then every few words, and then word-by-word. The positive and negative practice demonstrates mastery / control over the abnormal/ nonorganic voice production.

If possible, this process should occur with patient, clinician, and family/ friends in attendance. Other doctors, speech pathologists, pulmonologists, and allergists who may have previously attempted to help the patient using medical rather than behavioral treatments should also be made aware of the nature of the patient’s diagnosis, the purely behavioral approach to it, and the idea that behavioral intervention to resolve this problem completely should not normally exceed three visits to a speech pathologist, to avoid his or her becoming a co-dependent or source of secondary gain.

Listen to a few demonstrations below:

Mucosal Chatter

Mucosal chatter is an audible phenomenon of injured vocal cord vibration. It is commonly heard in the softly-sung upper voice of persons with nodules, polyps, etc.

Hoarseness or roughness are broad and nonspecific descriptors useful only for severe injuries. Small injuries that are nevertheless impairing the singing range may leave the speaking voice sounding normal. I suppose “hoarseness of singing range” could be used, but again, that would be an unsophisticated and basic description of vocal phenomenology. To hear more useful phenomena of injury, we elicit and thereby investigate the upper range of singing (even in nonsingers) because high, soft singing makes the phenomenology apparent.  This is why we have described “vocal cord swelling checks” and created a video to teach how to elicit them, and also how to evaluate and communicate the phenomenology that results. In particular, delays of phonatory onset (“onset delays”) above approximately C5 (523 Hz) may indicate mucosal injury even when speaking voice sounds normal. Also heard is air-wasting, where there is a “scratchiness” to the excess airflow. Segmental vibration is also a common audible phenomenon of a mucosal disorder can also be easily taught and recognized.

Vocal cord mucosal chatter adds an extremely rapid “shudder” on top of the pitch of the voice. I have used “chatter” rather than “shudder” because the latter suggests a lower frequency than the former. It could be called a very fine-grained diplophonia…but typical diplophonia, caused by independent vibrating segments, is a much grosser vocal phenomenon. While chatter is more subtle, once it is pointed out and taught briefly, most people can easily distinguish between onset delays, diplophonia, segmental vibration, the transient “squeaking” of a micro-segmental vibration, the crackling sound of mucus dancing on the vocal cords, and “chatter.”  Those who master recognition of these phenomena can easily communicate them to colleagues.

For our purposes, let me stress again that the above phenomena—and chatter in particular—do not happen in the normal larynx, where vocal cord margins match perfectly and the mucosa oscillates normally. When heard—even in the person with a normal speaking voice—the examiner can strongly suspect a mucosal abnormality even before examining the vocal cords. In fact, where these phenomena are heard and initial examination looks normal, it would be a good idea to “look harder.”

Patient examples:

Segmental Vibration

In the normal larynx, segmental vibration occurs when both chest and falsetto (head) registers are produced by vibration of the anterior 2/3 of the vocal cords. The posterior 1/3 is “inhabited” by the arytenoid cartilage and does not vibrate.

In certain pathological circumstances such as displayed in the photo sequences below, only a small part of the vocal cords vibrates.

This segmental vibratory phenomenon is typically seen in vocal cords that are damaged—such as by vocal nodules, polyps, cyst, scarring, etc. In such persons, upper voice is typically particularly impaired, until, as the person continues to try to ascend the scale, suddenly a crystal-clear “tin whistle” kind of voice emerges and may continue upwards to very high pitches.

Some in the past have talked about flagelot, flute, bell, or whistle register.  We suspect that this was in the days before videostroboscopy and at least in some cases may have been segmental vibration.

The best way to determine if what sounds like a “tin whistle” upper voice extension is due to segmental vibration is by videostroboscopic examination during that kind of phonation. The other way is for the individual to produce their “tin whistle” kind of voice very softly and then try to crescendo. If full length vibration, smooth crescendo will be possible. If segmental, there will be a sudden “squawk” as the vocal cords try to go (unsuccessfully) from segmental to full-length vibration.


Segmental Vibration Compared to Full-length

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Translucent polypoid swellings (1 of 4)

A younger man with chronic hoarseness due to large translucent polypoid swellings, not seen well at closed phase of full-length vibration at E3 (165 Hz).

Open phase, E3 (2 of 4)

Open phase of vibration at the same pitch showing that the full length of both cords swings laterally. Now the large polyp left vocal cord (right of photo) is easily seen.

Closed phase, E4 (3 of 4)

At E4 (330 Hz), vibration is damped (not allowed) except for the short anterior segment indicated by arrows.

Open phase, E4 (4 of 4)

At the same pitch, but open phase of vibration of that same short segment.

Whistle Register or Tin-whistle Segmental Vibration?

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Closed phase (1 of 4)

Closed phase of vibration at C4 (~ 262Hz) in a woman who is chronically hoarse and is a "vocal overdoer". Note the early contact at the bilateral swellings (right greater than left), and the MTD posturing (separation of vocal process "grey" zone posteriorly).

