Vocal Cord Paresis
Vocal cord paresis is the partial loss of voluntary motion for one or more of the muscles that move the vocal cords. Paresis is to be distinguished from paralysis, which refers to a complete loss of motion. Sometimes, however, the terms “paralysis” or “paralyzed” are used less precisely to encompass any kind of loss of motion, partial or complete. But we prefer the term “paresis” whenever it applies, and below we suggest a way to use this term when describing more complicated cases of vocal cords with reduced or no mobility.
Paresis or paralysis of a muscle or muscle group is caused by damage to its nerve supply. In other words, the underlying cause of a paretic or paralyzed muscle’s immobility is not a disorder of that muscle per se, but a disorder of the nerve supplying that muscle. Perhaps for this reason, it is common to speak of paralysis according to the nerve involved, rather than the muscle or muscles; in the world of laryngology, for example, we speak of “paralysis of the recurrent nerve.” However, it seems more logical to describe paralysis or paresis according to what is actually immobilized: the muscles. For example: if in a given case only the posterior cricoarytenoid (PCA) muscle is immobilized, then instead of calling that “paralysis of the recurrent nerve,” we would call it “PCA-only vocal cord paresis.”
In that example, though, some might wonder if it would be better for us to say “paralysis” instead of “paresis.” In other words, should we describe the nature of the immobility of the PCA muscle alone (so that, if the PCA is totally immobile, we would say “PCA-only vocal cord paralysis”) or that of the vocal cord’s entire set of muscles (which as a group is only partially immobile, so we would stick with “PCA-only vocal cord paresis”)? We think that, in general, it is more helpful to do the latter. To illustrate, here is an imaginary conversation: “Is this vocal cord paralyzed or paretic?” “Paretic.” “Which kind of paresis is it?” “PCA-only.”
It is surprisingly easy to diagnose the different variants of vocal cord paresis with a straightforward visual examination. Click on a particular variant to learn more:
- Vocal cord paresis, TA + LCA
- Vocal cord paresis, TA-only
- Vocal cord paresis, LCA-only
- Vocal cord paresis, PCA-only
- Vocal cord paresis, IA-only
Vocal Cord Paresis (Thyroarytenoid Muscle) Accentuated by Disuse
This woman illustrates that vocal cords are inhabited by muscle (thyroarytenoid muscle, to be precise). If that muscle atrophies due to paresis (partial loss of nerve supply), this alone can weaken the voice. That is what happened to her 10 years ago, in her fifties, after thyroid surgery. Initially the left cord did not move (paralysis). Then movement returned and along with it, her voice gradually gained in strength. When recovery was maximal, the vocal cord abducted (opened) and adducted (closed) normally. She also regained “90%” of her voice; while the muscle within the vocal cord did not recover fully, there was sufficient strength and tone to mostly “keep up” with the demands of her moderate voice use. Technically, she began with paralysis (of TA, LCA, and PCA) but after recovery, had a TA-only paresis as shown in photos 1-3 below. All was well for 10 years as she had a perfectly functional voice.Ten years later, now in her sixties, she developed a bad URI (not Covid-19) and voice deteriorated in the midst of hard bouts of coughing. At the same time, due to retirement, and self-quarantine, she was using voice very little. Two months later, still using voice very little and even intentionally “resting it,” her voice is extremely weak. The explanation is that by figuratively putting her voice in bed, she has added disuse atrophy to the longstanding paresis. How do we know this? The answer is in photos 4-5 below. And the appropriate initial treatment? Voice building exercises.
Conus bulge in the larynx (1 of 5)
This photo represents the larynx during her 10 years of functional voice. The normal right cord has a “conus (muscle) bulge” marked by the dotted ellipse just below the margin. On the left, due to TA paresis and atrophy, there is no conus bulge, denoted by the “?” Note further that the ventricle is capacious on the left, a second indicator of atrophic muscle. Compare the length of the bracket on each side. Why is the voice then so good? Because the right cord is strong and the residual muscle in the paretic left cord (right of photo) though of reduced bulk, has good tone and strength. See also photo 3.
