Laryngopedia

To educate about voice, swallowing, airway, coughing, and other head and neck disorders

Inability to burp or belch

Posted on September 26, 2016 by admin

Inability to burp or belch

Inability to burp or belch occurs when the upper esophageal sphincter (cricopharyngeus muscle) loses its ability to relax in order to release the “bubble” of air. The sphincter is a muscular valve that encircles the upper end of the esophagus just below the lower end of the throat passage. If looking from the front at a person’s neck, it is just below the “Adam’s / Eve’s apple” and more specifically, directly behind the cricoid cartilage. If you care to see this on a model, look at the photo below. That sphincter muscle relaxes for about a second every time we swallow saliva, food, or drink. All of the rest of the time it is contracted. Whenever a person belches, the same sphincter needs to let go for a split second in order for the excess air to escape upwards. In other words, just as it is necessary that the sphincter “let go” to admit food and drink downwards in the normal act swallowing, it is also necessary that the sphincter be able to “let go” to release air upwards for belching. The formal name for this disorder is retrograde cricopharyngeus dysfunction (R-CPD).

People who cannot release air upwards are miserable. They can feel the “bubble” sitting at the mid to low neck with nowhere to go. Or they experience gurgling when air comes up the esophagus only to find that the way of escape is blocked by a non-relaxing sphincter. It is as though the muscle of the esophagus continually churns and squeezes without success. The person so wants and needs to burp, but continues to experience this inability to burp. Sometimes this can even be painful. Such people often experience abdominal bloating as the air must make its way through the intestines before finally being released as flatus.

Approaches for treating the inability to burp:

For people who experience this problem of R-CPD to the point of discomfort and reduced quality of life, here is one approach: First, a consultation to determine whether or not the criteria for diagnosing R-CPD are met. Next, a simple Videoendoscopic swallow study which incorporates a neurological examination of tongue, pharynx (throat) and larynx muscles. This establishes that the sphincter works normally in a forward (antegrade) swallowing direction, but not in a reverse (retrograde) burping or regurgitating fashion. Along with the symptoms described above, this straightforward office consultation and swallowing evaluation establishes the diagnosis of retrograde cricopharyngeus dysfunction (non-relaxation).

The second step is to place Botox into the malfunctioning sphincter muscle. The desired effect of Botox in muscle is to weaken it for at least several months. The person thus has many weeks to verify that the problem is solved or at least minimized. The Botox injection could potentially be done in an office setting, but we recommend the first time (at least) placing it during a very brief general anesthetic in an outpatient operating room. That’s because the first time, it is important to answer the question definitively, that is, that the sphincter’s inability to relax when presented with a bubble of air from below, is the problem. Furthermore, based upon an experience with more than 130 patients as of March 2019, a single injection appears to “train” the patient how to burp. More than 60% of patients have maintained the ability to burp long after the effect of the Botox has dissipated. That is, long past 6 months from the time of injection.

Patients treated for R-CPD as just described should experience dramatic relief of their symptoms. And to repeat, our experience in treating more than 130 patients (and counting) suggests that this single Botox injection allows the system to “reset” and the person may never lose his or her ability to burp. Of course, if the problem returns, the individual could elect to pursue additional Botox treatments, or might even elect to undergo endoscopic laser cricopharyngeus myotomy. To learn more about this condition, see Dr. Bastian’s description of his experience with the first 51 of his much larger caseload at https://journals.sagepub.com/doi/full/10.1177/2473974X19834553.

Photos of the cricopharyngeus muscle:

1. The highlighted oval represents the location of the cricopharyngeus muscle.
2. The cricopharyngeus muscle in the open position.
3. The cricopharyngeus muscle in the contracted position.
inability to burp Where have patients traveled from?

