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Laryngopedia

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

Laryngopedia By Bastian Medical Media

Multimedia Encyclopedia


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Vallecula

Literally, the “little valley,” formed between the base of the tongue and the anterior face of the upright epiglottis.



Vallecular Cyst

A vallecular cyst is a mucus-containing cyst in the vallecula. Such cysts are relatively common. Vallecular cysts are almost always asymptomatic and found during examination for another issue, such as a voice problem.


Photos of Vallecular Cyst:

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Vallecular cysts (1 of 2)

Panoramic view of the laryngopharynx, showing two vallecular cysts (arrows), between the base of the tongue and epiglottis.

Vallecular cysts (2 of 2)

Closer view. These cysts were an incidental finding during an examination for an unrelated complaint. They were not causing the patient any problems and could be left alone.

Vallecular Cysts don’t Disturb Swallowing—Except When They Do

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Vallecular cyst (1 of 4)

Enormous vallecular cyst in this young woman. Swallowing of solids is affected. Food seems to catch and then expectorate back up to the mouth. No problem with liquids.

Evaluation of function (2 of 4)

Palate, pharynx, and larynx function are all normal. There is no pooling of saliva in the hypopharynx.

Applesauce residue (3 of 4)

An organized ring of applesauce remains after trying to swallow blue-stained applesauce.

Water wash (4 of 4)

Water wash is very effective in clearing the applesauce away. Vallecular cysts are usually left alone; here, the plan is to remove it with the thulium laser and see if swallowing is restored.

Laser for A Type of Lesion Usually Left Alone

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Vallecular cyst (1 of 8)

A large vallecular cyst in an older man with awareness of a “foreign body” sensation when swallowing.

Beginning swallow (2 of 8)

As a swallow begins, note the posterior pressure on the epiglottis and lateral pressure on the pharyngeal wall. Normally we leave these alone, but with careful discussion he wanted to be rid of this to see if it would diminish his symptoms.

Laser coagulation (3 of 8)

With the patient sitting in a chair under only topical anesthesia, office laser coagulation begins with a wide area.

Cyst wall (4 of 8)

Coagulation now involves the full thickness of the cyst wall. When it sloughs off, the cyst will be widely unroofed.

Contents spilling out (5 of 8)

Cyst contents are spilling out.

Concluding coagulation (6 of 8)

At the conclusion of the procedure the cyst has evacuated its contents and collapsed in size. The coagulated surface will detach over the next week or two.

3 weeks later (7 of 8)

Three weeks later, the vallecula is normal and the patient says symptoms are reduced “50%.”

Collapsed cyst (8 of 8)

The collapsed cyst with nearby unrelated and typical vallecular cyst requiring no treatment.


Valsalva Maneuver

The transient, somewhat forceful exhalation of air against an intentionally blocked airway. In a common variant of this maneuver, a person blocks the exhaled air by sealing the lips and plugging the nose, which forces air up the Eustachian tube and “pops the ears”; this variant is often performed when on a plane that is descending for landing. In a second variant, a person blocks the exhaled air by closing the vocal cords; this variant is often performed sub-consciously when a person lifts a heavy weight. This second variant of the Valsalva maneuver is also sometimes elicited by a physician during a cardiac or neurological evaluation.



Verrucous Carcinoma

Verrucous carcinoma is a variant of squamous cell carcinoma (SCCA). In the head and neck, this uncommon subtype of SCCA is seen most often in the oral cavity or on the vocal cords. Visually, it tends to have an exophytic (outward-growing) and wartlike, irregular surface. This variant of SCCA is typically less aggressive than other squamous cell carcinomas. Local recurrence tends to be the issue more than distant metastasis. Surgery tends to be the most effective treatment, though of course every patient’s circumstance is individualized and considered in the light of three treatment options: surgery, radiation therapy, and chemotherapy.


Photos:

Verrucous Carcinoma, Before and After Laser Treatment

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Verrucous carcinoma (1 of 5)

Verrucous carcinoma, left vocal cord, persistent after radiotherapy elsewhere, in a patient unable to undergo general anesthesia due to severe lung disease.

Verrucous carcinoma, after laser treatment (3 of 5)

After several Thulium Laser ablations, using topical and injected local anesthesia, with patient sitting in examination chair, thereby avoiding general anesthesia.

