TA + LCA Paresis
TA + LCA paresis is weakness or paralysis of both the thyroarytenoid (TA) and lateral cricoarytenoid (LCA) muscles of one vocal cord, but with normal function of that cord’s posterior cricoarytenoid (PCA) muscle. The TA muscle “inhabits” the vocal cord and normally provides bulk and internal tone to the cord. The LCA muscle helps to bring the vocal cord to the midline for voice production and, more specifically, to bring the “toe” of the arytenoid cartilage to the midline.
Indicators of TA + LCA Paresis
- Movement: Position is normal during breathing, but the vocal cord does not move closer than the intermediate position for voicing. In other words, it is further lateral than the paramedian position one would see with paralysis of all three muscles: TA + LCA + PCA.
- Position and appearance: Due to the TA paralysis, the margin of the cord is slightly concave, the ventricle is capacious, and the conus area below the free margin is lacking in bulk. Due to the LCA paralysis, there is lateral turning of the vocal process. This lateral turning is seen best in low voice, and is a little less apparent with very high voice.
- Appearance during voicing (under strobe lighting): Flaccidity as indicated by increased amplitude of vibration; the lateral excursions become exaggerated and the mucosal wave increases. One may also see chaotic fluttering. The gap between the cords is particularly large because of the unopposed lateral pull of the intact PCA muscle. TA and LCA paresis is often mistaken for complete vocal cord paralysis (TA + LCA + PCA). To avoid this mistake, the examiner must notice this lateral position. The examiner can also try to make any such lateral pulling more evident by asking the patient to inhale sharply or, better yet, to sniff, which exaggerates the abductory movements of the patient’s vocal cords.
- Voice quality: Exceedingly weak and air-wasting. After successful medialization, the obligate falsetto and luffing may disappear, while some of the breathy-pressed quality may persist.
Other variants of vocal cord paresis include LCA-only, TA-only, PCA-only, and IA-only (interarytenoid muscle).
Visual Cues of Paresis Validated by their Change with Recovery!
TA weakness (1 of 6)
Dramatic breathy voice change after intubation/ cardiac surgery in an elderly woman. Breathing position clearly shows left TA weakness (bowed margin and subtle spaghetti-linguini difference) when compared with the right vocal cord as indicated by brackets. It appears that abductory function (PCA) is good, and LCA function cannot be determined until the patient attempts makes voice.
LCA weakness (2 of 6)
During phonation, lateral turning of the left vocal process (right of photo, compare arrows) caused by LCA weakness of that side. The vibratory blur is wider on the left (right of photo) as well, suggesting larger amplitude of vibration due to flaccidity.
Six weeks later (3 of 6)
Six weeks later, the patient thinks her voice has returned to normal. In this abducted position, margin bowing is less, and the spaghetti-linguini difference appears to have gone away. Subtle medial turning of the vocal process may be due to full recovery of LCA possibly unmasking subtle weakness of PCA, or just an artifact… Compare with photo 1.
LCA muscle recovered (4 of 6)
Now the vocal processes both point straight anteriorly (arrows) because left LCA muscle (right of photo) has recovered. Compare with photo 2. It would still be good to verify, however, that TA is fully recovered, given the subtle bowing that remains in the prior photo (3).
Closed phase (5 of 6)
Closed phase of vibration, strobe light at low pitch. Incomplete closure anteriorly suggests atrophy but to an equal degree for both vocal cords.
Open phase (6 of 6)
Open phase of vibration shows that the amplitude of vibration (lateral excursion) is approximately the same bilaterally, validating that left TA function (right of photo) has returned fully.
Paresis, TA + LCA, before and after Placement of an Implant
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.
Paresis, TA + LCA, before and after Injection of Voice Gel
Normally functioning PCA muscle (1 of 8)
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 2
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 3
TA + LCA paresis (1 of 4)
TA + LCA paresis left vocal cord (right of photo). Note atrophy, concave margin. Lateralization is full, indicating that the PCA muscle is working normally. Hence, the anterior branch of the recurrent laryngeal nerve is not working.
Breathy voice (2 of 4)
The same patient, attempting to phonate. There is a large gap between the cords. There may be IA weakness along with the LCA, since the gap is so large. The voice here is extremely breathy / air-wasting.
