Laryngocele

A disorder in which the laryngeal saccule is inflated and becomes abnormally enlarged. A common symptom of a laryngocele is hoarseness.

How it develops:

The laryngeal saccule, or laryngeal appendix, is a very small blind sac—a dead-end corridor, so to speak—which is located just above the vocal cords, one on each side, and is lined with glands that supply lubrication to the cords. When a person makes voice, it is possible for a little bit of the air being pushed up out of the trachea to slip into this saccule. If over time enough air enters the saccule with enough force, the saccule may begin to be inflated and stretched out, leading to a laryngocele.

In some cases, the air that slips into and inflates the laryngocele will slip back out again as soon as the person stops making voice, so that the laryngocele abruptly inflates and deflates with each start and stop of speech or voice-making. (The photos and video below are an example of this.) In other cases, the air cannot exit as easily, but it may be reabsorbed slowly during quiet times or during sleep—only to be inflated again at the next instance of more active speaking.

Laryngocele vs. saccular cyst:

A much more common disorder of the laryngeal saccule (compared with a laryngocele) is a saccular cyst, which can occur if the entrance to the laryngeal saccule becomes blocked. In this scenario, air is absorbed, but secretions build up and gradually expand the saccule.

Symptoms and treatment for laryngocele:

A common symptom is hoarseness, because while the saccule is inflated, it may press press down on the vocal cords, not allowing them to vibrate freely, or it may block the laryngeal vestibule just above the cords and partially muffle the sound produced by the cords. Standard treatment is surgical removal, through one of two approaches: a small incision on the neck that leads into the larynx from the outside, or a laryngoscope that is inserted through the mouth and down into the larynx so that the laryngocele can be removed using a laser.


Photos:

Laryngocele

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Laryngocele (1 of 5)

Before phonation begins: the laryngocele is not visible.

Saccule (2 of 5)

Phonation begins: the saccule suddenly begins to inflate.

Saccule blocks airway (3 of 5)

The saccule is at peak inflation. Note how this obstructs the laryngeal airway.

Phonation ending (4 of 5)

The saccule is deflating. Note the motion blur; inflation and deflation each happens in a fraction of a second.

Phonation ended (5 of 5)

The laryngocele is again fully deflated and hidden from view.

Bilateral Laryngocele, Before and After Removal

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Bilateral laryngocele (1 of 8)

Vocal cords approaching point of best closure possible (due to left cord paresis). Faint dotted lines outline the approximate boundary of each laryngeal saccule, which not yet inflated.

Bilateral laryngocele (2 of 8)

As air just begins coming upward between the cords, one can see subtle inflation (dotted lines), particularly of the right saccule (left of image).

Bilateral laryngocele (3 of 8)

As phonation continues, inflation of the (now diagnosable) laryngocele becomes obvious, and the left laryngocele (right of image) is now more obviously inflated than before, again indicated by the dotted lines.

Bilateral laryngocele (4 of 8)

Near the end of a sustained period of voicing, maximum inflation of the laryngoceles is seen (dotted lines). On the right side (left of image), the stretching mucosa is so thinned as to appear translucent.

Bilateral laryngocele, after removal (5 of 8)

Same patient, breathing position, 12 weeks after complete removal of the bilateral laryngoceles via false cord incisions (lines of incision shown by dotted lines). This patient also has long-standing paralysis of the right vocal cord (left of image) and limited mobility of the left cord, so the cords don’t open fully for breathing.

Bilateral laryngocele, after removal (6 of 8)

Phonatory position. Note the lack of inflation of the now-absent laryngoceles, and compare that with photos 3 and 4 of this series.

Bilateral laryngocele, after removal (7 of 8)

Closer view of the posterior ends of the true vocal cords during maximal abduction for breathing. Space between the vocal cords is an estimated 50% of normal, because of the paralyzed right cord and the limited mobility of the left cord.

Bilateral laryngocele, after removal (8 of 8)

Same close-up view, but during phonation. The left vocal cord (right of image) has shifted slightly toward the midline, but the cords do not actually close and, thus, the patient cannot produce glottic (true vocal cord) voice. An implant could help to close this gap, but the patient will first try developing a “false cord voice.”

