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:
Interarytenoid (IA) Weakness
Another Interarytenoid (IA) Muscle Paresis or Is It Avulsion?
Watch the Progression of A Rare Laryngeal Paresis Scenario Including Interarytenoid (IA) Muscle
Idiopathic Subglottic Stenosis
Idiopathic subglottic stenosis has different levels: Series of 4 photos
Another way to inject idiopathic subglottic stenosis: Series of 3 photos
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.
Check out our list of resources containing peer-reviewed articles, patient stories and more!
Photos of the cricopharyngeus muscle:
Esophageal Findings: Series of 3 photos
Abdominal Distention of R-CPD: Series of 3 photos
A Rare “abdominal crisis” Due to R-CPD (inability to burp)
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.
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.
More Interesting Esophageal Findings of R-CPD (Inability to Burp)
Dramatic Lateral Dilation of the Upper Esophagus: Series of 3 photos
What the Esophagus Can Look Like “Below A Burp”: Series of 3 photos
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;
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
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:
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
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.
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
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.
Breathing Tube Injury—A Rare Complication of Intubation for General Anesthesia
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
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 Causing Partially Frozen Cricoarytenoid Joints
Forcing the Larynx to Give Up Its (Paresis and Intubation Injury) Secrets
Intubation Injury, Including A Subglottic Synechia
Vocal Cord “Tear” and Granuloma
Injured Adult Larynx from Intubation In Infancy
Intubation Injury to Voice, Airway, from Decades Ago
Injury at Two Levels from Breathing Tube-Particularly Clear
Subglottic Granulation and Curving Airstream
Double Whammy: Intubation Injury + Glottic Furrows
Sometimes You DO Remove Granulation to Avoid Tracheotomy
Who Knew…? Many Such Injuries Are Never Found
A Strapping Young Man Whose Larynx Was Injured As A 1-lb Preemie!
An “Inner Voice” Problem Viewed As An End-Organ Problem
Intubation Scar With Pseudo-Polyp
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.