Vocal cord paralysis (1 of 2)
Paralysis of left vocal cord (right of image), breathing position. Note that the left cord is bowed and atrophied as compared with the right.

Vocal cord paralysis (2 of 2)
Same patient during phonation, showing that the cords do not approximate; this correlates with a weak, breathy, air-wasting voice quality.

Vocal cord paralysis (1 of 5)
This person has an extremely weak and air-wasting voice. Here, with the vocal cords in breathing position, the cause of this voice problem is not yet evident.

Vocal cord paralysis (2 of 5)
Phonation. The cause of the problem is still not evident.

Vocal cord paralysis (3 of 5)
Closer view. The explanation becomes more apparent. As will ultimately be seen, this patient has paralysis of the left vocal cord (right of image); that is, the TA, LCA, and PCA muscles on that side are all affected. Best seen here is evidence of TA weakness (bowing of free margin, loss of left cord bulk especially in the area of the “conus”, and enlarged ventricle). The cord is paramedian, suggesting that the PCA muscle is not working, too. The LCA muscle is hard to evaluate in this view, however.

Vocal cord paralysis: evidence of LCA weakness (4 of 5)
Phonation in the low chest register (note the wide zone of blurring of the vocal cord's free margin). Here, the vocal process is clearly seen to turn laterally (arrow), indicating LCA weakness, in addition to the TA and PCA weakness seen in photo 3.

Vocal cord paralysis 5 of 5)
Phonation at very high pitch (thus, the vibratory blur narrows). The antero-posterior lengthening of the left cord at this high pitch turns the left vocal process back towards the midline (compare with photo 2), masking the LCA weakness. This low voice/high voice difference in the posterior commissure is routinely but not universally seen with LCA weakness.

Vocal cord paralysis: before medialization (1 of 12)
A classic example of “spaghetti-linguine” vocal cords, here in breathing position. The “linguine” cord (left of image) is normal; the “spaghetti” cord (right of image) is paralyzed, likely since birth. On the paralyzed side, notice the deep and broad ventricle, mild bowing of the margin of the cord, and reduced width of the upper surface of the cord (“spaghetti”-like), as compared with the non-paralyzed side.

Vocal cord paralysis: before medialization (2 of 12)
Phonation, more distant view, under standard light. Notice the considerable gap between the vocal cords. This gap correlates with the patient’s weak and air-wasting voice quality.

Vocal cord paralysis: before medialization (3 of 12)
Open phase of vibration, under strobe light. The paralyzed cord (right of image) has a much increased amplitude (lateral or outward excursion) and exaggerated bowing, due to its flaccidity.

Vocal cord paralysis: before medialization (4 of 12)
“Closed” phase of vibration, which is of course not closed at all, because the paralyzed cord (right of image) cannot come fully to the midline.

Vocal cord paralysis: 1 week after medialization (5 of 12)
One week after surgical medialization of the paralyzed cord (right of image), using a silastic implant buried deeply within the cord. Notice that the ventricle is no longer capacious, and the free margin is no longer bowed. Furthermore, in contrast with photo 1 of this series, the “spaghetti-linguine” description of these vocal cords is no longer apt.

Vocal cord paralysis: 1 week after medialization (6 of 12)
Phonation, under standard light. The gap between the cords is no longer seen (compare with photo 2), and the patient's spontaneous speaking voice sounds normal. She can recruit loudness effectively without any luffing or observable weakness.

Vocal cord paralysis: 1 week after medialization (7 of 12)
Open phase of vibration, under strobe light. The lateral or outward excursion of the paralyzed cord (right of image) is now similar to that of the non-paralyzed cord. Compare with photo 3.

Vocal cord paralysis: 1 week after medialization (8 of 12)
The closed phase of vibration is much more closed than preoperatively. Compare with photo 4.

Vocal cord paralysis: 5 months after medialization (9 of 12)
Five months after medialization. Compare this partially abducted position with photos 1 and 5 of this series.

