Multimedia Encyclopedia
Pachyderma
Literally, “elephant skin.” Used in laryngology to refer to rough or thick mucosa. Most often seen in the interarytenoid area and is thought to be indicative of acid reflux or, sometimes, chronic bacterial infection. Pachyderma does not typically affect the voice, though the underlying cause of the pachyderma can (e.g., chronic inflammation from acid reflux or chronic bacterial laryngitis). In such a case, the true vocal cords themselves appear intensely red.
Photos:
Pachyderma, caused by laryngitis sicca: Series of 3 photos
Elephant skin: Series of 1 photo
Palate
A structure which serves as both the roof of the mouth and the floor of the nasal cavity and nasopharynx. The palate has two parts: the hard palate and the soft palate. The hard palate, which is the anterior two-thirds of the palate, begins just behind the upper central teeth and is made up of bone. The soft palate, which is the posterior one-third of the palate, is made up of muscle; the soft palate is therefore movable, and it elevates to help with swallowing and speech.
Palate deviation
A phenomenon in which, when the palate is lifted, the midline deviates to the normal side and the weak side droops. Palate deviation is seen in individuals who have paresis or paralysis of a hemi-palate due to Vagus nerve injury or dysfunction. It can be observed from either the oral cavity or nasopharynx view; subtle cases sometimes seem easier to see from the nasopharynx view.
Photos of palate deviation:
Palate paralysis (1 of 1)
View of the upper surface of the palate from within the nasopharynx. Due to this patient's hemi-palate paralysis, the palate deviates to one side, such that its midline (darker dotted line) no longer matches the nasopharynx's midline (lighter dotted line).
Palate elevation
Lifting of the soft palate so that its edge rests against the posterior pharyngeal wall, functionally separating the nasopharynx and oropharynx. Palate elevation occurs with each swallow to keep food or liquid from entering the back of the nose. It also occurs during speech with any non-nasal sounds (in English, all sounds except for “n,” “m,” and “ng”), keeping the sounds non-nasal by keeping air from passing out through the nose.
Photos:
Palate, down (1 of 2)
View from within the nasopharynx. The palate (upper surface seen at the bottom edge of the photo) is down, as the patient is breathing.
Palate, elevated (2 of 2)
The patient changes to voicing a high-pitched "eee", at which the palate elevates.
Palate paralysis
Loss of motion of the muscle in the soft palate, so that the palate does not properly elevate. Normally, the soft palate elevates to seal the nasopharynx when swallowing or when pronouncing any non-nasal sounds (in English, all sounds except for “n,” “m,” and “ng”). However, if the vagus nerve is damaged high in its course, near the base of skull, then the palate on that side can lose its ability to lift, and it remains down during the aforementioned tasks.
A patient with palate paralysis might experience not only hypernasality (speech resonance quality resembling that heard with cleft palate) but also nasal regurgitation, especially of liquids (“water comes out my nose when I swallow”), and also nasal emissions (a slight hissing sound that comes through the nose when the person produces strong consonants).
Photos:
Palate paralysis (1 of 1)
View of the upper surface of the palate from within the nasopharynx. Due to this patient's hemi-palate paralysis, the palate deviates to one side, such that its midline (darker dotted line) no longer matches the nasopharynx's midline (lighter dotted line).
Palate branch of the vagus nerve (1 of 4)
This young woman sustained facial bone and skull base fracture during an auto accident. In this nasopharynx view, note that her right palate (left of photo) elevates fully (long arrow), while the left side only partially (short arrow). The palate branch of the vagus nerve is injured on the left (right of photo).
Pharynx branch of the vagus nerve (2 of 4)
At rest, the pharynx appears flat and symmetrical, but there is a question whether the midline may have migrated to the patient’s right (left of photo). The vagal branch to the pharynx is also injured on the left (right of photo).
Damage to left vagal nerve function (3 of 4)
By eliciting a very high-pitched voice, a pharynx contraction is recruited and now we can see that the pharyngeal wall pulls to the right (horizontal arrow) and the constrictor muscle squeezes inward only on the right (long arrow at left of photo). This confirms good right vagal function (left of photo) and damage on the left (not pictured).
Residue during swallowing test (4 of 4)
After eating a cracker and attempting to wash it away with water, the residue is primarily in the vallecula and left pyriform sinus. Arrows show how the pharynx can squeeze during swallowing in order to clear out the right pyriform sinus (left of photo). With no active muscle on the left (right of photo) to clear out the pyriform sinus, it pools food.
Paralytic falsetto
See obligatory falsetto.
Paralyzed vocal cords
See vocal cord paralysis, unilateral and vocal cord paralysis, bilateral.
Parkinson’s disease-related voice change
Voice change that accompanies Parkinson’s disease (PD) typically has two components. One component is a change to the “inner engine” of the voice. It is as if the inner motivation or vitality of communication or voice is damped down; think of the “motor” being limited mostly to “idle” rather than “first, second, third, and fourth” gears. When coaxed or even goaded to produce more vigorous voice, a person with advanced PD may find it hard to impossible (depending upon severity) to increase loudness. If the average person can “choose” vocal loudness settings of 1 through 5, it is as though levels 2 through 5 become inaccessible to the person with PD.
A second component of PD-related voice change is that the larynx becomes weak and atrophied. This is not surprising, since any body part will tend to atrophy if it is never used in a vigorous way. The phenomenology of PD-related voice change is that the voice is overly quiet and soft-edged, and though speech does not tend to become slurred, it can lose its crispness of articulation, and the pace of speech may diminish.
Photos:
Parkinson’s-related voice change (1 of 3)
Larynx of person with severe Parkinson’s disease; breathing position. Note the remarkable atrophy of the vocal cords, manifested in particular by the capacious ventricles (green dotted lines), the margin bowing (arrows), loss of “conus” bulk, and increased visibility of the contours of the vocal processes (blue dotted lines).
Parkinson’s-related voice change (2 of 3)
Phonatory (voicing) position. In addition to the bowing of the vocal cords, especially the left cord (right of image), note the slight scissoring of the left vocal process to overlap the right vocal process, as indicated by the arrows.
Parkinson’s-related voice change (3 of 3)
Cords coming into phonatory position, magnified view. Here can be seen even more clearly that, due to Parkinson’s-related atrophy, the contours of the vocal processes are more visible (blue dotted lines), like an emaciated person’s ribs. Note also that the LCA muscles have contracted slightly before the IA: the “toes” (T’s) of the arytenoid cartilages are in contact before the “heels” (H’s).
Voice Building:
Voice Building (shorter version):
PCA-only paresis
Weakness or paralysis of the vocal cord’s posterior cricoarytenoid (PCA) muscle, but with normal function of the vocal cord’s other muscles. The PCA muscle abducts (lateralizes) the vocal cord for breathing. The following are indicators of PCA-only paresis:
- Movement: The vocal cord closes normally for voicing, but it does not abduct for breathing. It remains motionless at the midline.
- Position and appearance: Position is normal during phonation, but the vocal cord does not open (lateralize) for breathing. Because the cord does not appear to move (it adducts or closes normally, but from an already-adducted position), PCA-only paresis is often mistaken for complete vocal cord paralysis—TA (thyroarytenoid), LCA (lateral cricoarytenoid), and PCA. Key points of difference between PCA-only paresis and complete paralysis are that, in the former case, the tip of the vocal process is in a normal medial position and the vocal cord has normal bulk and tone.
- Appearance during voicing (under strobe lighting): Completely normal, because the adductors of the cord (TA and LCA muscles) are intact. Hence, as with a normal cord, there is no flaccidity or asymmetry of vibration.
- Voice quality: Entirely normal. Many individuals are told this is due to “compensation” of the opposite cord, but actually it is because the muscles used for voicing (TA + LCA) are intact.
Other variants of vocal cord paresis include LCA-only, TA-only, TA + LCA, and IA-only (interarytenoid muscle).