Laryngocele, Seen in a CT Image

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Laryngocele, seen in a CT image (1 of 1)

The patient’s left-sided saccule is dilated and filled by air, forming a laryngocele (the largest black spot in the image). The right-sided saccule is not seen because it is of normal size. The two smaller black spots show air in the pyriform sinuses (a normal finding).

Videos:

Laryngocele: A Cause of Hoarseness
A laryngocele is a disorder of the saccule, or laryngeal appendix, in which air abnormally expands it. Watch this video to see how a laryngocele behaves in real-time, and why that can affect the voice.

Stenosis

Abnormal narrowing of a passageway in the body. At our practice, stenosis typically refers to narrowing in the breathing passage, such as for narrowing in the glottic, subglottic, or tracheal areas.

Stenosis in the airway can be the result of prolonged endotracheal intubation, external trauma such as gunshot wound, crush injury, or tracheotomy, an inflammatory or auto-immune process, surgical resection of part of the airway for tumor, or other causes. Persons with airway stenosis will note a reduced capacity for exercise. Often the clinician hears noisy breathing on inhalation, especially when the patient is asked to fill the lungs quickly. Esophageal stenosis gives symptoms of difficulty swallowing solids more so than liquids.


Photos of Stenosis:













 



















Nuances of Endotracheal Tube Injury

This woman with high-risk comorbidities of diabetes and obesity, was in ventilated in ICU more than a month for pulmonary complications of Covid-19 infection. She had an orotracheal tube in place for 3.5 weeks, and then a tracheotomy tube was placed. Now at her first visit a year later, she remains tracheotomy-dependent, and is told she has bilateral vocal cord paralysis (disproven in the following photo series).

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Maximum glottic opening (1 of 8)

Is it paralysis, as diagnosed elsewhere? At a fairly distant view, the maximum opening between the vocal cords at any phase of breathing appears to be approximately a 4mm glottic opening.

Undersurface mucosa indraws (2 of 8)

When the patient inspires rapidly with tracheotomy tube plugged, the vocal cord undersurface mucosa indraws (grey bands at dotted lines), further narrowing the glottic chink. One sees a faint suggestion of breathing tube injury (divot) at the arrow. Notably, there is a very low pitched rumbling sound heard that does not come from the glottis.

Phonation (3 of 8)

During phonation, the cords approximate fully, and in fact the voice is remarkably normal-sounding and she even has an excellent upper range.

Posterior commissure divot (4 of 8)

At close range while breathing with trach plugged, the posterior commissure divot subtly visible in Photo 2 is confirmed. A divot in the right posterior cord “always” indicates that the tube was taped to the left corner of the mouth. The patient’s mother confirmed that this was so.

Further evidence of scarring (5 of 8)

Angling farther posteriorly, additional evidence of inter-arytenoid and possible joint capsule injury is seen. Faint dotted lines outline this area. The problem is not bilateral vocal cord paralysis but posterior commissure scarring, tethering the arytenoids together.

View into trachea (6 of 8)

Looking now into the subglottis and trachea, there is narrowing only at trach entry site, accentuated functionally because the membranous trachea (MT) moves in and out with respiratory phase.

Vibration of trachea (7 of 8)

When the patient plugs the trach tube and inspires rapidly, the deep rumbling sound is again heard, and comes from vibration of the membranous trachea indrawing (arrows) and vibrating (zigzag line).

Open trachea beyond the tube (8 of 8)

A view past the tip of the trach tube shows no secondary area of tracheal stenosis.

The plan here is posterior commissuroplasty, followed by placement of a smaller trach tube and a trial of plugging. If plugging is tolerated during the day, she will need a sleep study with it plugged at night, given the tracheomalacia and her obesity.


Videos of Stenosis:

Tracheal Stenosis: Before and After
In this video, trachea (windpipe) blockage causes shortness of breath until the narrowed segment is removed. You will see views of the trachea before and after surgical repair.
Post-Radiation Hypopharyngeal Stenosis
People with larynx or pharynx (voice box or throat) cancer often undergo radiation therapy as part of their treatment regimen. An uncommon complication is stenosis (narrowing, scarring) of the entrance to the upper esophagus at the junction of the throat and esophagus. This video provides an example of this disorder.