Verrucous carcinoma, several weeks after laser treatment (4 of 5)

Approximately six weeks later, durable resolution of tumor. Yellow material is mucus.

Verrucous carcinoma, several weeks after laser treatment (5 of 5)

During voicing. Arytenoid moves, but much of membranous vocal cord has been ablated as intended.


Vibrato

In the voice, a pulsating effect produced by small variations of pitch, typically occurring five or six times per second. The opposite of singing with vibrato is to sing with straight tone.




Videoendoscopic Swallowing Study (VESS)

A method of evaluating a person’s swallowing ability by means of a video-documented physical examination, looking from inside the throat. Also called the fiberoptic endoscopic evaluation of swallowing (FEES). The videoendoscopic swallowing study (VESS) is to be distinguished from the videofluoroscopic swallowing study (VFSS), which is an x-ray-based assessment.

How it works:

To perform a VESS, a clinician uses a fiberoptic or distal-chip nasolaryngoscope. The clinician begins by examining the structure and function of the patient’s palate, tongue, pharynx, and larynx, including sensation, if desired. Next, to assess the patient’s swallowing capabilities and limitations, the clinician positions the tip of the nasolaryngoscope just below the nasopharynx and, looking downward into the throat, asks the patient to swallow a series of colored substances with a range of consistencies (e.g., blue-stained water, blue-stained applesauce, and orange-colored crackers).

As the patient swallows these substances, the clinician watches to see if any significant traces remain in or reappear in the space above, around, or within the larynx, rather than disappearing into the entrance to the esophagus. If significant traces remain in view, or if any material spills into the opening of the larynx or down the trachea, the patient may have presbyphagia. If significant traces initially disappear but then re-emerge upward from the esophageal entrance, the patient may have cricopharyngeal dysfunction, with or without a Zenker’s diverticulum.

Benefits of the videoendoscopic swallowing study:

This method has particular value for patients who are bedfast and cannot travel to the radiology suite, or for patients whose swallowing function is rapidly evolving (improving, usually), such as those recovering from a mild stroke. For clinicians experienced with this technique, VESS can also often be used with new patients complaining of dysphagia during the initial consultation as a robust and—depending on patient history—potentially stand-alone method of diagnosis and management. Sometimes, the VESS findings, along with a patient history of solid food lodgment at the level of the cricoid cartilage or cricopharyngeus muscle, will indicate when VFSS should also be obtained to assess for possible cricopharyngeal dysfunction. Even in this latter circumstance, when VFSS is called upon to confirm a suspected diagnosis, VESS will have already oriented the examiner to the nature and severity of the problem. In most follow-up circumstances other than after cricopharyngeal myotomy, VESS is generally more efficient and inexpensive than VFSS.


Photos:

VESS Assesses Equipment, Secretions, then Swallowing Ability

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Part Ia: Palate elevates normally (1 of 7)

This man has symptoms of cricopharyngeus muscle dysfunction (CPD), with frequent lodgment of solid food (never soft or liquid material) at the level of mid-to-low neck. This VESS sequence demonstrates his propulsive or “pitcher” ability. Here in VESS part Ia, palate elevates normally (arrows). Left palate is not drooping and there is no deviation.

Part Ib: phonation (2 of 7)

In Part Ib of VESS, the patient makes voice, to prove normal movement and good closure of the vocal cords. In addition, no secretional pooling is seen in vallecula or pyriform sinuses.

Part Ic: High pitch elicited (3 of 7)

Part Ic: Very high pitch is elicited. Pharyngeal walls contract inward (arrows), closing the pyriform sinuses. Part Ia,b, and c (Photos 1, 2, and 3) verify that there is good function of swallowing equipment, i.e. palate, pharynx, and larynx (and tongue).

Part IIa: applesauce (4 of 7)

Part IIa: Blue-stained applesauce is first, because puree is the “easiest” material for the majority of patients, whatever their diagnosis. Here, one sees only minimal residue after several boluses are swallowed.

Part IIb: cracker (5 of 7)

Part IIb: After an orange (cheese) cracker, lodgment in the vallecula, and…

Part IIb: continued (6 of 7)

...on the pharyngeal walls (arrows).

Part IIc: water (7 of 7)

Part IIc: After several boluses of blue-stained water, all cracker is washed away and there is no blue staining or residue within the laryngeal vestibule, subglottis, or high trachea. Given this man’s CPD symptoms, VFSS may show a cricopharyngeus muscle bar, indicating incomplete relaxation of the upper esophageal sphincter.

