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.
Paresis, PCA-only (1 of 4)
PCA muscle of the right vocal cord (left of image) is not working. TA and LCA are perceived as intact, based on the combination of: 1) normal voice; 2) the right cord is not bowed; 3) ability to medially turn or at least keep in line the right vocal process (see also photo 2); and 4) the right cord is not atrophied, nor is the right ventricle unusually capacious.
Paresis, PCA-only (2 of 4)
During phonation, there is no sign of lateral turning of the right vocal process, which would indicate LCA weakness. Furthermore, vibratory blurring (in this standard-light view) appears to be fairly equal on each side, suggesting there is no flaccidity of the right cord, contrary to what one would expect were the TA weak on that side.
Paresis, PCA-only (3 of 4)
Strobe light, closed phase of vibration, again showing that there is no lateral turning of the vocal process.
Paresis, PCA-only (4 of 4)
Strobe light, open phase of vibration. The amplitude of vibration for each cord appears to be equal, just as it did (based on blurring) in photo 2. This finding confirms that the TA is not weak, as such weakness would make the right cord flaccid and increase its amplitude of vibration.
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.
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).
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.
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 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.
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.
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.
(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.
(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.
(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.