Voice gel injection (3 of 4)
After injection with voice gel to plump and medialize the left cord (right of photo). The needle has just been withdrawn. Compare with photo 1.
Injection complete (4 of 4)
Also after injection, when making voice, the patient can approximate the cords (the gap is gone) and voice is dramatically strengthened.
TA + LCA Paresis
TA + LCA paresis (1 of 4)
This photo verifies that both PCA muscles are working (note the wide, bilaterally equal abduction of the cords). It also indicates TA weakness on the left (right of photo): the left side (right of photo) is “spaghetti” differing from the right side’s (left of photo) “linguini.” Furthermore, the conus bulge (indicated by ‘X’) is missing on the left (right of photo). LCA function has not yet been determined.
Weak left vocal cord (2 of 4)
At the beginning of adduction for voicing, note that the right cord (left of photo) has already come to the midline, and vocal process is turning medially. Left side (right of photo) will come somewhat to the midline likely due to IA function due to its bilateral innervation, and also perhaps CT function.
Vocal process points laterally (3 of 4)
Strobe light during phonation. “Most closed” phase of vibration is in fact not closed, due to unopposed pull (even if just baseline tone) of left PCA muscle (right of photo). Note as well that the vocal process on the left (right of photo) points laterally due to LCA weakness; on the right, intact LCA side (left of photo, the vocal process turns medially.
Strobe light during phonation (4 of 4)
Open phase reveals the increased amplitude of vibration of left cord (right of photo), validating in a second way the weakness of the left TA muscle (right of photo).
Paresis, TA + LCA, with Recovery
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.
Paresis, TA + LCA, before and after Medialization
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.
TA + PCA-only Paresis
Breathing position (1 of 5)
Abducted (breathing) position, shows the bowed contour of the left cord (right of photo), and loss of mass due to wasting of muscle within the cord. The left vocal process points medially ( see arrow), suggesting that the LCA muscle is still active.
Phonatory position (2 of 5)
During attempted phonation, note the gap (see arrows) that remains between the cords, accounting for her breathiness. In this view, vocal processes are reasonably antero-posterior in orientation, again suggesting good LCA function. In addition, note the lateral buckling of the left cord (right of photo), due to its flaccidity.
Voice gel injection (3 of 5)
At the moment just before voice gel injection into this flaccid cord. Blood is due to the cricothyroid membrane puncture moments before, for the purpose of providing topical anesthesia.
Plumped vocal cord (4 of 5)
Needle hub pulls the false cord laterally and true vocal cord is noticeably plumped up by the gel.
After voice gel injection (5 of 5)
Phonation, immediately after voice gel injection. Notice that the vocal cords come into much better contact. Voice is correspondingly dramatically improved.
Example 2
Breathing position (1 of 6)
This male singer is complaining of loss of edge/ body/ strength of voice, with onset several months ago. This distant view, in breathing position, shows no obvious abnormalities.
Phonation (2 of 6)
Here in phonation at D4 (294 Hz) there is still no obvious abnormality seen.
Closed phase, A3 (3 of 6)
Viewed up close, at A3 (220 Hz), closed phase of vibration, subtle lateral turning of the left vocal process (right of photo) is suspected, but this middle voice pitch would tend to obscure that finding.
Open phase, A3 (4 of 6)
Also at A3, but open phase, the lateral turning looks a little more evident and note as well a subtle increased degree of lateral excursion “bowing” of the left cord (right of photo).
Closed phase, C3 (5 of 6)
Lower pitch C3 (131 Hz) is elicited to reveal paresis findings, if truly present. In this closed phase strobe view, lateral turning is about the same, but it looks like the line of contact of the cords is not straight.
Open phase, C3 (6 of 6)
Also at C3, lateral turning of the vocal process is still a little subtle at best, but the flaccidity of the left true cord (right of photo) is obvious, and consistent with TA paresis. A reasonable diagnosis here is “definite left TA paresis, and subtle LCA as well.”
Telescope Panoramic Views are Routinely not Adequate for Assessing Paresis!
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.
