TA + LCA Paresis
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. The following are 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.
Photos of TA + LCA paresis:
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.
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 (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.
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.
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 (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.
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.
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.
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.
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.
Weakness or paralysis of the vocal cord’s thyroarytenoid (TA) muscle, but with normal function of the vocal cord’s other muscles. The TA muscle “inhabits” the vocal cord and normally provides bulk and internal tone to the cord. The following are indicators of TA-only paresis:
- Movement: The vocal cord opens normally for breathing and closes normally for voicing.
- Position and appearance: Position is normal. Typically, the margin of the cord is slightly concave, the ventricle is capacious, and the conus area below the free margin is lacking in bulk.
- Appearance during voicing (under strobe lighting): Closure at the posterior commissure is complete and symmetrical bilaterally. Under strobe light, one sees flaccidity as indicated by increased amplitude of vibration; the lateral excursions become exaggerated and the mucosal wave increases. One may also see chaotic fluttering.
- Voice quality: Weak and air-wasting and often indistinguishable from a case of complete vocal cord paralysis—TA, LCA (lateral cricoarytenoid), and PCA (posterior cricoarytenoid).
Photos of TA-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 (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.
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.
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.
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.
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.
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.
(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.
At our practice, we use a 7-point interval scale upon which the patient and family will rate the patient’s degree of talkativeness.
(1) signifies an individual who is unusually quiet and uncommunicative;
(4) represents an averagely talkative person;
(7) describes someone who is unusually extroverted and even a “life of the party” type.
Technology-driven diagnostic model
A term used somewhat interchangeably with the reductionistic diagnostic model. The idea of a technology-driven diagnostic model is that technology is generally the answer to difficult diagnostic dilemmas. The hope is also looking to make voice diagnosis more “scientific” or “objective.” Inherent to the technology-driven model is the idea that the disorder will be better understood if only we can make enough measures of various sorts. By extension, if we don’t understand a voice disorder completely by the end of a large battery of measurements, we need more measures. While the clinicians at our practice make use of state-of-the-art technology, the integrative diagnostic model is preferred.
A synthetic material, polytetrafluoroethylene, most popularly associated with non-stick cooking pans. Until 25 or so years ago, it was common to treat paralyzed vocal cords by injecting a paste of Teflon particles deep within the cords. It was an effective treatment for its time, but it occasionally caused granuloma formation and required late debulking.
Today, injected materials such as hyaluronic acid gel or hydroxyapatite particles suspended in hyaluronic acid are typically used instead for temporary or somewhat permanent rehabilitation. For permanent rehabilitation of permanent paralysis, surgically implanted silastic wedges are used most often, though other materials are also used optionally.
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.
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.
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.
Audio with photos:
The patient describes original problem with Teflon granuloma/ overinjection, and the improvement after debulking Teflon.
Teflon bulge (1 of 5)
Abducted (breathing) position. 25 years ago, this woman had left vocal cord paralysis and was injected with Teflon paste. Unfortunately, this bulge of Teflon is below the cord’s margin, rather than within its center, which is disrupting the person’s voice (see next photo and caption). Space for breathing is diminished but adequate.
Teflon bulge (2 of 5)
Phonation, open phase of vibration, with strobe light. Voice quality is poor, because the Teflon bulge interferes with vocal cord vibration by deflecting the pulmonary air stream, stretching and stiffening the tissue, and putting the vocal cords out of symmetry with each other. Treatment will involve removing part of the Teflon bulge.
Teflon bulge: after treatment (4 of 5)
A few months after debulking of the Teflon. The contour of the undersurface of the left cord (right of image) is still abnormal, but much less so. Compare with photo 1.
The prototype is water. Other examples include black coffee and apple juice. There is little consistency or viscosity to thin liquids, making them difficult to manage when there is an issue with bolus control or inability to close the larynx fully when swallowing, as with unilateral vocal cord paralysis.
A little-known inflammatory condition of the lateral thyrohyoid ligament and nearby tissues in the neck. The connective tissues in this area comprise in practical terms a floating “joint” that attaches the larynx to the hyoid bone. Inflammation of unknown cause can lead to a syndrome similar to tennis elbow, so that the point of attachment becomes chronically sore. Thyrohyoid syndrome is also known as hyoidynia, hyoid bursitis, or lateral thyrohyoid ligament syndrome.1
A patient with this condition typically (but not always) has a history of placing stress on this connective tissue in his or her profession or activities—trumpet playing, for example. Diagnosis is confirmed with finger or thumb pressure to find a point of acute tenderness over the greater horn of the hyoid bone and sometimes the upper border of the thyroid cartilage. The clinician may find it helpful also, by way of comparison, to apply gentle pressure on the submandibular gland or carotid artery so as to confirm that the point of tenderness is truly greatest at the lateral thyrohyoid ligament, hyoid bone, or thyroid cartilage.