Photos:
Paresis, PCA-only (1 of 4)
PCA muscle of the right vocal cord (left of image) is not working. TA and LCA are perceived as intact, based on the combination of: 1) normal voice; 2) the right cord is not bowed; 3) ability to medially turn or at least keep in line the right vocal process (see also photo 2); and 4) the right cord is not atrophied, nor is the right ventricle unusually capacious.
Paresis, PCA-only (2 of 4)
During phonation, there is no sign of lateral turning of the right vocal process, which would indicate LCA weakness. Furthermore, vibratory blurring (in this standard-light view) appears to be fairly equal on each side, suggesting there is no flaccidity of the right cord, contrary to what one would expect were the TA weak on that side.
Paresis, PCA-only (3 of 4)
Strobe light, closed phase of vibration, again showing that there is no lateral turning of the vocal process.
Paresis, PCA-only (4 of 4)
Strobe light, open phase of vibration. The amplitude of vibration for each cord appears to be equal, just as it did (based on blurring) in photo 2. This finding confirms that the TA is not weak, as such weakness would make the right cord flaccid and increase its amplitude of vibration.
PCA-only paresis years after thyroid lobectomy (1 of 6)
Several years after right (left of photo) thyroid lobectomy. Voice was drastically altered for a few months but then seemed to recover fully. Panoramic view during sniff maneuver shows midline but immobile right vocal cord (left of photo). No apparent atrophy of the cord itself, and the vocal process turns medially (arrow) suggesting that voicing muscles TA, LCA are intact and not balanced by PCA, because PCA muscle is paralyzed. This would explain patient’s normal voice, yet immobile cord.
PCA-only paresis years after thyroid lobectomy (2 of 6)
Closer view, with same findings as in photo 1.
PCA-only paresis years after thyroid lobectomy (3 of 6)
View of posterior commissure just before reaching contact for phonation. Note that both vocal processes are aligned antero-posteriorly (see arrows). This indicates a functioning LCA muscle on the right, and not only on the left.
PCA-only paresis years after thyroid lobectomy (4 of 6)
During phonation, standard light, the cords appear to approximate firmly.
PCA-only paresis years after thyroid lobectomy (5 of 6)
Closed phase of phonation, strobe light, at very low pitch (E3, or 165 Hz). The lowest part of patient pitch range would be expected to accentuate flaccidity, if present.
PCA-only paresis years after thyroid lobectomy (6 of 6)
Open phase of vibration, still at E3 (165 Hz). Vibratory amplitude is equal between the cords, demonstrating no increase of flaccidity of right cord (left of photo) as another way of “proving” that TA musculature is normal.
Abducted breathing position (1 of 4)
As the patient is taking a breath, only the right cord (left of photo) abducts (though not yet fully in this photo). Left cord (right of photo) remains at midline and vocal process remains in line with the membranous cord, suggesting that the LCA muscle on the left (right of photo) is working.
Full approximation of cords, TA is intact (2 of 4)
Full approximation of the cords, and furthermore there is no enlargement of the ventricle (at 'X') and this also suggests left TA muscle is also intact.
Phonation, LCA is intact (3 of 4)
The posterior commissure during phonation. Note that there is no lateral turning of the vocal process, validating that the left LCA muscle (right of photo) is intact.
Phonation under strobe light, PCA-only paresis (4 of 4)
During phonation, strobe light, open phase of vibration. Left TA (right of photo) function again validated in that the amplitude of vibration on the left (right of photo) is not greater than on the right (left of photo). If the left TA muscle were paralyzed, then the amplitude on the left (right) would be greater than on the right (left).
Unequal lateralization (1 of 4)
The vocal cords appear equally lateralized, but are not. The right one (left of photo) is paramedian and does not abduct, and the left (right of photo) is abducted, and moves to the midline with phonation, as seen in photos 3 and 4.
PCA not working (2 of 4)
Shifting the view posteriorly, it is easier to see that the right PCA muscle does not work, and without its lateralizing pull, the unopposed LCA muscle turns the vocal process sharply medially (arrow). Right TA is intact despite pseudobowing, caused here by exaggerated LCA action.
Phonation, closed phase (3 of 4)
Under strobe light. The vocal cords push against each other equally, and IA muscle pulls the “heels” of both arytenoid cartilages together, causing the right vocal process (left of photo) to point anteriorly, just like on the left (right of photo).
Phonation, open phase (4 of 4)
Open phase of vibration. Amplitude of vibration is greater on the right (left of photo) but not due to TA muscle atrophy, but instead as a result of mucosal stiffness on the left (right of photo) The explanation: superficial laser cordectomy performed years earlier for early cancer. Medial-to-lateral capillary reorientation is the visual clue of mucosal regeneration/ scarring.
Post thyroidectomy (1 of 4)
After thyroidectomy, this individual’s voice was breathy for several months postoperatively, but then recovered fully. Yet, her right vocal cord appears to be paralyzed, rather than paretic. Here note that PCA on the left (right of photo) pulls that (normal) cord fully laterally, while the right cord (left of photo) remains midline and with slight medial turning of the vocal process to suggest right LCA muscle is intact.
Phonatory view (2 of 4)
Making voice under standard light, the cords appear to close at the midline, consistent with intact IA and bilaterally intact LCA muscles. Equal vibratory blur between the two sides suggests that the both TA muscles are also intact.
LCA and TA muscles working (3 of 4)
Under strobe light, closed phase of vibration: Medial compression appears equal and the vocal processes (indicated by lines) point straight anteriorly, again confirming that both LCA muscles are working, and suggesting that both TA’s are also working.
PCA-only paresis (4 of 4)
Open phase with equal amplitude (lateral excursion) of vibration of both cords, indicating that the TA muscle is not atrophic or flaccid. Put all of the above findings together, and this is classic PCA-only paresis of the right vocal cord.
PCA not working, TA is weak (1 of 3)
The patient reported a voice quality of about "50%" after neck surgery a few months earlier and has (so far) recovered to "75%." The patient's difficulty tolerating the examination despite extensive topical anesthesia results in incomplete (though sufficient) information. Here it appears that PCA is not working on the right (left of photo), as the vocal cord position is paramedian rather than fully lateralized. Right TA muscle (left of photo) appears weak, too, as indicated by "spaghetti-linguini" bulk asymmetry (brackets), mild vocal cord bowing (dotted line) and capacious right ventricle (left of photo). This view does not permit evaluation of conus for atrophy, nor of LCA function.
LCA recovered (2 of 3)
Visual finding of full closure during phonation in this distant view, along with good ability to increase loudness at low pitch without audible luffing both suggest but do not prove that LCA is likely recovered, and also that there is some tone in the atrophied TA muscle.
TA partially recovered (3 of 3)
A sub-optimal view of open phase of vibration also suggests that the TA muscle is partially recovered. In all, this is a barely-adequate examination but when an examiner can invest deeply in subtle and even distant findings, an examination such as this that does not meet an examiner's standard of quality, can yet suffice for diagnosis and treatment planning.
Sense of instability (1 of 3)
This person had a major voice change after thyroidectomy for a large goiter. Within 2 months, voice recovered fully--except for a sense of instability. The PCA-only paresis is not the explanation because voice-making muscles (TA + LCA) are intact. And in fact vocal capability testing shows that both yell and projected voice are normal. The visual finding here of vocal cord bowing and capacious ventricle do not count as a breathing position finding with PCA-only paresis due to the unopposed action of LCA muscle, combined with an uncontracted TA muscle, both of which cause pseudo-bowing.
Vibratory amplitude (2 of 3)
During phonation under strobe light, with TA tensing, "bowing" disappears. Furthermore the vibratory "blur" at the margin of the left fold (right of photo) is equal to the right (left of photo), telling us that vibratory amplitude is approximately the same on both sides.
Spasm (3 of 3)
An audible/ visible spasm occurs when the right vocal cord jerks laterally for 4 frames (~ 1/8th of a second). The problem isn't PCA weakness on the left (right of photo), but instead an abductory spasm on the right (left of photo), fully mobile cord!