Open phase (2 of 4)

Open phase of vibration, shows that the entire length of the vocal cord margin participates in vibration at this pitch.

Segmental vibration (3 of 4)

Segmental vibration at F5 involves only the short anterior segment (brackets). The vocal cord swellings do not vibrate, nor does the posterior vocal cord. This is the closed phase of vibration.

Whistle register (4 of 4)

Open phase of that tiny anterior segment. This imparts a truly tiny "tin whistle" quality that cannot be maximized to a volume above beyond pianississimo. In some cases, singers who have not seen their vocal cords at this kind of high magnification under strobe light believe this to be a normal "whistle register".

Search not Only for Nodules, but Also for Segmental Vibration and Look at the Posterior Commissure for MTD

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Open phase (1 of 4)

In a young pop-style singer, the open phase of vibration under strobe light at C#5 (554 Hz). This magnified view is best to see the large fusiform nodules.

Closed phase (2 of 4)

Closed phase of vibration at the same pitch shows touch closure—that is, that the nodules barely come into contact.

Segmental vibration (3 of 4)

Even when patients are grossly impaired in the upper voice as is the case here, the clinician always requests an attempt to produce voice above G5 (784 Hz), in order to detect segmental vibration. Here, the pitch suddenly breaks to a tiny, crystal-clear D6 (1175 Hz) Only the anterior segment (arrows) vibrates.

Posterior commissure (4 of 4)

A more panoramic view that intentionally includes the posterior commissure to show that the vocal processes, covered by the more ‘grey’ mucosa (arrows), do not come into contact. This failure to close posteriorly is a primary visual finding of muscular tension dysphonia posturing abnormality.

Sulcus and Segmental Vibration

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Glottic sulci (1 of 4)

Closed phase of vibration, strobe light, at G3 (196 Hz) in a young high school teacher/ coach who is also extremely extroverted. Faint dotted lines guide the eye to see the lateral lip of her glottic sulci.

Open phase (2 of 4)

Open phase of vibration at the same pitch, showing full-length oscillation.

Closed phase (3 of 4)

Closed phase of vibration at E-flat 5 (622 Hz). Arrows indicate closure of the short oscillating segment.

Segmental vibration (4 of 4)

Open phase of vibration also at E-flat 5, Only the tiny segment opens significantly. As expected the patient’s voice has the typical segmental “tin whistle” quality.

Open Cyst and Sulcus; Normal and Segmental Vibration

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Margin swelling (1 of 6)

Breathing position of the vocal cords of a very hoarse actor. Note the margin swelling of both sides. The white material on the left vocal cord (right of photo) is keratin debris emerging from an open cyst. Find the sulcus of the right vocal cord (left of photo) which is more easily seen in the next photo.

Narrow band light (2 of 6)

Further magnified and under narrow band light. The right sulcus is within the dotted outline. Compare now with photo 1.

Open phase, strobe light (3 of 6)

Under strobe light, open phase of vibration at A3 (220 Hz). The full length of the cords participate in vibration.

Closed phase, same pitch (4 of 6)

At the same pitch, the closed phase again includes the full length of the cords.

Segmental vibration (5 of 6)

At the much higher pitch of C5 (523 Hz) a “tin whistle” quality is heard and only the anterior segment (at arrows) is opening for vibration. The posterior opening is static and not oscillating, as seen in the next photo.

Closed phase (6 of 6)

The closed phase of vibration involves only the tiny anterior segment of the vocal cords, at the arrows. The posterior segment is not vibrating and is unchanged.

Tiny Vibrating Segment Gives Tiny Tin Whistle Voice

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Prephonatory instant (1 of 6)

This young woman has been hoarse for many years. This preparatory posture shows marked separation of the cords posteriorly, suggesting MTD as well.

Phonation (2 of 6)

Now producing voice, with vibratory blur of the entire length of the cords on both sides.

Gaps due to nodules (3 of 6)

Under strobe light at a lower pitch of A4 (440 Hz), closed phase of vibration. Large gaps anterior and posterior to the polypoid nodule(s) explain breathy quality and short phonation time.

Open phase (4 of 6)

Open phase of vibration also at A4 (440 Hz) shows that the full length of the vocal cords are vibrating. Compare with the following two photos.

"Tin whistle" sound (5 of 6)

Now at A5 (880 Hz), the patient can only make an extremely tiny (tin whistle) quality. The only segment vibrating is within the circle (here, closed phase). The posterior segment does not vibrate.

"Tin whistle" at open vibration (6 of 6)

Still at A5 (880 Hz), the open phase of vibration, again of *only* the tiny anterior segment.

Phonatory Gap

Phonatory gap occurs when the vocal cords fail to close during phonation. A phonatory gap may be seen in patients who have muscle tension dysphonia, vocal cord paresis or paralysis, loss of tissue, or vocal cord flaccidity.