Treatment of thyrohyoid syndrome is typically supportive and may include reduction of percussive or aggressive use of voice, non-steroidal anti-inflammatory drugs, or (by far most effective) an injection of 0.5 ml of Kenalog 40 mg per ml at the lateralmost point of the hyoid and upper border of the thyroid cartilage2, requiring care and experience, as this is just anterior to the carotid artery. This injection may cause soreness on top of the thyrohyoid syndrome pain for a day or two, followed by considerable, if not complete, relief for about three weeks. After this time, pain may return, though not usually to the original level. In some cases a single injection suffices; in others, a series of three injections, performed three or four weeks apart, is more effective.
Sinha P, Grindler DJ, Haughey BH. A pain in the neck: lateral thyrohyoid ligament syndrome. Laryngoscope. 2014;124(1):116-8. ↩
Tonic Variant Spasmodic Dysphonia
A variant of spasmodic dysphonia (SD) in which the spasms (and their effect on the voice) are sustained rather than intermittent. Tonic variant spasmodic dysphonia is to be distinguished from classic variant SD.
Individuals with a tonic variant of adductor SD have a sustained strained-sounding voice. Individuals with a tonic variant of abductor SD have a voice that is more or less continuously breathy. Tonic variant SD goes undiagnosed or misdiagnosed far more frequently than does classic variant SD.
“Pure” tonic-variant adductory Spasmodic Dysphonia
Four subtypes of adductor SD, tonic variant :
Non dysphonic variant
Stage whisper variant
Vocal fry variant
A benign bony growth on the medial surface (tongue side) of the mandible or jaw bone. Also known as mandibular torus. Mandibular tori are usually seen on both the left and right sides (bilaterally). They often require no treatment unless they interfere with denture fitting.
In laryngology, mandibular tori come to attention because, when large, they can make it difficult or impossible for the clinician to gain a view of the vocal folds during microlaryngoscopy. That difficulty arises because during a microlaryngoscopy, the floor of the mouth is normally compressed by the laryngoscope to allow the scope to angle anteriorly at the viewing end, but mandibular tori, being composed of bone, do not compress.
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.
The ultimate surgical option for larynx cancer, in which the entire voice box is removed. Options used to avoid total laryngectomy are endoscopic laser surgery; partial laryngectomy; radiation; and chemo/radiation. Today, total laryngectomy is most often a salvage procedure, performed after failure of the initial treatment. It is still, however, a good primary option for very advanced tumors not likely to respond to chemo/radiation.
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.
Aspiration to a very limited degree, in which perhaps no more than a few drops or particles of liquid or food material enter the airway. If a person only has occasional trace aspiration, there is no real risk of aspiration pneumonia, especially if the person responds with coughing.
The trachea, or windpipe in layman’s terminology, begins on its upper end just below the larynx and extends inferiorly into the chest where it splits into the right and left mainstem bronchi; delivering inspired air to the right and left lungs, respectively.
The tracheal rings comprise approximately two-thirds of the circumference of the trachea, anteriorly and laterally. The remaining posterior one-third “membranous” tracheal mucosa is the anterior surface of the “party wall” it shares with the esophagus.
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.
Tracheal resection and reanastomosis
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.
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).
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.
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.
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.
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.
Tracheoesophageal Party Wall
The membranous shared wall between the trachea and esophagus. The tracheoesophageal party wall is also known as the membranous trachea. This membranous wall makes up one-third of the trachea’s circumference; the other two-thirds is bolstered and stiffened by cartilaginous rings. These stiff cartilaginous rings help to keep the trachea open, whereas the membranous wall has some flexibility and may momentarily bulge into and narrow the tracheal passageway, as during a cough or a Valsalva maneuver.
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.
Tracheoesophageal Voice Prosthesis (TEP)
A device that is placed in the wall that separates the trachea and esophagus in order to enable a total laryngectomy patient to make voice. The tracheoesophageal voice prosthesis (TEP) uses a one-way valve to let air pushed up from the lungs to pass through from the trachea and enter the esophagus, causing the walls of the esophagus to vibrate as a new voice, but without letting food or liquids to pass through the other way, from the esophagus to the trachea.
