The pharynx (loosely “throat”) has a “foodway” function to convey food and liquid from the mouth to the esophagus. It also serves as part of the “airway,” also from mouth into the larynx and trachea. These foodway/airway functions are kept separate so food and liquid do not enter the airway towards the lungs. At the moment of swallowing, vocal cords clamp firmly together and epiglottis drops over the entrance of the larynx to divert food and liquid into the esophagus. During each swallow, lasting perhaps a second, breathing is briefly suspended. Once the food/liquid has gone by, the larynx re-opens and breathing resumes.

A thin sheet of muscle surrounds the pharynx, and squeezes to narrow the pharynx and help to propel swallowed material. That contraction lasts for approximately one second, each time the person swallows. The muscle is innervated bilaterally by the pharyngeal branch of the vagus nerve and so one side or both sides can be paralyzed by tumor, fracture at the base of the skull, viral injury, etc.

This diagnosis is often overlooked, because clinicians may not be clear on how to make the diagnosis. The best way is to obtain a clear panoramic view of the laryngopharynx as seen in the photo series below, and ask the patient to produce a very high pitch. This maneuver “recruits” contraction of the pharynx outside of the act of swallowing and allows the examiner to see clearly the difference in the contraction of the two sides. The paralyzed side is pulled to the non-paralyzed side, again as seen below.

Some with unilateral pharynx paralysis can compensate and continue to swallow (with limitations). Others are completely unable to surmount the impediment of this kind of paralysis.

Pharyngeal Paralysis, Seen with Pharynx Contraction

Pharyngeal paralysis (1 of 2)

View of the laryngopharynx. This patient has pharyngeal paralysis on one side, which is already slightly evident because the posterior pharyngeal wall's midline (dotted line) is deviating here slightly to one side, even at rest.

Pharyngeal paralysis, more obvious with pharynx contraction (2 of 2)

The pharynx is contracted, and the posterior pharyngeal wall (midline again at dotted line) now deviates dramatically toward the non-paralyzed side of the pharynx. This pharynx contraction was elicited via extremely high-pitched voicing.

Pharyngeal Paralysis

Pharyngeal paralysis (1 of 1)

Panorama of the laryngopharynx. Note the capacious left pyriform sinus (right of photo), one strong indicator of paralysis of the pharynx on that side.

Pharyngeal paralysis (1 of 1)

Blue-stained water swallowed by the patient has preferentially pooled in the left pyriform sinus (right of image), due to weakness of the left inferior pharyngeal constrictors.

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.

Other variants of vocal cord paresis include TA-only, TA + LCA, PCA-only (posterior cricoarytenoid muscle), and LCA-only (lateral cricoarytenoid muscle).

Photos of IA-only paresis:

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 (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.

Interarytenoid (IA) Weakness

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.

View of posterior commissure (4 of 4)

Very close-range view in the posterior commissure as the patient phonates, showing that the arytenoids do not come into contact. The tips of vocal processes are touching but out of view at the bottom of the photo (below the dots).

Another Interarytenoid (IA) Muscle Paresis or Is It Avulsion?

Breathy and weak voice (1 of 8)

Bowing (2 of 8)

Pre-phonatory view (3 of 8)

Phonatory view (4 of 8)

Posterior commissure (5 of 8)

TA function (6 of 8)

IA mucosa (7 of 8)

IA avulsion (8 of 8)

Watch the Progression of A Rare Laryngeal Paresis Scenario Including Interarytenoid (IA) Muscle

Full abduction (1 of 5)

Large gap during phonation (2 of 5)

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

Arytenoids no longer touch (4 of 5)

Breathy voicing (5 of 5)

Voice change that accompanies Parkinson’s disease (PD) typically has two components. One component is a change to the “inner engine” of the voice. It is as if the inner motivation or vitality of communication or voice is damped down; think of the “motor” being limited mostly to “idle” rather than “first, second, third, and fourth” gears. When coaxed or even goaded to produce more vigorous voice, a person with advanced PD may find it hard to impossible (depending upon severity) to increase loudness. If the average person can “choose” vocal loudness settings of 1 through 5, it is as though levels 2 through 5 become inaccessible to the person with PD.

A second component of PD-related voice change is that the larynx becomes weak and atrophied. This is not surprising, since any body part will tend to atrophy if it is never used in a vigorous way. The phenomenology of PD-related voice change is that the voice is overly quiet and soft-edged, and though speech does not tend to become slurred, it can lose its crispness of articulation, and the pace of speech may diminish.

