IA-only paresis refers to weakness or paralysis of the larynx’s interarytenoid (IA) muscle—an unpaired muscle spanning between the bodies of both arytenoid cartilages—but 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.
Photos of IA-only paresis:
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, 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.
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.
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.
Bowing (2 of 8)
The abducted vocal cords for breathing show vocal cord bowing but otherwise nothing particularly noteworthy.
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.
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?
Posterior commissure (5 of 8)
Deep inside the posterior commissure during phonation. The large chink persists.
TA function (6 of 8)
Closed phase of vibration at B3 (247 Hz) shows good thyroarytenoid (TA) function.
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.
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.
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 (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.)
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 (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.)
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.
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).
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.
Rich vascular pattern (3 of 4)
The rich vascular pattern accompanying the lesion is seen better and is a visual finding of inflammation.
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.
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.
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
Here is the most efficient way forward: First, a consultation to determine whether or not the criteria for diagnosing R-CPD are met. Next, a simple office-based videoendoscopic swallow study which incorporates a neurological examination of tongue, pharynx (throat) and larynx muscles and often includes a mini-esophagoscopy. This establishes that the sphincter works normally in a forward (antegrade) swallowing direction, but not in a reverse (retrograde) burping or regurgitating fashion. Along with the symptoms described above, this straightforward office consultation and swallowing evaluation establishes the diagnosis of retrograde cricopharyngeus dysfunction (non-relaxation).
The second step is to place Botox into the malfunctioning sphincter muscle. The desired effect of Botox in muscle is to weaken it for at least several months. The person thus has many weeks to verify that the problem is solved or at least minimized.
The Botox injection could potentially be done in an office setting, but we recommend the first time (at least) placing it during a very brief general anesthetic in an outpatient operating room. That’s because the first time, it is important to answer the question definitively, that is, that the sphincter’s inability to relax when presented with a bubble of air from below, is the problem. Furthermore, based upon an experience with more than 190 patients as of August 2019, a single injection appears to “train” the patient how to burp. Approximately 80% of patients have maintained the ability to burp long after the effect of the Botox has dissipated. That is, long past 6 months from the time of injection.
Patients treated for R-CPD as just described should experience dramatic relief of their symptoms. And to repeat, our experience in treating more than 190 patients (and counting) suggests that this single Botox injection allows the system to “reset” and the person may never lose his or her ability to burp. Of course, if the problem returns, the individual could elect to pursue additional Botox treatments, or might even elect to undergo endoscopic laser cricopharyngeus myotomy. To learn more about this condition, see Dr. Bastian’s description of his experience with the first 51 of his much larger caseload at https://journals.sagepub.com/doi/full/10.1177/2473974X19834553.
Check out our list of resources containing peer-reviewed articles, patient stories and more!
Photos of the cricopharyngeus muscle:
1. The highlighted oval represents the location of the cricopharyngeus muscle.
2. The cricopharyngeus muscle in the open position.
3. The cricopharyngeus muscle in the contracted position.
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
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.
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. 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.”
Bloated Abdomen (2 of 3)
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.
(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.
(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.
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.”
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.
Where have patients traveled from?
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 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:
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.
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.
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.
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 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:
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.
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 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.
Also known as inhalation. 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.
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.
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.
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:
- 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.
- 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.
- 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.
- 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:
- 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.”
- 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.
- 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.
- 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
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):
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.
Intubation injury (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.
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.
Intubation injury (3 of 3)
Maximum phonatory closure. 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 (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 (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.
Intubation injury (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 (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 (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 (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.)
Intubation injury (2 of 4)
During phonation, the vocal cords appear to come together reasonably well, but as already mentioned, the voice sounds breathy.
Intubation injury (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.
Intubation injury (4 of 4)
During phonation. 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.
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.
Intubation injury (1 of 4)
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 4)
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 4)
During phonation, seen at closer range, the granuloma rides upward and nearly fills the laryngeal vestibule.
Anterior commissure (4 of 4)
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
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.
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.
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.
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.
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.
Intubation injury (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.
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.
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).
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.
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.
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.
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).
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.
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.
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.
(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).
(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.
(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.
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 involuntary inspiratory phonation 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.