Dysphagia / Delayed Swallow Reflex

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Dysphagia / Delayed swallow reflex (1 of 3)

Panoramic view of laryngopharynx before administering blue-stained applesauce.

Dysphagia / Delayed swallow reflex (2 of 3)

Same view after first bolus of blue-stained applesauce. The vallecula fills with material before the swallow “happens”—signifying a delayed swallow reflex.

Dysphagia / Delayed swallow reflex (3 of 3)

After several rapidly-administered boluses (to assess patient’s “limits”), note hypopharyngeal pooling, but none within the laryngeal vestibule.

Zenker’s Diverticulum

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Zenker's diverticulum (1 of 3)

This view is a moment after a completed swallow of blue-stained applesauce.

Postcricoid area (2 of 3)

Same view, a second later, as blue-stained applesauce emerges from the Zenker's diverticulum upward (toward the camera) into the postcricoid area.

Hypopharynx (3 of 3)

Another second later, applesauce continues to re-emerge into the hypopharynx.

Reflux Into Hypopharynx, Characteristic of Cricopharyngeal Dysfunction

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Reflux into hypopharynx (1 of 3)

The patient has swallowing problems typical of cricopharyngeal dysfunction. This swallow study reinforces that impression as well as the likely presence of a Zenker's diverticulum. In this photo, blue-stained water has just been swallowed, and the vocal cords are beginning to open. At this point, the hypopharynx contains no residue.

Reflux into hypopharynx (2 of 3)

One second later, the blue-stained water begins to emerge from just above the cricopharyngeus muscle into the "swallowing crescent".

Reflux into hypopharynx (3 of 3)

Another two seconds later, the larynx has fully opened post-swallow. The post-swallow hypopharyngeal re-emergence of the blue-stained water is apparent.

Hypopharynx Pooling After Swallow

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Hypopharynx pooling

Hypopharynx pooling after swallow (1 of 1)

Shows trace of blue-stained applesauce remaining behind after the patient has swallowed.

Laryngeal Penetration

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Laryngeal penetration (1 of 1)

After the patient swallowed several boluses of blue-stained applesauce, there were traces visible on the laryngeal surface of the epiglottis, indicative of penetration into the earliest part of the airway. By itself, soiling of the laryngeal vestibule to this minor degree does not threaten the person’s ability to eat by mouth.

Zenker’s Diverticulum and VESS

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Zenker’s diverticulum (1 of 4)

This middle-aged woman has had a known Zenker’s diverticulum for several years. She has now reached a point of frustration that has motivated her to proceed with cricopharyngeus myotomy. The series that follows explains some of the reason for her frustration. In this view, the patient has just completed a swallow of her saliva.

Saliva from Zenker's sac (2 of 4)

A few seconds later, saliva begins to return upwards into the post-arytenoid area (at arrow) from the Zenker’s sac.

More saliva (3 of 4)

Less than a second later, more saliva comes upward from the Zenker’s sac.

Forced to re-swallow (4 of 4)

A few seconds later, sufficient saliva has welled up from the sac that the patient is forced to re-swallow, taking her back to the appearance of the first photo in this series, only to begin the same cycle depicted in these four photos again and again.

Vallecular Cysts don’t Disturb Swallowing—Except When They Do

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Vallecular cyst (1 of 4)

Enormous vallecular cyst in this young woman. Swallowing of solids is affected. Food seems to catch and then expectorate back up to the mouth. No problem with liquids.

Evaluation of function (2 of 4)

Palate, pharynx, and larynx function are all normal. There is no pooling of saliva in the hypopharynx.

Applesauce residue (3 of 4)

An organized ring of applesauce remains after trying to swallow blue-stained applesauce.

Water wash (4 of 4)

Water wash is very effective in clearing the applesauce away. Vallecular cysts are usually left alone; here, the plan is to remove it with the thulium laser and see if swallowing is restored.

Pill Lodgment Due to Swallowing Disability

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Lodged pill (1 of 4)

This older woman swallowed a pill that lodged low in her throat. In spite of repeated swallows and attempts at expectoration, she couldn't move it for many hours. On examination a few days later, this superficial ulceration is seen due to mild chemical burn. Note as well the redness of the left arytenoid and pyriform sinus (right of photo).