LCA working, TA partially working (1 of 4)
Many years earlier, this man had thoracic surgery for patent ductus arteriosis repair. Immediately postoperatively, voice was down to “20%.” Within several months it had recovered to about “50%” where it has remained for 30 years. Two notable findings: bowing of left vocal cord (right of photo) along with subtle twitching, but without a significant “spaghetti” sign of atrophy as compared with the right, and medial turning of the left vocal process (right of photo). The conclusion: LCA appears to be working, and TA is working at least partially.
Closer view (2 of 4)
Close visualization of the posterior commissure during “sniff” confirms that PCA is not working on the left (right of photo); LCA action is confirmed with exaggerated medial turning of the vocal process.
Closed phase (3 of 4)
Under strobe light, showing closed phase at low pitch. Posterior folds close completely, confirming LCA function. The left vocal cord (right of photo) looks to be at a slightly lower level, confirming at least some level of atrophy.
Open phase (4 of 4)
Open phase of vibration shows larger amplitude of vibration of left vocal cord (right of photo). Putting all of these findings together in big picture terms: LCA is working “fully,” TA partially, and PCA not at all.
(1 of 3)
After neck surgery, this person's voice was grossly abnormal (weak, whispery) for several months. Now voice is normal, and the patient is being seen only for laryngopasm. In this view, the right vocal cord (left of photo) is midline, because the PCA muscle on that side is not working to lateralize it. This suggests that the posterior branch of the recurrent laryngeal nerve has not recovered.
(2 of 3)
Closed phase of vibration under strobe light shows that the cords close fully, suggesting that the right sided TA and LCA muscles necessary for normal voice (served by anterior branch of the recurrent laryngeal nerve) have recovered fully. The open phase of vibration (next photo) will verify (or disprove) this speculation.
(3 of 3)
In fact, the lateral excursions of the vocal cords are the same (compare the lateral "distance" from the midline (indicated by the dotted line).. This verifies that there is no weakness (flaccidity) of the right TA muscle. The lack of lateral turning of the vocal process verifies that the LCA muscle is also working on that side. Hence, PCA-only paresis.
Pedunculated
Pedunculated, meaning attached by a stalk; the opposite of sessile.
Pemphigoid
Pemphigus vulgaris (Pemphigoid) is the result of one’s immune system attacking healthy cells in the skin rather than foreign invaders. It creates blisters or sores on the skin which are prone to rupturing and infection. Though it is a skin disease, it often has laryngeal manifestations, which can make it difficult to swallow or eat.
Bullus pemphigoid is different than pemphigus vulgaris in that the blisters do not rupture as easily, making infection less likely. It also may have laryngeal manifestations. It is, however, more rare than pemphigus vulgaris.
The cause of either disease is unknown.
Photos:
Perimenopausal voice change
Perimenopausal voice change is a syndrome that seems to be related to the effect on voice of declining estrogen levels. Some women seem to escape this problem almost entirely; others experience pronounced symptoms. When severe, the affected woman will note the following: (1) upper range is either lacking, or extremely effortful; (2) there is paralaryngeal discomfort and muscular tension when she attempts to sing in the upper range; (3) there is a tendency to sing flat in the upper range. May be counteracted with varying degrees of success through vocal exercise and/or estrogen replacement therapy.
Pharyngeal deviation
Pulling of the posterior pharyngeal wall to one side, as sometimes seen when a patient performs the “pharyngeal squeeze.” This finding accompanies paresis or paralysis of the constrictor muscles of one side of the pharynx. In these cases, elicitation of the pharyngeal squeeze will reveal that the pharyngeal wall pulls to the normal (non-paralyzed) side. On the normal side, one will typically see bulging of normally functioning muscle to fill one pyriform sinus; meanwhile, the other pyriform sinus will appear capacious and almost dilated. The midline pharyngeal raphe, which joins the pharyngeal constrictor muscles, moves far to the normal side. A person with these findings normally experiences considerable swallowing difficulty, with pooling of saliva or ingested materials, particularly in the pyriform sinus on the paretic or paralyzed side.
Photos:
Pharyngeal paralysis (1 of 2)
View of the laryngopharynx. This patient has pharyngeal paralysis on one side, which is already slightly evident because the posterior pharyngeal wall's midline (dotted line) is deviating here slightly to one side, even at rest.
Pharyngeal paralysis, more obvious with pharynx contraction (2 of 2)
The pharynx is contracted, and the posterior pharyngeal wall (midline again at dotted line) now deviates dramatically toward the non-paralyzed side of the pharynx. This pharynx contraction was elicited via extremely high-pitched voicing.
Pharyngeal paralysis
Pharyngeal paralysis (1 of 2)
View of the laryngopharynx. This patient has pharyngeal paralysis on one side, which is already slightly evident because the posterior pharyngeal wall's midline (dotted line) is deviating here slightly to one side, even at rest.
Pharyngeal paralysis, more obvious with pharynx contraction (2 of 2)
The pharynx is contracted, and the posterior pharyngeal wall (midline again at dotted line) now deviates dramatically toward the non-paralyzed side of the pharynx. This pharynx contraction was elicited via extremely high-pitched voicing.
Pharyngeal paralysis (1 of 1)
Panorama of the laryngopharynx. Note the capacious left pyriform sinus (right of photo), one strong indicator of paralysis of the pharynx on that side.
Pharyngeal paralysis (1 of 1)
Blue-stained water swallowed by the patient has preferentially pooled in the left pyriform sinus (right of image), due to weakness of the left inferior pharyngeal constrictors.
Pharyngocele
A dilated outpouching from the normal contour of the pharynx.
Photos:
Pharyngocele: view at vocal cord level (1 of 6)
A 20-year-old man complains that his neck expands and that he has pain while playing the trumpet. This radiographic image is at the level of the vocal cords, during quiet breathing; at this point, the pharyngeal dilation and pharyngocele are not yet seen. Compare with image 2.
Pharyngocele: view at vocal cord level (2 of 6)
Same view as in image 1, except that the patient is performing a Valsalva maneuver, to simulate trumpet playing. Whereas in image 1 the pharynx is completely collapsed, here it is inflated with air. A true pharyngocele, seen on the right side of the image, is beginning to develop. Also, compare the neck’s surface contour between this image and image 1.
Pharyngocele: view at supraglottic level (3 of 6)
This view is at the supraglottic level, during quiet breathing, and already shows mildly dilated pyriform sinuses. Compare with image 4.
Pharyngocele: view at supraglottic level (4 of 6)
The patient again performs a Valsalva maneuver, during which the pharynx dilates dramatically. Compare with image 3.
Pharyngocele: view at base of tongue level (5 of 6)
Higher view yet, at the base of the tongue opposite the tip of the epiglottis, during quiet breathing. Compare with image 6.
Pharyngocele: view at base of tongue level (6 of 6)
The patient again performs a Valsalva maneuver, during which the hypopharynx expands dramatically; the beginning of a true pharyngocele can be seen again, this time on the left of image. If this young man were to continue playing trumpet, one would expect the pharynx to expand more and more over time.
Pharyngocutaneous fistula
The leaking of saliva outside of the pharynx (“throat” part of the swallowing passage) through a defect in the pharyngeal mucosa lining. This may occur transiently in up to 20% of persons who have undergone total laryngectomy, with the sixth postoperative day the peak time of incidence. Prior radiation therapy seems to increase the risk of fistulization.
Traditionally, the treatment was to make a midline incision directly, insert a penrose drain, and then use pressure dressings. Modern treatment uses suction drains to control salivary leakage and allow the rest of the skin flap to adhere to the neck1. Then, the drain is removed, shortened, and replaced a series of times to allow the tract to close from top to bottom.
Pharyngocutaneous fistula (1 of 3)
Panorama of reconstructed hypopharynx one week after laryngectomy for persistent cancer after radiotherapy. (PPW = posterior pharyngeal wall. PE = pseudo-epiglottis, often seen after reconstruction. F's arrow = fistula. E = esophageal entrance.)
Pharyngocutaneous fistula (2 of 3)
Closer view of fistula opening and esophageal entrance, with salivary pooling.