Cryptococcus Neoformans

Cryptococcus neoformans laryngitis is a rare fungal infection of the larynx. The infection usually occurs as a primary pulmonary infection but can spread to other regions of the body. Common characteristics of cryptococcus neoformans include longstanding hoarseness, sore throat, or edema of the vocal cords. Cryptococcus neoformans laryngitis is treated with oral anti-fungal medications such as fluconazole.


Photos of cryptococcus neoformans:

Cryptococcus infection of the larynx: Series of 4 photos

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laryngeal vestibule

Panoramic view (1 of 4)

Panoramic view of laryngeal vestibule in a man with very longstanding hoarseness and sore throat. Note intense redness and bumpy mucosal surface. Biopsy revealed Cryptococcus neoformans.
rough surfaced vocal cords

Closer view (2 of 4)

Closer view of the vocal cords shows similar intense inflammation and rough surface.
smooth mucosal surface

One year later (3 of 4)

After a one-year course of fluconazole, an oral anti-fungal medication. Symptoms are gone. The larynx is no longer inflamed, and the mucosal surface is smooth. White area of scarring (dotted surround), and scar band (parallel dotted lines).
healthy vocal cords

One year later, close-up (4 of 4)

Close-up of the vocal cords shows similar resolution of redness and cobblestoned surface.

SLAD-R

SLAD-R (Selective laryngeal adductor denervation-reinnervation). This procedure was introduced by Dr. Gerald Berke of UCLA in the late 1990’s. It is a surgical option for adductory spasmodic dysphonia. The concept is to sever the anterior branch of the recurrent laryngeal nerve. This denervates the spasming laryngeal adductors (particularly thyroarytenoid and lateral cricoarytenoid muscles). The squeezed, strained quality and/ or “catching, cutting out, stopping” of the voice are replaced initially with an extremely breathy and weak voice. This initially weak voice is analogous to what one might sound like after a Botox injection that is far too high a dose. To return strength to the voice, a branch of the ansa cervicalis nerve that normally supplies some relatively “unimportant” neck muscles is anastomosed (connected) to the severed nerve. It takes 3 months to a year for tone to begin to return to the adductory muscles. Since the “unimportant” neck muscles were not affected by the dystonia, the hope is that the new nerve supply to the laryngeal muscles may not be affected by dystonia.


Photos:



Videos:

One Man’s Experience Over Time with SLAD-R
SLAD-R is a surgical alternative to ongoing “botox” injections for treatment of adductory spasmodic dysphonia. The surgery involves intentionally cutting the nerves that close the vocal cords for voice and reconnecting a different nearby nerve supply (reinnervating the nerves). This surgery requires the patient’s willingness to endure an extremely breathy voice for many months after the procedure, while awaiting reinnervation.

Pharyngeal Paralysis

The pharynx (loosely “throat”) has a “foodway” function to convey food and liquid from the mouth to the esophagus. It also serves as part of the “airway,” also from mouth into the larynx and trachea. These foodway/airway functions are kept separate so food and liquid do not enter the airway towards the lungs. At the moment of swallowing, vocal cords clamp firmly together and epiglottis drops over the entrance of the larynx to divert food and liquid into the esophagus. During each swallow, lasting perhaps a second, breathing is briefly suspended. Once the food/liquid has gone by, the larynx re-opens and breathing resumes.

A thin sheet of muscle surrounds the pharynx, and squeezes to narrow the pharynx and help to propel swallowed material. That contraction lasts for approximately one second, each time the person swallows. The muscle is innervated bilaterally by the pharyngeal branch of the vagus nerve and so one side or both sides can be paralyzed by tumor, fracture at the base of the skull, viral injury, etc.

This diagnosis is often overlooked, because clinicians may not be clear on how to make the diagnosis. The best way is to obtain a clear panoramic view of the laryngopharynx as seen in the photo series below, and ask the patient to produce a very high pitch. This maneuver “recruits” contraction of the pharynx outside of the act of swallowing and allows the examiner to see clearly the difference in the contraction of the two sides. The paralyzed side is pulled to the non-paralyzed side, again as seen below.

Some with unilateral pharynx paralysis can compensate and continue to swallow (with limitations). Others are completely unable to surmount the impediment of this kind of paralysis.




Croup

Also known as laryngotracheitis or laryngotracheobronchitis, croup1 is a primarily pediatric viral disease affecting the larynx and trachea. Though it may resemble a simple cold at first, the infection causes a loud barking cough and stridor (unusual, high-pitched breathing noises indicating partial airway obstruction). The majority of cases are caused by parainfluenza viruses (types 1, 2, and 3) but a variety of other viruses can lead to croup symptoms.