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Marfan syndrome

Posted on October 13, 2014 by admin

A genetic connective tissue disorder caused by a defect in gene FBN1, which codes for abnormal structure of fibrillin-1, a protein crucial for formation of normal connective tissue. Most critical is Marfan syndrome’s effect on heart and blood vessels, which tend to dilate and be at risk of rupture. Connective tissue in bones, ligaments, and other parts of the body is also affected.

Laryngologists may encounter Marfan syndrome because parts or all of the aorta may need to be replaced over time, due to abnormal dilation of the weakened arterial wall, with risk of rupture. When such surgery is done, the left recurrent nerve is at risk of injury, and this would lead to left vocal cord paralysis. With Marfan syndrome, it is rare to live to age 70.

Photos:

Marfan syndrome: Series of 5 photos

Marfan syndrome (1of 5)
70-year-old patient whose left vocal cord (right of photo) was implanted 15 years ago with a silastic wedge to rehabilitate paralysis. Voice was reported as "normal" for many years, but in recent months has deteriorated.

Marfan syndrome (2 of 5)
As the right vocal cord (left of photo) moves toward the midline, the arytenoid cartilage (white dotted line) appears to emerge from the right vocal cord without bringing the membranous segment (green dotted line) with it.

Marfan syndrome (3 of 5)
At close range, one can see more clearly that the connective tissue attachment between the arytenoid cartilage and soft tissue of the vocal cord itself has been completely lost. As in photo 2 the white dotted line marks the arytenoid cartilage and the green dotted line marks the vocal cord's membranous segment.

Marfan syndrome (4 of 5)
A different view, showing again the vocal process of the arytenoid cartilage detaching from the vocal ligament/muscle of the membranous portion of the vocal cord.

Marfan syndrome (5 of 5)
Panoramic view of the hypopharynx, showing aneurysmal dilation of the internal carotid artery (bulge on right side of photo). Epiglottis is at the center and left.

Presbyphonia

Posted on November 8, 2013 by admin

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.

Presbylarynx

Posted on November 8, 2013 by admin

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: Series of 4 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: Series of 3 photos

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.

Bilateral vocal cord fixation

Posted on July 20, 2012 by admin

Immobility of both vocal cords due to a scarring rather than paralytic cause. The scarring might manifest as a synechia that tethers the vocal cords to each other and prevents them from separating during breathing. Or it could mean that both cricoarytenoid joints are ankylosed, or “frozen.”

The commonest cause of bilateral vocal cord fixation is prolonged endotracheal intubation, such as in gravely ill or injured persons, who may spend weeks in an intensive care unit and on a ventilator. Vocal cord fixation can rarely be caused by rheumatoid arthritis. It is also seen infrequently as a progressive, late complication of radiation therapy for larynx cancer.

Photos:

Bilateral vocal cord fixation: Series of 2 photos

Bilateral vocal cord fixation (1 of 2)
After bilateral posterior cordotomies, “keyhole” shaped glottis. Size of opening at posterior commissure is exaggerated by the wide-angle lens of the distal-chip video-endoscope.

Bilateral vocal cord fixation (2 of 2)
Persistent posterior opening, but musculomembranous cords come into good contact and have not been damaged by either the original endotracheal tube or the posterior cordotomies, and voice is very serviceable.

Necrosis

Posted on July 20, 2012 by admin

The death of cells or tissue. In laryngology, necrosis is seen most commonly after radiation therapy to the larynx for cancer treatment. Radiation kills the tumor but at the same time damages the blood supply of normal tissue on a permanent basis. Necrosis in this instance is called “radionecrosis.” Or, necrosis could result from trauma (a physical wound) that disrupts blood supply, or occasionally in the context of ulcerative laryngitis, which seems to necrose the superficial layers of the vocal cords. Necrotic tissue typically sloughs off down to viable (living) tissue.

Photos:

Necrosis, before and after discontinuing bevacizumab: Series of 6 photos

Necrosis (1 of 6)
Biopsy of hazy, superficially ulcerated lesion on right vocal cord (left of image) shows only “necrosis.” There is no proof but only a question whether this necrosis may be a side effect of the bevacizumab (Avastin) the patient is taking for lung cancer.