The need for a TEP:
A patient who undergoes a total laryngectomy procedure will have the entire larynx removed and the end of the trachea redirected to an opening—called a stoma—created in the front of the neck. The result is that the patient can now breathe through this stoma, but would be unable to make any voice, because the larynx (voice box) is gone, and the air for voicing that once passed up through the larynx, causing the vocal cords to vibrate and thereby making voice, now simply exits the trachea at the stoma. Such a patient can obtain an alternate voice by using a TEP device.
The placement of a TEP:
In order to place a TEP device into the wall that separates the trachea and esophagus (the tracheoesophageal party wall), a puncture must first be made, into which the device can fit. This puncture can be made during the laryngectomy procedure (primary tracheoesophageal puncture) or else afterward in a separate procedure (secondary tracheoesophageal puncture), typically some weeks after the laryngectomy. Some clinicians prefer to place the device itself as part of the primary puncture. Others first place a catheter to hold the puncture open and allow for tube feedings while the pharynx heals, and then they place the actual device in an office setting 10 days or more later.
The use of a TEP:
When a patient with a TEP device wants to speak, he or she must momentarily cover the stoma in the front of the neck, so that air coming up from the lungs is redirected through the TEP and into the esophagus to make voice. Some patients will simply cover the stoma as needed with their thumb, if their stoma is normally left entirely open, or is only concealed from view with a small, unobtrusive, breathable cloth. More commonly, however, the patient’s stoma is fitted with a housing, into which is placed a heat and moisture exchanger (HME); in these cases, the HME, which looks like a flat, plastic button, can be pushed as needed to block the stoma and enable voicing. Whatever the case, speaking with a TEP device is a learned skill and requires training through speech therapy.
TEP: Series of 4 photos
TEP voicing: Series of 4 photos
TEP’s that want to become buried: Series of 4 photos
How the one-way flapper valve works in a TEP prosthesis: Series of 3 photos
Flaccidity of the trachea, due to injury or congenital defect, such that the tracheal passageway fails to stay open at its normal diameter, especially during inspiration. In adults, tracheomalacia is most commonly seen after a prolonged intubation in which the endotracheal tube balloon was (sometimes necessarily) over-inflated and, consequently, exerted too much pressure on the tracheal rings, damaging and thereby weakening them; infection can also exacerbate this weakening of the tracheal rings. Intubation is a less common cause of tracheomalacia now, however, since the advent years ago of high-volume, low-pressure endotracheal tube and tracheotomy tube cuffs. In neonates, tracheomalacia can be congenital or a sign of incomplete development of the trachea.
Tracheomalacia should be distinguished from nonorganic breathing disorder, tracheal, which differs from tracheomalacia in that the tracheal collapse which occurs is functional or volitional, and is sometimes used to amplify asthmatic wheezing, or to masquerade as asthma, in each case for secondary gain.
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.
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 (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.
Photos of Tracheotomy:
Tracheotomy dependence is the state of having no choice but to breathe through a tracheotomy tube, because of an obstruction of the normal “pathway” for breathing, through nose and/or mouth, through the larynx, and only then into the trachea. Tracheotomy dependence may occur because part or all of the larynx has been removed, e.g., for cancer, or because of severe scarring or inflammation.
A tracheotomy tube is a device that is surgically placed into the trachea low in the neck, with its tip well inside the trachea and its other end anchored to a faceplate that sits on the surface of the neck. A tracheotomy tube allows an individual to breathe directly from the neck opening into the trachea as an alternative to normal breathing through the nose and/or mouth. “Trach” is the colloquial term used by clinicians to refer to a tracheotomy tube.
A fenestrated tracheotomy tube allows voicing when there is stenosis
Traditional diagnostic model (for voice disorders)
The traditional diagnostic model (for voice disorders) is the method of diagnosis used up to recent decades, and still by far the most prevalent model worldwide. Here, the clinician collects a patient history and then proceeds directly to mirror examination, or possibly one using the fiberscope. Unfortunately, many diagnoses may be missed due to missing information. See also: the integrative diagnostic model for voice disorders.
Some polyps are covered by mucosa that is opaque. Some are filled with blood (hemorrhagic polyp). On the other hand, some have a thin and delicate mucosa, and a watery content that is not transparent, yet transmits some light. Unlike a blister, which they could be construed as resembling, and which typically resolves itself, most translucent polyps end up requiring surgery for their resolution.
Photos of translucent polyps:
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).
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.
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.
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.