Photos:

Parkinson’s-related Voice Change

Parkinson’s-related voice change (1 of 3)

Larynx of person with severe Parkinson’s disease; breathing position. Note the remarkable atrophy of the vocal cords, manifested in particular by the capacious ventricles ( green dotted lines), the margin bowing (arrows), loss of “conus” bulk, and increased visibility of the contours of the vocal processes (blue dotted lines).

Parkinson’s-related voice change (2 of 3)

Phonatory (voicing) position. In addition to the bowing of the vocal cords, especially the left cord (right of image), note the slight scissoring of the left vocal process to overlap the right vocal process, as indicated by the arrows.

Parkinson’s-related voice change (3 of 3)

Cords coming into phonatory position, magnified view. Here can be seen even more clearly that, due to Parkinson’s-related atrophy, the contours of the vocal processes are more visible (blue dotted lines), like an emaciated person’s ribs. Note also that the LCA muscles have contracted slightly before the IA: the “toes” (T’s) of the arytenoid cartilages are in contact before the “heels” (H’s).

Voice Building:

Voice Building (shorter version):

Weakness or paralysis of the vocal cord’s posterior cricoarytenoid (PCA) muscle, but with normal function of the vocal cord’s other muscles. The PCA muscle abducts (lateralizes) the vocal cord for breathing. The following are indicators of PCA-only paresis:

• Movement: The vocal cord closes normally for voicing, but it does not abduct for breathing. It remains motionless at the midline.
• Position and appearance: Position is normal during phonation, but the vocal cord does not open (lateralize) for breathing. Because the cord does not appear to move (it adducts or closes normally, but from an already-adducted position), PCA-only paresis is often mistaken for complete vocal cord paralysis—TA (thyroarytenoid), LCA (lateral cricoarytenoid), and PCA. Key points of difference between PCA-only paresis and complete paralysis are that, in the former case, the tip of the vocal process is in a normal medial position and the vocal cord has normal bulk and tone.
• Appearance during voicing (under strobe lighting): Completely normal, because the adductors of the cord (TA and LCA muscles) are intact. Hence, as with a normal cord, there is no flaccidity or asymmetry of vibration.
• Voice quality: Entirely normal. Many individuals are told this is due to “compensation” of the opposite cord, but actually it is because the muscles used for voicing (TA + LCA) are intact.

Other variants of vocal cord paresis include LCA-only, TA-only, TA + LCA, and IA-only (interarytenoid muscle).

Photos:

Paresis, PCA-only

Paresis, PCA-only (1 of 4)

Paresis, PCA-only (2 of 4)

Paresis, PCA-only (3 of 4)

Paresis, PCA-only (4 of 4)

PCA-only Paresis Years after Thyroid Lobectomy

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.

Left PCA-only Paresis

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).

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Sharp Observation Required to Sort out this PCA-only Paresis and Cancer Scar Combo

Unequal lateralization (1 of 4)

The vocal cords appear equally lateralized, but are not. The right one (left of photo) is paramedian and does not abduct, and the left (right of photo) is abducted, and moves to the midline with phonation, as seen in photos 3 and 4.

PCA not working (2 of 4)

Shifting the view posteriorly, it is easier to see that the right PCA muscle does not work, and without its lateralizing pull, the unopposed LCA muscle turns the vocal process sharply medially ( arrow). Right TA is intact despite pseudobowing, caused here by exaggerated LCA action.

Phonation, closed phase (3 of 4)

Under strobe light. The vocal cords push against each other equally, and IA muscle pulls the “heels” of both arytenoid cartilages together, causing the right vocal process (left of photo) to point anteriorly, just like on the left (right of photo).

Phonation, open phase (4 of 4)

Open phase of vibration. Amplitude of vibration is greater on the right (left of photo) but not due to TA muscle atrophy, but instead as a result of mucosal stiffness on the left (right of photo) The explanation: superficial laser cordectomy performed years earlier for early cancer. Medial-to-lateral capillary reorientation is the visual clue of mucosal regeneration/ scarring.

Classic Findings Again of PCA-only Paresis

Post thyroidectomy (1 of 4)

After thyroidectomy, this individual’s voice was breathy for several months postoperatively, but then recovered fully. Yet, her right vocal cord appears to be paralyzed, rather than paretic. Here note that PCA on the left (right of photo) pulls that (normal) cord fully laterally, while the right cord (left of photo) remains midline and with slight medial turning of the vocal process to suggest right LCA muscle is intact.

