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Laryngopedia By Bastian Medical Media

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IA-Only Paresis

IA-only paresis refers to weakness or paralysis of the larynx’s interarytenoid (IA) musclean unpaired muscle spanning between the bodies of both arytenoid cartilagesbut with normal function of the other muscles in the larynx. The IA muscle helps to bring the posterior commissure together for voice production and, more specifically, to bring the bodies or “heels” of the arytenoid cartilages on each side simultaneously to the midline. The following are indicators of IA-only paresis:

  • Movement: The vocal cord opens normally for breathing. From a distance, it can appear to close normally for voicing, but more intense and up-close inspection shows a persistent posterior commissure opening not only for voicing but also at the moment of cough and Valsalva maneuver. Without confirming that the heels of the arytenoids cannot come together regardless of task, the possibility of a functional posturing abnormality (such as seen for nonorganic voice disorders) cannot be ruled out. If voice change has occurred abruptly, and the above criteria pertain, IA-only paralysis can be considered; if of very gradual onset, the clinician will first want to rule out a deformity of the cricoarytenoid joints, such as can be seen with cricoid chondrosarcoma.
  • Position and appearance: Position is normal during breathing, but the posterior commissure cannot be brought to full closure whether during voicing, cough, or Valsalva maneuver.
  • Appearance during voicing (under strobe lighting): Vibration of the vocal cords can be normal, though, again, the persistent posterior commissure gap will be seen. The tone and bulk of the vocal cords themselves are normal.
  • Voice quality: Air-wasting, and with shortened phonation time, but without the luffing and diplophonia often apparent when the thyroartyenoid (TA) muscle is also paralyzed.

Other variants of vocal cord paresis include TA-only, TA + LCA, PCA-only (posterior cricoarytenoid muscle), and LCA-only (lateral cricoarytenoid muscle).

Photos of IA-only paresis:

IA-Only Paresis

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IA-only paresis (1 of 5)

This patient describes his voice as being extremely weak with an abrupt onset that was unrelated to intubation or any other injury. The patient's voice sounds extremely breathy regardless of vocal task. The amount of bowing seen here cannot fully explain the breathy (air-wasting) dysphonia that is heard.

IA-only paresis (2 of 5)

An intense visualization of the posterior commissure begins to reveal the mystery. While the "toes" (indicated by each letter T), or vocal processes of the arytenoids, come into full contact, the "heels" (indicated by each letter H), or bodies of the arytenoid cartilages, do not.

IA-only paresis (3 of 5)

An even closer view shows the persistent posterior commissure gap.

IA-only paresis, during a cough (4 of 5)

The elicited cough shown in this image proves that the patient is physically unable to close the posterior commissure.

IA-only paresis, during a Valsalva maneuver (5 of 5)

An elicited Valsalva maneuver, which also fails to close the posterior commissure. High-resolution CT was performed to prove there was no abnormality of the cricoid or arytenoids which might account for this finding of apparent interarytenoid paresis or avulsion.

Interarytenoid (IA) Weakness

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PCA muscles intact (1 of 4)

After SLAD-R surgery. The PCA muscles are intact, explaining normal abduction of both vocal cords for breathing.

Pre-phonatory instant (2 of 4)

At the pre-phonatory instant, one can see partial recovery of LCA muscles, explaining the ability of tips of vocal processes (at dots) to turn medially as the patient prepares to produce voice. Bowing is due to continuing TA weakness.

IA weakness (3 of 4)

The tips of the vocal processes (again at dots) are touching; the gap that remains posterior to them suggests that the interarytenoid muscle (IA) is not yet contracting sufficiently to bring the “heels” of the arytenoids together.

View of posterior commissure (4 of 4)

Very close-range view in the posterior commissure as the patient phonates, showing that the arytenoids do not come into contact. The tips of vocal processes are touching but out of view at the bottom of the photo (below the dots).

Another Interarytenoid (IA) Muscle Paresis or Is It Avulsion?

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good vocal cords in a middle aged man

Breathy and weak voice (1 of 8)

Middle aged man with fairly abrupt weakening of voice with no explanation that occurred a year before this examination. Voice is very breathy, air-wasting, and weak. He also has a tendency to cough on liquids. Distant view at high pitch shows good vocal cord closure and symmetrical pharyngeal squeeze.
bducted vocal cords

Bowing (2 of 8)

The abducted vocal cords for breathing show vocal cord bowing but otherwise nothing particularly noteworthy.
medial turning of the vocal processes

Pre-phonatory view (3 of 8)

As the vocal cords move towards each other on the way to producing voice, note the medial turning of the vocal processes (arrows), suggesting LCA muscles to be intact. The bodies of arytenoids, their “heels” as compared with the vocal process “toes” do not yet approach each other.
vibratory blur of the cords

Phonatory view (4 of 8)

Now producing voice (see vibratory blur of the cords under this standard light) shows that vocal processes are in contact (arrows) but the ‘heels’ of the arytenoids still do not approximate. Is this nonorganic? Neurogenic? Orthopedic (cricoarytenoid joints)? Myogenic?
Deep inside the posterior commissure during phonation

Posterior commissure (5 of 8)

Deep inside the posterior commissure during phonation. The large chink persists.
good thyroarytenoid (TA) function

TA function (6 of 8)

Closed phase of vibration at B3 (247 Hz) shows good thyroarytenoid (TA) function.
interarytenoid (IA) mucosa is blown away from the chink

IA mucosa (7 of 8)

The interarytenoid (IA) mucosa is blown away from the chink here by uncontrollable blast of air even while the patient tries to Valsalva /breath hold. Tight closure of not only true, but also false cords verifies his level of effort.
interarytenoid mucosa has oscillated anteriorly

IA avulsion (8 of 8)

During same Valsalva maneuver 1/5th of a second (6 frames) later, the interarytenoid mucosa has oscillated anteriorly (arrow). Why can’t the arytenoid “heels” come together? The best thought here is interarytenoid avulsion which could have sudden onset. Denervation seems possible but less likely given presumed bilateral innervation of that muscle, and a bilaterally symmetrical joint problem of rapid onset also seems unlikely.

Watch the Progression of A Rare Laryngeal Paresis Scenario Including Interarytenoid (IA) Muscle

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hitish lesion of the right cord is a red herring finding

Full abduction (1 of 5)

Three months ago, this otherwise healthy woman experienced an abrupt change in voice. The vocal phenomenology is that of weakness and air-wasting. Here, in full abduction, the vocal cords look slender and the whitish lesion of the right cord (left of photo) is a red herring finding. (Compare with Photo 3.)
Large gap during phonation

Large gap during phonation (2 of 5)

During phonation (note blurring of the vocal cord margins), there is a large gap between the cords. Interarytenoid muscle seems to be functioning, in that the “heels” of the arytenoids come into quite good contact (horizontal arrows, above). The tips of vocal processes, or “toes” of the arytenoid cartilages, point laterally, (diverging arrows, below) suggesting LCA weakness. (Compare with photo 4.)
vocal cords appear to be hyper-abducted

Two months later—voice is even worse (3 of 5)

Two months later, the patient reports that her voice is even worse. Note that while breathing, the vocal cords appear to be hyper-abducted. It is as though more of the ability to adduct (come together) has been lost; put another way, that abduction is less “balanced” by any tone from adductory (voicing) muscles. (Compare with photo 1.)
Arytenoids no longer touch

Arytenoids no longer touch (4 of 5)

Here, at the prephonatory instant, just before vibratory blurring commences, notice that the heels of the arytenoids no longer touch. It is as though IA muscle is denervated. (Compare with photo 2.)
Extremely breathy voicing

Breathy voicing (5 of 5)

Extremely breathy voicing has commenced. Note the blurring of the right cord margin (left of photo). If anything, the posterior glottis is even farther apart. Radiographic/diagnostic questions: Is there a mass lesion anywhere? No. Is the cricoid cartilage deformed? No. What is causing this? Unknown.