Pharyngocutaneous fistula (3 of 3)
Patient receiving suction drain treatment. The suction tubing evacuates saliva drop by drop as it forms, eliminating the need for wound dressings and long term antibiotics. This treatment also prevents infection and causes less discomfort for the patient than traditional treatment.
Larynx losing function (1 of 4)
This man underwent supraglottic laryngectomy and radiotherapy nearly 20 years ago. A biopsy was done some years later elsewhere, and triggered radionecrosis. Hyperbaric oxygen treatments back then saved the day. This larynx has continued to lose function slowly over time, necessitating tracheotomy, and with deteriorating voice quality. The latest problem is coughing on liquids, and they are coming out his tracheotomy tube. Here, you see the arytenoid apices (each marked with A). Epiglottis and false vocal cords are surgically absent. Base of tongue (BoT) was pulled down to the level of the vocal cords. Click to enlarge this photo to see the dots marking the upper surface of each cord.
Swallowing (2 of 4)
Now looking deep into the surgically-minimized laryngeal vestibule, the two larger dots are again on the vocal cords, for comparison with photo 1. The fine dotted line encircles a fistula. When the patient swallows, food or liquid can enter in the direction of the arrow. Where it goes next is seen in the following photos.
View from between vocal cords (3 of 4)
The scope has entered between the cords (between the dots in photo 2), and is now viewing the subglottis. “T” near the top of the photo marks where the tracheotomy tube is seen entering the trachea. The anterior subglottic fistula is seen at the bottom of the photo with the sidewall of the tracheotomy tube seen at the lower-case “t.”
Swallowing water (4 of 4)
Remaining in the anterior subglottis while the patient swallows pale blue-stained water, you see a part of the bolus “exploding” through the fistula, and this series of 4 photos taken together fully explain why this man is having so much difficulty with liquids that he swallows coming out his tracheotomy tube.
Bastian RW, Park AH. Suction drain management of salivary fistulas. Laryngoscope. 1995;105(12 Pt 1):1337-41. ↩
Pharynx contraction
Contraction of the pharyngeal constrictor muscles that surround the throat. Or, the “pharyngeal squeeze.” It is the primarily the middle and inferior constrictor muscles that contract. When these muscles contract, they tense and narrow the pharynx. This action is particularly important for swallowing.
The pharynx also contracts when a person produces voice above a certain pitch in his or her range. The threshold for pharynx contraction depends in part on a person’s sex and age, and in women with peri-menopausal voice change (a condition in which they lose some capability and comfort in their upper vocal range), the pharynx will contract at a much lower pitch than otherwise expected. Thus, a clinician trying to diagnose peri-menopausal voice change can endoscopically view a patient’s pharynx and elicit different vocal tasks to see if the voice’s “muscular ceiling”—where the pharynx begins to contract—has lowered or not.
Photos:
Pharynx contraction (1 of 2)
The pharyngeal constrictor muscles are relaxed during low-pitch phonation. Notice the open pyriform sinuses.
Pharynx contraction (2 of 2)
During high-pitch phonation, the pharyngeal constrictor muscles contract (in direction of green arrows) to obscure the pyriform sinuses; the midline is now evident (blue arrow).
Panoramic view, A3 (1 of 3)
Panoramic view of laryngopharynx of an older middle-aged woman singing A3 (220 Hz). Pharynx here is uncontracted and both pyriform sinuses (within dotted lines) are maximal in size.
Contraction, A4 (2 of 3)
At A4 (440 Hz), the pharynx has begun to contract, and the pyriform sinuses have begun to close.
Maximal contraction, F5 (3 of 3)
At F5 (698 Hz), the pharynx is nearly maximally contracted and pyriform sinuses nearly closed completely. Sustained singing at this pitch and above will be effortful and cause discomfort, unless this singer can learn to “de-recruit” pharynx contraction via technical changes of voice production.
Pharyngeal paralysis (1 of 2)
View of the laryngopharynx. This patient has pharyngeal paralysis on one side, which is already slightly evident because the posterior pharyngeal wall's midline (dotted line) is deviating here slightly to one side, even at rest.
Pharyngeal paralysis, more obvious with pharynx contraction (2 of 2)
The pharynx is contracted, and the posterior pharyngeal wall (midline again at dotted line) now deviates dramatically toward the non-paralyzed side of the pharynx. This pharynx contraction was elicited via extremely high-pitched voicing.
Pharynx contraction (1 of 2)
At low vocal pitch, the pharynx is uncontracted; pyriform sinuses are both widely open.
Pharynx contraction (2 of 2)
At high pitch, the pharynx contracts and surrounds the larynx more closely; pyriform sinus capacity is reduced.
Pharynx contraction (1 of 2)
Laryngopharyngeal view of a young woman, phonating at F4 (~349 Hz). Here the pharynx is relaxed: notice the broad arc of the pharyngeal wall (green dotted line) and the widely open pyriform sinuses (blue dotted lines).
Pharynx contraction (2 of 2)
Same patient, now phonating at C5 (~523 Hz). The pharynx has contracted: notice the narrower, more pointed arc of the pharyngeal wall (green dotted line) and that the pyriform sinuses (blue dotted lines) are nearly closed. In this relatively young soprano, this degree of pharyngeal contraction should not occur until she sings as high as G5 (~784 Hz) or higher. This singer is experiencing loss of expected upper range—a lowered “muscular” ceiling of the voice.
Phases of swallowing
The different phases that together make up the act of swallowing. Actually, swallowing is a rapid and seamless act, and dividing that act into distinct phases is somewhat arbitrary. But one simple scheme for the phases of swallowing, among many that have been codified, would be:
Phases of swallowing:
- Oral preparatory phase: food is masticated (chewed), mixed with saliva, and then “gathered” into a softened mass (called a bolus) between the tongue and palate.
- Oral transit phase: the bolus is sent posteriorly toward the base of the tongue. This sending of the bolus is a volitional (technically conscious) action, though it may be performed without really thinking about it.
- Oro-pharyngeal phase: the bolus arrives at the base of the tongue and triggers the swallow reflex, which is non-volitional, or automatic.
- Pharyngeal phase: the bolus travels down from the base of the tongue past the closed and elevated larynx and to the entrance of the esophagus. This is a continuation of the automatic swallow reflex.
- Esophageal phase: the cricopharyngeus muscle relaxes to allow the bolus into the upper esophagus, from where it is passed downward by waves of muscle contraction through the lower esophageal sphincter (LES) and into the stomach. All of the muscular action in this phase is also non-volitional.
Videos:
This video gives an overview of how swallowing works, how it can sometimes go wrong (presbyphagia or cricopharyngeal dysfunction), and possible ways to treat those problems (swallowing therapy or cricopharyngeal myotomy).
Phonation
Phonation is the process of making vocal sound by bringing vocal cords together while a stream of pulmonary air passes between them, causing them to vibrate. Roughly, this means to “make voice.”
Phonatory arrest
A phonatory arrest is a manifestation of spasmodic dysphonia, a part of its phenomenology, in which the voice suddenly “chokes off” in the middle of an intended sound, causing a brief instant of silence before the voice starts again.
Phonatory gap
When the vocal cords fail to close during phonation. A phonatory gap may be seen in patients who have muscle tension dysphonia, vocal cord paresis or paralysis, loss of tissue, or vocal cord flaccidity.
In addition, however, a phonatory gap occasionally occurs in patients who have none of the above conditions. In this type of case, the patient will struggle with onset delays, but delays that “pop” followed by relatively clear voice rather than the scratchier or hoarser-sounding onset delays associated with vocal cord mucosal swelling. Also, if asked to perform our vocal cord swelling checks, such a patient will tend to struggle more with the “Happy birthday” task than the descending staccato task (the opposite is true for patients with mucosal swelling).
Photos:
Phonatory gap (1 of 4)
At the prephonatory instant, D4 (~294 Hz), standard light. Notice how separated the vocal cords are.
Phonatory gap (2 of 4)
Phonation, a moment later, with vibratory blur. The cords remain separated. The question is whether this gap is due to: 1) a posturing problem, such as muscular tension dysphonia (MTD); 2) flaccidity-induced bowing; 3) some other cause.
