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 (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 (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.

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.

TA + LCA paresis (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. 

TA + LCA paresis (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.

TA + LCA paresis (4 of 4)
Strobe light during phonation. 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 (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 of 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.

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 (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.

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 (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.”

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.

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.

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.

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 (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.

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.

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.

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.

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.

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.

(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.

(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.

Teflon bulge (1 of 4)
Abducted, breathing position, standard light. The left vocal cord (right of image) was injected with Teflon paste decades ago, before contemporary materials and techniques were available. Note the bulge in the ventricle, and also at the free margin of the cord (arrows).

Teflon bulge (2 of 4)
Phonatory view, strobe light. Notice how the right vocal cord (left of image) must “wrap around” the convex left vocal cord.

Teflon bulge: after removal (3 of 4)
A few weeks after microsurgical “excavation” of part of the Teflon. Straighter free margin, and reduced bulge within the ventricle.

Teflon bulge: after removal (4 of 4)
Phonation, strobe light. In spite of blurring, can see that the match of the cords is improved, and this correlates with the patient’s much improved voice.

Tethered vocal cords (1 of 5)
This man has right vocal cord paralysis and a history decades ago of Teflon injection into the right vocal cord, resulting in posterior commissure synechiae. He is short of breath, partly due to the tissue band and partly because it tethers the vocal cords closer together than they would otherwise need to be as seen in photo 4 after the band is removed. See also photo 5.

At closer range (2 of 5)
At closer range.

Before laser removal (3 of 5)
The thulium laser fiber (F) is touching the synechiae, with laser energy about to be delivered.

Immediately after laser (4 of 5)
This is just after the thulium laser division of the band using topical anesthesia only, with patient sitting in a chair.

One month post-op (5 of 5)
A month later, no residue of the synechiae is seen, and the vocal cords can spring farther apart than in photo 1.

Strained and pressed sounding voice (1 of 4)
At speech pitch of B3 (247 Hz), the not only true, but also false cords are continually compressed together and voice is very strained and pressed-sounding.

False cords relax (2 of 4)
Just a note higher, at C4 (262 Hz), false cords relax a little to reveal the true cords.

Voice quality less strained (3 of 4)
An octave above, in falsetto, true cords are now nearly completely seen. Voice quality is less strained. This exemplifies the common but not universal finding that falsetto is less affected by the dystonia than chest register.

Adductory tone during breathing (4 of 4)
This patient's larynx also demonstrates marked adductory tone during breathing, though not to the point of classifying this individual as having a respiratory dystonia component.

Torus mandibularis (1 of 2)
View inside the mouth, focused on the floor of the mouth, with tongue retracted. The “mounds” seen in the foreground are unusually large tori, which are touching anteriorly.

Torus mandibularis (2 of 2)
Looking more directly downward onto the tori, with the tongue now pointing upward at the roof of the mouth.

Lesion (1of 3)
Nearly 80-year old man in whom CT for another reason shows this lesion just below the vocal cords, left upper trachea. Comparison with CT 18 months earlier shows the same lesion, and it is now only a few mm larger than then. Note that this man has had partial pharyngectomy and postoperative radiotherapy 40 years earlier for a pharyngeal wall cancer.

Decisions (2 of 3)
A week after attempted removal with the laser in the O.R. Removal was only partial due to difficult anatomy. The pathology result was "papilloma, with focus of invasive squamous cancer." Radiotherapy is not an option. Tracheal distortion is from tracheotomy 40 years before.

Removal (3 of 3)
The dilemma: Do a total laryngectomy with no cartilage destruction, the papilloma component, and such minimal progression over 18 months? Thus, the decision to do this aggressive laser ablation in the videoendoscopy procedure room. Surveillance will be intense, and total laryngectomy may still be necessary. More, later...

Open (1 of 2)
After total laryngectomy, the upper esophageal sphincter is open here for a brief moment, allowing one to see beyond into the esophagus.

Contracted (2 of 2)
A moment later, the sphincter contracts, as though the purse string of a velvet jewelry bag had been tightened.

Trachea (1 of 2)
View from just below the vocal cords. Note the u-shaped cartilaginous tracheal rings that give the trachea some firmness and resistance to collapse. The membranous third of the circumference puts a flat "lid" on the trachea, but can bulge inward when a person coughs.

Trachea (2 of 2)
View from the middle of the trachea in a different patient. Here the tracheal rings are shaped more like an “o” but the top of the “o” is completed by the membranous tracheal wall marked by the blue line. Also, the carina is seen distally and marked by an "x". This is where the trachea divides into right and left mainstem bronchi.