Necrosis (2 of 6)
Open phase of vibration (strobe light) shows that only the left cord (right of image) oscillates.

Necrosis (3 of 6)
Closed phase of vibration (strobe light) shows that closure is result of left cord excursion.

Necrosis, after discontinuing bevacizumab (4 of 6)
Several months after discontinuing bevacizumab, the right vocal cord ulcer has healed.

Necrosis, after discontinuing bevacizumab (5 of 6)
Narrow band illumination accentuates the ingrowth of new capillaries.

Necrosis, after discontinuing bevacizumab (6 of 6)
Phonatory match (standard light) is improved, but the right vocal cord (left of image) remains stiff, as the ulcer has been replaced by scar tissue.

Radionecrosis: Series of 4 photos

Radionecrosis (1 of 4)
This patient was originally treated for early vocal cord cancer with radiation. Tumor persistence required hemilaryngectomy. Then nearly a year later, he developed a neck metastasis (in a lymph node). Neck dissection was performed, but the tumor was found to have penetrated the capsule of the lymph node (a high-risk finding for recurrence), so he received “insurance policy” proton beam radiotherapy of the right side of the neck. Unfortunately the posterior edge of the thyroid cartilage became necrotic due to the “double dose” of radiation. In this view, one only sees swelling of the right arytenoid mound, but the pyriform sinus is closed and the necrotic area cannot yet be seen.

Radionecrosis (2 of 4)
Here, the patient is performing the trumpet maneuver to splay open the right pyriform sinus. The area of necrosis is beginning to be seen at arrow.

Radionecrosis (3 of 4)
The necrotic tissue is seen here at a much closer range.

Radionecrosis (4 of 4)
An even closer view into the necrotic pyriform sinus. Multiple biopsies have been taken from this area to be sure there is no cancer. Eventually, this larynx had to be removed not for cancer, but for this radiation complication.

Anterior commissure-to-subglottis fistula complication of radiation: Series of 4 photos

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.

Phonatory insufficiency

Posted on July 19, 2012 by admin

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: Series of 3 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: Series of 4 photos

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: Series of 4 photos

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. ↩

Arytenoid chondritis / perichondritis

Posted on July 18, 2012 by admin

An infectious or inflammatory response with ongoing ulceration or granulation on the superstructure of the arytenoid cartilage. Here we are talking of the arytenoid cartilage and/ or its thin “envelope” of fibrous tissue called perichondrium. The root chondr- refers to cartilage.

A similar and much more common disorder, contact granuloma or contact ulcer, occurs on the medial surface of the arytenoid cartilage, but low and at the level of the vocal process. When arytenoid chondritis or perichondritis occurs, it causes significant chronic pain (in contrast to contact granuloma, which can be pain-free or bring only minor discomfort). We have never diagnosed the underlying cause. Treatment tends to require definitive removal of the area of cartilage involved (not the entire arytenoid, of course), and then typically the area will heal, though often only after a time of re-granulation.

Photos:

Arytenoid chondritis, before and after removal: Series of 5 photos

Arytenoid chondritis (1 of 5)
Festering arytenoid chondritis of over a year's duration. Several biopsies done elsewhere showed only inflammation.

Arytenoid chondritis, removed (2 of 5)
Two weeks after aggressive partial arytenoid superstructure excision, in an attempt to get down to healthy cartilage.

Arytenoid chondritis, removed and healed (3 of 5)
After complete healing. Note loss of anterior arytenoid prominence on the operated side as compared with the unoperated side.

Arytenoid chondritis, removed and healed (4 of 5)
At this point, patient is entirely symptom-free. Notice resolution of the lesion and inflammation. The arytenoid mound is a little lower on right (left of image) than on left (right of image), due to surgical removal of part of the superstructure of the arytenoid.