Phonatory gap (3 of 4)
The most “closed” phase of vibration, as seen under strobe light, at the relatively low pitch of F4 (~349 Hz); again, the cords are not actually closed. This is not the picture of MTD, however; with MTD, there would be a greater gap between the vocal processes of the arytenoid cartilages (at arrows).
Phonatory gap (4 of 4)
Open phase of vibration, at the same pitch as photo 3. The lateral amplitude of each cord's vibration is equal, and relatively small (midline shown by a dotted line), which would not be seen with vocal cord flaccidity. Hence, neither MTD nor flaccidity is the explanation for this patient's gap. Also, this patient's voice manifests "popping" onset delays that are similar to other phonatory gap patients who have neither MTD nor flaccidity.
Closed phase at a high pitch (1 of 4)
A mezzo soprano is singing at A5 (880 Hz). This is the “closed” (or rather “more closed,” since a slight gap remains) phase of vibration as seen under strobe light.
Open phase at a high pitch (2 of 4)
Here the voice is at the same pitch, but at the open phase of vibration. The amplitude of vibration (distance moved from the midline) is small.
Closed phase at a low pitch (3 of 4)
Now singing 2 octaves lower at A3 (220 Hz). This is the closed phase of vibration. The vocal cords are short and “fat.” In contrast to stringed instruments and the piano where high pitches are made with short and thin strings, the voice produces high pitches with long and thin. For an analogy, twang a rubber band stretched to different lengths and hear the change in pitch.
Open phase at a low pitch (4 of 4)
Still at A3, but now during the open phase of vibration. The amplitude (distance moved from the midline) is also typically greater for low pitches, at similar loudness level.
Phonatory insufficiency
When the vocal cords cannot close sufficiently or vibrate adequately to produce a serviceable voice. An inability to close is usually evidenced by air-wasting phenomenology.
This phonatory insufficiency could have one of several causes. It could be due to the loss of part or all of one or both vocal cords, such as after removal of a vocal cord cancer. Or it could follow prolonged intubation and resulting pressure necrosis of the posterior ends of the vocal cords 1. Another possibility might be scarring of the anterior joint capsule of the cricoarytenoid joints, also as a complication of prolonged endotracheal intubation due to grave illness. Yet another cause might be vocal cord paralysis or paresis. The latter problems not only interfere with the cords’ ability to close, but also make the affected cord flaccid, so that it blows out of the way too easily, further wasting the air stream.
When a person with any of these causes of poor vocal cord closure tries to produce voice, maximum phonation time is typically reduced, because only a fraction of the air pushed up from the lungs is converted to sound, with the remainder of the air quickly “wasted.”
The second main category of phonatory insufficiency, in which the vocal cords cannot vibrate adequately, is seen in a person with stiff or scarred vocal cords. Such a person may not waste air, but just be unable to produce other than a harsh whispery sound, because the stiffened vocal cords (now more like thick leather rather than like, as is normal, plastic wrap overlying a thin layer of jello) cannot vibrate as freely or at all.
Photos:
Phonatory insufficiency (1 of 3)
Abducted breathing position. Note the divots at the posterior commissure (arrows), likely due to pressure necrosis caused by intubation of long duration. Dotted lines indicate the lines of the normal cord, to show the divots more clearly.
Phonatory insufficiency (2 of 3)
The irregular white line along the length of the vocal cords (arrows) suggests that there may have been pressure necrosis of the musculo-membranous portion of the vocal cord and that now the mucosa adheres directly to muscle, with no intervening vocal ligament layer.
Phonatory insufficiency (3 of 3)
Maximum phonatory closure. Note that the posterior commissure defect is hidden by the partial closure of the arytenoid cartilages. Even so, the arytenoid cartilages are unable to come into contact. The musculomembranous cords are quite far apart due partly to tissue loss. Furthermore, the cords are stiff and inflexible. No glottic voice is possible.
Phonatory insufficiency (1 of 4)
After 15 days of intubation, this voice is sounding both breathy (air-wasting) and pressed. From a distance it appears that the right cord (left of image) is paralyzed. (Compare with image 2)
Phonatory insufficiency (2 of 4)
During phonation, the voice again sounds breathy and pressed.
Phonatory insufficiency (3 of 4)
A close up view shows the posterior divot of the right cord (left of image). The absence of atrophy, bowing, or flaccidity, confirms that the problem is right cord fixation due to scarring of the right cricoarytenoid joint, not paralysis.
Phonatory insufficiency (4 of 4)
During phonation, the posterior commissure deficit caused by pressure necrosis from the endotracheal tube is seen with the dotted line. The small green circles represent the vocal processes not approximating thus validating the joint injury.
Phonatory insufficiency due to loss of vibration-capable tissue (1 of 4)
The larynx is in an open position for breathing, though the right half of the larynx has been removed to treat cancer. On the right (left of photo) there is a pseudocord, which is tissue used to replace the right cord, but not a type of tissue that can vibrate. Only the middle of the left cord (right of photo) has been preserved.
Phonatory insufficiency due to loss of vibration-capable tissue (2 of 4)
Here the patient produces voice by bringing the remnant of the left cord (right of photo) into partial contact with the pseudocord (left of photo). You can see vibratory blurring of the left cord, but no blurring of the pseudocord. In addition, closure is incomplete.
Phonatory insufficiency due to loss of vibration-capable tissue (3 of 4)
This image shows voice use under strobe lighting. During the closed phase of vibration the cords do not fully close as the left cord cannot quite reach the pseudocord. This accounts for air-wasting.
Phonatory insufficiency due to loss of vibration-capable tissue (4 of 4)
Still under strobe lighting, this image shows the open stage of vibration. The pseudocord appears the same, but the remnant of left cord has oscillated laterally. Due to the shortened length of the cord, the pitch of the voice is higher than expected for this person.
Bastian RW, Richardson BE. Postintubation phonatory insufficiency: an elusive diagnosis. Otolaryngol Head and Neck Surg. 2001; 124(6): 625-33. ↩
Pill dysphagia
Difficulty or inability to swallow pills. For some individuals with pill dysphagia, swallowed pills may tend to lodge in the person’s vallecula, due to presbyphagia. For others, swallowed pills may tend to lodge at the level of the cricopharyngeus muscle, due to cricopharyngeal dysfunction. Yet other individuals may experience pill dysphagia from childhood, perhaps due in part to fear, such that the person cannot commit to swallowing a pill without gagging at the prospect.
Pitch
Where voice is concerned, pitch refers to the highness or lowness of a tone, perceived through the sense of hearing, that correlates with the fundamental frequency or rate of vibration of the vocal folds.
Polypoid degeneration
Diffuse swelling of the vocal cords, due to build-up of edema fluid within the mucosa. Polypoid degeneration is also referred to as Reinke’s edema or smoker’s polyps. This condition is most often seen in long-term smokers who are also somewhat talkative. In other words, polypoid degeneration is rare in talkative non-smokers and also rare in taciturn smokers.
Symptoms of polypoid degeneration:
Polypoid degeneration tends to virilize (masculinize) the quality and capabilities of the voice, and this effect is most noticeable in women. Also, in more severe cases, polypoid degeneration can induce involuntary inspiratory phonation or a fluttering, almost snoring sound during sudden inhalation.
Appearance of polypoid degeneration:
Polypoid degeneration typically appears as pale, watery bags of fluid attached to the superior surface and margins of the vocal cords. In less severe cases, the swelling might be more subtle, but if the patient is instructed to inhale while making voice, then the polypoid tissue will be drawn away from the cords into the glottic aperture, giving each vocal cord margin a convex contour and thereby becoming more noticeable (see two such examples in the photos below).
Treatment for polypoid degeneration:
The patient is encouraged to give up smoking. Short-term voice therapy can help in some cases, reducing the turgidity of the polypoid tissue and thereby improving the voice to a small but noticeable extent. However, the polypoid degeneration itself is permanent, so if the voice quality remains unacceptable to the patient even after voice therapy, then surgery is necessary.