The central problem for patients with croup is the swelling of the subglottic region of the larynx, which is the narrowest part of the airway in children. It can vary in its severity and can last anywhere from three days to two weeks. Most patients do not require hospitalization, as home treatment or prescribed antibiotics or steroids are typically sufficient.


Croup, aka Laryngotracheitis:

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Croup

Croup, aka laryngotracheitis (1 of 4)

Though croup is most often seen in children, this woman developed a barking cough and mild, non-anxiety provoking stridor in the context of an upper respiratory infection. In this panoramic view note in particular the prominence and redness of the conus part of the vocal cords (indicated by white lines).
laryngotracheitis

Croup, aka laryngotracheitis (2 of 4)

Closer view. Dotted lines signify normal airway diameter.
redness and narrowing of the posterior subglottic airway

Croup, aka laryngotracheitis (3 of 4)

Even closer view showing redness and narrowing of the posterior subglottic airway.
Croup

Croup, aka laryngotracheitis (4 of 4)

View within the posterior subglottic narrowing.

  1. Meyer, Anna. “197. Pediatric Infectious Disease” Cummings Otolaryngology Head and Neck Surgery. Ed. Paul Flint. 6th ed. Vol. 3. Philadelphia, PA: Elsevier, 2015. 3045-3054. 

Chondroma

Chondroma is a benign growth composed of cartilage cells.


Chondroma of thyroid cartilage

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CT scan of the larynx, showing the thyroid cartilage

CT scan of the larynx (1 of 4)

CT scan of the larynx, showing the thyroid cartilage (outlined by gray dotted lines) and an abnormality deforming the thyroid cartilage on one side (between the white arrows). Note how the thyroid cartilage bulges on that side, as compared with the opposite side, and the black speck which indicates varying densities in the cartilage.
Chondroma of thyroid cartilage

Endoscopic View of the Larynx (2 of 4)

Same patient, endoscopic view of the larynx, again showing the abnormality (at arrows). Here the abnormality looks similar to a saccular cyst, but the scan (and subsequent biopsy) shows that it is cartilaginous and a chondroma, not chondrosarcoma.
Closer view of the chondroma

Chondroma of thyroid cartilage (3 of 4)

Closer view of the chondroma, showing an almost bi-lobed appearance.
Chondroma of thyroid cartilage

Left Vocal Cord Sits Lower Then the Right (4 of 4)

Under strobe lighting, which shows that the left vocal cord (right of photo) is apparently at a lower level than the opposite cord.

Thyrohyoid Syndrome

A little-known inflammatory condition of the lateral thyrohyoid ligament and nearby tissues in the neck. The connective tissues in this area comprise in practical terms a floating “joint” that attaches the larynx to the hyoid bone. Inflammation of unknown cause can lead to a syndrome similar to tennis elbow, so that the point of attachment becomes chronically sore. Thyrohyoid syndrome is also known as hyoidynia, hyoid bursitis, or lateral thyrohyoid ligament syndrome.1

A patient with this condition typically (but not always) has a history of placing stress on this connective tissue in his or her profession or activities—trumpet playing, for example. Diagnosis is confirmed with finger or thumb pressure to find a point of acute tenderness over the greater horn of the hyoid bone and sometimes the upper border of the thyroid cartilage. The clinician may find it helpful also, by way of comparison, to apply gentle pressure on the submandibular gland or carotid artery so as to confirm that the point of tenderness is truly greatest at the lateral thyrohyoid ligament, hyoid bone, or thyroid cartilage.

Treatment of thyrohyoid syndrome is typically supportive and may include reduction of percussive or aggressive use of voice, non-steroidal anti-inflammatory drugs, or (by far most effective) an injection of 0.5 ml of Kenalog 40 mg per ml at the lateralmost point of the hyoid and upper border of the thyroid cartilage2, requiring care and experience, as this is just anterior to the carotid artery. This injection may cause soreness on top of the thyrohyoid syndrome pain for a day or two, followed by considerable, if not complete, relief for about three weeks. After this time, pain may return, though not usually to the original level. In some cases a single injection suffices; in others, a series of three injections, performed three or four weeks apart, is more effective.