Of unknown cause. This term is used most often in laryngology to refer to vocal cord paralysis, after a mass lesion along the course of the recurrent laryngeal nerve is ruled out.

Idiopathic Subglottic Stenosis

A subtype of subglottic stenosis that is inflammatory. One view is that this entity is actually a limited expression of Wegener’s Granulomatosis (aka Granulomatosis with polyangiitis).



Idiopathic subglottic stenosis has different levels: Series of 4 photos

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dilation of idiopathic subglottic stenosis

Post dilation (1 of 4)

Six months after dilation of idiopathic (inflammatory) subglottic stenosis, the patient has noted only slight deterioration, and breathing ability remains acceptable to her.
closer view of idiopathic subglottic stenosis

Closer view (2 of 4)

At closer range, the inflammatory component appears more evident.
vascular pattern

Rich vascular pattern (3 of 4)

The rich vascular pattern accompanying the lesion is seen better and is a visual finding of inflammation.
congested capillaries

"Sharing" the airway (4 of 4)

Here, the scope has been passed through the area of maximal narrowing and the patient becomes acutely aware of greater difficulty breathing. "Sharing the airway" is a way of 'measuring' it functionally. Note again the congested capillaries.

Another way to inject idiopathic subglottic stenosis: Series of 3 photos

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idiopathic inflammatory subglottic stenosis

Idiopathic inflammatory subglottic stenosis (1 of 3)

This patient is about to receive a triamcinolone (steroid) injection into her idiopathic inflammatory subglottic stenosis, while sitting in a chair under topical anesthesia. Dotted circle is for reference with Photo 2.
infused medication into cricoid

Priot to injection (2 of 3)

A needle has been passed through anterior neck skin and its tip rests out of sight, submucosally just inferior to the anterior cricoid ring. Note that the milky white medication has been infused submucosally within the dotted ring.
needle in tracheal wall

Injection (3 of 3)

Here, the 27-gauge needle traverses the trachea in order to inject the posterior tracheal wall. The submucosal white medication appears at the *.

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.

Check out our list of resources containing peer-reviewed articles, patient stories and more!

Photos of the cricopharyngeus muscle:

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Location of the cricopharyngeus muscle

Cricopharyngeus Muscle (1 of 3)

The highlighted oval represents the location of the cricopharyngeus muscle.
Retrograde Cricopharyngeus Dysfunction (R-CPD)

Cricopharyngeus Muscle (2 of 3)

The cricopharyngeus muscles in the open position.
Contracted Cricopharyngeus Muscle

Contracted Cricopharyngeus Muscle (3 of 3)

The cricopharyngeus muscle in the contracted position.

Esophageal Findings: Series of 3 photos

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Reperti esofagei (1 di 3)

A view of the mid-esophagus in a young person (early 30’s). The esophagus is kept open by the patient’s un-burped air. Note the “aortic shelf” at A, delineated by dotted lines.

Esophageal Findings (2 of 3)

A moment later, additional air is pushed upwards from the stomach to dilate the mid-esophagus even more. A bony “spur” in the spine is thrown into high relief by the stretched esophagus.

Esophageal Findings (3 of 3)

A view of the upper esophagus (from just below the cricopharyngeus muscle sphincter) shows what appears to be remarkable lateral dilation (arrows) caused over time by the patient’s unburpable air. Dilation can only occur laterally due to confinement of the esophagus by trachea (anteriorly) and spine (posteriorly), as marked.

Abdominal Distention of R-CPD: Series of 3 photos

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Gastric Air Bubble (1 of 3)

This abdominal xray of an individual with R-CPD shows a remarkably large gastric air bubble (dotted line), and also excessive air in transverse (T) and descending (D) colon. All of this extra air can cause abdominal distention that increases as the day progresses.

Bloated Abdomen (2 of 3)

Flatulence in the evening and even into the night returns the abdomen to normal, but the cycle repeats the next day. To ask patients their degree of abdominal distention, we use pregnancy as an analogy in both men and women. Not everyone describes this problem. Most, however, say that late in the day they appear to be “at least 3 months pregnant.” Some say “6 months” or even “full term.” In a different patient with untreated R-CPD, here is what her abdomen looked like late in every day. Her abdomen bulges due to all of the air in her GI tract, just as shown in Photo 1.

Non-bloated Abdomen (3 of 3)

The same patient, a few weeks after Botox injection. She is now able to burp. Bloating and flatulence are remarkably diminished, and her abdomen no longer balloons towards the end of every day.

A Rare “abdominal crisis” Due to R-CPD (inability to burp)

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X-Ray of Abdominal Bloating (1 of 2)

This young man had an abdominal crisis related to R-CPD. He has had lifelong symptoms of classic R-CPD: inability to burp, gurgling, bloating, and flatulence. During a time of particular discomfort, he unfortunately took a “remedy” that was carbonated. Here you see a massive stomach air bubble. A lot of his intestines are air-filled and pressed up and to his right (left of photo, at arrow). The internal pressure within his abdomen also shut off his ability to pass gas. Note arrow pointing to lack of gas in the descending colon/rectum. NG decompression of his stomach allowed him to resume passing gas, returning him to his baseline “daily misery” of R-CPD.

X-Ray of Abdominal Bloating (2 of 2)

X-Ray without markings

Can’t Burp: Progression of Bloating and Abdominal Distention – a Daily Cycle for Many with R-CPD

This young woman has classic R-CPD symptoms—the can’t burp syndrome. Early in the day, her symptoms are least, and abdomen at “baseline” because she has “deflated” via flatulence through the night.  In this series you see the difference in her abdominal distention between early and late in the day.  The xray images show the remarkable amount of air retained that explains her bloating and distention.  Her progression is quite typical; some with R-CPD distend even more than shown here especially after eating a large meal or consuming anything carbonated.

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Side view of a bloated abdomen (1 of 6)

Early in the day, side view of the abdomen shows mild distention. The patient’s discomfort is minimal at this time of day as compared with later.

Mild distension (2 of 6)

Also early in the day, a front view, showing again mild distention.

Front view (3 of 6)

Late in the same day, another side view to compare with photo 1. Accumulation of air in stomach and intestines is distending the abdominal wall.

Another view (4 of 6)

Also late in the day, the front view to compare with photo 2, showing considerably more distention. The patient is quite uncomfortable, bloated, and feels ready to “pop.” Flatulence becomes more intense this time of day, and will continue through the night.

X-ray of trapped air (5 of 6)

Antero-posterior xray of the chest shows a very large stomach air bubble (at *) and the descending colon is filled with air (arrow).

Side view (6 of 6)

A lateral view chest xray shows again the large amount of excess air in the stomach and intestines that the patient must rid herself of via flatulence, typically including through the night, in order to begin the cycle again the next day.

Shortness of Breath Caused by No-Burp (R-CPD)

Persons who can’t burp and have the full-blown R-CPD syndrome often say that when the bloating and distention are particularly bad—and especially when they have a sense of chest pressure, they also have a feeling of shortness of breath. They’ll say, for example, “I’m a [singer, or runner, or cyclist or _____], but my ability is so diminished by R-CPD.  If I’m competing or performing I can’t eat or drink for 6 hours beforehand.”  Some even say that they can’t complete a yawn when symptoms are particularly bad.  The xrays below explain how inability to burp can cause shortness of breath. 

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X-ray of trapped air (1 of 2)

In this antero-posterior xray, one can see that there is so much air in the abdomen, that the diaphragm especially on the left (right of xray) is lifted up, effectively diminishing the volume of the chest cavity and with it, the size of a breath a person can take.