For surgery on polypoid degeneration, it was once common to strip away the polypoid tissue, but this approach often leads to an unacceptably high-pitched, thin-sounding, and husky voice. A better method is to reduce the tissue more conservatively, potentially leaving some fractional residual polypoid tissue. This way, although the voice might remain mildly virilized, it also retains a richer and more effortless quality.
Audio with photos:
Voice sample of a patient with smoker’s polyps, BEFORE surgery (see this patient’s photos just below):
Same patient, two months AFTER surgery (the occasional syllable dropouts are due to the recentness of surgery):
Smoker's polyps, BEFORE surgery (1 of 4)
Even during quiet breathing, the convexity of the vocal cord margins (dotted lines show where normal margins would be) reveal the presence of smoker's polyps.
Smoker's polyps, BEFORE surgery (2 of 4)
During inspiratory phonation: the polyps are drawn inward and are easier to see.
Smoker's polyps, AFTER surgery (3 of 4)
Two months after surgery, during quiet breathing. The vocal cord margins are now straight.
Smoker's polyps, AFTER surgery (4 of 4)
During inspiratory phonation: the margins are drawn into a mildly convex contour, but far less than preoperatively. The patient's voice is also much improved, albeit the occasional syllable dropouts due to recentness of surgery (listen to this patient's voice samples in the audio section of the encyclopedia entry).
Photos:
Smoker’s polyp / Reinke’s edema (1 of 2)
Quiet breathing, under standard light. The edematous mucosa is not yet evident.
Smoker’s polyp / Reinke’s edema (2 of 2)
Elicited inspiratory phonation in-draws and thereby reveals the edematous mucosa, greater on the right (left of image) than the left. The dashed lines indicate the normal location and contour of the vocal cords' free margins.
Smoker’s polyps / Reinke’s edema (1 of 3)
This patient is a long-term smoker, and also is talkative. Her voice has been gradually deepening for years. Here, with the vocal cords in abducted breathing position, one can only see somewhat underwhelming, broad-based, low-profile swelling, along with some hazy leukoplakia in the mid-cord.
Smoker’s polyps / Reinke’s edema (2 of 3)
Phonation. Again, there is only very low-profile, broad-based convexity of the margins, and again, the hazy leukoplakia in the mid-cords.
Smoker’s polyps / Reinke’s edema (3 of 3)
Elicited inspiratory phonation. Now, one can see that, contrary to the appearance in the prior two views, this patient in fact has moderate-sized “smoker's-type” polyps, aka Reinke’s edema. The increased mass explains the virilization of the sound of this woman’s voice.
Smoker’s polyps in various “poses” (1 of 4)
Vocal cord abduction for breathing, during expiratory phase. Left polyp (right of photo) appears to be the only finding. This is in a middle aged smoker with several years of gradually deepening / masculinized and now rough voice. The black dot and white "X" are reference points, facilitating comparisons with the other photos.
Smoker’s polyps in various “poses” (2 of 4)
At the beginning of elicited rapid inspiration, showing the polyp beginning to be displaced from upper surface to the margin. That is, previously-unseen polypoid tissue (at "X") is now indrawing from upper surface of the right cord (left of photo) as well, and margin has become convex rather than straight as it was in photo 1.
Smoker’s polyps in various “poses” (3 of 4)
The left-sided polyp (right of photo) is now displaced below the margin of that cord. The right polyp (left of photo) is now fully displaced/ indrawn to the margin of the right cord (left of photo).
Smoker’s polyps in various “poses” (4 of 4)
During voice-making, most of the edematous tissue relocates back to the upper surface of the cords where it vibrates chaotically to add not only masculine but also rough voice quality.
Videos:
This video illustrates how smoker’s polyps can be seen more easily when the patient makes voice while breathing in (called inspiratory phonation). During inspiratory phonation, the polyps are drawn inward and become easier to identify.
Pontocaine
Pontocaine is the chemical name for the most common topical anesthetic used at our practice to anesthetize the nasal passage in preparation for passage of the flexible videoendoscope or fiberscope. When applied topically, pontocaine numbs the mucosa for between 15 and 30 minutes.
Pooling
Pooling occurs when a person’s swallow does not successfully send the entire mass of food or liquid into the esophagus, so that some or all of the material remains in the hypopharynx. In such cases, the material commonly pools in the vallecula and pyriform sinuses. It can also cling to the base of the tongue or the pharyngeal walls. Pooling is often caused by presbyphagia, and its occurrence may put a patient at risk of aspiration.
Popping onset
Positive/ Negative practice
This behavioral treatment is prescribed primarily for patients with nonorganic voice disorders. A patient with a nonorganic voice disorder has been diagnosed with aberrant voice production due to the abnormal use of a normal mechanism, often due to stress or some sort of secondary gain. She or he may have been ‘stuck’ with the abnormal voice for months to years, or may lurch between normal and abnormal voice production on an apparently involuntary basis. To help patients first “find” their normal voices, the clinician guides the patient through a variety of vocal elicitations such as: a yell, glissando, siren, or vocal fry. All of this may be with or without clinician digital manipulation of the laryngeal framework. After preliminarily ‘settling in’ the patient’s reestablished normal voice, the clinician quickly asks the patient to alternate between the re-established normal voice and the old abnormal voice. First, the patient alternates upon clinician cue, again optionally with or without digital manipulation, and then the patient demonstrates the ability to switch between the two kinds of voice production at the sentence level, and then every few words, and then word-by-word. The positive and negative practice demonstrates mastery / control over the abnormal/ nonorganic voice production. If possible, this process should occur with patient, clinician, and family/ friends in attendance. Other doctors, speech pathologists, pulmonologists, and allergists who may have previously attempted to help the patient using medical rather than behavioral treatments should also be made aware of the nature of the patient’s diagnosis, the purely behavioral approach to it, and the idea that behavioral intervention to resolve this problem completely should not normally exceed three visits to a speech pathologist, to avoid his or her becoming a co-dependent or source of secondary gain.
Listen to a few demonstrations below:
Post-radiation telangiectasia
Atypical dilation or formation of capillaries as a mid- or long-term response to radiation. These are a benign but sometimes impressive-looking tissue change. Often, post-radiation telangiectasias do not appear until a year or more following the end of the course of radiation.
Photos:
Soon after end of radiotherapy (1 of 4)
Early after conclusion of radiotherapy for a left anterior vocal cord cancer. There is a small amount of resolving radiation mucositis (white patches) in the interarytenoid area.
1 year later: slight post-radiation telangiectasia (2 of 4)
Nearly a year later, with mild vascular prominence, especially left vocal cord (right of image).
2 years later: post-radiation telangiectasia (3 of 4)
Now nearly two years after end of radiotherapy, much more prominent vascularity, called post-radiation telangiectasia. This side effect of radiation often begins to happen between one and two years after the end of radiotherapy. Notice that the post-radiation telangiectasias involve all areas that received radiation (including false vocal cords, etc.), and not just the area of original tumor. Voice remains very good.
3 years later: post-radiation telangiectasia (4 of 4)
Just over three years after the radiotherapy, telangiectasia now exuberant, but fairly stable. Voice remains very good.
Inflammation with moderate dysplasia (1 of 8)
Hoarseness began 2 years prior to this initial examination photo. This middle aged man has never smoked; has no reflux symptoms, nor has he had any response to empiric reflux therapy. Biopsy shows inflammation with moderate dysplasia. HPV testing was negative. No explanation for this chronic inflammation is ever found. A series of KTP laser treatments of stippled vascular areas and leukoplakia ensues.
Squamous cell carcinoma-in situ (2 of 8)
A year later, similar findings except appearance of a slight anterior commissure inflammatory web. Eventually, after an additional 2 years (5 years after onset of hoarseness) a second biopsy is triggered by aberrant, “corkscrew” capillaries. The diagnosis: squamous cell carcinoma-in situ. Laser excision is typically preferred for well-demarcated early vocal cord cancer, but the diffuse, superficial and bilateral abnormalities suggested radiotherapy instead.
Post radiation (3 of 8)
Six weeks after the end of his 30 radiation treatments, healing of the superficial ulceration (within dotted lines) is underway.