Trumpet maneuver (2 of 4)

At closer range, while having the patient perform a trumpet maneuver, a well-demarcated superficial ulcer is seen again.

VESS (3 of 4)

Administration of blue-stained applesauce during VESS shows that a partial reason for lodgment may be reduced propulsive strength, indicated by pooling of material in the vallecula.

Incomplete relaxation of CPD (4 of 4)

After sips of blue-stained water, note the fairly organized crescent of pooled water in the pyriform sinuses and post-arytenoid area. This can suggest a functional outlet obstruction caused by incomplete relaxation of the cricopharyngeus muscle (CPD).

Delayed Swallow Reflex: Compare Blue Applesauce and Blue Water

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VESS (1 of 4)

During VESS, blue-stained applesauce falls down to the posterior base of tongue. If the swallowing reflex were normal, the patient would have swallowed before the applesauce arrived here.

Delayed swallow reflex (2 of 4)

Because of the viscosity of the material it "hangs" for a moment and does not fall down into the entrance of the larynx. Even with a delayed swallow reflex, there is still a second or two to swallow before that happens. The patient will tend to cough less with this consistency than with water.

Blue-stained water (3 of 4)

Here, blue-stained water is flowing into the right pyriform sinus (left of photo at arrow). Movement is rapid (note the blur) due to the low viscosity of water; there is less time to react and swallow than with applesauce, explaining why coughing on water is more common than purée or solid.

No residue (4 of 4)

Still, at the end of several boluses of applesauce and water, stained with blue food coloring, there is no stain or residue inside the entrance of the airway. The delayed swallowing reflex is a liability but without a risk of pneumonia.

Scarring Diverts Swallowed Materials Directly into the Larynx

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Post tonsillectomy (1 of 4)

A young woman struggles to swallow after extensive cauterization of severe bleeding after tonsillectomy elsewhere. The arrows here show the path food and liquid should follow to get into the esophagus (opening indicated by flat oval).

Closer view (2 of 4)

Closer view shows that the epiglottis is tethered to base of tongue at the dotted line. Furthermore, the "ski jump" scar appears to be ready to divert swallowed material directly into the larynx ( arrow) rather than into the pyriform sinus at *.

The "chute" (3 of 4)

A closer view shows even better the "chute" into the larynx.

Abnormal diversion (4 of 4)

While swallowing blue-colored water, arrows indicate the normal path on the left (right of photo) and the abnormal diversion into the larynx on the right (left of photo). The patient manages, but must swallow carefully, especially since the epiglottis cannot invert since it is scarred to the base of tongue as shown in photo 2.

Skull Base Fracture and Vagus Nerve Injury—Note Pharynx Contraction and Impact on Swallowing

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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.

VESS in 6 Still Photos

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Assessing the patient's swallowing (1 of 6)

Step 1 is assessment of the patient's swallowing "equipment." Here we see that the palate elevates symmetrically against the posterior pharyngeal wall.

Observing the pharynx (2 of 6)

The next step is to observe the pharynx squeeze with inferior constrictors bulging to surround the larynx. The vocal cords close fully.

Patient secretions (3 of 6)

Next is the assessment of patient secretions. This hypopharyngeal pooling of saliva (foamy bubbles) predicts that there will be similar pooling of swallowed food materials during the next step of VESS.

Pooling of swallowed pureed food (4 of 6)

As predicted, blue-stained applesauce (purée consistency) pools in the pyriform sinuses. There is no laryngeal soiling (penetration, aspiration).

Swallowing solids (5 of 6)

The next test is the cheese cracker (solid consistency). After swallowing, the residue is seen especially in the vallecula.

Residue after foods (6 of 6)

After several boluses of blue-stained water, a small amount remains in the pyriform sinuses and post-arytenoid area.

VESS (Videoendoscopic Swallow Study) Findings after Radiotherapy

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Narrowed pharyngeal wall (1 of 7)

After radiation and chemotherapy for larynx cancer several years earlier. Note the dry secretions. There is narrowing of the pharyngeal wall (dotted line) due to radiation scarring.

Swallowing applesauce (2 of 7)

After the second bolus of blue-stained applesauce. The propulsive ability ("pitcher of swallowing") is inadequate, leaving a lot of post-swallow residue.