  1. Sinha P, Grindler DJ, Haughey BH. A pain in the neck: lateral thyrohyoid ligament syndrome. Laryngoscope. 2014;124(1):116-8. 

  2. Kunjur J, Brennan PA, Ilankovan V. The use of triamcinolone in thyrohyoid syndrome. British Journal of Oral and Maxillofacial Surgery. 2002;40:450-451. 

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.




  1. Bastian RW, Park AH. Suction drain management of salivary fistulas. Laryngoscope. 1995;105(12 Pt 1):1337-41. 

IA-Only Paresis

IA-only paresis refers to weakness or paralysis of the larynx’s interarytenoid (IA) musclean unpaired muscle spanning between the bodies of both arytenoid cartilagesbut with normal function of the other muscles in the larynx. The IA muscle helps to bring the posterior commissure together for voice production and, more specifically, to bring the bodies or “heels” of the arytenoid cartilages on each side simultaneously to the midline. The following are indicators of IA-only paresis:

  • Movement: The vocal cord opens normally for breathing. From a distance, it can appear to close normally for voicing, but more intense and up-close inspection shows a persistent posterior commissure opening not only for voicing but also at the moment of cough and Valsalva maneuver. Without confirming that the heels of the arytenoids cannot come together regardless of task, the possibility of a functional posturing abnormality (such as seen for nonorganic voice disorders) cannot be ruled out. If voice change has occurred abruptly, and the above criteria pertain, IA-only paralysis can be considered; if of very gradual onset, the clinician will first want to rule out a deformity of the cricoarytenoid joints, such as can be seen with cricoid chondrosarcoma.
  • Position and appearance: Position is normal during breathing, but the posterior commissure cannot be brought to full closure whether during voicing, cough, or Valsalva maneuver.
  • Appearance during voicing (under strobe lighting): Vibration of the vocal cords can be normal, though, again, the persistent posterior commissure gap will be seen. The tone and bulk of the vocal cords themselves are normal.
  • Voice quality: Air-wasting, and with shortened phonation time, but without the luffing and diplophonia often apparent when the thyroartyenoid (TA) muscle is also paralyzed.

Other variants of vocal cord paresis include TA-only, TA + LCA, PCA-only (posterior cricoarytenoid muscle), and LCA-only (lateral cricoarytenoid muscle).


Photos of IA-only paresis:

IA-Only Paresis

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IA-only paresis (1 of 5)

This patient describes his voice as being extremely weak with an abrupt onset that was unrelated to intubation or any other injury. The patient's voice sounds extremely breathy regardless of vocal task. The amount of bowing seen here cannot fully explain the breathy (air-wasting) dysphonia that is heard.

IA-only paresis (2 of 5)

An intense visualization of the posterior commissure begins to reveal the mystery. While the "toes" (indicated by each letter T), or vocal processes of the arytenoids, come into full contact, the "heels" (indicated by each letter H), or bodies of the arytenoid cartilages, do not.

IA-only paresis (3 of 5)

An even closer view shows the persistent posterior commissure gap.

IA-only paresis, during a cough (4 of 5)

The elicited cough shown in this image proves that the patient is physically unable to close the posterior commissure.

IA-only paresis, during a Valsalva maneuver (5 of 5)

An elicited Valsalva maneuver, which also fails to close the posterior commissure. High-resolution CT was performed to prove there was no abnormality of the cricoid or arytenoids which might account for this finding of apparent interarytenoid paresis or avulsion.

Interarytenoid (IA) Weakness

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PCA muscles intact (1 of 4)

After SLAD-R surgery. The PCA muscles are intact, explaining normal abduction of both vocal cords for breathing.

Pre-phonatory instant (2 of 4)

At the pre-phonatory instant, one can see partial recovery of LCA muscles, explaining the ability of tips of vocal processes (at dots) to turn medially as the patient prepares to produce voice. Bowing is due to continuing TA weakness.

IA weakness (3 of 4)

The tips of the vocal processes (again at dots) are touching; the gap that remains posterior to them suggests that the interarytenoid muscle (IA) is not yet contracting sufficiently to bring the “heels” of the arytenoids together.