Left vocal cord adducts normally (2 of 5)
During phonation, the atrophic left cord (right of photo) also adducts normally. Closure appears to be “tight” with a thin dark line of approximation.
Voice remains strong despite atrophy (3 of 5)
Though paretic and atrophied, lack of flaccidity is shown in the strobe photo. The lateral excursion of the left cord (right of photo) is no greater than the right, validating good tone and strength despite the atrophy.
Smaller conus bulge (4 of 5)
Due to the patient’s retirement, self-isolation due to the threat of Covid-19, arrival to her sixties, and self-prescribed voice rest, muscle bulk including in the normal right cord has visibly diminished. See here the noticeably smaller conus bulge, consistent with reduced muscle mass. Both ventricles are larger as well, also indicating atrophy of the thyroarytenoid muscles on both sides.
Atrophy + Flaccidity (5 of 5)
While there is no strobe image available, this view during phonation shows a wider zone of blurring than in photo 2 as another indicator of not only atrophy but also flaccidity. Voice building should restore her voice to baseline.
High Vagus Nerve Injury
The vagus (10th cranial) nerve originates from the medulla (part of the brainstem), exits from the base of the skull through the jugular foramen, and among other things, supplies branches to the musculature of palate, pharynx, and larynx. Location of vagus nerve injury is sometimes evident by palate and pharynx findings. But these findings are sometimes overlooked as in this case, especially if palate and pharynx are weak but not completely paralyzed.
Case study: This 50-something woman developed a weak voice and moderate difficulty swallowing upon awakening 5 months prior to this visit. Fortunately, her symptoms of weak voice and difficulty swallowing were not devastating, and are improving. But up to this examination, there has been no diagnosis. This examination reveals a “lesion” of her right vagus nerve and it has to be at the base of the skull because palate, pharynx, and larynx muscles are all weak. Voice is functional but lacks the ability to project and has a “soft-edged” quality. A sophisticated listener can also hear mild hypernasality. The examination below prompts a scan with special attention to base of skull to be sure there is no mass lesion there.
Nasopharynx (1 of 7)
This view of the nasopharynx shows that soft palate elevates and deviates to the left (curved arrow). The right side of the palate is atrophic and there is a gap (straight arrow) when she speaks. Saliva on the back wall of the nasopharynx (where it doesn’t belong) is also a clue.
Saliva pooling in right pyriform sinus (2 of 7)
Initial view of the hypopharynx shows saliva pooling preferentially in the right pyriform sinus at *. This is a typical finding of right pharynx paresis or paralysis.
Pharynx contracts (3 of 7)
To “prove” that the pharynx is weak on the right, the patient is asked to produce a very high pitch to recruit pharynx contraction. The midline (dashed line) has deviated far to the left (right of photo). Pharynx contracts on the left (arrows), closing the pyriform sinus on that side. There is no corresponding contraction on the patient’s right (left of photo).
Swallowing blue applesauce (4 of 7)
Blue-stained applesauce the patient has attempted to swallow replaces the saliva in the right pyriform sinus, but there is no soiling of the laryngeal vestibule (initial opening to the airway).
Unilateral pharynx contraction (5 of 7)
Elicitation of the “pharyngeal squeeze” with high pitched voice re-demonstrates unilateral pharynx contraction (arrows).
Right vocal cord paresis (6 of 7)
Closer inspection of larynx shows right vocal cord paresis (LCA and TA seem mostly intact explaining reasonably functional voice).
Vocal cord is paretic, not paralyzed (7 of 7)
Phonation shows fairly good vocal cord approximation, again showing that the cord is paretic rather than paralyzed, and explaining the fairly functional voice. Despite having swallowed several boluses of blue applesauce and water, the laryngeal vestibule shows no soiling, explaining why the patient is managing her swallowing even though she is aware that it is abnormal.
