TA-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).
TA-only Paresis after Botox Injection for Spasmodic Dysphonia
This man with adductory spasmodic dysphonia, has had consistent results during 15 years of botulinum toxin injections, administered several times per year. After his most recent (routine, and unremarkable) injection with his longstanding dose, his initial weakness was exaggerated and is only beginning to subside after six weeks. This dramatic “outlier” result that cannot be attributed to botox targeting. As seen in the photos below, the explanation is instead a right TA-only paresis.
The only reasonable interpretation is that the needle tip has “sheared” the branch of the recurrent laryngeal nerve supplying the thyroarytenoid muscle (leaving branches to the posterior cricoarytenoid and lateral cricoarytenoid muscles (PCA + LCA) undisturbed.
In a practice that supplies treatment to approximately 100 patients per month and ~1200 injections per year, this phenomenon occurs perhaps twice per year. The voice “always” recovers back to baseline SD symptomatology, but excessive breathiness starts to resolve only 6 weeks after the injection.
Right Thyroarytenoid Atrophy (1 of 3)
At close range, notice the findings, from lateral to medial, of right (left of photo) thyroarytenoid atrophy: a) capacious ventricle; b) “spaghetti” compared to the left vocal cord’s “linguini” morphology; c) margin concavity; and D) flat conus contour. Notice that the cord is fully lateralized, due to intact PCA (posterior cricoarytenoid) function.
Sharp medial turning (2 of 3)
In a closer view, the right vocal cord begins to move to the midline. Notice the sharp medial turning of the vocal process, again validating that the LCA muscle is functioning.
Right vocal process overlaps left vocal process (3 of 3)
At the moment before voice begins, with the right cord at the midline, the margin bowing is again accentuated. Notice again the medially turned right vocal process also overlaps the left vocal process.
Paresis, TA-only
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.
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
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.
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)
This man had a paretic left vocal cord. At diagnosis, the arytenoids did not match. After placing a vocal cord implant, he regained good strength, but his voice quality remained gravelly. At close range in abducted position, the “bulk” of both vocal cords appears similar.
Vocal processes (2 of 5)
At middle distance, with the vocal cords beginning to close, the tips of the vocal processes do not seem aligned (asterisks), similarly to pre-implant.
Vocal processes do not match when touching (3 of 5)
Just as the vocal processes arrive in contact with each other, one can see more clearly that the tips of the vocal processes do not match (see dotted lines).
Vocal cords out of alignment (4 of 5)
Now in full phonatory (voicing) contact, the right arytenoid rides up over top of the left vocal cord. And the tips of the vocal processes remain unaligned as well (dotted lines). The posterior ventricles also do not match (curved lines).
Asymmetrical vibration (5 of 5)
With different effective length of membranous cords, and overlap of right cord on top of left, not to mention that the implant in the left cord, asymmetrical vibration is not surprising. The voice is strong, but gravelly.
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.
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