Trachea (1 of 1)
Radiographic view at the upper chest level. The horseshoe-shaped anterior segment of the trachea’s wall, two-thirds of the total circumference, is the trachea’s cartilaginous component. The posterior one-third is the membranous trachea, which also constitutes the anterior one-third of the esophagus, and is also called the tracheoesophageal party wall. The esophagus is dilated with air; this patient has undergone a total laryngectomy.

View into mid-trachea, diagnosis unknown (1 of 4)
View into the middle of the trachea in a man being evaluated for an unrelated problem. Note the remarkable projections (compare with normal trachea elsewhere on site). At initial examination the diagnosis was not known. The 'X' in subsequent photos marks the same place on the carina.

Spicules found in the tracheal wall (2 of 4)
A little farther down the trachea, and a closer view of the spicules projecting from the tracheal wall, whose nature at this examination was still unknown.

Diagnosis revealed (3 of 4)
View within the trachea just above the carina, where the trachea divides into right and left mainstem bronchi. Attempted biopsy revealed the extremely hard and unyielding nature of the projections, subsequently shown to be “bone.” Literature review revealed the diagnosis of tracheobronchopathia osteochochondroplastica, which essentially means “disease in trachea and bronchi due to bony change/ growth in cartilage rings.”

Biopsy reveals bone tissue (4 of 4)
Attempt to biopsy these projections with a flexible scope was unsuccessful due to their bony nature. Biopsy in the operating room made the diagnosis by revealing bone tissue. Copy and paste the link below to view the definition of tracheobronchopathia osteochochondroplastica: http://www.ncbi.nlm.nih.gov/pubmed/25013916

Mild tracheobronchopathia osteochochondroplastica (1 of 2)
A milder expression of this disorder. This person has been followed for years for a different problem, so these are incidental findings. Across the years, there has been no change in the lesions seen here in the trachea.

Mild tracheobronchopathia osteochochondroplastica (2 of 2)
Closer view of the enlargement of the cartilaginous rings of the trachea.

Trachea, with tracheotomy tube (1 of 2)
Upper trachea, with tracheotomy tube in view.

Trachea, with tracheotomy tube (2 of 2)
When the patient exhales fully, the posterior (back-side) tracheoesophageal party wall flexes anteriorly (frontward) to obstruct the trachea just above tracheotomy tube entry.

Tracheal stenosis (1 of 8)
This view from the level of the vocal cords shows high-grade tracheal stenosis, involving rings two, three, and four; the airway here is an estimated 30% of its normal diameter. For reference, a dotted line marks the level of the cricoid cartilage.

Tracheal stenosis (2 of 8)
Slightly closer view. This patient is very short of breath with minimal activity and, even at rest, has audible stridor. Elsewhere, across a span of several prior weeks, she had undergone three dilation procedures with only minimal, transient benefit.

Tracheal stenosis (3 of 8)
Close-up view shows scarring, collapse of tracheal walls, and some granulation tissue.

Just below the tracheal stenosis (4 of 8)
The trachea just beyond the stenosis is normal.

Tracheal stenosis, 5 days after surgery (5 of 8)
Five days after tracheal resection and primary reanastomosis. Compare with photo 1. Note that the airway’s diameter has at least tripled (part of the opening is obscured by tenacious mucus). The patient’s shortness of breath is now gone, as is the stridor.

Tracheal stenosis, 5 days after surgery (6 of 8)
Close-up of the line of anastomosis, with a couple of sutures visible. Compare with photo 3. Again, tenacious mucus in the upper part of the photo is obscuring part of the view.

Tracheal stenosis, 2 months after surgery (7 of 8)
Another eight weeks later. The airway is wide-open and has also now healed since the surgery. Compare this view with photo 1 (pre-surgery) and photo 5 (early follow-up).

Tracheal stenosis, 2 months after surgery (8 of 8)
Compare this view with photo 2.

Upper tracheal stenosis, before repair (1 of 6)
View from above the level of the vocal cords, showing severe narrowing and deformity of the upper trachea, caused by a “difficult” tracheotomy many years earlier. This man is frustrated by activity limitations, and difficulty coughing up accumulated mucus.

Upper tracheal stenosis, before repair (2 of 6)
View from just below the level of the vocal cords, showing the deformity and stenosis more clearly.