Arytenoid chondritis, removed and healed (5 of 5)
The area of festering chondritis has completely healed. The arrow shows center of where the lesion was.

Arytenoid chondritis: Series of 3 photos

Arytenoid chondritis (1 of 3)
This person has twinges of pain every time she swallows, like “ground glass” or “razor blades.” She locates the sensation by pointing precisely to the upper part of the thyroid cartilage on the left. The exam reveals an arytenoid ulcer (upper right of image), with surrounding erythema.

Arytenoid chondritis (2 of 3)
A closer view shows more clearly the central depression and rolled border of the lesion.

Arytenoid chondritis (3 of 3)
Using narrow-band illumination at even closer range.

Arytenoid chondritis: Series of 1 photo

Arytenoid chondritis (1 of 1)
Small ulcer with surrounding erythema, right arytenoid superstructure.

[Gallery not found]

Arytenoid chondritis at the glottic level NOT likely from reflux!: Series of 3 photos

2 weeks post dilation (1 of 3)
Two weeks after dilation of this inflammatory subglottic stenosis. Treatment elsewhere with esomeprazole for 2 years had not resolved this. This is likely forme fruste Wegener’s-type stenosis, which in this patient has required dilation every few years, with marked resolution of shortness of breath/ noisy breathing.

Ulcer not caused by tube or reflux (2 of 3)
There was no postoperative pain at all until on the 4th postoperative day, when she developed left throat pain radiating to the left ear. Note within dotted line a flat ulcer with surrounding redness, resembling an apthous ulcer more than endotracheal tube injury or acid reflux. Observation was counseled, and even discontinuation or reduction of her esomeprazole.

3 months later, ulcer is gone (3 of 3)
Within a few weeks, the pain resolved. Here, 3 months later, the ulcer and erythema are gone. Dotted lines indicate where the ulcer would be if still present. Compare with photo 2.

Arytenoid perichondritis: Series of 5 photos

Arytenoid perichondritis (1 of 5)
Singer with constant right throat pain and vocal impairment, worsened by singing and speaking. Examination finding: arytenoid perichondritis. Note the erosion exposing the arytenoid cartilage, and the associated swelling.

Pseudopolyp (2 of 5)
Swelling creates a “pseudopolyp” (at arrow) that interferes with vocal cord closure and vibration.

Phonation (3 of 5)
Phonatory view under strobe light.

Two weeks post treatment (4 of 5)
Two weeks after antibiotic treatment. He has intermittent mild discomfort only when singing, and his voice is much improved. Minimal residual erosion (see arrow), with mild inflammatory changes.

Normal voice (5 of 5)
Pseudopolyp has resolved and no longer interferes with voice. At follow-up 6 weeks later, his voice is entirely normal and he has no pain.

Arytenoid perichondritis awaiting surgery: Series of 2 photos

Inflammation (1 of 2)
Spontaneous onset of sore throat, laryngitis, without any other URI symptoms approximately 6 months earlier. Biopsy elsewhere showed 'acute and chronic inflammation.' Note the inflamed, rolled border outlined by dotted line, and a sense of central excavation.

Surgery likely (2 of 2)
At closer range. The solution here will likely be to remove the lesion to include a central "festering" area of perichondrium, as for the other cases on this page. Cause of this kind of lesion is always unknown.

Arytenoid perichondritis going...coming...gone!: Series of 4 photos

Throat pain (1 of 4)
Very localized throat pain, left mid-neck, has been present for about 5 months with no sign of improvement despite trials of antibiotics, and fluconazole elsewhere. The location of pain correlates well to the lesion (bold arrow). The pain is very troublesome, fluctuating between 5 and 7 on a ten-point scale, worse with talking and tending to increase as the day progresses. The patient was also experiencing frequent laryngospasm. The patient was offered further observation vs. excision at her option.

