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Laryngopedia By Bastian Medical Media

Multimedia Encyclopedia

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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:


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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A view of the mid-esophagus

Esophageal Findings (1 of 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.
A bony spur in the spine

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.
dilation of the upper 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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x-ray of Gastric Air Bubble

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.

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?


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; and 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.

Photos of Indicator Lesions:

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:

Injection laryngoplasty

Injection laryngoplasty is a procedure during which an implant in paste form, typically a product called Cymetra™, is injected through a needle and into a paralyzed vocal cord. The purpose of an injection laryngoplasty is two cord. The first is to fatten the vocal cord so that it moves toward the other vocal cord and diminishes the gap between them that is causing the air-wasting dysphonia. The second reason is to fortify the tissue so that the paralyzed cord is less flaccid and can “stand up” to the pressure from the other vocal cord and the air passing between them.

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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Abducted, breathing position of vocal cords

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

Inspiratory phonation (2 of 4)

Inspiratory phonation in-draws the mild Reinke’s edema (smoker’s type polyp formation).
Open phase, faint translucency

Open phase, faint translucency (3 of 4)

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

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.

Intubation injury audio with photos:

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



“Tattoo” of blood after detachment of intubation granuloma

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intubation granuloma on vocal cords

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.
granuloma becoming pedunculate

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 has detached

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 left from granduloma

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 on vocal cord

Blood Tattoo (5 of 5)

A closer view of the “blood tattoo.”

Subglottic granulation and curving airstream

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Proud flesh within cricoid ring

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 of granulation tissue

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.
subglottic scar band

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).
anterior border of the scar band

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.

  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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