Looking from below the stenosis (3 of 6)
The trachea below the area of stenosis is normal.

After tracheal repair (4 of 6)
View from just above the level of the vocal cords, six weeks after tracheal resection and primary anastomosis, showing final result. Patient feels he breathes completely normally. Compare with photo 1.

After tracheal repair (5 of 6)
View from just below the level of the vocal cords. The tracheal caliber is now virtually normal. A broken, absorbable suture is seen at 2 o’clock, and a tiny remaining unhealed area is at 11 o'clock. Compare with photo 2.

After tracheal repair (6 of 6)
A close-up view shows the circular line of the anastomosis more clearly.

Tracheal stenosis and collapse (1 of 2)
Due to a life-threatening illness, this person had an endotracheal tube in place for a few weeks. When she got stronger, a tracheotomy tube (not seen as it is below this level of the trachea) was inserted. The result is severe scarring in the trachea. The expected diameter of the tracheal opening is indicated by the dotted line. The “X” marks the same location in each of the two photos.

Tracheal stenosis and collapse (2 of 2)
When this person exhales fully through her tracheotomy tube, or if she attempts to speak, the membranous tracheal wall also bulges forward, and obliterates the tiny residual opening. Dilation has been performed but helped minimally. The indicated procedure, if her severe medical condition will allow, is removal of the damaged segment of the trachea with reconstruction (aka tracheal resection, primary reanastomosis).

Tracheotomy (1 of 4)
This woman was gravely ill and intubated longterm. A tracheotomy was required. Now she wants the tube removed.

View below vocal cords (2 of 4)
The tip of the scope has been taken below the vocal cords. Note the fenestrated tracheotomy tube within the high trachea.

Fenestra (3 of 4)
When the patient plugs her trach tube with a finger, air comes into the distal tip of the tube (dark circle within the tube), passes up and out of the fenestra (window) and can power the vocal cords which are above our view. The trachea surrounds the tube as a whole without any "blow-by". If there were no fenestra, the patient would be unable to speak.

Patient post-trach (4 of 4)
After tracheal resection and re-anastomosis, the tracheotomy is no longer needed. The circular scar is at the dotted line. The M denotes overlying mucus. The patient now breathes normally.

Distant view of vocal cords (1 of 3)
Wide-angle view of vocal cords and subglottis, with white tracheotomy tube in evidence. This person was sent for resection of a stenotic (scarred, narrowed) tracheal segment, and repair. The patient can barely breathe when her trach tube is plugged for one or two breaths as a test. In this distant view, we can't evaluate the trachea, but do see posterior vocal cord tissue loss caused by a prior endotracheal tube injury (area enclosed by dotted lines).

Trach tube (2 of 3)
Sometimes, as depicted here, the tube itself obstructs a stenotic segment that, without the tube, might be large enough that tracheal resection/ reanastomosis is not needed.

Smaller tube (3 of 3)
The #6 tube in photo 2 has been replaced here with a #4 (smaller) tube. The posterior thrust of the curvature of the smaller tube is less; furthermore, the diameter is smaller. For both reasons, there is much more space for "blow-by" and the patient can breathe quite well with the tube plugged. If she can tolerate it plugged 24/7 except for routine cleaning, the tube can be removed, giving even more space for passage of air. This careful process may remove the need for surgical repair.

Tracheobronchial cough vibration (1 of 2)
Patient with SNC who is treated for presumed infection because of her congested rumbling “productive-sounding” cough. The "X" marks the same place in this photo and the following photo.

Tracheobronchial cough vibration (2 of 2)
Patient is at the moment of a deep, productive-sounding cough, but in fact it is not productive. Her many courses of antibiotics are probably unnecessary. The narrowing of the lumen is due to inward bulging of the membranous tracheal wall. The blur is caused by vibration during this cough.

Abducted breathing position (1 of 5)
Normal laryngeal entrance, with vocal cords in abducted (breathing) position.

View of mid-trachea (2 of 5)
View in normal mid-trachea. Note that the cartilaginous rings make up approximately 2/3 of the circumference and that the membranous trachea (upper photo at 'X') is more flat.

View just above the carina (3 of 5)
View just above the carina, where the distal trachea splits into left and right mainstem bronchi. Anterior take-off of carina at the 'X'.  The straight line delimits the membranous (flexible) tracheal wall.

Wheezing begins (4 of 5)
With Valsalva maneuver to accentuate patient’s functional expiratory wheezing. Note that the membranous tracheal and bronchial walls bulge inward on a functional basis to narrow the airway. Wheezing begins to be heard. The 'X' again marks the anterior take-off of the carina. Compare with Photo 3.