View of posterior commissure (4 of 4)

Very close-range view in the posterior commissure as the patient phonates, showing that the arytenoids do not come into contact. The tips of vocal processes are touching but out of view at the bottom of the photo (below the dots).

Another Interarytenoid (IA) Muscle Paresis or Is It Avulsion?

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good vocal cords in a middle aged man

Breathy and weak voice (1 of 8)

Middle aged man with fairly abrupt weakening of voice with no explanation that occurred a year before this examination. Voice is very breathy, air-wasting, and weak. He also has a tendency to cough on liquids. Distant view at high pitch shows good vocal cord closure and symmetrical pharyngeal squeeze.
bducted vocal cords

Bowing (2 of 8)

The abducted vocal cords for breathing show vocal cord bowing but otherwise nothing particularly noteworthy.
medial turning of the vocal processes

Pre-phonatory view (3 of 8)

As the vocal cords move towards each other on the way to producing voice, note the medial turning of the vocal processes (arrows), suggesting LCA muscles to be intact. The bodies of arytenoids, their “heels” as compared with the vocal process “toes” do not yet approach each other.
vibratory blur of the cords

Phonatory view (4 of 8)

Now producing voice (see vibratory blur of the cords under this standard light) shows that vocal processes are in contact (arrows) but the ‘heels’ of the arytenoids still do not approximate. Is this nonorganic? Neurogenic? Orthopedic (cricoarytenoid joints)? Myogenic?
Deep inside the posterior commissure during phonation

Posterior commissure (5 of 8)

Deep inside the posterior commissure during phonation. The large chink persists.
good thyroarytenoid (TA) function

TA function (6 of 8)

Closed phase of vibration at B3 (247 Hz) shows good thyroarytenoid (TA) function.
interarytenoid (IA) mucosa is blown away from the chink

IA mucosa (7 of 8)

The interarytenoid (IA) mucosa is blown away from the chink here by uncontrollable blast of air even while the patient tries to Valsalva /breath hold. Tight closure of not only true, but also false cords verifies his level of effort.
interarytenoid mucosa has oscillated anteriorly

IA avulsion (8 of 8)

During same Valsalva maneuver 1/5th of a second (6 frames) later, the interarytenoid mucosa has oscillated anteriorly (arrow). Why can’t the arytenoid “heels” come together? The best thought here is interarytenoid avulsion which could have sudden onset. Denervation seems possible but less likely given presumed bilateral innervation of that muscle, and a bilaterally symmetrical joint problem of rapid onset also seems unlikely.

Watch the Progression of A Rare Laryngeal Paresis Scenario Including Interarytenoid (IA) Muscle

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hitish lesion of the right cord is a red herring finding

Full abduction (1 of 5)

Three months ago, this otherwise healthy woman experienced an abrupt change in voice. The vocal phenomenology is that of weakness and air-wasting. Here, in full abduction, the vocal cords look slender and the whitish lesion of the right cord (left of photo) is a red herring finding. (Compare with Photo 3.)
Large gap during phonation

Large gap during phonation (2 of 5)

During phonation (note blurring of the vocal cord margins), there is a large gap between the cords. Interarytenoid muscle seems to be functioning, in that the “heels” of the arytenoids come into quite good contact (horizontal arrows, above). The tips of vocal processes, or “toes” of the arytenoid cartilages, point laterally, (diverging arrows, below) suggesting LCA weakness. (Compare with photo 4.)
vocal cords appear to be hyper-abducted

Two months later—voice is even worse (3 of 5)

Two months later, the patient reports that her voice is even worse. Note that while breathing, the vocal cords appear to be hyper-abducted. It is as though more of the ability to adduct (come together) has been lost; put another way, that abduction is less “balanced” by any tone from adductory (voicing) muscles. (Compare with photo 1.)
Arytenoids no longer touch

Arytenoids no longer touch (4 of 5)

Here, at the prephonatory instant, just before vibratory blurring commences, notice that the heels of the arytenoids no longer touch. It is as though IA muscle is denervated. (Compare with photo 2.)
Extremely breathy voicing

Breathy voicing (5 of 5)

Extremely breathy voicing has commenced. Note the blurring of the right cord margin (left of photo). If anything, the posterior glottis is even farther apart. Radiographic/diagnostic questions: Is there a mass lesion anywhere? No. Is the cricoid cartilage deformed? No. What is causing this? Unknown.