Side view (2 of 2)

The lateral view again shows the line of the thin diaphragmatic muscle above the enormous amount of air in the stomach. The diaphragm inserts on itself so that when it contracts it flattens. That action sucks air into the lungs and simultaneously pushes abdominal contents downward. But how can the diaphragm press down all the extra air? It can’t fully, and the inspiratory volume is thereby diminished. The person says “I can’t get a deep breath.”

More Interesting Esophageal Findings of R-CPD (Inability to Burp)

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Stretched Esophagus

Stretched Esophagus (1 of 4)

Using a 3.7mm ENT scope with no insufflated air, note the marked dilation of the esophagus by swallowed air the patient is unable to belch. T = trachea; A = aortic shelf; S = spine
posterior wall of the trachea

Tracheal Wall (2 of 4)

The posterior wall of the trachea (T) is better seen here from a little higher in the esophagus. A = aorta
stretched esophagus

Over-dilation (3 of 4)

The photo is rotated clockwise at a moment when air from below is pushed upward so as to transiently over-dilate the esophagus. Note that the esophagus is almost stretching around the left side of the trachea in the direction of the arrow.
left mainstem bronchus is made visible

Bronchus (4 of 4)

Now deeper in the esophagus (with it inflated throughout the entire examination by the patient’s own air), it even appears that the left mainstem bronchus (B) is made visible by esophageal dilation stretching around it.

Dramatic Lateral Dilation of the Upper Esophagus: Series of 3 photos

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lateral dilation of the throat at C6 of the spine

(1 of 3)

This photo is at the level of (estimated) C6 of the spine (at S). This person has known cervical arthritis, accounting for the prominence. Opposite the spine is the trachea (T). Note the remarkable lateral dilation (arrows) in this picture obtained with with no insufflated air using a 3.6mm ENF-VQ scope. It is the patient’s own air keeping the esophagus open for viewing.
air from below further dilates the upper esophagus

(2 of 3)

At a moment when air from below further dilates the upper esophagus, the tracheal outline is particularly well-seen (T) opposite the spine (S). The “width” of the trachea indicated further emphasizes the degree of lateral dilation, which is necessary because spine and trachea resist anteroposterior dilation.
aortic shelf at the mid-esophagus

(3 of 3)

Just for interest, at mid-esophagus, the familiar aortic “shelf” is seen. Again, this esophagus is being viewed with a 3.6 mm scope with only the patient own (un-burped) air allowing this view.

What the Esophagus Can Look Like “Below A Burp”: Series of 3 photos

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Mid-esophagus of a person with R-CPD

Baseline (1 of 3)

Mid-esophagus of a person with R-CPD who is now burping well after Botox injection into the cricopharyngeus muscle many months earlier. The esophagus remains somewhat open likely due to esophageal stretching from the years of being unable to burp and also a “coming burp.”
esophagus dilates abruptly

Pre-burp (2 of 3)

A split-second before a successful burp the esophagus dilates abruptly from baseline (photo 1) as the excess air briefly enlarges the esophagus. An audible burp occurs at this point.
burp in the esophagus

Post-burp (3 of 3)

The burp having just happened, the esophagus collapses to partially closed as the air that was “inflating it” has been released.

Where have no-burpers traveled from?


R-CPD patients BVI treated across the USA

World Map of RCPD Patients

Inability to Initiate Swallow

When a person feels unable to initiate the swallow. Normally, after the oral preparatory phase of swallowing (chewing, mixing with saliva), a person can voluntarily initiate the swallow reflex by moving the liquid or chewed food back to the base of the tongue, triggering the reflex. Occasionally, however, a person with otherwise normal swallowing feels unable to start or commit to the swallow. They often say, “The food just stays in my mouth; I can’t seem to get myself to swallow.” This problem can be neurogenic, but can also reflect a kind of phobia or sense of vulnerability about swallowing.

Indicator Lesions

Indicator lesions are visual findings of vibratory injury in a person who has no current voice complaints, and whose “swelling checks” are normal.


Individuals who fit the “vocal overdoer profile” may only notice vocal limitations caused by vibratory injury on an occasional and transient basis. These episodes may be brushed off as insignificant, because they are so brief, and recovery so complete. Even while asymptomatic, however, such individuals may have subtle visual findings of vibratory injury—“Indicator lesions.” Unless discovered during a screening examination for entry to music studies, the individual may be unaware of these findings. What if indicator lesions are found? Suggested responses:

1. Make sure the individual understands that these are indicator lesions and as such constitute a “yellow flag” suggesting at least occasional overuse of voice.

2. Define the “vocal overdoer syndrome” for the person as the combination of and interaction between an expressive, talkative, extroverted personality and a “vocally busy” life. Said another way, there may be both intrinsic, personality-based and extrinsic, vocal commitment based reasons that amount and forcefulness of voice may be excessive. A 7-point talkativeness scale can be used to estimate the intrinsic risk, where “1” represents Clint Eastwood, “4” the averagely talkative person, and “7” the life of the party. The extrinsic risk is addressed by making a list of vocal commitments such as for occupation, childcare, hobbies, social activities, religious practice, athletics/ sports, and rehearsal and performance.

3. Discuss the symptom complex of mucosal injury:

a) Loss/ impairment of high, pianissimo singing;

b) Day-to-day variability of vocal clarity and capability;

c) A sense of increased effort to produce voice;

d) Reduced mucosal endurance, or becoming “tired” vocally from amount/ manner of voice use that does not seem to induce this in others;

e) Phonatory onset delays—the slight hiss of air that precedes the beginning of the sound, especially if high and soft. Speaking voice hoarseness can be a fairly late and gross symptom of mucosal injury.

4. Talk about managing the amount, manner, and spacing of voice use to reduce unnecessary wear and tear on the vocal cord mucosa.

5. Teach vocal cord swelling checks as a means of detecting even subtle injury. Respond to what they tell you!

Singers are understandably distressed when they discover even the tiniest mucosal swelling such as indicator lesions. That is because for true singers, singing is not just what they do; the term “singer” also defines who they are. So injury threatens both activity and identity. Consequently, discuss indicator lesions with great care and sensitivity. Keep in mind that some doctors speak of “small vocal nodules that do not interfere with singing.”

Small nodules that are but a tiny step above indicator lesions, especially when spicule-shaped rather than fusiform, always exact a penalty to the singing voice (see #3 above), but limitations can often be concealed by warming up, and singing more loudly. Singers often say “I have a big voice that doesn’t do pianissimo.” That is, pp becomes p; mp becomes p; mf becomes f; and so forth. Alternatively, the singer considers the missing pianissimo to be a technical fault.

Indicator Lesions and MTD

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Breathy voice (1 of 6)

Distant view at the prephonatory instant in young female singer. There is a wide gap between the cords. The explanation for this gap is not immediately evident, but the voice is breathy.

Phonation (2 of 6)

Phonation has started with margin blurring, and the sense of extra space between the cords remains.

Open phase (3 of 6)

Strobe light, open phase of vibration at B4 (494 Hz)

Closed phase (4 of 6)

Closed phase of vibration, still at B4. Note the incomplete closure posteriorly caused by MTD. Arrows indicate the vocal processes.

Open phase, indicator lesions (5 of 6)

Open phase of vibration, strobe light, at F#5 (740 Hz). Here, the subtle indicator lesions are seen more clearly; vocal cord margins are not perfectly straight.

"Closed" phase, MTD (6 of 6)

“Closed” phase of vibration is not really closed and the vocal processes do not come into full closure, again consistent with MTD.

Indicator Lesions

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Middle-aged teacher (1 of 4)

Middle-aged teacher who also sings. She is aware of effortfulness to sing; this is hard to interpret because she is pre-menopausal and also not actively singing/ grooming her voice. Extraordinarily subtle margin swellings could easily be overlooked in this view.