Photos of TA + LCA Vocal Cord Paresis:
Paresis, TA + LCA (1 of 6)
Distant view shows lesser normal-appearing abduction left cord (right of image) during breathing, suggesting that the left posterior cricoarytenoid muscle is working. Note the lesser bulk of the left vocal cord as compared with the right, although this is subtle at this viewing distance.
Paresis, TA + LCA (2 of 6)
At closer range, still in breathing position, one can see more easily the “linguine” of the right vocal cord (left of image) compared with the “spaghetti” and slight bowing of the left. These findings correlate with left thyroarytenoid (TA) muscle weakness and atrophy.
Paresis, TA + LCA (3 of 6)
In phonatory position under strobe light, the bowing of the left cord (right of image) is more evident, as is the lateral turning of the left vocal process, consistent with weakness of the left lateral cricoarytenoid (LCA) muscle. Lines denote the direction each vocal process is pointing.
Paresis, TA + LCA: 1 week after implant is placed (4 of 6)
One week after placement of a large silastic implant into the left vocal cord (right of image). Notice the temporary eversion of the left ventricle, almost simulating a large polyp.
Paresis, TA + LCA: 3 months after implant is placed (5 of 6)
A few months later, fullness of left vocal cord (right of image) remains, but eversion / edema of ventricular mucosa has resolved. Compare with image 1.
Paresis, TA + LCA: 3 months after implant is placed (6 of 6)
During phonation, much better closure (with markedly improved voice) but still slightly lateral turning of the left vocal process (right of image). Compare with image 3.
Example 2
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Panorama shows normally functioning PCA muscle (supplied by posterior branch), indicated by abduction of both vocal cords to a fully lateralized position.
Paresis, TA + LCA (2 of 8)
As vocal cords just begin to move to adducted, phonatory position, note that the left cord (right of image) leads medially with the tip of the vocal process, while right vocal process remains turned laterally due to paralysis of the LCA muscle.
Paresis, TA + LCA (3 of 8)
Close-up of posterior commissure during phonation shows continuing lateral pointing of the right vocal process (left of image), again due to a paralyzed LCA muscle.
Paresis, TA + LCA (4 of 8)
Panoramic view during phonation shows lateral buckling due to flaccidity of paralyzed TA muscle, left vocal cord (right of image).
Paresis, TA + LCA: voice gel injection (5 of 8)
A needle is being inserted into the TA muscle to inject voice gel as a temporary implant to plump up the cord so that the left cord (right of image) will be able to ” reach” it during phonation—and also, to counteract the flaccidity seen in photo 4 above.
Paresis, TA + LCA: after voice gel injection (6 of 8)
After plumping of the right vocal cord (left of image) with voice gel is completed.
Paresis, TA + LCA: after voice gel injection (7 of 8)
Phonation after voice gel injection, standard light. Note better closure of the cords.
Paresis, TA + LCA: after voice gel injection (8 of 8)
Phonation under strobe light, open phase of vibration. This view shows that the voice gel has abolished the flaccidity seen above in photo 4.
Example 3
Paresis, TA + LCA (1 of 5)
Right vocal cord paresis (left of image). Note marked atrophy as compared with the left cord. Highly lateralized position denotes some persistent action of the right posterior cricoarytenoid muscle.
Paresis, TA + LCA (2 of 5)
Initiation of phonation. Note medical turning off left vocal process of arytenoid (right of image), and absent movement of the right vocal cord. Neither thyroarytenoid nor lateral cricoarytenoid muscles are innervated.
Paresis, TA + LCA: voice gel injection (3 of 5)
Immediately following injection of right vocal cord (left of image) with voice gel, with patient in videoendoscopy room chair, under topical anesthesia. Note bulging of right vocal cord.
Paresis, TA + LCA: 1 month after voice gel injection (4 of 5)
A month later, showing plumping up of the right vocal cord (left of image) with voice gel. Vocal cord continues to abduct fully, due to functioning posterior branch of recurrent nerve, which innervates the posterior cricoarytenoid muscle.