Left bronchus blocked (5 of 5)
As bulging inward continues, the left mainstem bronchus is particularly blocked. This explains why, on auscultation of the chest, wheezing sounds louder on the left than the right. Compare with photos 3 and 4.

Tracheoesophageal voice prosthesis (1 of 4)
Tracheal flange beginning to embed (at arrows) because the TEP device is too short.

Tracheoesophageal voice prosthesis (2 of 4)
Esophageal flange is bowing outward because the TEP device is too short.

Tracheoesophageal voice prosthesis, corrected fitting (3 of 4)
Same patient, with normal (now flat) esophageal flange fitting.

Tracheoesophageal voice prosthesis, during voicing (4 of 4)
During TEP voicing, pulmonary air comes up the trachea, is diverted through the center of the TEP device and, when the one-way valve opens, comes into the esophagus to bring its walls into vibration.

Hypopharynx of a tracheoesophageal voice prosthesis patient (1 of 4)
Panoramic view of the hypopharynx, in a patient who has undergone total laryngectomy. The entrance to the esophagus is at the line of arrows.

Hypopharynx, as the tracheoesophageal voice prosthesis patient makes voice (2 of 4)
Air has been diverted from the trachea and through the tracheoesophageal voice prosthesis (shown in the next two images) so that the hypopharyngeal tissue here is now vibrating (thus, is blurred) and making voice.

Tracheoesophageal voice prosthesis (3 of 4)
Seen here is the inner (esophageal) flange of the tracheoesophageal prosthesis, with its central flutter valve in closed (swallowing or resting) position.

Tracheoesophageal voice prosthesis, as the patient makes voice (4 of 4)
The patient has capped his tracheostome and is diverting air into the esophagus through the now-open central flutter valve. The pharyngoesophageal tissues are now vibrating (as seen in photo 2), and this vibration is blurring the image.

TEP buried (1 of 4)
This man’s TEP voice is becoming gradually more effortful, choppy, and strained. The explanation is that tissue (mucosa) is slowly burying the inner (esophageal) flange of the device. Half of the circumference is hidden under the mucosal flap indicated by dotted line.

Re-inserted and re-positioned TEP (2 of 4)
After re-inserting and re-positioning, now the entire circumference is visible, and voice has returned to effortless baseline.

Tissue overgrowing flange (3 of 4)
In a different patient, tissue (at X’s) is also trying to overgrow the internal (esophageal) flange.

Flange partially buried (4 of 4)
The anterior (tracheal) flange is partially buried. The area indicated by dotted line should all be visible device, rather than tissue.

Tracheomalacia (1 of 2)
Even at its maximum functional caliber, this trachea is severely narrowed (stenotic), due to injury from long-term intubation and tracheotomy. Not yet visible here is the tracheomalacia component (illustrated in image 2). A small granuloma is also visible on the right edge of the image.

Tracheomalacia (2 of 2)
Additional functional collapse (the tracheomalacia component), with both inspiration and expiration.

Tracheal hyperflexibility (1 of 6)
This patient has COPD as well as a "wet and productive" sounding cough. The explanation for this is not actual mucus, but tracheal vibration that sounds like a mucus-y cough. This panoramic view shows inspiration and normal abduction of the vocal cords. As we will see in photo 3, the trachea is patent at this moment.

Tracheal hyperflexibility (2 of 6)
Expiratory partial closure of the true vocal cords, similar to the lip-pursing maneuver persons with COPD often use to prevent lower airway collapse. As we see in photo 4, collapse is happening in spite of this lip-pursing maneuver.

Tracheal hyperflexibility (3 of 6)
Mid-trachea during deep inspiration, corresponding to the vocal cord position in photo 1. The white arrow indicates a speck of mucus which will also be seen in photo 4.

Tracheal hyperflexibility (4 of 6)
Mid-trachea, showing the same position as photo 3 but now during expiration. The membranous tracheal wall is bulging inward and nearly blocking the trachea. A wheezing sound is heard as air whistles though this narrow lumen (the expected lumen is indicated by the curved dotted line). The same speck of mucus that was seen in photo 3 is indicated again by the white arrow.

Tracheal hyperflexibility (5 of 6)
A little farther down the trachea, during inspiration.