Phonatory view (2 of 4)

During phonation at E-flat 4 (311 Hz) with vibratory blurring under standard light. The subtle narrowing of the blurred dark line between the folds could still be overlooked.

Pre-phonatory instant (3 of 4)

Use of the pre-phonatory instant by having the patient do repeated staccato at the same pitch. Here, very small, low-profile, and broad-based swellings can be seen.

Indicator swellings (4 of 4)

At much higher pitch, E5 (659 Hz) and using strobe light. In this view of the open phase of vibration, at high magnification, the rounded “indicator swellings” are seen best.

Indirect vs. Direct Laryngoscopy

Direct laryngoscopy refers to viewing the larynx directly, in a straight line, through a hollow, lighted tube, with the patient typically under general anesthesia. Indirect laryngoscopy refers to visualization of the larynx with the patient sitting in a chair, by using a mirror, fiberscope, videoendoscope, or laryngeal telescope more in the manner of a perisocope that “looks around the corner” – in this case, the base of the tongue.


Indole-3-carbinol (I3C) is a phytochemical (plant chemical) found in significant quantities in cruciferous vegetables (cabbage, broccoli, cauliflower, Brussels sprouts, kale, collards, kohlrabi). Capsules of I3C may be purchased without prescription as a nutritional supplement. This compound alters estrogen metabolism and the result is anti-proliferative. I3C has been widely used as a treatment for recurrent respiratory papillomatosis (RRP), though our physicians have found the benefit in their adult patients to be underwhelming.


Toward the lower end of a person’s body. For example: the feet are inferior to the head. The opposite of superior.

Inflammatory Stenosis

Inflammatory stenosis is narrowing in a lumen or passageway caused by an inflammatory process. This term is used most commonly at our practice to refer to stenosis in the high trachea or subglottis, thought to be an incomplete expression (forme fruste) of Wegener’s granulomatosis.

Photos of Inflammatory Stenosis:

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Rheumatoid arthritis (1 of 4)

Young woman diagnosed several years earlier with rheumatoid arthritis, but 8 months ago noted noisy breathing and exercise intolerance. This medium-range view shows inflammatory subglottic narrowing.

Inflammatory subglottic stenosis (2 of 4)

At closer range, this inflammatory subglottic stenosis is seen better.

One week after dilation (3 of 4)

A week after outpatient dilation, steroid injection, the patient’s symptoms are dramatically reduced. Adherent mucus makes the caliber look smaller than it is. Compare with photo 1.

Mucus (4 of 4)

At closer range, the lumen is much enlarged, especially if adherent mucus were not present ('M' stands for mucus). Compare with photo 2.

Injection Laryngoplasty

Injection laryngoplasty is a procedure during which the vocal cord is injected (filled) with an implant material.  The most common reason for this is a paralyzed vocal cord, but it might also be used for severe vocal cord bowing unresponsive to voice building. There are also other diagnoses such as atrophy or tissue loss. In each of these diagnoses, the patient is motivated by a weak, air-wasting (breathy or diplophonic) voice quality that is highly limiting to his or her ability to communicate.

Materials available for injection are a temporary gel (various brands), a semi-permanent calcium hydroxyapatite paste, micronized human collagen, the patient’s own fat, usually harvested from around the umbilicus, or in an earlier era, Teflon™ paste.  The particular material used usually depends upon whether temporary or more permanent voice strengthening is needed.

The purpose of injection laryngoplasty is two-fold:

First, to fatten the cord and shift its static position toward the midline so that the other (mobile) vocal cord can “reach it.”  The second reason is to fortify the tissue so that the deficient cord is less flaccid and can “stand up” to the air pressure below and passing between the two cords when they are positioned together to create voice.

The vocal cord can be injected in three ways:

1) With the help of extensive topical anestheisa, In an “office” videoendoscopy room, using a curved cannula inserted through the mouth, over the back of the tongue, and down into the cord through its upper surface.

2)  In an “office” videoendoscopy room, injecting through the anterior neck while viewing the vocal cords video-endoscopically on a monitor screen.

3)  In an outpatient operating room and during brief general anesthesia, viewing through a laryngoscope placed through the mouth to visualize the vocal cords, and injecting in a straight line through the upper surface of the vocal cord(s).

Which method is used depends on surgeon and patient preference, as well as the circumstance.  For example, a medically-fragile patient might be best done under topical anesthesia in an “enhanced office” setting.  A person having more permanent material injected, and certainly if it is to be bilateral, may need exquisite symmetry of injection more suitably done under brief general anesthesia.

Injection Laryngoplasty with Temporary Gel

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Laryngoplasty (1 of 4)

This person awakened with a weak, whispery voice after emergency abdominal surgery. Now 3+ months later, voice is returning by degrees but is still very weak. In this photo, the patient is breathing quietly. The weak left vocal cord is more bowed than the right.
whispery air-wasting voice

Reason for air-wasting (2 of 4)

When she tries to produce voice, the left vocal cord comes only part of the way to the midline, leaving a large gap, and explaining her whispery air-wasting voice quality.
Voice gel injected into vocal cord

Voice gel injected into vocal cord (3 of 4)

On the same day, due to pressing patient need, the left vocal cord was “plumped” with voice gel. That material typically provides temporary benefit of 6 to 12 weeks, gradually absorbing during that time.
Vocal cords close completely

Vocal cords close completely (4 of 4)

Voice is dramatically improved, now that her vocal cords can more fully close to reduce the air-wasting and transform the voice from whispery to strong. Compare with photo 2.

Injection Laryngoplasty

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Vocal cord paralysis

Vocal cord paralysis (1 of 7)

This person has a whispery voice due to right vocal cord paralysis. The right cord (left of photo) does not move from this lateralized position, whether she is breathing or attempting to make voice. The left cord (right of photo) is mobile and lateralized in this breathing position but can come to midline (see photo 3) when she makes voice. Here you see a needle poised to inject the slender, paralyzed lateralized cord with a filler material, in this case voice “gel.”
Voice gel injection

Voice gel injection (2 of 7)

After the cord has been plumped up with injected voice gel. The injected cord is now within reach of the left cord during voicing, and it is also more firm.
Strong voice

Success (3 of 7)

The needle is withdrawn, and the patient is producing strong voice.
Plump right vocal cord

Plump right vocal cord (4 of 7)

A month later, as expected, the right cord (left of photo) remains plump.
posterior gap due to LCA weakness

Posterior gap (5 of 7)

Voice remains very good, due to ability to press the cords together. The upper surface of the injected cord is at a higher level than the left cord, due to the expected bulging “superiorly” and not only medially. Incidentally noted is the posterior gap due to LCA weakness. See the tell-tale lateral turning of the right vocal process at arrow.
right cord does not fully lateralize

PCA Weakness (6 of 7)

A little over a year after injection, the right cord appears to remain somewhat plump, as though some voice gel remains in a “pool” that protects from resorption. Though not well shown here, the right cord does not fully lateralize, suggesting residual PCA weakness.
vocal process has come back into line

LCA muscle recovered (7 of 7)

Voice remains very good, and the cords come into good approximation. The upper surface bulging is no longer seen. The most telling finding is that the LCA muscle appears to have recovered, and very likely, the TA muscle with it. Note that the vocal process has come back into line with the rest of the cord (arrow), and the posterior commissure gap seen in photo 5 is no longer seen. The patient’s excellent voice is explained by recovery of voicing muscles (TA and LCA) more than by residual voice gel.

Inpatient surgery

Inpatient surgery is surgery performed in a hospital in which the patient is expected to stay over at least one night. Most often, the patient reports early the morning of surgery for admission to the hospital, undergoes the procedure, and then is taken from recovery room back to their hospital bed for one or more days of recovery.