Paresis, TA + LCA: 1 month after voice gel injection (5 of 5)
Phonation. There is some movement to the midline due to the bilaterally innervated interarytenoid muscle. The lateral cricoarytenoid muscle is paralyzed, as seen in lateral turning of the vocal process. Voice is dramatically improved as compared with pre-injection. The voice gel will be expected to gradually absorb over three to nine months, during which time the anterior branch of the recurrent nerve may recover its function.
Example 4
Paresis, TA + LCA, with recovery (1 of 4)
Left vocal cord “paralysis” (TA, LCA, primarily, with suggestion of slight PCA activity). In breathing position, one can see the left cord (right of photo) bowing and the capacious ventricle, indicating TA weakness. Intermediate abducted position of left cord suggests some PCA function remains.
Paresis, TA + LCA, with recovery (2 of 4)
During phonation, lateral turning of the left vocal process (right of photo) indicates LCA weakness, as does the large phonatory gap.
Paresis, TA + LCA, with recovery (3 of 4)
Six weeks later, there is definite improvement of voice, though it remains abnormally weak. In this abducted (breathing) position, note that the left cord (right of photo) is less bowed and the ventricle is less capacious. This would be viewed as more than a “soft” finding, requiring skeptical, nuanced observation and some suspension. Compare with photo 1.
Paresis, TA + LCA, with recovery (4 of 4)
During phonation, one can see closer approximation. The vocal process on the left (right of photo) no longer turns laterally, even when using low pitch in an attempt to accentuate this finding.
Example 5
Vocal cord paresis (1 of 2)
Paresis, right vocal cord (left of image). Notice the slight loss of muscle bulk on the right cord as the upper surface dips subtly into the ventricle, whereas it remains a more flat upper surface farther laterally into the ventricle on the left.
Vocal cord paresis (2 of 2)
Phonation under strobe light: the right vocal cord process turns slightly laterally due to LCA muscle weakness. The membranous cord also buckles laterally due to its underlying TA muscle atrophy and flaccidity.
Example 6
Paresis, TA + LCA (1 of 7)
This patient has idiopathic right TA + LCA paresis. From a distant view, the unopposed pull of the right PCA (left of photo) can already be detected, but is better seen in the next photo.
Paresis, TA + LCA (2 of 7)
At closer range and in a breathing position, both PCA muscles work to fully lateralize the cords. The right (left of photo, in red) TA paralysis/atrophy is seen via a spaghetti-linguini difference in the cords and a larger, deeper right ventricle. Most notably, the right vocal process pulls laterally because the paralyzed LCA does not resist unopposed pull of the active PCA.
Paresis, TA + LCA (3 of 7)
Beginning to approach phonation position, the cords begin to move to the midline via function of the IA muscles, and the left cord (right of photo) reaches the midline via function of the left LCA muscle. Absent function of the right LCA and TA (left of photo) continues to be seen clearly in this view.
Paresis, TA + LCA (4 of 7)
During phonation, vibratory blur is seen under standard light, and lateral buckling of the flaccid right cord (left of photo).
Paresis, TA + LCA: after medialization (5 of 7)
Soon after a simple medialization of right cord (left of photo) with a silastic wedge, resulting in the plumpness of the right cord. Compare with photos 1 and 2.
Paresis, TA + LCA: after medialization (6 of 7)
Again beginning to approach phonation position. See again the plumpness of the right cord (left of photo). Compare with photo 3.
Paresis, TA + LCA: after medialization (7 of 7)
During phonation, there is much better contact between the cords, and the right cord (left of photo) is no longer flaccid. Compare with photo 4.
Example 7
TA weakness (1 of 4)
94 year-old with gradual weakening of voice across 2 years. Breathing (abducted) position shows left PCA muscle (right of photo) to be intact. In spite of distant view, spaghetti-linguini, capacious ventricle, and margin bowing are obvious indicators of TA weakness.