After sipping water (3 of 7)

After three sips of blue-stained water, much of the applesauce has been washed away.

Gravity aiding in swallowing (4 of 7)

Additional water washes nearly all of the residue in the "swallowing crescent" away--mostly by gravity as seen in the next photo.

Lifting larynx (5 of 7)

Each swallow looks like this. The pharynx "bird swallow" mechanism lifts larynx forward so that the swallowing crescent opens down to the cricopharyngeus muscle, indicated by double dotted lines. (PC = post-cricoid.)

A closer look (6 of 7)

At closer range, the cricopharyngeus muscle bulge is seen more clearly, along with the small opening into the esophagus.

Gravity aiding again in swallowing (7 of 7)

Blue-stained water flowing into the esophagus mostly by gravity.

Cervical Osteophytes do not by Themselves Seem a Major Impediment to Swallowing

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Protruding osteophytes (1 of 2)

This 95 year-old man has large cervical osteophytes (bony proliferation due to arthritis). These osteophytes protrude into the pharynx (dotted lines). It would seem they would be a major impediment to swallowing.

Rapid swallowing (2 of 2)

After an initial test swallow, eight boluses of blue applesauce are administered rapidly. The purpose of this is to serve as a “stress test” so that we see his swallowing at its worst…But he has only a small amount of residue, and passes the test. Most individuals with cervical osteophytes are of advanced age. When swallowing is impaired, the explanation is usually more than just the osteophyte.

Aspiration, and Fountain of Returned Aspirate after Coughing

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Salivary pooling (1 of 5)

This young man has a chromosome disorder. He has trouble swallowing but no history of pneumonia. The palate, pharynx, and larynx motor function is normal, but the salivary pooling seen here predicts what follows…

After applesauce (2 of 5)

After several boluses of blue-stained applesauce, there is significant pooling (residue), but nothing down at the level of the vocal cords.

After cheese cracker (3 of 5)

After chewing and swallowing a cheese cracker, a part is lodged in the vallecular.

After water (4 of 5)

During administration of blue-stained water, a large drip is seen falling downwards, directly into the laryngeal vestibule.

Cough expels the water from airway (5 of 5)

A moment later, a cough sprays the aspirated blue-stained water upwards and out of the airway.

Zenker’s Diverticulum Returns Its Contents Upwards to the Throat After Each Swallow

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VESS (1 of 3)

During Videoendoscopic swallow study (VESS), this patient has just swallowed blue applesauce. It has disappeared downwards (arrows) into the upper esophagus but part of it is retained in a Zenker's diverticulum (out of view).

Swallowing Crescent (2 of 3)

Exactly one second later blue applesauce appears in the swallowing crescent as the sac empties a part of its contents upwards.

Applesauce spills into airway (3 of 3)

One second later, even more blue applesauce has emerged. If it were more liquid, it would spill forward to enter the airway. This explains the constant throat clearing and re-swallowing of persons with Zenker's diverticula (caused by antegrade cricopharyngeus dysfunction).

Three Views of the Entrance to the Esophagus from far Away to Close-up

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Swallowing Crescent (1 of 3)

During swallowing, the “the swallowing crescent”—outlined by the dotted line—receives swallowed food or liquid in order to funnel it into the esophagus (not open in this view). The asterisks are reference points to compare all three photos. One does not want any material to enter the laryngeal vestibule (hashed lines).

Closed esophagus (2 of 3)

A closer view. The esophagus is still not open in this view. Compare asterisk with prior and following photo.

Open Esophagus (3 of 3)

At the moment of a dry swallow, the esophagus opens as shown here. Again, the asterisks allow comparison with photos 1 and 2.

Videos:

Videoendoscopic Swallowing Study (VESS)
This video features an example of a 100-year-old patient undergoing VESS.


Videoendoscopy

Videoendoscopy is the coupling of video-documenting technology to an endoscope, so that the examination of the larynx, trachea, or esophagus, as the case may be, is permanently recorded for later review and possible comparison with prior endoscopy examinations.



Videofluoroscopic Swallowing Study (VFSS)

An x-ray-based method of evaluating a person’s swallowing ability. The videofluoroscopic swallowing study (VFSS) is also sometimes called the modified barium swallow, or the “cookie swallow.”