The act of drawing air from the environment into the nose or mouth and down into the air sacs (alveoli) of the lungs, where the exchange of oxygen and carbon dioxide happens. En route to the lungs, this in-drawn air passes down through the laryngeal vestibule, between the vocal cords, and then down the trachea and bronchi on their way to the air sacs. Also known as inhalation.

Inspiratory Phonation

When voice is produced using inhaled air. By contrast, normal voice production uses exhaled air. Voice production with inhaled air is often involuntary or unintentional—for example, a gasp of surprise, or with a person whose vocal cords are scarred or paralyzed in a nearly closed position. Inspiratory phonation is also more limited with respect to pitch range and loudness than is normal, expiratory phonation.


Reinke’s (smoking-related) edema and how to see it: Series of 4 photos

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Convexed vocal cords (1 of 4)

Abducted, breathing position. Note that the margin of both vocal cords is slightly convex. See dotted line for normal, perfectly straight margin.

Inspiratory phonation (2 of 4)

Inspiratory phonation in-draws the mild Reinke’s edema (smoker’s type polyp formation).

Open phase, faint translucency (3 of 4)

Strobe illumination, at E4 (approximately 330 Hz), mostly open phase.

Closed phase, faint translucency (4 of 4)

Note again in closed phase.


Smoker’s Polyps (aka Polypoid Degeneration or Reinke’s Edema)
This video illustrates how smoker’s polyps can be seen more easily when the patient makes voice while breathing in (called inspiratory phonation). During inspiratory phonation, the polyps are drawn inward and become easier to identify.

Integrative diagnostic model

The integrative diagnostic model is a powerful, three-part methodology for diagnosis: a voice-focused history; assessment of vocal capabilities and vocal limitations via elicitation; and intense laryngeal examination. Once these three parts of the evaluation are accomplished, the information gleaned from them must be integrated and correlated to arrive at a sound diagnosis.

Background of the integrative diagnostic model:

In an attempt to use only what is necessary and sufficient from the remarkable list of options available for evaluation, this model was developed and refined as an accurate and efficient process for diagnosing voice disorders. There are, of course, other models: a “traditional” one might include only a patient history and then proceed directly to examination of the larynx.

The history, as told by the patient and family, is the “story line” of the problem. The examination is performed either with the time-honored laryngeal mirror or a fiberscope. In some circumstances, this traditional model is sufficient, such as when the disorder is obvious or acute. For chronic or elusive disorders, this traditional model often or even routinely does not provide enough information to make a complete diagnosis and to support patient understanding of their problem.

The inadequacy of the traditional model has led some to dramatically expand the diagnostic process, and to divide an expanded list of diagnostic tasks among two or more clinicians. That is, different clinicians (laryngologist, speech pathologist, neurologist, etc.) may each take a separate history, and then assess basic characteristics of the voice using auditory perception; they may then make acoustic, aerodynamic, electroglottographic, and even electromyographic machine measures of the acoustic, airflow, and neurophysiological output of the larynx; and finally examine the vocal folds using a state-of-the-art technique called laryngeal videostroboscopy. This dramatic expansion of the diagnostic process could be dubbed the technology-driven or reductionistic model. It can be argued that some items on the expanded list of diagnostic modalities are superfluous for diagnostic evaluation – and only encumber the process. Even when this technology-driven approach arrives at an accurate diagnosis, it may have done so with much more time and expense than necessary. Furthermore, unless machine measures are collected at the extremes of vocal capability and these various kinds of data are then skillfully integrated, the diagnosis may still be missed.

Simplicity is a virtue; hence, the formulation of the integrative diagnostic model. Based on extensive review of available diagnostic modalities and years of experience, some laryngologists may find it appropriate to “swim against the current” and resist, for purposes of diagnosis, methodologies that contribute little to the diagnostic process.

How the integrative diagnostic model works:

  1. In the first step, the patient’s history (story line of the problem) is mined for crucial, insight-giving information. It is not the quantity but the relevance of historical details that makes the difference. A focused, voice-relevant history attempts to go directly to necessary information and organize it in a coherent fashion. By the time the history has been completed, the physician should have generated a list of the two or three most likely diagnoses and be ready to move into the second step of the diagnostic process.
  2. In the second step, the voice itself is assessed via a vocal capability battery. The idea here is to ask the voice to accomplish various tasks, each of which helps the physician assess one or another extreme of a particular vocal capability. We are interested, more than anything else, in the extremes of capability because that is where the “abnormal phenomenology” of each particular voice disorder is typically most clearly revealed. The vocal phenomenology that one hears during the vocal capability battery tends to support one or another of the preliminary diagnoses that came to mind during the history. At this point, the clinician is often already focusing in on the single most likely diagnosis, and rarely two or more remain in play.
  3. In the third step, the larynx itself is subjected to intense visual imaging using the latest scopes available, and at times, topical anesthesia to permit a very close-up and precise view. Most often this includes videoendoscopic or videostroboscopic pictures of the larynx, subglottis, and trachea. Often, laryngeal examination is performed during the patient’s performance of the same extremes of vocal capability where abnormal vocal phenomenology was heard during vocal capability elicitation.
  4. After the historical, vocal phenomenology, and laryngeal image information is collected from steps 1, 2, and 3, the physician must synthesize a diagnosis which  fits the information gleaned from each part of the model. Infrequently, the physician will need to keep two potential diagnoses open, though one is usually favored over the other. In such a case, the patient is asked to see the speech pathologist who, through an extended interaction with the patient’s voice and vocal phenomenology, can add additional insight. Almost always, however, a firm diagnosis is reached at the conclusion of the initial consultation using the integrative diagnostic model, and its results are shared with the patient and family, along with the proposed treatment plan – whether medical treatment, behaviorial treatment (speech therapy), surgery, or multiple methods.

In an ideal world, key features of the model are:

  1. All three parts of the model preferably should be mastered by a single individual, rather than spreading it between two or three individuals who see the patient separately or “as a committee.”
  2. Each step of the three-part model should be applied in a codified sequence within the same consultation to make the necessary integration and synthesis of the diagnosis as efficient as possible, within a single clinician visit.
  3. The diagnostic model steadfastly keeps at bay other components beyond the crucial three, eliminating evaluations that might clutter the process of coming to an efficient and precise diagnosis by using only necessary and sufficient methods. Measurements or evaluations that do not fit the requirements of this diagnostic model continue to be seen as primarily for research purposes or for therapy monitoring or biofeedback, rather than as part of the diagnostic process itself.
  4. The individual best able to master the diagnostic model due to innate capabilities and/or motivation in any particular site is the one who should take primary responsibility for diagnosis, whether that individual is a physician or speech pathologist. (In the latter case, there must of course be physician oversight, especially for medical and structural abnormalities.)

Interferon (or Alpha-interferon)

Interferon is a glycoprotein produced especially in white blood cells in response to stimuli such as exposure to virus, bacterium, or parasite. Humans make endogenous (self-made) interferon in relatively small amounts. Exogenous (made outside the body, as by the pharmaceutical industry) interferon may be administered to assist in fighting infection or cancer. In laryngology, interferon has been used against HPV infection that causes recurrent respiratory papillomatosis (RRP).

Intermittent Whisper Phonation

Intermittent whisper phonation is a term that describes the vocal phenomenology of abductor spasmodic dysphonia (AB-SD).

Intubation Injury

Injury, typically to the posterior part of both vocal cords, caused by an endotracheal tube1. An endotracheal tube may be used briefly during general anesthesia for surgery, but may be in place for much longer in persons suffering respiratory failure or neurological injury. When severe, the hallmark vocal phenomenology of intubation injury is breathy-pressed phonation.