1 week post removal (2 of 4)
After waiting an additional month, the patient became motivated to have the lesion removed. This examination is one week after excision of perichondrium and a small amount of cartilage, seeking to remove the “festering point.” The surgical wound is indicated by small dotted line on the left (right of photo). The patient’s pain is already much reduced, in spite of this wound, but peculiarly, she now has just a slight similar pain on the right. Note the small lesion indicated by the arrow, and visible in retrospect, in photo 1.

5 weeks post removal (3 of 4)
Five weeks after surgical removal, left-sided pain is still gone, and after a course of antibiotics and steroids, right sided lesion (arrow) and pain are nearly gone. It is not known whether healing was spontaneous or the result of steroid and antibiotic. This is because treatment of longstanding lesions often fails, and early, minimal lesions like this one sometimes heal without treatment.

3 months post removal (4 of 4)
Now 3 months after surgical excision, the larynx is entirely healed; pain and laryngospasm are gone.

Flaccidity of vocal cords

Posted on July 16, 2012 by admin

Photos of Flaccidity:

Flaccid vocal cords: Series of 4 photos

Flaccid vocal cords (1 of 4)
Pre-phonatory instant, standard light.

Flaccid vocal cords (2 of 4)
Vibratory blur with standard light. Note relatively wide "gray" zone of blur.

Flaccid vocal cords (3 of 4)
Dramatic lateral excursions due not only to bowing, but also flaccidity.

Flaccid vocal cords (4 of 4)
Eventual recoil towards midline, but cords never come into full contact before they are again thrown to their maximum lateral vibratory excursion, as in photo 3.

Flaccid vocal cords: Series of 3 photos

Flaccid vocal cords (1 of 3)
Open phase of vibration showing large amplitude in middle voice.

Flaccid vocal cords (3 of 3)
Between open and closed phase, showing vibratory contact is aberrant.

Vocal cord bowing: Series of 4 photos

Vocal cord bowing (2 of 4)
Partially closed phase, strobe light. Notice that the anterior cords 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 is an incidental finding an not related to the patient’s rough voice quality.

Vocal cord bowing (3 of 4)
Coming to closed phase, but with persistent anterior open segment.

Vocal cord bowing (4 of 4)
Closed phase of vibration, strobe light.

Flaccidity without bowing: Series of 4 photos

Flaccidity without bowing (1 of 4)
The patient exhibits typical symptoms of bowing/atrophy/flaccidity, but in this case there is little bowing or atrophy—primarily flaccidity is seen. In this view, the abducted vocal cords appear full, with no exaggeration of the ventricles. (The apparent asymmetry between the vocal cords is due to the viewing angle; both cords are the the same.)

Flaccidity without bowing (2 of 4)
Now seen under the strobe light, the amplitude of vibration of the vocal cords is excessive. These flaccid vocal cords lack the firmness to "recoil" back to the mid-line, until maximal separation of the cords is reached.

Flaccidity without bowing (3 of 4)
As the patient is reaching the closed phase of the vibratory cycle, the anterior cords are arriving late to closure, a typical finding with flaccid vocal cords.

Flaccidity without bowing (4 of 4)
Now at the maximum closed phase of vibration, a pinhole of incomplete closure is seen. In this case, there is no independent oscillatory vibration of the anterior segment of the vocal cord.

False cord phonation: Series of 5 photos

False cord phonation due to flaccid true cords (1 of 5): before false cords begin to vibrate
An elderly man, quiet by nature who uses the voice little, complains of weak, gravelly voice quality. This view of phonation, standard light, shows a slightly wider dark line of phonatory blurring. Also, the false vocal cords are overly approximated, but not yet participating in vibration (for that, see images 4 and 5).

False cord phonation due to flaccid true cords (2 of 5): before false cords begin to vibrate
Strobe light reveals an unusually wide amplitude of vibration, denoting flaccidity of the true vocal cords.