In a radiology suite under fluoroscopy (which creates moving rather than still x-ray images), the patient is asked to swallow barium in thin liquid and paste consistencies, and then in paste on a cookie or cracker. The barium bolus is followed radiographically through the mouth, throat, and into the esophagus. Both lateral and anteriorposterior views are recorded and, depending on the facility, a simple screening sequence of the subsequent movement down the esophagus is also recorded.


Photos:

Cricopharyngeal dysfunction, before and after myotomy: Series of 2 photos

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Lateral x-ray of the neck while swallowing barium

Cricopharyngeal dysfunction: before myotomy (1 of 2)

Lateral x-ray of the neck while swallowing barium (seen as a dark column). The non-relaxing cricopharyngeus muscle (light-grey bulge outlined by a dotted line) is causing narrowing of the upper esophageal passageway, as highlighted by the narrowed stream of dark barium at that point (arrow). Liquids and very soft foods can squeak through this narrow opening, but solid foods tend to get stuck.
X-ray after myotomy

Cricopharyngeal dysfunction: after myotomy, resolved (2 of 2)

After myotomy. The surgically divided muscle can no longer narrow the upper esophageal passageway, as seen by the widened stream of dark barium at the level of the muscle (arrows).

Cricopharyngeal dysfunction, before and after myotomy: Series of 2 photos

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VFSS of the neck while swallowing barium

Cricopharyngeal dysfunction: before myotomy (1 of 2)

Lateral x-ray of the neck while swallowing barium (the dark material seen here in the throat). The non-relaxing cricopharyngeus muscle (light-grey bulge outlined by a dotted line) is causing narrowing of the upper esophageal passageway, as highlighted by the narrowed stream of dark barium at that point (arrow). Liquids and very soft foods can squeak through this narrow opening, but solid foods tend to get stuck.
urgically divided muscle can no longer narrow the upper esophageal passageway

Cricopharyngeal dysfunction: after myotomy, resolved (1 of 2)

After myotomy. The surgically divided muscle can no longer narrow the upper esophageal passageway, as seen by the widened stream of dark barium at the level of the muscle (arrows).

Videos:

Barium Swallow (Barium Esophagram)
This video presents a clear visual example of a barium swallow, a test that involves having the patient swallow a barium solution while using x-rays to observe the flow of the barium, which can reveal swallowing deficiencies.
Cricopharyngeal Dysfunction: Before and After Cricopharyngeal Myotomy
This video shows x-rays of barium passing through the throat, first with a narrowed area caused by a non-relaxing upper esophageal sphincter (cricopharyngeus muscle), and then after laser division of this muscle. Preoperatively, food and pills were getting stuck at the level of the mid-neck, and the person was eating mostly soft foods. After the myotomy (division of the muscle), the patient could again swallow meat, pizza, pills, etc. without difficulty.


Viral Laryngitis

Infection or inflammation of the vocal cord mucosa, caused by viral infection. The mucosa becomes pink or red, and the normally thin mucus blanket increases in volume and can become more viscous. If the mucosa becomes sufficiently inflamed and edematous, an individual can lose his or her voice transiently (for one to three days, typically). An analogy for these tissue and secretional changes in the larynx is viral “pink-eye.” For treatment, antibiotics are of no benefit; instead, as the patient waits for the infection to pass, supportive measures such as voice rest and hydration are suggested.



Vocal aberration

A vocal event or phenomenon that is unexpected and abnormal. It is “something the voice does that it shouldn’t.” These sorts of findings, in combination with vocal capabilities and vocal limitations, are listened for during the vocal capability battery.



Vocal capabilities

Vocal capabilities refer to the full extent of the voice’s abilities in terms of loudness, range, steadiness and control, rapid repetitive sound-making, high soft singing, and so forth. Understanding of any voice’s capabilities (and limitations) requires much elicitation by the examiner. Also required is an understanding of expected capabilities for sex and age, so that an individual’s capabilities can be compared with what is expected.



Vocal capability battery

The vocal capability battery is a variable set of vocal tasks that the clinician elicits from the patient in order to understand the individual’s vocal capabilities and vocal limitations. During the vocal capability battery, the clinician might assess average/anchor pitch, maximum range, ability to add loudness, sustained phonation (for stability), swelling checks of mucosal injury, maximum phonation time, and response to brief trial therapy.