Breathing Tube Injury—A Rare Complication of Intubation for General Anesthesia

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Inflamed vocal cord (1 of 5)

This patient had severe voice change after intubation for a 2-hour surgical procedure. She says voice was 100% before surgery and she awakened at 15%, a whisper with a bit of voice mixed in. Fortunately, across six weeks she has recovered partially to “70%.” The right cord (left of photo) looks “inflamed.”

Closer view (2 of 5)

At closer range, a little more detail is seen.

Scarring from intubation tube (3 of 5)

Under narrow band light, it appears that there is scarring of that fold likely from a laceration upon insertion of the tube. (She was told intubation was difficult.) A key finding, however: the right vocal process is turned slightly laterally, suggesting weakness of the LCA muscle.

Mucosal Injury (4 of 5)

Under strobe light, closed phase of vibration, it is almost as if there is loss of mucosa upper surface of right cord.

Flaccidity of right vocal cord (5 of 5)

Open phase of vibration shows flaccidity of the right cord, with a much larger lateral excursion / amplitude of open phase on the right (left of photo).

Conclusion: While we try to explain abnormality due to one cause, here, the patient has a mucosal injury and paresis of right TA and LCA muscles, which can also follow intubation. This explains why the initial postop voice was so weak and whispery, and also the rapid partial improvement. This voice will likely continue to improve and be very functional as a speaking voice. Fortunately, this person is not a singer, as clarity especially in upper notes, will likely be remain impaired even after full recovery.

“Tattoo” of blood after detachment of intubation granuloma

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Intubation granuloma (1 of 5)

This woman was intubated for 5 days due to severe illness. Afterwards, she had no voice for several weeks. It has recovered nearly fully, but she was told elsewhere that there was a “growth” that needed to be removed.

Intubation granuloma (2 of 5)

In this closer view with forced inspiration, one can see that this is a granuloma, with point of attachment at arrows becoming pedunculated. Since granulomas typically mature, pedunculate (become attached by a progressively thinner stalk), and fall off on their own, she was advised to return in 4 months, at which point it would likely be gone.

Granuloma is gone (3 of 5)

4 months later: In this distant view, it appears that the granuloma has indeed detached. (Typically patients do not know when this happened; rarely, they cough out a pink piece of tissue and a bit of blood at the time of detachement.)

Blood tattoo (4 of 5)

In this mid-range view, a “blood tattoo” is seen where the pedicle detached from the granuloma (arrow). This “blood spot” often persists for months or years.

Blood Tattoo (5 of 5)

A closer view of the “blood tattoo.”


Intubation injury audio with photos:

Voice sample of a patient with a cricoartyenoid joint intubation injury (see this patient’s photos just below):

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Intubation injury (1 of 3)

Abducted breathing position. Note the divots at the posterior commissure (arrows), likely due to pressure necrosis caused by intubation of long duration. Dotted lines indicate the lines of the normal cord, to make it easier to see the divots.

Intubation injury (2 of 3)

The irregular white line along the length of the vocal cords (arrows) suggests that there may have been pressure necrosis of the musculo-membranous portion of the vocal cord and that now the mucosa adheres directly to muscle, with no intervening vocal ligament layer.

Maximum phonatory closure (3 of 3)

Note that the posterior commissure defect is hidden by the partial closure of the arytenoid cartilages. Even so, the arytenoid cartilages are unable to come into contact. The musculomembranous cords are quite far apart, due partly to tissue loss. Furthermore, the cords are stiff and inflexible. No glottic voice is possible.

Intubation Injury Causing Partially Frozen Cricoarytenoid Joints

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Intubation injury (1 of 4)

Maximum abduction (separation of the vocal cords for breathing) in a man with a posterior commissure injury due to several days of endotracheal intubation.

Intubation injury (2 of 4)

During voicing. The posterior vocal cords come only slightly closer together (leaving a dark V-shaped gap here); the membranous cords (lower part of the photo) appear to come close enough together that the expiratory air stream brings them into oscillation, seen as a blur under standard light.

Closed phase of vibration (3 of 4)

During voicing, closed phase of vibration, under strobe light. The anterior cords touch, but there remains a very large posterior commissure opening: the vocal processes (at *) do not touch each other as they should during voicing. This is not so much from pressure necrosis as it is from cricoarytenoid joint injury.

Open phase of vibration (4 of 4)

The vocal processes (again, at *) remain in the same orientation to each other as in photo 3.

Intubation Injury

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Abducted, breathing position (1 of 2)

Abducted, breathing position, standard light. Note the large defects in the posterior vocal cord, presumably caused by a long-term endotracheal tube (breathing tube), used when the patient had a life-threatening illness that required ventilation for many weeks.

Intubation injury (2 of 2)

When the patient tries to produce voice, the vocal cords remain far apart due to injury of the crico-arytenoid joints. The posterior divots add to the leakage of air.
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Intubation injury (1 of 3)

Panoramic view shows that the vocal cords abduct (open) fairly fully. At this distance, only a hint of the intubation injury is seen: on one side, at the arrow.

Posterior commissure divots (2 of 3)

Same patient at much closer range, as he is about to make voice. Now the significant posterior commissure divots are seen clearly on both sides. If this were the closest he could get the vocal cords, this would indicate injury to the joints as well.

Intubation injury (3 of 3)

As he actually makes voice, however, the vocal cords do come completely together, proving that the joints can move to fully adducted (closed) position.
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Intubation injury (1 of 4)

After 15 days of intubation, this voice is sounding both breathy (air-wasting) and pressed. From a distance, it appears that the right cord (left of image) is paralyzed. (Compare with image 2.)

Breathy Voice (2 of 4)

During phonation, the vocal cords appear to come together reasonably well, but as already mentioned, the voice sounds breathy.

Vocal cord fixation (3 of 4)

A close-up view shows a posterior divot of the right cord (left of image, at arrows). This finding (along with the absence of atrophy, bowing, or flaccidity when viewed later under srobe light) confirms that the problem is right cord fixation due to scarring of the right cricoarytenoid joint, not paralysis.

During phonation (4 of 4)

The posterior commissure deficit caused by pressure necrosis from the endotracheal tube is shown by the dotted line and arrows. Also seen here is that the vocal processes ( at each pair of green dots) are not reaching each other, further validating the joint injury.

Forcing the Larynx to Give Up Its (Paresis and Intubation Injury) Secrets

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Intubation injury (1 of 4)

This young man was intubated for months at birth. For all of his life of more than 20 years, voice has been what he describes as “50%” of normal. Then after a recent URI, it descended to “20%. ” In this “breathing” position, one would say that abduction is normal, and evidence of intubation erosions is seen within dotted lines.

Forceful exhalation (2 of 4)

As he exhales forcefully, it appears that TA and LCA are normal on the left (right of photo). LCA cannot yet be evaluated on the right (left of photo). The medial dotted line indicates the free margin on each side, and the lateral one, the beginning of the ventricle. The posterior commissure divots are still seen (additional dotted lines).

Phonation begins (3 of 4)

As phonation begins, the flaccid right vocal cord (left of photo) buckles laterally. Posterior commissure visualization will add more information.

LCA (4 of 4)

The right vocal process (left arrow) turns laterally, suggesting that LCA is not working (along with previously-noted TA in photos 2 and 3). Left vocal process (right of photo) turns medially but the rest of the arytenoid more posteriorly appears to be eroded away as also seen in photos 1 and 2.

Intubation Injury, Including A Subglottic Synechia

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Intubation injury, including a subglottic synechia (1 of 2)

View of the vocal cords, in abducted position, in a patient with voice change after long-term intubation due to brain injury. Injury of the left posterior vocal cord (right of image) can be seen, where pressure from the breathing tube caused an erosion or divot (arrow). The synechia is not yet visible from this viewing perspective.

Intubation injury, including a subglottic synechia (2 of 2)

Same patient, just below the level of the cords. This synechia, located posteriorly, is additional evidence of breathing tube injury.

