PCA-only Paresis
PCA-only paresis is 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).
Paresis, PCA-only
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.
Evolution of Vocal Cord Paralysis To End as PCA-only Paresis
For some voice doctors, measurement is accorded more respect than observation. Both are legitimate, of course, yet, visual (observational) understanding of paralysis and paresis remains far more useful than EMG, acoustic, or aerodynamic measurements. This case strongly illustrates that point.
This older man underwent thoracic surgery but due to complications was also intubated for much of two days. Immediately upon awakening, his voice was altered. He said it was whisper only.
At his original office visit a month later, he thought his voice had improved to “10%” and examination showed left vocal cord paralysis (TA, LCA, and PCA muscles all non-functional). Three months later, his voice was by his description to 40% and improving further week by week. By month 8 post-surgery, verified at 18 months, he felt his voice was “99%” recovered; examination showed recovery of TA and LCA, but not PCA muscle.
The final diagnosis: Left PCA-only paresis. Rather than being entirely “out,” the PCA seems only to be weak.
Left Cord Margin Bowing (TA weakness) (1 of 11)
A month after thoracic surgery that took voice from “100%” preop to “0” postop (whisper only). Breathing position (partially open) shows bowing of the left cord margin (right of photo).
LCA Paresis Identified (2 of 11)
Just before vibration (phonation) begins, there is a large gap between the cords. The left TA-related bowing/atrophy remains obvious, and the tip of the vocal process (VP) is turned laterally, indicating weakness of the left LCA muscle.
Voice is Breathy! (3 of 11)
Now creating an exceedingly breathy voice (see vibratory blur) with a phonation time of mere seconds due to air wasting between the cords. Two critical muscles for producing voice, TA and LCA, are not working.
LCA Paresis Best View (4 of 11)
The key view is during voicing when LCA weakness is appreciated by noting lateral turning of the left vocal process (circled arrow).
4 Months Later, Glottis Open For Breathing (5 of 11)
Now at 4 months post-injury, this view is rotated; the left cord (right of photo is lateralized and the left (bowed) cord is actually midline. Is slight medial turning of the vocal process (VP) imaginary? That would correlate with the patient’s comment that voice is noticeably better and continuing to improve week by week.
Gap during phonation Less (6 of 11)
During phonation, the gap between the cords is less than in Photo 4, and lateral turning of the left vocal process (arrow) less exaggerated. This suggests slight recovery of the left LCA muscle.
PCA Weakness Is All That remains (7 of 11)
At 8 months from the injury, the patient says his voice is completely recovered. In this breathing position, one can see that the left PCA muscle which should lateralize that cord is still not working, explaining the midline position of the left cord (right of photo). But of course, the PCA muscle deficit does not affect voice, but only the size of the glottic aperture during breathing…But tone in the LCA muscle is clearly turning the vocal process medially.
LCA Recovered: The Vocal Process Now Turns Medially (8 of 11)
Both vocal process turn medially for phonation, suggesting recovery of the left LCA muscle, even though the right vocal process rides up on top of the left (seen not infrequentlyin older larynges).
At 18M, Left Cord Does Not Abduct Due To Continuing PCA Weakness (9 of 11)
At 18 months, and continuing to feel his voice is normal. In this breathing position, the glottic aperture is reduced because the left cord does not lateralize, consistent with ongoing weakness of the left PCA muscle. The bowing is not significant because PCA weakness coupled with normal TA and LCA create bowing while breathing, even in young people. See also the next photo.
Left PCA Can Muster Some Lateralization (10 of 11)
When the patient sniffs, his weak left PCA muscle does lateralize the cord, somewhat, abolishing the “bowing” seen in photo 9.
Full Recovery for Voicing, Despite PCA-Only Paresis (11 of 11)
At the prephonatory instant, both vocal processes come into straight-line contact (compare with photos 4 and 6. Keep in mind that PCA weakness alone does not affect voice but PCA-only paresis is seen only during breathing, as in Photo 10.
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).
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.
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