False cord phonation due to flaccid true cords (3 of 5): before false cords begin to vibrate
Maximum closed phase shows the telltale residual opening at the anterior commissure (from this perspective, the lowermost end of the true cords), also a potent indicator of flaccidity.

False cord phonation due to flaccid true cords (4 of 5): after false cords begin to vibrate
When asked to produce louder voice, the false cords begin to participate in vibration, and a rough, gravelly superimposed “godfather” quality arrives. Notice that the true cords are in at least partial open phase of vibration.

False cord phonation due to flaccid true cords (5 of 5): after false cords begin to vibrate
Now the false cords are in open phase of vibration, and the true cords are in maximum closed phase of vibration, with the same residual opening anteriorly seen in photo 3. False cord phonation is not to be seen most accurately as primary here, but as a secondary result of effort necessitated by flaccid true cords.

Flaccidity: Series of 5 photos

Flaccidity (1 of 5)
Under strobe light, the vocal cords begin opening at the area of flaccidity anteriorly. The patient has a husky and gravelly voice quality (view here rotated 90 degrees counterclockwise).

Flaccidity (2 of 5)
Vibratory separation continues and is still greatest anteriorly.

Flaccidity (3 of 5)
Open phase of vibration now complete. Distance of lateral excursions is large, indicating the flaccidity of cords.

Flaccidity (4 of 5)
The cords are returning to closed vibratory position, but anterior cords close late due to flaccidity. Sometimes this anterior segment vibrates independently and this causes a rough voice quality.

Flaccidity (5 of 5)
At maximum closed phase, there is still a tiny incomplete closure anteriorly.

Voice Building:

Voice Building (shorter version):

Vocal cord scissoring

Posted on July 16, 2012 by admin

Mismatching of the levels of the vocal cords. Vocal cord scissoring may in some cases be asymptomatic, but more often it introduces a rough quality to the voice, because the desired mirror-image bilateral symmetry of oscillation will be lost.

Photos:

Scissoring of the vocal cords: Series of 1 photo

Scissoring of the vocal cords (1 of 1)
The left vocal cord (right of image) rides up over the right, posteriorly.

Vocal cord scissoring, made more obvious by atrophy: Series of 4 photos

Vocal cord scissoring, made more obvious by atrophy (1 of 4)
The vocal processes in this patient are extremely visible because the rest of the vocal cord on each side is atrophic and bowed.

Vocal cord scissoring, made more obvious by atrophy (2 of 4)
The vocal cords approach each other for voicing. Note the evident asymmetry between the vocal processes. The left vocal process (right of image) projects further anteriorly than does the opposite process. It is also at a higher (more cephalad) level.

Vocal cord scissoring, made more obvious by atrophy (3 of 4)
Phonation, closed phase of vibration, under strobe lighting. Note the overlap (scissoring) of the left vocal process (right of image) on top of the other process.

Vocal cord scissoring, made more obvious by atrophy (4 of 4)
Phonation, at a higher pitch, at which the scissoring of the left vocal process (right of image) on top of the other becomes even more evident.

Scissoring arytenoids after years of vocal effort: Series of 4 photos

Voice remains effortful after radiation for carcinoma (1 of 4)
This man was severely hoarse for years, due to what looked like carpet-variant papillomas/ HPV effect. Each of many biopsies across many years confirmed “papilloma” often with severe atypia. Twice, the lesions tested negative for HPV DNA. After many years, he developed a carcinoma and received radiation with durable cure depicted here. Voice, however, remained rough and effortful.

Approaching phonatory position (2 of 4)
As he is approaching phonatory position (hence the blurring), right vocal process (left of photo) is overly turned medially.

Phonation (3 of 4)
As the vocal cords close, the overlap of right (left of photo) on top of left (right of photo) becomes very obvious.

Scissoring arytenoids (4 of 4)
The right vocal process (left of photo) rides up on top of the left vocal cord (right of photo). This, along with the stiffness of his cords caused by multiple prior surgical procedures and then radiation, accounts for his hoarse voice.