Post-Intubation Stenosis

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Endotrachel tube injury (1 of 4)

View of larynx of an individual in critical condition who was ventilated for 2 weeks via an endotracheal tube. See the erosion of the posterior right cord (left of photo) from pressure necrosis of the endotracheal tube, indicated by the white, semi-circle markings.

Closer view, between the posterior vocal cords (2 of 4)

With tip of endoscope positioned deeper within the larynx, between the posterior vocal cords, a small opening is visible several centimeters distally. Diameter of the opening is an estimated 20% of normal, which is below the level of the patient's tolerance, and explains why a (white) tracheotomy tube has been placed.

Even closer view, showing upper surface of the tube (3 of 4)

Closer view, showing more clearly the curved upper surface of the tracheotomy tube entering just below the stenosis and serving as a “back door” for breathing.

Non-inflammatory stenosis, caused purely by injury (4 of 4)

Note in this close-range view that this is a non-inflamed kind of stenosis caused purely by injury. Compare this with stenosis from presumed forme fruste Wegener’s granulomatosis.

Vocal Cord “Tear” and Granuloma

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Intubation injury (1 of 8)

Gross hoarseness was immediately evident after a surgical procedure involving endotracheal intubation. After a few months, this granuloma is evident. It appears to be pedunculated and attached only where indicated by the dotted line. The small "X" is for reference with photos 2 and 4.

Granuloma drawn into glottis (2 of 8)

Here, the granuloma is drawn downward into the glottis by the inspiratory airstream. The "X" is for reference with photos 1 and 4.

Phonation (3 of 8)

During phonation, seen at closer range, the granuloma rides upward and nearly fills the laryngeal vestibule.

Anterior commissure (4 of 8)

Closeup at the anterior commissure. Dotted line indicates anterior edge of the granuloma. The "X" is for reference with photos 1 and 2.

Granuloma detached (5 of 8)

A few months later, voice has improved. The granuloma has spontaneously detached. Pinkness remains.

Vocal cord blurring (6 of 8)

During voicing under standard light, note that there is vocal cord blurring on the right cord (left of photo) far more than on the left (blurring is indicated by thin, black lines). This suggests that the left side (right of photo) is not vibrating well.

Closed phase (7 of 8)

Low in the female range, at A3 (220 Hz), closed phase of vibration.

Open phase (8 of 8)

Open phase of vibration at the same pitch, showing that only the right cord (left of photo) vibrates.

Injured Adult Larynx from Intubation In Infancy

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Intubation injury (1 of 6)

This young woman has a very weak voice. More than 20 years earlier, she was intubated for a month due to prematurity. Distant view of open (breathing) position. It appears that the right cord (left of photo) does not abduct fully.

Phonation (2 of 6)

Phonation, still seen from a distance. The space between the cords can already be appreciated, but without much detail. Dotted line indicates line of partly missing aryepiglottic cord, likely due to pressure from the endotracheal tube.

Breathing position (3 of 6)

Closer view, breathing position shows a divot in the posterior right cord (left of photo); a similar divot on the left (right of photo) is out of view.

Prephonatory instant (4 of 6)

Closer view at prephonatory instant shows incomplete closure.

Phonatory blurring (5 of 6)

Two frames apart, showing phonatory blurring. This patient cannot bring the posterior cords closer together whether phonating, doing a Valsalva maneuver, breath-holding, etc. This indicates joint injury.

Scarring in subglottis (6 of 6)

Scarring in the subglottis is greater on the left (right of photo) than the right (left of photo).

Intubation Injury to Voice, Airway, from Decades Ago

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Severe intubation injury (1 of 5)

Almost 40 years earlier, long term intubation for a severe neurological problem. Severe injury is seen at both glottic (vocal cord) and subglottic levels. Dashed lines indicate the outline of the endotracheal tube-induced divots that partly explain weak voice. Dotted circle shows what the normal subglottic airway caliber should be.

Subglottic stenosis (2 of 5)

Closer view of subglottic stenosis.

Mid-distal trachea (3 of 5)

View past the subglottic stenosis shows normal mid- and distal trachea.

Posterior commissure keyhole (4 of 5)

As the vocal cords are arriving together for voicing, the posterior commissure keyhole is better appreciated. Dots are for reference with next photo.

Flaccidity (5 of 5)

Still under strobe light, now the flaccidity of right cord (left of photo) is indicated by its larger amplitude of vibration and bowed/ buckled margin.

Injury at Two Levels from Breathing Tube-Particularly Clear

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Posterior commissure divots (1 of 8)

Three months after a 6-day intubation, this man has noisy breathing and a weak, breathy voice. Note the posterior commissure divots from endotracheal tube pressure necrosis, and narrowed subglottic airway likely from balloon pressure.

Closed phase (2 of 8)

Closed phase of vibration under strobe light shows persistent posterior gap causing air-wasting (breathy) voice quality.

Open phase (3 of 8)

Open phase of vibration.

Subglottic stenosis (4 of 8)

Close-up view of the subglottic stenosis, with dotted lines showing what might be normal size. With a membranous component, it is always worth a single dilation to see whether a larger lumen might be gained. In similar cases, an increase of just 10 or 15% lumenal size is much noticed and appreciated by the patient.

Post dilation (5 of 8)

A few days after balloon dilation of the stenosis, with bruising and inflammation still evident.

Closer view (6 of 8)

Closeup of the just-dilated stenosis. Only the membranous (mucosal) band element seen here to have been stretched open will be subject to widening.

Final result (7 of 8)

Final result, seen from a distance, a few months later. Visually, this is not a dramatic change, but when the patient and family were given options “subtle, mild, moderate, or large” to describe the improvement, they both chose “moderate.” And the patient thought the improvement was sufficient for his needs. Compare with photo 1 and 5.

Closer view (8 of 8)

Closeup of final, healed view, showing a change of shape of the lumen. This man is content with his current “limited but acceptable” airway. If he became dissatisfied and therefore motivated, tracheal resection and reanastomosis would be his best option, though it would not be wrong to do one more dilation, to see if another slight improvement could be gained.

Subglottic Granulation and Curving Airstream

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Intubation injury (1 of 4)

After a 9-day intubation for serious illness, the patient has difficulty breathing due to this “proud flesh” response to injury within the cricoid ring, posteriorly. Breathing has improved in the past week, leading to a decision to await further maturation, rather than proceeding to microlaryngoscopic removal.

Lobules (2 of 4)

Close-up view of the lobules of granulation tissue. Air can easily pass around the obstruction as indicated by the arrows.

2 months later (3 of 4)

As predicted, breathing continued to improve to the point of seeming normal to the patient, and 2 months later, the granulation tissue has matured and detached, leaving behind a subglottic scar band (parallel lines).

Scar band (4 of 4)

Here is a close-up of the scar band. A solid line denotes the anterior border of the scar band for reference in all 4 photos, but compare especially to photo 2.

Double Whammy: Intubation Injury + Glottic Furrows

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Intubation injury + glottic furrows (1 of 4)

Extremely poor voice in elderly man after severe, life-threatening illness with complications; including an 18-day endotracheal intubation for purposes of ventilation. Now he is being evaluated for his very poor voice. Here, open (breathing) position at a distance does not show the findings as clearly as in subsequent photos. Small X's are for reference with remaining photos. The arrows denote tip of vocal processes.

Bilateral glottic furrows (2 of 4)

At closer range, divots begin to be appreciated (above the X's) and bilateral glottic furrows are more clearly noted.

Intubation injury (3 of 4)

As the vocal cords begin to close, this view (deep into the posterior commissure) shows clearly the divots caused by pressure necrosis outline where the breathing tube sat. Dotted lines show what would be the normal line of posterior vocal cords.