Phonatory view (2 of 4)

Making voice under standard light, the cords appear to close at the midline, consistent with intact IA and bilaterally intact LCA muscles. Equal vibratory blur between the two sides suggests that the both TA muscles are also intact.

LCA and TA muscles working (3 of 4)

Under strobe light, closed phase of vibration: Medial compression appears equal and the vocal processes (indicated by lines) point straight anteriorly, again confirming that both LCA muscles are working, and suggesting that both TA’s are also working.

PCA-only paresis (4 of 4)

Open phase with equal amplitude (lateral excursion) of vibration of both cords, indicating that the TA muscle is not atrophic or flaccid. Put all of the above findings together, and this is classic PCA-only paresis of the right vocal cord.

A Mediocre Examination for Paresis

PCA not working, TA is weak (1 of 3)

The patient reported a voice quality of about "50%" after neck surgery a few months earlier and has (so far) recovered to "75%." The patient's difficulty tolerating the examination despite extensive topical anesthesia results in incomplete (though sufficient) information. Here it appears that PCA is not working on the right (left of photo), as the vocal cord position is paramedian rather than fully lateralized. Right TA muscle (left of photo) appears weak, too, as indicated by "spaghetti-linguini" bulk asymmetry (brackets), mild vocal cord bowing (dotted line) and capacious right ventricle (left of photo). This view does not permit evaluation of conus for atrophy, nor of LCA function.

LCA recovered (2 of 3)

Visual finding of full closure during phonation in this distant view, along with good ability to increase loudness at low pitch without audible luffing both suggest but do not prove that LCA is likely recovered, and also that there is some tone in the atrophied TA muscle.

TA partially recovered (3 of 3)

A sub-optimal view of open phase of vibration also suggests that the TA muscle is partially recovered. In all, this is a barely-adequate examination but when an examiner can invest deeply in subtle and even distant findings, an examination such as this that does not meet an examiner's standard of quality, can yet suffice for diagnosis and treatment planning.

Laryngology 401: PCA-only Paresis, but the Actual Voice Problem Is Spasmodic Dysphonia

Sense of instability (1 of 3)

This person had a major voice change after thyroidectomy for a large goiter. Within 2 months, voice recovered fully--except for a sense of instability. The PCA-only paresis is not the explanation because voice-making muscles (TA + LCA) are intact. And in fact vocal capability testing shows that both yell and projected voice are normal. The visual finding here of vocal cord bowing and capacious ventricle do not count as a breathing position finding with PCA-only paresis due to the unopposed action of LCA muscle, combined with an uncontracted TA muscle, both of which cause pseudo-bowing.

Vibratory amplitude (2 of 3)

During phonation under strobe light, with TA tensing, "bowing" disappears. Furthermore the vibratory "blur" at the margin of the left fold (right of photo) is equal to the right (left of photo), telling us that vibratory amplitude is approximately the same on both sides.

Spasm (3 of 3)

An audible/ visible spasm occurs when the right vocal cord jerks laterally for 4 frames (~ 1/8th of a second). The problem isn't PCA weakness on the left (right of photo), but instead an abductory spasm on the right (left of photo), fully mobile cord!

Test your Mastery of Visual Nuances of Paresis with this Case

LCA working, TA partially working (1 of 4)

Many years earlier, this man had thoracic surgery for patent ductus arteriosis repair. Immediately postoperatively, voice was down to “20%.” Within several months it had recovered to about “50%” where it has remained for 30 years. Two notable findings: bowing of left vocal cord (right of photo) along with subtle twitching, but without a significant “spaghetti” sign of atrophy as compared with the right, and medial turning of the left vocal process (right of photo). The conclusion: LCA appears to be working, and TA is working at least partially.

Closer view (2 of 4)

Close visualization of the posterior commissure during “sniff” confirms that PCA is not working on the left (right of photo); LCA action is confirmed with exaggerated medial turning of the vocal process.

Closed phase (3 of 4)

Under strobe light, showing closed phase at low pitch. Posterior folds close completely, confirming LCA function. The left vocal cord (right of photo) looks to be at a slightly lower level, confirming at least some level of atrophy.

Open phase (4 of 4)

Open phase of vibration shows larger amplitude of vibration of left vocal cord (right of photo). Putting all of these findings together in big picture terms: LCA is working “fully,” TA partially, and PCA not at all.