Prephonatory instant (2 of 4)
Prephonatory instant and distant view are inadequate to assess LCA, which preliminarily looks like it may be working; that is, the left vocal process (right of photo) initially looks to be pointing straight anteriorly.
LCA not working (3 of 4)
Prephonatory instant at closer range shows the classic lateral turning of vocal process showing LCA is in fact not working.
Phonatory blur (4 of 4)
During phonatory blur, one can see additional lateral buckling of the left cord (right of photo), due to TA flaccidity. The lesson: distal chip or fiberoptic scopes with topical anesthesia are required for best assessment of vocal cord paresis, despite the greater optical resolution of rigid telescopes.
Example 8
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.
Photos of TA-only Vocal Cord Paresis
Paresis, TA-only (1 of 3)
Panoramic view of the larynx with the cords in full abduction. Note the asymmetry — particularly the bowed free margin on left (right of image), and capacious ventricle.
Paresis, TA-only (2 of 3)
Close-up at near-closure for phonation. Equal bilateral adduction and matching angles of medial line of aytenoid cartilages demonstrates that LCA muscles are working bilaterally. This appears to be a paresis of TA muscle alone.
Paresis, TA-only (3 of 3)
Close-up view, in abducted, breathing position. The “spaghetti” of the left cord (right of image) does not match the normal “linguini” of the right cord. Also, note the left cord bowing and capacious ventricle.
Example 2
Paresis, TA-only (1 of 5)
During abducted breathing position, note the atrophy of the left cord (right of image), mild margin convexity, and the capacious ventricle (at bottom-right), all of which indicate TA paresis. The cord abducts fully, demonstrating intact PCA fuction. LCA function cannot be determined in this view.
Paresis, TA-only (2 of 5)
Adducted position for phonation, with phonatory blurring as seen under standard light. LCA appears to be functioning, as indicated by the strict anterior-posterior direction of the left vocal process (right of image), just the same as for the right. This accounts for quite good approximation of the cords. The ventricle again appears capacious (dotted oval). Based upon these first two photos, we can surmise that this is a TA-only paresis.
Paresis, TA-only (3 of 5)
Under strobe light, showing increased amplitude of vibration of the left cord (right of image). This finding suggests in yet another way that the TA muscle is paralyzed.
Paresis, TA-only: after implant is placed (4 of 5)
After placement of an implant into the left cord (right of image). Note the bulging of that cord and straightening of the cord’s margin, and also that the ventricle on that side no longer appears capacious. Compare with photo 1.
Paresis, TA-only: after implant is placed (5 of 5)
Under strobe illumination. Note that the lateral excursion of both cords is the same, since the left cord (right of image) is now less flaccid. Compare with photo 3
Photos of LCA-only Vocal Cord Paresis
LCA weakness, in a patient with vocal cord paralysis (1 of 2)
Phonation in the low chest register (note the wide zone of vibratory blurring). Here, the vocal process is clearly seen to turn laterally (arrow), a tell- tale indicator of LCA weakness. As other views of this particular patient would indicate, she actually also has weakness of the TA and PCA muscles, not just LCA-only paresis, but this view alone would correspond to a patient who had LCA-only paresis.
LCA weakness, masked by high pitch (2 of 2)
Phonation at very high pitch (as expected, the vibratory blur narrows). The antero-posterior lengthening of the left cord (right of image) at this high pitch turns the vocal process on that side back towards the midline (compare with photo 1), masking the LCA weakness. This low voice/high voice difference in the posterior commissure is routinely but not universally seen with LCA weakness.
Photos of PCA-only Vocal Cord Paresis
Paresis, PCA-only (1 of 4)
PCA muscle of the right vocal cord (left of image) is not working. TA and LCA are perceived as intact, based on the combination of: 1) normal voice; 2) the right cord is not bowed; 3) ability to medially turn or at least keep in line the right vocal process (see also photo 2); and 4) the right cord is not atrophied, nor is the right ventricle unusually capacious.