In addition, however, a phonatory gap occasionally occurs in patients who have none of the above conditions. In this type of case, the patient will struggle with onset delays, but delays that “pop” followed by relatively clear voice rather than the scratchier or hoarser-sounding onset delays associated with vocal cord mucosal swelling. Also, if asked to perform our vocal cord swelling checks, such a patient will tend to struggle more with the “Happy birthday” task than the descending staccato task (the opposite is true for patients with mucosal swelling).


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Phonatory gap (1 of 4)

At the prephonatory instant, D4 (~294 Hz), standard light. Notice how separated the vocal cords are.

Phonatory gap (2 of 4)

Phonation, a moment later, with vibratory blur. The cords remain separated. The question is whether this gap is due to: 1) a posturing problem, such as muscular tension dysphonia (MTD); 2) flaccidity-induced bowing; 3) some other cause.

Not MTD (3 of 4)

The most “closed” phase of vibration, as seen under strobe light, at the relatively low pitch of F4 (~349 Hz); again, the cords are not actually closed. This is not the picture of MTD, however; with MTD, there would be a greater gap between the vocal processes of the arytenoid cartilages (at arrows).

Its Phonatory gap (4 of 4)

Open phase of vibration, at the same pitch as photo 3. The lateral amplitude of each cord's vibration is equal, and relatively small (midline shown by a dotted line), which would not be seen with vocal cord flaccidity. Hence, neither MTD nor flaccidity is the explanation for this patient's gap. Also, this patient's voice manifests "popping" onset delays that are similar to other phonatory gap patients who have neither MTD nor flaccidity.

The Same Vocal Cords Shown Short and Fat vs. Tall and Thin

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Closed phase at a high pitch (1 of 4)

A mezzo soprano is singing at A5 (880 Hz). This is the “closed” (or rather “more closed,” since a slight gap remains) phase of vibration as seen under strobe light.

Open phase at a high pitch (2 of 4)

Here the voice is at the same pitch, but at the open phase of vibration. The amplitude of vibration (distance moved from the midline) is small.

Closed phase at a low pitch (3 of 4)

Now singing 2 octaves lower at A3 (220 Hz). This is the closed phase of vibration. The vocal cords are short and “fat.” In contrast to stringed instruments and the piano where high pitches are made with short and thin strings, the voice produces high pitches with long and thin. For an analogy, twang a rubber band stretched to different lengths and hear the change in pitch.

Open phase at a low pitch (4 of 4)

Still at A3, but now during the open phase of vibration. The amplitude (distance moved from the midline) is also typically greater for low pitches, at similar loudness level.

Torus Mandibularis

Torus mandibularis is a benign bony growth on the medial surface (tongue side) of the mandible or jaw bone. Also known as mandibular torus. Mandibular tori are usually seen on both the left and right sides (bilaterally). They often require no treatment unless they interfere with denture fitting.

In laryngology, mandibular tori come to attention because, when large, they can make it difficult or impossible for the clinician to gain a view of the vocal folds during microlaryngoscopy. That difficulty arises because during a microlaryngoscopy, the floor of the mouth is normally compressed by the laryngoscope to allow the scope to angle anteriorly at the viewing end, but mandibular tori, being composed of bone, do not compress.


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Torus mandibularis (1 of 2)

View inside the mouth, focused on the floor of the mouth, with tongue retracted. The “mounds” seen in the foreground are unusually large tori, which are touching anteriorly.

Torus mandibularis (2 of 2)

Looking more directly downward onto the tori, with the tongue now pointing upward at the roof of the mouth.

Vocal Instability

Vocal Instability is a characteristic that might manifest most clearly during sustained phonation as a glitch, catch, wavering, tremor, in-and-out vocal fry, or other such finding. In each case, the patient would be unable, partially able, or only intermittently able to produce a steady and predictable voice.

Pharyngeal Deviation

Pharyngeal deviation is a pulling of the posterior pharyngeal wall to one side, as sometimes seen when a patient performs the “pharyngeal squeeze.” This finding accompanies paresis or paralysis of the constrictor muscles of one side of the pharynx. In these cases, elicitation of the pharyngeal squeeze will reveal that the pharyngeal wall pulls to the normal (non-paralyzed) side. On the normal side, one will typically see bulging of normally functioning muscle to fill one pyriform sinus; meanwhile, the other pyriform sinus will appear capacious and almost dilated. The midline pharyngeal raphe, which joins the pharyngeal constrictor muscles, moves far to the normal side. A person with these findings normally experiences considerable swallowing difficulty, with pooling of saliva or ingested materials, particularly in the pyriform sinus on the paretic or paralyzed side.


Pharyngeal Paralysis, Seen with Pharynx Contraction

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Pharyngeal paralysis (1 of 2)

View of the laryngopharynx. This patient has pharyngeal paralysis on one side, which is already slightly evident because the posterior pharyngeal wall's midline (dotted line) is deviating here slightly to one side, even at rest.

Pharyngeal paralysis, more obvious with pharynx contraction (2 of 2)

The pharynx is contracted, and the posterior pharyngeal wall (midline again at dotted line) now deviates dramatically toward the non-paralyzed side of the pharynx. This pharynx contraction was elicited via extremely high-pitched voicing.