PCA-only Paresis of Right Vocal Cord and Normal Voice

Ineffective PCA Muscle (1 of 3)

After neck surgery, this person's voice was grossly abnormal (weak, whispery) for several months. Now voice is normal, and the patient is being seen only for laryngopasm. In this view, the right vocal cord ( left of photo) is midline, because the PCA muscle on that side is not working to lateralize it. This suggests that the posterior branch of the recurrent laryngeal nerve has not recovered.

Vocal muscles are recovered (2 of 3)

Closed phase of vibration under strobe light shows that the cords close fully, suggesting that the right sided TA and LCA muscles necessary for normal voice (served by anterior branch of the recurrent laryngeal nerve) have recovered fully. The open phase of vibration (next photo) will verify (or disprove) this speculation.

Signs of PCA-only paresis (3 of 3)

In fact, the lateral excursions of the vocal cords are the same (compare the lateral "distance" from the midline (indicated by the dotted line).. This verifies that there is no weakness (flaccidity) of the right TA muscle. The lack of lateral turning of the vocal process verifies that the LCA muscle is also working on that side. Hence, PCA-only paresis.

Weakness or paralysis of the vocal cord’s thyroarytenoid (TA) muscle, but with normal function of the vocal cord’s other muscles. The TA muscle “inhabits” the vocal cord and normally provides bulk and internal tone to the cord. The following are indicators of TA-only paresis:

• Movement: The vocal cord opens normally for breathing and closes normally for voicing.
• Position and appearance: Position is normal. Typically, the margin of the cord is slightly concave, the ventricle is capacious, and the conus area below the free margin is lacking in bulk.
• Appearance during voicing (under strobe lighting): Closure at the posterior commissure is complete and symmetrical bilaterally. Under strobe light, one sees flaccidity as indicated by increased amplitude of vibration; the lateral excursions become exaggerated and the mucosal wave increases. One may also see chaotic fluttering.
• Voice quality: Weak and air-wasting and often indistinguishable from a case of complete vocal cord paralysis—TA, LCA (lateral cricoarytenoid), and PCA (posterior cricoarytenoid).

Other variants of vocal cord paresis include LCA-only, TA + LCA, PCA-only, and IA-only (interarytenoid muscle).

Photos of TA-only paresis:

Paresis, TA-only

Paresis, TA-only (1 of 3)

Paresis, TA-only (2 of 3)

Paresis, TA-only (3 of 3)

Paresis, TA-only: before and after an Implant

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

TA-only Paresis before and after Voice Gel Injection

TA weakness, intact LCA + PCA (1 of 5)

TA weakness indicated by bowed margin and “spaghetti-linguini” difference between the cords. Medial turning of vocal process (arrow) suggests intact LCA; abducted position suggests intact PCA function. Blood is from cricothyroid membrane puncture to instill topical anesthesia.

Prephonatory instant (2 of 5)

Before voice gel injection at prephonatory instant. Wasting of left cord (right of photo), and capacious ventricle on the left (right of photo) clearly evident.

Gel injection (3 of 5)

At beginning of voice gel injection (needle at white arrow).

Straight vocal cord margin (4 of 5)

At conclusion of voice gel, note straight left cord margin (right of photo). Compare with photos 1 and 3.

Phonation (5 of 5)

Phonation after injection complete. Voice dramatically strengthened. Compare with photo 2.

Just Bowing? No, TA-only Paresis

Prephonatory view (1 of 4)

As the cords approach voice-making position, in a man with weak voice symptoms. What details do you see?

Phonation (2 of 4)

Now closed for phonation, the right vocal cord margin (left of photo) is bowed as compared with the left (right of photo), more normal cord.

Bowing and Atrophy (3 of 4)

At closer range, not only bowing, but also absence of the "conus" bulge ("C") below the right cord (left of photo), indicates TA atrophy in a second way.

Open phase (4 of 4)

Under strobe light, at the open phase of vibration, the bowed margin of the right cord is seen even more clearly. Its greater lateral vibratory excursion adds flaccidity to previously-noted bowing and atrophy.

“Mostly-TA” Paresis

Atrophy (1 of 4)

After an upper respiratory infection, this man's voice was self-rated at "45%" of normal strength. After 3 weeks, it suddenly increased to "65%," and then very slowly improved over the next 5 months to "85%" at the time of this examination. Note subtle atrophy of the left fold (right of photo).

TA atrophy (2 of 4)

One finding of subtle TA atrophy is the smaller "conus" bulge on the left (right of photo). Compare the brackets on the two sides. Complete abduction suggests PCA function is intact.