Narrow band light (4 of 8)
Closer view, now under narrow band light: A fine vascular pattern has returned except in the areas bounded by dotted lines.
Regenerated vascular pattern (5 of 8)
Six weeks later (3 months after end of radiotherapy), the superficial ulceration has healed, and voice is very functional. Note the regenerated vascular pattern, and compare with photo 4.
Post-radiation telangiectasias (6 of 8)
“On schedule” a year after the end of successful radiation therapy, post-radiation telangiectasias are becoming evident. Compare progression of these telangiectasias in photos 4, 5, 6, 7, and 8.
Standard light (7 of 8)
Now 3 years from the end of radiotherapy, radiation telangiectasia are “maximal” and stable. Voice remains very good.
Narrow band light (8 of 8)
Same view, under narrow band light.
Post-radiation telangiectasias (1 of 4)
Years after radiotherapy for vocal cord cancer, the exaggerated capillaries are not typical capillary ectasia, but instead post-radiation telangiectasias. The "polyp" may be also radiation-related because there is no history of voice over-use.
Pulsed-KTP coagulation (2 of 4)
At the conclusion of pulsed-KTP coagulation of the "polyp."
"Polyp" pulled off (3 of 4)
The "polyp" has pulled off with the fiber.
Three weeks later (4 of 4)
Three weeks later, the vocal cords now match, voice is improved, and the site of surgery (arrow) is healed.
Post radiotherapy (1 of 2)
More than five years after radiotherapy for early vocal cord cancer, the post-radiation telangiectasias seen here are maximal and not expected to increase further. What can occasionally increase, are small polyp-like elevations (arrow to the left).
Narrow band lighting (2 of 2)
Narrow band light at closer range dramatically accentuates vascularity. Intense red becomes almost black; pink becomes blue-green.
Post-surgical laryngitis
Post-surgical laryngitis is inflammation of the larynx, not from infectious organisms, but from irritation caused by a surgical procedure. By analogy, think of the redness around a knuckle that has an abrasion but is not infected. Post-surgical laryngitis is typically transient and lasts only a few days following surgery. A typical time of recovery after nodule surgery is about four days, which explains why the suggested time of complete silence after surgery is four days, with gradually increasing amounts of voice use beginning on postoperative day four or five.
Post-swallow hypopharyngeal reflux
Refers to when, shortly after a person swallows, some swallowed material returns from below the esophageal entrance back up into the hypopharynx. This finding is an almost certain diagnostic indicator of cricopharyngeal dysfunction, usually with an associated Zenker’s diverticulum.
If this reflux occurs during a videoendoscopic swallowing study, the clinician will see that, though there may be little to no hypopharyngeal residue immediately after the swallow, a moment later some swallowed material (e.g., blue-stained applesauce or water) reappears and wells up in the post-arytenoid area and into the pyriform sinuses. If this reflux occurs during a videofluoroscopic swallowing study, the clinician will see barium remaining in the Zenker’s sac and, immediately after each swallow, moving back upward into the hypopharynx.
Photos:
Dysphagia and possible Zenker's (1 of 5)
This middle-aged man has solid > liquid dysphagia, and x-rays elsewhere (not available at this visit) reportedly showed a Zenker’s diverticulum. Even without that prior knowledge, the highly organized hypopharyngeal salivary pooling is strongly suggestive of this diagnosis, but subsequent photos of VESS even more so.
After a complete swallow (2 of 5)
During VESS, after completing a swallow of blue-stained applesauce, note the residue in the post-arytenoid area.
Additional material (3 of 5)
A third of a second later, additional material has emerged from below, likely ejected upwards from the Zenker’s sac.
Hypopharyngeal residue (4 of 5)
At the end of another swallow of the blue applesauce, the hypopharyngeal residue is again seen, but more important is that...
Two seconds later (5 of 5)
...again, about 2 seconds later, the left pyriform sinus fills from below as the material in the sac is ejected upwards.
VESS (1 of 7)
In a patient with a known Zenker's Diverticulum, who has just finished swallowing blue-stained applesauce during VESS.
Reflux (2 of 7)
Less than a second later, the applesauce and some saliva bubbles reflux upwards from the Zenker's sac into the postarytenoid area.
Post-swallow (3 of 7)
Here, the patient has just swallowed a cheese cracker.
Reflux of cracker (4 of 7)
About a second and a half later, this material, mixed with saliva, returns from the sac.
VFSS (5 of 7)
Just after the patient has swallowed a bolus of barium
A second later, barium is "squishing" upwards from the sac.
Continued reflux (7 of 7)
Additional barium has come upwards into the postarytenoid area (compare with Photos 2 and 4).
Posterior
Toward the back side of a person’s body. For example: the heel is posterior to the toes. The opposite of anterior.
Posterior commissure
The flat, front-facing surface of the glottic aperture that lies between the vocal cord’ posterior ends. When the vocal cords are in abducted (breathing) position, the posterior commissure is at its widest, since the cord’ posterior ends are spread furthest apart from each other. When the vocal cords have come together into adducted (voicing) position, the posterior commissure is essentially just the point of contact between the posterior ends of the cords.
In individuals who have acid reflux or other inflammatory conditions, the mucosa at the posterior commissure may thicken (pachyderma).
See also: anterior commissure.
Posterior commissuroplasty
An endoscopic procedure performed for individuals who have difficulty breathing, due to either bilateral vocal cord paralysis or bilateral vocal cord fixation. These individuals’ vocal cords are immobile or fixed in a mostly closed position, which inhibits breathing and often causes noisy inspiration.
In a posterior commissuroplasty, the clinician uses a carbon dioxide laser to take small divots from the posterior ends of both vocal cords. These divots create more space between the cords so that, during breathing, air can pass through more easily. This procedure can avoid the need for a tracheotomy. It also preserves the voice’s functionality better than a transverse cordotomy typically does.
Photos:
Involuntary inspiratory voice (1 of 6)
This elderly man is tracheotomy-dependent due to inability to open the vocal cords. Here while breathing in, there is a posterior “keyhole” from the divots caused by pressure necrosis of the breathing tube. Still, due to inspiratory airstream, he produces involuntary inspiratory voice. General anesthesia for laser widening of the airway (posterior commissuroplasty) would be very risky due to his diabetes and many other medical problems. Hence, the decision to attempt this with patient awake and sitting in a chair.
Laser posterior commissuroplasty (2 of 6)
The posterior right vocal cord is injected with lidocaine with epinephrine, in preparation for office laser posterior commissuroplasty. F = false vocal cord. T = true vocal cord, near its posterior end. The left vocal cord is injected similarly prior to the procedure that follows.
During the commissuroplasty (3 of 6)
The thulium laser fiber is being used to excavate the posterior commissure. Note the existing divot of the opposite (right) vocal cord (dotted lines) which will also be enlarged (next photos).
Deepening divot (4 of 6)
With view rotated clockwise approximately 45 degrees, work is commencing to deepen the right vocal cord divot.
Inspiratory indrawing decreased (5 of 6)
At the conclusion of the procedure. Not only is the ‘keyhole’ seen in photo 1 larger, but inspiratory indrawing of the rest of the vocal cords is greatly diminished.
Phonation (6 of 6)
Now phonating, voice is similar to the beginning of the procedure, because the vibrating part of the vocal cord was not disturbed. Of course, number of words per breath is slightly lower, due to increased use of air through the keyhole—air wasting.
Posterior pharyngeal wall
The posterior pharyngeal wall is the back wall of the swallowing passage. The upper part of the posterior pharyngeal wall can be seen when one looks through an opened mouth, beyond the soft palate, uvula, and tonsils. There is a layer of mucosa, then muscle, and then the bodies of the cervical vertebrae.