Paresis, PCA-only (2 of 4)
During phonation, there is no sign of lateral turning of the right vocal process, which would indicate LCA weakness. Furthermore, vibratory blurring (in this standard-light view) appears to be fairly equal on each side, suggesting there is no flaccidity of the right cord, contrary to what one would expect were the TA weak on that side.
Paresis, PCA-only (3 of 4)
Strobe light, closed phase of vibration, again showing that there is no lateral turning of the vocal process.
Paresis, PCA-only (4 of 4)
Strobe light, open phase of vibration. The amplitude of vibration for each cord appears to be equal, just as it did (based on blurring) in photo 2. This finding confirms that the TA is not weak, as such weakness would make the right cord flaccid and increase its amplitude of vibration.
Example 2
PCA-only paresis years after thyroid lobectomy (1 of 6)
Several years after right (left of photo) thyroid lobectomy. Voice was drastically altered for a few months but then seemed to recover fully. Panoramic view during sniff maneuver shows midline but immobile right vocal cord (left of photo). No apparent atrophy of the cord itself, and the vocal process turns medially (arrow) suggesting that voicing muscles TA, LCA are intact and not balanced by PCA, because PCA muscle is paralyzed. This would explain patient’s normal voice, yet immobile cord.
PCA-only paresis years after thyroid lobectomy (2 of 6)
Closer view, with same findings as in photo 1.
PCA-only paresis years after thyroid lobectomy (3 of 6)
View of posterior commissure just before reaching contact for phonation. Note that both vocal processes are aligned antero-posteriorly (see arrows). This indicates a functioning LCA muscle on the right, and not only on the left.
PCA-only paresis years after thyroid lobectomy (4 of 6)
During phonation, standard light, the cords appear to approximate firmly.
PCA-only paresis years after thyroid lobectomy (5 of 6)
Closed phase of phonation, strobe light, at very low pitch (E3, or 165 Hz). The lowest part of patient pitch range would be expected to accentuate flaccidity, if present.
PCA-only paresis years after thyroid lobectomy (6 of 6)
Open phase of vibration, still at E3 (165 Hz). Vibratory amplitude is equal between the cords, demonstrating no increase of flaccidity of right cord (left of photo) as another way of “proving” that TA musculature is normal.
Example 3
Abducted breathing position (1 of 4)
As the patient is taking a breath, only the right cord (left of photo) abducts (though not yet fully in this photo). Left cord (right of photo) remains at midline and vocal process remains in line with the membranous cord, suggesting that the LCA muscle on the left (right of photo) is working.
Full approximation of cords, TA is intact (2 of 4)
Full approximation of the cords, and furthermore there is no enlargement of the ventricle (at ‘X’) and this also suggests left TA muscle is also intact.
Phonation, LCA is intact (3 of 4)
The posterior commissure during phonation. Note that there is no lateral turning of the vocal process, validating that the left LCA muscle (right of photo) is intact.
Phonation under strobe light, PCA-only paresis (4 of 4)
During phonation, strobe light, open phase of vibration. Left TA (right of photo) function again validated in that the amplitude of vibration on the left ( right of photo) is not greater than on the right (left of photo). If the left TA muscle were paralyzed, then the amplitude on the left (right) would be greater than on the right (left).
Photos of IA-only Vocal Cord 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 (3 of 5)
An even closer view shows the persistent posterior commissure gap.
IA-only paresis, during a cough (4 of 5)
The elicited cough shown in this image proves that the patient is physically unable to close the posterior commissure.
IA-only paresis, during a Valsalva maneuver (5 of 5)
An elicited Valsalva maneuver, which also fails to close the posterior commissure. High-resolution CT was performed to prove there was no abnormality of the cricoid or arytenoids which might account for this finding of apparent interarytenoid paresis or avulsion.
Example 2
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.
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