LCA intact (3 of 4)

As the vocal cords are coming to midline for phonation, the bowed left vocal cord margin, indicating TA atrophy, is accentuated. Left vocal process is turning medially, suggesting preserved LCA function.

Closed phase (4 of 4)

An extremely subtle finding of flaccidity is the incomplete closure of the left anterior cord during the closed phase of vibration under strobe light. A highly speculative interpretation? Perhaps a complete left vocal paralysis, with early recovery of left LCA and some TA. Then more gradual recovery to this subtle TA-only paresis.

TA-only Paresis, before and after Recovery

Bowing and atrophy (1 of 4)

Mediastinal lymphoma has just been discovered as the cause of this middle-aged man’s marked vocal weakness. He describes it as “50%” of normal. Note bowing of the right cord (left of photo) and atrophy (“spaghetti-linguini larynx”).

Dramatic flaccidity (2 of 4)

Under strobe light, showing dramatic flaccidity and increased lateral excursion of vibration of the right cord (left of photo) as compared with the left (right of photo). Vocal processes are fairly symmetrical suggesting LCA is at least mostly intact.

Bowing reduced (3 of 4)

After several cycles of chemotherapy, the patient feels well and voice had recovered to “100%” but is at this moment only “75%” due to an upper respiratory infection (see pinkness). Note as well that the right vocal cord (left of photo) has recovered much of its bulk, bowing is reduced, and the “spaghetti-linguini” appearance is virtually gone.

Equalized amplitude (4 of 4)

Under strobe light, the amplitude of vibration is equalized between the two sides and it almost looks like the lateral excursion is greater on the left (originally normal) vocal cord.

Another TA-only Paresis

Left vocal cord paralysis (1 of 4)

This person noted abrupt and severe voice change about six months earlier. Examination elsewhere at that time showed a “paralyzed left vocal cord.” The patient remembers seeing that one vocal cord did not move at all suggesting that perhaps TA + LCA + PCA were initially paralyzed. Voice is partially recovered by the time of this examination, but still moderately weak. Note that PCA muscles are working bilaterally. Left TA (right of photo) is clearly atrophied (spaghetti – linguini comparison), margin bowing, etc. We can’t yet decide about LCA function.

Working LCA muscles (2 of 4)

As the vocal cords approach each other just before phonation, the vocal processes turn medially on both sides, though perhaps a little better on the right than the left. Now we know that LCA muscles are both working.

Deficient TA muscle (3 of 4)

At the pre-phonatory instant, just before vibratory blurring, the normal right cord (left of photo) has a straight margin, while the left (right of photo) is bowed (TA is deficient). Both vocal processes are in a line—NOT pointing laterally on the left as would be the case if the LCA were not working. We see again that the only muscle not working is the left TA.

Open phase of vibration (4 of 4)

Here, under strobe light, at open phase of vibration, note that the lateral amplitude of the left vocal cord (right of photo) is greater, due to flaccidity of the atrophied left TA muscle.

Arytenoid Mismatch Makes for Gravelly Voice Quality Is Hard to Fix in Some Cases of Vocal Cord Paralysis

One could medialize more aggressively posteriorly on the left, hoping to raise the level of the cord, but often attempts to compensate for arytenoid mismatch such as that seen here are only modestly successful. Arytenoid superstructure is not useful for assessment of match; instead, the examiner should judge match at the vocal processes.

Arytenoids do not align (1 of 5)

Vocal processes (2 of 5)

Vocal processes do not match when touching (3 of 5)

Vocal cords out of alignment (4 of 5)

Asymmetrical vibration (5 of 5)

Vocal Cord Atrophy Goes Away when Nerve Supply to the Thyroarytenoid Muscle Returns

Bowed Margin (1 of 2)

After open-heart surgery, the left vocal cord is highly paretic. The evidence in the left vocal cord (right of photo) includes a) bowed vocal cord margin; b) capacious ventricle (V); and c) the "spaghetti" caliber of the left vocal cord as compared with the "linguini" caliber on the right (left of photo). Compare bracket length.

Thyroarytenoid muscle (2 of 2)

Notice after recovery of the nerve that the margin bowing on the left is no longer seen. The ventricle (V) is no longer capacious; and the "spaghetti-linguini" disparity between the caliber of the cords has become "linguini-linguini" due to recovery of normal bulk of the thyroarytenoid muscle within the left vocal cord.