Phonatory position (4 of 4)

Now in closed voice-making position, posterior defect is out of view, but the vocal processes remain visible and come into contact at arrows. This shows that the endotracheal tube injuries are divots only without scarring of the joint capsules (that if present would prohibit contact of the vocal processes at arrows). There is air wasting through the posterior keyhole not visible here, and the bilateral glottic furrows and pseudo-bowing are extremely evident. They cause additional air-wasting, and adherence of mucosa at the depth of the furrows interferes with the mucosa’s vibratory ability.

Sometimes You DO Remove Granulation to Avoid Tracheotomy

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Granulation (1 of 8)

Prior to this first visit, this person suffered extensive burns, was intubated for 10 days, and then underwent tracheotomy, and then was decannulated (tracheotomy removed). She has scarring of the posterior commissure outlined by the dotted line. The granulation extends well down into the subglottis. She is uncomfortable with a marginal airway and noisy breathing. Laser and microdebrider are planned to try to avoid having to reinsert the tracheotomy.

Closer view (2 of 8)

Tip of the iceberg view of granulation and scarred area.

Post microlaryngoscopies (3 of 8)

After a series of microlaryngoscopies purely to improve airway and avoid tracheotomy, the granulation has finally matured. Airway is no longer marginal, but is still very limited for significant activity.

Scarring (4 of 8)

At close range, the area of posterior scarring is again indicated by dotted line; the dark area of the actual airway is narrow and slit-like.

Post posterior commissuroplasty (5 of 8)

A month after posterior commissuroplasty, breathing is improved due to the widened space posteriorly. Compare the dark area for breathing with photo 3.

Breathing improved (6 of 8)

Six months after posterior commissuroplasty, breathing remains much improved. Compare dark airway contour again with photo 3 above.

Closer view (7 of 8)

A closer view of the airway, which is much wider posteriorly than preoperatively (photo 4).

Phonatory view (8 of 8)

When patient makes voice, there is a persistent space posteriorly, where the airway was surgically widened, but again, this has not significantly affected the voice.

Who Knew…? Many Such Injuries Are Never Found

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Coughing evaluation (1 of 6)

An octogenarian is being evaluated for recent coughing of months duration. To evaluate her complaint of major mucus production, an “exam of opportunity” mini-bronchoscopy was done. Salivary pooling (see bubbles) is seen, likely due to interference with swallowing caused by topical anesthesia.

Intubation scars (2 of 6)

Just barely through the vocal cords, two circumferential scars are seen at 1 and 2. This prompted a conversation during which the patient noted that decades earlier, she had been intubated for 11 days during a grave illness.

Stenosis (3 of 6)

At closer range, the zone of stenosis is seen better. This is an incidental finding at this time, and is not responsible for her sensory neuropathic cough. She has no shortness of breath or sense of exercise limitation.

Further down trachea (4 of 6)

The trachea beyond the lower edge of the scarred segment is of normal caliber but turns to the patient’s left, giving the illusion of distal narrowing.

Below stenosis (5 of 6)

Just below the stenosis, the normalcy of the distal trachea is better seen. The carina is at C.

Carina (6 of 6)

Right at the carina, and looking into both mainstem bronchi. Many persons who have been intubated for a long period of time likely have asymptomatic and therefore undetected and inconsequential scars like those seen in photos 2, 3, and 4.

A Strapping Young Man Whose Larynx Was Injured As A 1-lb Preemie!

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Intubated as preemie (1 of 4)

Born at 25 weeks weighing 1 pound and 5 ounces, this man had been intubated for 30 days in a neonatal ICU. He survived, has thrived, and has a functional but breathy-pressed voice. This distant view begins to show why. Focus on the damaged left vocal cord (right of photo) for the rest of this series.

Left vocal cord (2 of 4)

At closer range, the right vocal cord (left of photo) appears normal; the left (right of photo) appears to have much less bulk.

Vascular pattern (3 of 4)

Under strobe light, open phase of vibration, note the typical post-injury vascular pattern at the arrow. The vascular pattern of the right cord (left of photo) is normal.

"Closed" phase (4 of 4)

Closed phase of vibration isn't fully closed; the left cord (right of photo) is a at a lower level, and doesn't oscillate due to its scarred mucosa, and a divot possibly from long-ago endotracheal tube pressure, is seen more clearly at dotted line.

An “Inner Voice” Problem Viewed As An End-Organ Problem

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Atrophied right vocal cord (1 of 4)

This young woman was in an auto accident with traumatic brain injury 6 months earlier. Immediately after the injury, an endotracheal tube was used for several days. Now, months later, voice remains quiet, and post-intubation laryngeal injury or neurological deficit is suspected. Here, the right vocal cord (left of photo) appears atrophied (spaghetti-lunguini larynx).

Vocal cords at high volume (2 of 4)

When the patient is coached to yell, her voice can be surprisingly loud. Posterior closure is good (at arrows) and there are no “divots” such as those seen when the endotracheal tube has created pressure necrosis. But why isn’t the voice weak, given the apparent right cord atrophy? The strobe images that follow explain.

Strobe light, closed phase (3 of 4)

Under strobe light, during the closed phase of vibration, vocal cord closure appears to be firm and equal bilaterally.

Open phase (4 of 4)

Correlating with the patient’s ability to produce loud voice, the open phase of vibration reveals equal amplitude and mucosal wave. While the right cord appeared atrophied, it shows no flaccidity. Her soft voice is a central “executive” problem; the primary explanation of the weak voice is the loss of the vitality and energy commanding the end organ. Nothing needs to be done to the larynx here; instead, the patient is taught a strategy for revving the “inner engine” of voice.

Intubation Scar With Pseudo-Polyp

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Posterior swelling (1 of 3)

This person is chronically hoarse 6 months after abdominal surgery. Placement of her breathing tube was said to be difficult. In this view with vocal cords abducted for breathing, the left vocal cord (right of photo) manifests an increase in vascularity and a margin swelling posteriorly (at arrow).

White scar (2 of 3)

A closer view appears to show a white “scar” lateral to the margin swelling. Its lateral extent is indicated by faint dotted line. Strong speculation is that there was a small laceration from endotracheal tube insertion (a fluke event), and that mucosa medial to this laceration was elevated and “relaxed” to the margin, creating a pseudopolyp. Look again at photo 1 to see the white “scar” again in that view.

Pseudopolyp (3 of 3)

During phonation, the pseudopolyp is clearly posterior to where an ordinary polyp from vibratory injury would occur. White-out of the large area of the upper surface is mostly from over-illumination. The different “width” of the vocal cords is not real, but just the result of camera angle. To improve voice significantly, the pseudopolyp will be resected to normalize the “match” of the margins, but vibratory stiffness from scarring will remain

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

Involuntary Inspiratory Phonation

Involuntary inspiratory phonation is a vocal phenomenon in which an involuntary vocal sound is made when one breathes in. In other words, a vocal noise such as one might hear from a person who is startled, takes an inward breath, and “gasps.” Inspiratory phonation becomes involuntary (necessary or impossible to abolish) when two conditions are met:

1) The vocal cords are unable to abduct (separate) normally during inspiration.
2) The speed of inspiratory airflow is sufficient to in-draw the cords and set them vibrating.

Conditions that may be associated with this include glottic stenosis, bilateral vocal cord paralysis, chemical denervation of both posterior cricoarytenoid muscles after Botox injection for abductory spasmodic dysphonia. In some cases, involuntary inspiratory phonation is heard only during the elicitations of the vocal capability battery, when the patient is asked to empty the lungs (breathe out fully) and then to fill them completely as rapidly and quietly as possible.


Example of involuntary inspiratory phonation:
Other than when she speaks, the vocal sounds are while breathing in.


Inspiratory phonation- How marginal is this airway?
In the video, the physician “shares” the patient’s airway with a flexible scope in order to determine the degree to which the airway is marginal.

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