Vocal cord paralysis: 5 months after medialization (10 of 12)
Phonation, under standard light, showing vibratory blur. Compare with photos 2 and 6 of this series.

Vocal cord paralysis: 5 months after medialization (11 of 12)
Open phase of vibration, under strobe light. As in photo 7 of this series, and in contrast to photo 3, the implant does not permit the paralyzed cord (right of image) to “buckle” laterally, or outward. If anything, the vibratory excursion of the non-paralyzed (and un-implanted) cord is greater than that of the paralyzed, implanted cord.

Vocal cord paralysis: 5 months after medialization (12 of 12)
The closed phase of vibration is now virtually normal, similar to photo 8 and in contrast with photo 4.

Extrusion of vocal cord implant (1 of 3)
Patient with a paralyzed left vocal cord (right of image), who several years ago had successful medialization of that cord with a silastic wedge. More recently, several months ago, she noticed pain and swelling during some intense aerobic activity and then a persistently roughened voice quality. This view shows that the left cord is inflamed.

Extrusion of vocal cord implant (2 of 3)
Strobe lighting. Note the convex shape of the left cord’s anterior end (the lower end, in this photo). This convexity is not caused by over-medialization, but instead by the inflammatory reaction.

Extrusion of vocal cord implant (3 of 3)
Closer view shows that the problem is exposure of the silastic implant. The actual silastic is bare at the arrow. Whitish exudate covers the remaining exposed implant. This is a rare event after medialization with a silastic implant.

Paralysis of left vocal cord (1 of 4)
An older man with left vocal cord paralysis (right of photo) after chest surgery involving the upper mediastinum. This is maximum adduction at the prephonatory instant showing bowing and atrophy of the left cord (right of photo). Voice is exceedingly weak and air-wasting.

Vocal gel injection (2 of 4)
At the beginning of voice gel injection in a voice lab, with the patient sitting in an examination chair. The trajectory of the 27-gauge needle is indicated with the dotted line. A second bolus of gel will be injected farther posteriorly.

Cord closer to midline (3 of 4)
At the conclusion of the injection, the left cord has been plumped up and also shifted towards the midline.

Complete adduction of cords (4 of 4)
The vocal cords can close completely now for voice production. Voice is dramatically stronger and the patient can say many more words on a breath before running out of air.

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.

Breathing position, bowed left cord (1 of 4)
Drastically weak voice since age 21 in a man now in his upper seventies. Breathing position. The normal right cord (left of photo) is fully lateralized, has a relatively straight margin (see line) and conus muscle bulge (pinker undersurface of cord marked by “C”) is fairly full. The abnormal left cord (right of photo) is paramedian (slightly lateral to midline), bowed (see line), and its conus muscle bulge practically nonexistent (marked by "C").

Approaching voicing position (2 of 4)
Approaching voicing position under standard light. Right cord (left of photo) has come almost to midline. Vocal process points slightly medially (arrow). Left cord (right of photo) shows lateral pointing of vocal process (arrow), bowed margin (see line), and its ventricle is capacious. Ventricle extends laterally from dotted line on each cord.

Vocal cord closure, large gap (3 of 4)
Voicing under strobe light, at maximum vibratory closure. Large gap explains major air-wasting dysphonia. Note directionality of vocal processes that appear to indicate LCA is working on the right (left of photo), and is not on the left (right of photo); note also the bowing of the left cord (right of photo).

Open phase of vibration, flaccidity of right cord (4 of 4)
Open phase of vibration shows what appears to be flaccidity (very large lateral excursion) of the right (neurologically intact) cord (left of photo). Flaccidity in working cord is often seen: the question is whether that is functionally “necessary” to allow vibration. I.E. would a normally tensed cord fail to oscillate with so little “grip” of the airstream? Or is it flaccid due to age and lack of a working partner to help keep it strong?