Tracheal hyperflexibility (6 of 6)
At the same position as photo 5, during a cough. The membranous trachea not only bulges inward, but it also vibrates impressively (note blur), creating a deep and rumbling cough whose "wet" quality is not actually from mucus, but from vibration of the tracheoesophageal party wall.

Trachea, with tracheotomy tube (1 of 2)
Upper trachea, with tracheotomy tube in view.

Trachea, with tracheotomy tube (2 of 2)
When the patient exhales fully, the posterior (back-side) tracheoesophageal party wall flexes anteriorly (frontward) to obstruct the trachea just above tracheotomy tube entry.

Tracheotomy (1 of 4)
This woman was gravely ill and intubated longterm. A tracheotomy was required. Now she wants the tube removed.

View below vocal cords (2 of 4)
The tip of the scope has been taken below the vocal cords. Note the fenestrated tracheotomy tube within the high trachea.

Fenestra (3 of 4)
When the patient plugs her trach tube with a finger, air comes into the distal tip of the tube (dark circle within the tube), passes up and out of the fenestra (window) and can power the vocal cords which are above our view. The trachea surrounds the tube as a whole without any "blow-by". If there were no fenestra, the patient would be unable to speak.

Patient post-trach (4 of 4)
After tracheal resection and re-anastomosis, the tracheotomy is no longer needed. The circular scar is at the dotted line. The M denotes overlying mucus. The patient now breathes normally.

Translucent polyp (1 of 4)
Close-range view with vocal cords in abducted position.  This is not the best view to see translucence but faintly “grey” tone of polyps (circled by dotted lines) is indicator of translucence.

Translucent polyp (2 of 4)
As vocal cords are coming towards adduction, grey indicator of translucence. 

Translucent polyp (3 of 4)
Similar view, with elicitation of rapid inspiration to reveal polyps better, especially on left (right of image).

Translucent polyp (4 of 4)
During strobe illumination, translucence especially of the right vocal cord (left of image), is seen best.  Note that the larger polyp rides on the margin of the left vocal cord (right of image).

Extroverted elementary teacher (1 of 6)
Elementary teacher and major extrovert is grossly hoarse. Here you can see the fibrotic-appearing injuries bilaterally and an extra translucent polypoid component on the left cord (right of photo).

Submucosal fibrosis (2 of 6)
Under narrow band light, the white area is not hazy leukoplakia, but instead submucosal fibrosis, deposited as a protection against mucosal vibratory collision/ shearing injury.

Phonatory view (3 of 6)
Under strobe light, closure is imperfect due to the mid-cord elevations.

Open phase (4 of 6)
Open phase of vibration with small amplitude and absent “mucosal wave” due to stiffness of the mucosa.

Post microsurgery, open phase (5 of 6)
A week after vocal cord microsurgery, voice is markedly improved. No attempt was made to remove all of the fibrosis, but only to straighten the vocal cord margins. Open phase of vibration at F5.

Post microsurgery, closed phase (6 of 6)
Closed phase of vibration at same pitch shows that some margin swelling remains. The patient also has MTD; posterior cords are widely separated.

Vocal cord injuries (1 of 4)
Vocal cord injuries of overuse are often bilaterally similar, but here we have two quite different expressions of injury: fibrosis and capillary ectasia on left (right of photo); translucent polypoid injury (not a cyst) on the right (left of photo).

Narrow band lighting (2 of 4)
Now under narrow band light, the left cord (right of picture) has a flatter, fibrotic expression with tiny ectatic capillaries.

Strobe lighting (3 of 4)
Under strobe light, the translucent, polypoid nodule of the right cord (left of photo) distorts vibratory closure.

Phonation (4 of 4)
This is the best closure this grossly hoarse person can achieve.

Vocal cord polyp (1 of 4)
This singer has had marked vocal impairment for many months. In this standard light abducted position at medium distance, a polyp is seen on the left vocal cord (right of photo).

Distant view (2 of 4)
In a more distant view under strobe light, translucence is noted as the darker, more grey center of the polyp ‘looking through’ to the darkness below the polyp.

Translucent polyp with mucus (3 of 4)
At higher magnification still under strobe light, notice that the linear antero-posterior blood vessels in the floor of the polyp can, remarkably, be seen through the overlying polyp. The white ‘blobs’ (arrows) are mucus.

Different phase of vibration (4 of 4)
At a different phase of vibration also at C#4 (277 Hz), the dark center of the polyp is the result of 'seeing through' this nearly transparent polyp to the dark glottal chink below it. The arrows again indicate mucus.