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.
Transnasal esophagoscopy (TNE)
Transnasal esophagoscopy (TNE) is a diagnostic procedure that involves passing a slender, flexible videoendoscope through a topically anesthetized nasal passage into the back of the nose, down past the larynx, and through the whole length of the esophagus. Formerly, esophagoscopes were much larger in diameter than the newer scope. This makes passage of the scope relatively pain-free so that topical anesthesia is all that is required. Occasionally, anxious patients are slightly sedated for the procedure; more commonly, sedation is not needed and, in this latter instance, the patient may not only drive to the examination, but drive back to work or home afterwards.
Transverse cordotomy is a surgical procedure on the posterior part of the vocal cord, first described to our knowledge by Dr. Haskins Kashima of Johns Hopkins University many years ago. The procedure is done for bilateral vocal cord paralysis, or for glottic stenosis caused by injury and resultant scarring of the vocal cords together. Typically, an individual undergoes this procedure because of tracheotomy dependence or because of marked exercise intolerance. The procedure is performed endoscopically, using the laser to make an incision across the posterior end of the most damaged or least functioning vocal cord. Inherent to this problem, and to this solution, is the idea that one trades away a little bit of voice to gain a little bit better airway.
Treatment for Sensory Neuropathic Cough
Begin with the medication marked with the large “X.” If, over time, the first prescription fails to provide adequate benefit, you will of course let us know this during a phone or encrypted email followup communication. At that point, we would create a new prescription that you would pick up at your pharmacy. You will follow the same procedure, if necessary, for a third medication if the first two do not reduce cough sufficiently. (see Voice Mail and Portal Email Instructions, below).
_______ Option 1: Amitriptyline (Elavil) OR Desipramine (Norpramin): begin with 10 mg 2 hours before bed.
1. If grogginess occurs, this often resolves if you persist in taking the medication for two weeks.
2. If you experience some response, but less than 80% reduction of your symptoms, please double to 20 mg. (2 pills) 2 hours before bed.
3. If there is still less than 80% reduction, you may increase step-wise up to 80 mg. (8 pills) 2 hours before bed.
4. If you have afternoon “breakthrough” coughing, you may try adding 10 or 20 mg (1 or 2 pills) at noon.
5. Please leave voicemail or encrypted email for your doctor 14 days after beginning,
as instructed below at *.
______ Option 2: Gabapentin (Neurontin): 300 mg (1 pill) at bedtime for 3 days; then 300 mg noon and bedtime for three days; then 300 mg breakfast, mid-afternoon and bedtime for 3 days; then breakfast, lunch, dinner, and bedtime (300 mg 4 times per day for a total of 1200 mg per day). You may increase slowly in like manner to as much as 600 mg (2 pills) four times a day, assuming side effects allow.
1. You must “taper on” and “taper off” this medication as described above.
2. Side effects are dramatically different between individuals. Some experience none in spite of high dose; a few notice significant side effects with even one pill per day.
3. Main side effect is sleepiness, or a mild feeling of being “drunk.” Also occasionally swelling of feet.
4. To minimize side effects, take the medication with food.
5. If you cannot tolerate side effects, back off to the next lower dose and maintain until you are tolerating the medication well, then try to increase again by one pill.
6. Please leave voicemail or encrypted email for your doctor approximately 14 days after beginning, as instructed below at *.
______ Option 3: Citalopram (Celexa): Start at 20 mg (1 pill) every evening. After one week, increase to 2 pills (40 mg)
1. You must “taper on” and “taper off” this medication, and do not make sudden large changes in dose.
2. Main side effects include drowsiness and dry mouth.
3. Please leave a voicemail for your doctor 7-10 days after beginning, as instructed below.
Information we need from you each time you call/email:
a. Your name (Please spell).
b. Name of medication and how long you have been taking it.
c. Your current dose level.
d. What % reduction of symptoms you are experiencing.
e. Side effects, if any.
f. Daytime and evening phone numbers.
g. Any other comments you wish to make, or questions you have.
Sample Voicemail: “This is John Doe, I’ve been on the amitryptyline 10 days. I increased to 50 mg (5 pills) each evening. My symptoms are diminished by 50%. Side effects are: ________________. My phone numbers are_______________ and _____________. I’d like to know what to do next.”
The use of a variety of brief therapy approaches during the initial diagnostic encounter to assess the vocal phenomenology that results, and also to see what changes of voice production appear to be possible for the patient, versus which ones seem not to be, due to physical limitation or nonorganic interference.