Classic TA + LCA-only Paresis, Right Vocal Cord
Atrophy of the conus (1 of 5)
This middle-aged woman awakened with a drastically altered, weakened voice. In this abducted position we can say both PCA muscles are normal. We can’t assess LCA in this view. It appears that TA is weak on the right cord (left of photo). There is a faint “spaghetti – linguini” difference (white brackets) but the right ventricle does not seem particularly capacious, nor is there any significant margin bowing. The most convincing finding is atrophy of the “conus” part of the vocal cord covered by the darker “purplish” mucosa delineated by the red brackets.
Inability to adduct (2 of 5)
Forced expiration should bring normal cords into slight “mirror image” adduction. In this view, the normal left cord (right of photo) adducts significantly, but the right does not. Now we know for sure that the right LCA muscle is not working. The phonation viewings that follow will allow us to further assess both LCA and TA function.
LCA weakness (3 of 5)
Low pitch phonation at F3 (175 Hz) with posterior commissure and vocal process mucosa in clear view, provides the “proof” of LCA weakness. Note that the right vocal process fails to turn medially. By contrast, the left vocal process is in line with the rest of the vocal cord and almost over-rotates medially to compensate.
Further review (4 of 5)
Now more than an octave higher at A-flat 4 (415 Hz), the vocal process is pulled a little bit more in line by the anteroposterior stretch, but the failure to point straight anteriorly (as does the normal left side) again indicates LCA weakness.
Luffing (5 of 5)
Under a strobe light, the patient is asked to produce voice at low pitch and as loudly as possible. This overwhelms the weak right cord. The audible luffing and the large amplitude and chaotic vibration of the right cord are virtually pathognomonic of vocal cord paralysis and every form of paresis other than PCA-only paresis.
Breathing Tube Injury—A Rare Complication of Intubation for General Anesthesia
Inflamed vocal cord (1 of 5)
This patient had severe voice change after intubation for a 2-hour surgical procedure. She says voice was 100% before surgery and she awakened at 15%, a whisper with a bit of voice mixed in. Fortunately, across six weeks she has recovered partially to “70%.” The right cord (left of photo) looks “inflamed.”
Closer view (2 of 5)
At closer range, a little more detail is seen.
Scarring from intubation tube (3 of 5)
Under narrow band light, it appears that there is scarring of that fold likely from a laceration upon insertion of the tube. (She was told intubation was difficult.) A key finding, however: the right vocal process is turned slightly laterally, suggesting weakness of the LCA muscle.
Mucosal Injury (4 of 5)
Under strobe light, closed phase of vibration, it is almost as if there is loss of mucosa upper surface of right cord.
Flaccidity of right vocal cord (5 of 5)
Open phase of vibration shows flaccidity of the right cord, with a much larger lateral excursion / amplitude of open phase on the right (left of photo).
Conclusion: While we try to explain abnormality due to one cause, here, the patient has a mucosal injury and paresis of right TA and LCA muscles, which can also follow intubation. This explains why the initial postop voice was so weak and whispery, and also the rapid partial improvement. This voice will likely continue to improve and be very functional as a speaking voice. Fortunately, this person is not a singer, as clarity especially in upper notes, will likely be remain impaired even after full recovery.
PCA working; TA and LCA Are not in this Paresis Subtype
Capacious ventricle, bowed margin (1 of 4)
A year earlier, after thyroid surgery, this older man experienced dramatic vocal weakness, unchanged to the present. In this breathing position, we can see that both PCA muscles appear to be working. Capacious ventricle (V) on the right vocal cord (left of photo) and bowed margin suggest TA is not working on that side. The position during voice-making will tell us more.
Pre-phonatory (2 of 4)
The patient is at the pre-phonatory instant, just before vibratory blurring. This is an inadequate view to assess LCA, however. See the next photo instead.
Posterior view (3 of 4)
This clear posterior commissure view at the pre-phonatory instant tells all: With medial turning of the vocal process indicated by the arrow at right of photo, we can see that left LCA is working; right vocal process (arrow at left of photo) still points laterally signifying that right LCA is not working. Right TA is not working; left TA is, despite margin bowing.
Right TA + LCA-only paresis (4 of 4)
Here the patient makes a weak, breathy voice, and we can see vibratory blurring. We can see again that this man has right TA + LCA-only paresis.
Share this article