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:


Photos of TA + LCA vocal cord paresis:

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normal-appearing abduction left cord

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.
thyroarytenoid muscle weakness and atrophy

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.
bowing of the left cord

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.
One week after placement of a large silastic implant

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.
eversion / edema of ventricular mucosa has resolved

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.
slightly lateral turning of the left vocal process

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.
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normally functioning PCA muscle

kb1-21020706

Panorama shows normally functioning PCA muscle (supplied by posterior branch), indicated by abduction of both vocal cords to a fully lateralized position.
paralysis of the LCA muscle

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.
posterior commissure

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.
lateral buckling due to flaccidity of paralyzed TA 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).
needle is being inserted into the TA muscle to inject voice gel

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.
vocal cord filled with voice gel

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.
Phonation after voice gel injection, standard light.

Paresis, TA + LCA: after voice gel injection (7 of 8)

Phonation after voice gel injection, standard light. Note better closure of the cords.
voice gel has abolished the flaccidity

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.
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Right vocal cord paresis

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.
Note medical turning off left vocal process of arytenoid

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.
injection of right vocal cord with voice gel

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.
plumping up of the right vocal cord with voice gel.

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.
bilaterally innervated interarytenoid 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.
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Left vocal cord paralysis

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.
lateral turning of the left vocal process

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.
left cord is less bowed and the ventricle is less capacious

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.
vocal process on the left no longer turns laterally

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.
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Paresis, right vocal cord

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.
ight vocal cord process turns slightly laterally due to LCA muscle weakness

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.
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plumpness of the right cord

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.
plumpness of the right cord

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.
better contact between the cords

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.
TA + LCA paresis

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.
right vocal process pulls laterally

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.
cords begin to move to the midline

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.
lateral buckling of the flaccid right cord

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).
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eft PCA muscle is intact

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

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.
Prephonatory instant

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.
lateral buckling of the left cord

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.
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Intubation injury (1 of 4)

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

Forceful exhalation (2 of 4)

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

Phonation begins (3 of 4)

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

LCA (4 of 4)

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

Photos of TA-only vocal cord paresis:

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Panoramic view of the larynx

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 of TA muscle

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.
left cord bowing and capacious ventricle

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.
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increased amplitude of vibration of the left cord

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.
TA paresis

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

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.
placement of an implant into the left cord

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

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:

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Phonation in the low chest register

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

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:

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PCA muscle of the right vocal cord is not working

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

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.
no lateral turning of the vocal process

Paresis, PCA-only (3 of 4)

Strobe light, closed phase of vibration, again showing that there is no lateral turning of the vocal process.
The amplitude of vibration for each cord appears to be equal

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.
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PCA muscle is paralyzed

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

PCA-only paresis years after thyroid lobectomy (2 of 6)

Closer view, with same findings as in photo 1.
posterior commissure just before reaching contact for phonation

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.
cords appear to approximate firmly

PCA-only paresis years after thyroid lobectomy (4 of 6)

During phonation, standard light, the cords appear to approximate firmly.
Closed phase of phonation

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.
Vibratory amplitude is equal between the cords

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.
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only the right cord abducts

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.
no enlargement of the ventricle

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.
posterior commissure during phonation

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.
PCA-only paresis

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:

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IA-only paresis (1 of 5)

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

IA-only paresis (2 of 5)

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

IA-only paresis (3 of 5)

An even closer view shows the persistent posterior commissure gap.

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

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

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

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

Breathy and weak voice (1 of 8)

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

Bowing (2 of 8)

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

Pre-phonatory view (3 of 8)

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

Phonatory view (4 of 8)

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

Posterior commissure (5 of 8)

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

TA function (6 of 8)

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

IA mucosa (7 of 8)

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

IA avulsion (8 of 8)

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

Full abduction (1 of 5)

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

Large gap during phonation (2 of 5)

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

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

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

Arytenoids no longer touch (4 of 5)

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

Breathy voicing (5 of 5)

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

Videos:

Injection Medialization for Vocal Cord Paresis
See an example of one variant of vocal cord paresis and how it limits the voice. Then watch a medialization procedure in which voice gel is injected into the vocal cord affected by paresis, and hear how the voice thereafter improves.