Postoperative Voice Use
Voice Use Following Vocal Fold Micro-Surgery in Singers
During the first 4 days following surgery–NO TALKING. During this time communicate instead using a dry erase board, pencil and paper or sign language. You may attempt to do gentle “gliding sounds” throughout your range every few hours for a few seconds, of course expecting to be hoarse! Your surgeon or speech pathologist will demonstrate what is meant by this. Day 4 following surgery (which begins week one of voice use): you may begin limited voice use according to the table below:
Note that we use a 1 through 7 scale to designate amount of talking. On this scale, 1 = someone who is quiet, introverted, and says little. 7 = someone who is sociable, extroverted, and who by nature talks a lot.
| Quality of Talking | Quality of Singing (if you sing) |
|---|---|
| WEEK ONE (days 4 through 11) Be a “2.” This means minimal voice use to get the “business of life” done. Perhaps 5 minutes of talking for any 30 minute period of the day. |
Vocalize gently 5 minutes twice a day. Begin to establish baseline for your “swelling tests.” (If needed, see also instruction sheet on this subject.) |
| WEEK TWO Be a “3.” Simple conversations. Up to 10 minutes within A 30 minute period. | Vocalize gently up to 15 minutes twice a day. Be sure to check “swelling tests” at least 2 x per day. |
| WEEK THREE Be a “4.” Limit talking to 15 minute stretches with a 15 minute rest period. | Vocalize up to 20 minutes three times per day. Swelling tests! |
| WEEK FOUR Be a “5.” Near-normal amounts of voice use but continue to beware of overdoing it! Twenty minutes of talking should be followed by some “down time.” | Vocalize/sing up to 30 minutes 3 x per day. |
| WEEK FIVE Continue to use voice at near-normal amounts, but with a sense of prudence and caution in noisy environments. | Begin to resume normal rehearsal and practice schedule, but not exceeding 90 minutes per day. It is critical that you perform swelling tests every morning and evening and compare to your baseline performance of these tasks. |
| WEEK SIX and beyond PUBLIC PERFORMANCE MAY RESUME | Normal rehearsal and practice schedule. Continue twice-daily swelling tests, especially if you are innately a “six” or “seven.” |
Presbylarynx
Literally, “old age larynx.” The term presbylarynx is used to signify vocal cord changes (and, by extension, vocal limitations) that accompany aging. Typically, these vocal cord changes include bowing of the cords, atrophy, flaccidity, and sometimes reduced wetness and lubrication of the vocal cords. The symptoms of these changes include foggy or weak voice quality, difficulty being heard in noisy places, and decreased vocal endurance.
Such findings are by no means universal in older individuals, however, and some of these changes may be resisted with vocal conditioning exercises. Moreover, some “presbylarynx” changes can be seen in individuals who are only 40 or 50, due to disuse of the voice or familial predisposition. For these reasons, presbylarynx does not seem to be a very useful term; instead, a precise description of the patient’s vocal cords seems to be more useful.
Photos:
Vocal cord bowing (1 of 4)
Open phase vibration, strobe light. Notice the large amplitude of vibration. The wide lateral excursions suggest flaccidity, especially when this is seen in middle voice.
Vocal cord bowing (2 of 4)
Partially closed phase. Notice that the anterior cords (arrows) are more flaccid, with delayed return to midline contact. When this is seen, that anterior segment may vibrate independently and cause a rough, gravelly voice quality. The capillary ectasia, left vocal cord (right of image), is an incidental finding and not related to the patient’s rough voice quality.
Vocal cord bowing (3 of 4)
Coming to closed phase, but with the persistent anterior open segment.
Vocal cord bowing (4 of 4)
Closed phase of vibration.
Flaccid vocal cords (1 of 3)
Open phase of vibration showing large amplitude in middle voice.
Flaccid vocal cords (2 of 3)
Maximum closed phase, but with persistent open area anteriorly (at arrow) If this area of exaggerated flaccidity oscillates independently, a rough quality is added to the voice.
Flaccid vocal cords (3 of 3)
Between open and closed phase, showing vibratory contact is aberrant.
Presbyphagia
Presbyphagia is a term used to describe swallowing difficulty of the sort that can be associated with the aging process: the process of swallowing as a whole is inefficient and reduced in vigor. Common findings include globally (as opposed to focally) reduced muscle bulk, often seen in vocal cords and not just pharyngeal wall musculature; globally reduced strength of contraction of the pharynx; and tendency for retention or pooling of a part of swallowed food or liquid in the vallecula or pyriform sinuses. Presbyphagia may be associated with cricopharyngeal dysfunction and, when severe, aspiration.
Photos:
Pooling (1 of 4)
This man coughs frequently especially when drinking. While his palate elevation, pharynx squeeze, and vocal cord functions are intact (as determined during VESS part 1A), note the pooling of saliva especially in the right pyriform sinus (left of photo) and on the pharyngeal wall (arrows) as well as within the laryngeal vestibule (bottom, left arrow). This predicts that his swallowing of blue-stained applesauce, water, and cracker will also be abnormal.
Residue (2 of 4)
As predicted by the information in photo 1, after administration of blue-stained applesauce, we see here an amount and location of residue that mirrors that of the saliva in photo 1. Greater residue in the right pyriform sinus (left of photo) is often seen with right-sided pharynx weakness, but that is not the case here.
Cracker (3 of 4)
After administration of cheese cracker, some of it remains in the vallecula, where it has displaced some of the applesauce.
Blue-stained water (4 of 4)
After administration of blue-stained water, most of cracker and applesauce are washed through. Some minimal blue-staining of the laryngeal vestibule explains why coughing tends to occur when drinking (especially thin liquids).
Presbyphonia
Literally, “old age voice.” See also presbylarynx. As with presbylarynx, to describe precisely the voice’s capabilities, limitations, and aberrations seems much more useful than to use this term.
Primary treatment
Primary treatment refers to the first or main treatment of a condition. Example: An individual with larynx cancer may have surgery as primary treatment; later, radiation therapy might follow as an additional treatment.
Projected voice
A voice that is perceptibly “thrown” or “called out,” as when talking to a group of 20 or more people. A clinician might ask a patient to project the voice during the vocal capability battery in order, for example, to reveal weakness not evident or only slightly apparent at normal speaking voice volume, to detect vocal inhibition, or to unmask a nonorganic voice disorder.
Pseudo-asthma
A disorder that mimics asthma but is not asthma. One such disorder is nonorganic breathing disorder, tracheal.
Puberphonia
Puberphonia is the inappropriate persistence of higher-pitched prepubertal voice long after puberty and normal voice change. Also called mutational falsetto. Such individuals maintain something like their high-pitched, childhood voice by speaking in falsetto register.
The cause of puberphonia is never known with precision. Some think the condition arises more often in men whose voices mutate to the normal and mature male quality suddenly and precipitously, dropping abruptly into the bass or bass-baritone range. It is as though the person isn’t given time to adapt to the new sound of the voice. Some individuals with puberphonia can produce normal voice on request, but consider it “ugly,” or even their “monster voice.” Others need considerable coaching to find the normal voice. Once convinced by voice experts that the “monster” voice actually sounds great and is the “normal” one, most individuals can adopt the new voice fairly rapidly. The process of normalization typically involves only two or three sessions of speech/voice therapy, provided the therapist is highly experienced and voice therapy-qualified.
Photos:
Falsetto vs chest registers at the same pitch—this is worth careful study: Series of 6 photos
Pulmonary function tests (PFTs)
A set of tests that evaluate the mechanical and functional capabilities of the lung and airways. PFTs may non-invasively investigate breathing problems, establish severity, assess risk for general anesthesia, and help determine whether a patient is a candidate for conservation cancer surgery.
Pulse register
Vocal fry is the name given to a quality of sound produced at low pitch (generally below 90 Hz, or around E2 or F2 in musical notation). Vocal fry is produced in what some call pulse register, as compared with chest and falsetto registers.
Pyriform sinus
Pyriform sinus refers to the pear-shaped fossa (Latin for “trench”) just lateral to the laryngeal entrance. Its medial surface is the aryepiglottic cord; laterally it is bounded by the thyroid cartilage, and posteriorly by the low posterior pharyngeal wall. The pyriform fossas and post-arytenoid area together constitute the “swallowing crescent,” which channels swallowed material just before it enters the esophagus, behind the larynx.
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