Vocal commitments

Events or circumstances that permit, invite, or demand much voice use. A person’s vocal commitments could include his or her occupation, childcare, rehearsals and performances, hobbies or even volunteer activities to which a person is highly committed, sports, and so forth. Heavy vocal commitments and innative talkativeness are the two potential sources of vocal overuse and, unsurprisingly, are often seen together.



Vocal Cord Bowing

“Bowing” is a descriptive term to specify that the vocal cords are not matching in a straight line, with only a thin dark line between them at the moment of pre-phonation. Instead, the cords become gently concave or bowed outwards. At the moment of pre-phonation, there is a wider, oval slit between the cords.

Bowing can be physiologic, asymptomatic, and a genetic “given.” In this physiologic type, the bowing will be subtle to mild and there will be good vibratory pattern. When moderate or severe, bowing may more likely be the result of aging, vocal disuse, Parkinson’s disease, or other conditions. Moderate and severe bowing correlate with a degree of vocal cord atrophy and the vibratory pattern can be more flaccid. The voice tends to have a soft-edged quality, a little higher in pitch than normal, and can fade with use. Voice building is the primary treatment, but very occasionally severe bowing is treated with bilateral vocal cord implants.


Photos:

Vocal Cord Bowing

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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.
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Vocal cords at the prephonatory instant

Vocal cord bowing (1 of 3)

Vocal cords at the prephonatory instant under standard light. Note the highly bowed glottic gap.
vibratory blur consistent with bowing

Vocal cord bowing (2 of 3)

After vibration begins. Note the very wide “vibratory blur,” consistent with bowing under standard light.
Open phase of vibration under strobe light

Vocal cord bowing (3 of 3)

Open phase of vibration under strobe light, showing unusually wide lateral excursions of the cords resulting from their flaccidity.
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Vocal cord bowing

Vocal cord bowing (1 of 2)

Vocal cord bowing, at the prephonatory instant.
Vocal cord bowing

Vocal cord bowing (2 of 2)

Immediately after phonation, showing better closure, but only due to vibratory blur.
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bowing at prephonatory instant

Vocal cord bowing (1 of 4)

Bowing of vocal cords as seen under continuous light, at prephonatory instant, just before vibratory blur.
bowing under strobe light

Vocal cord bowing (2 of 4)

Under strobe illumination, at maximum open phase (greatest lateral excursion).
Maximum closed phase of vibration

Vocal cord bowing (3 of 4)

Maximum "closed" phase of vibration, which is not fully closed; greatest medial vibratory excursion does not bring the cords into full contact.
Vocal cord bowing

Vocal cord bowing (4 of 4)

Due to vocal weakness, when effort is increased the false cords come into near contact, and can even add a rough second sound to the voice.
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Vocal cord bowing (1 of 4)

Prephonatory instant shows an oval gap between the cords, rather than a thin line.

Vocal cord bowing (2 of 4)

Bowing, as seen in abducted, breathing position.

Vocal cord bowing (3 of 4)

Strobe light, maximum closed phase, with poor closure especially anteriorly. The greater flaccidity anteriorly may cause an independent vibratory segment and chaotic vibration with rough, gravelly quality.

Vocal cord bowing (4 of 4)

Strobe light, maximum open phase of vibration.
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Bowed vocal cords

Vocal cord bowing (1 of 5)

Bowed vocal cords, abducted breathing position.
bowing of the musculomembranous

Vocal cord bowing (2 of 5)

As the cords begin to adduct, medial turning of vocal processes accentuates the bowing of the musculomembranous (anterior 2/3) of the vocal cords.
bowed free margins and an elliptical gap

Vocal cord bowing (3 of 5)

The prephonatory instant under continuous illumination, showing bowed free margins and an elliptical gap rather than the straight-line match of more normal vocal cords.
open phase of vibration

Vocal cord bowing (4 of 5)

Under strobe illumination, open phase of vibration.
cords' return to midline is flaccid

Vocal cord bowing (5 of 5)

Under strobe illumination, closed phase of vibration. The closure here isn't complete because the cords' return to midline is flaccid.

Bowing of vocal cords and effect of pitch

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prephonatory instant at a low pitch, D3

Weak voice (1 of 8)

This patient has a weak, air-wasting, and gravelly voice. In this distant view, prephonatory instant at a low pitch, D3 (147 Hz), severe bowing can be seen.
producing voice at D3

Phonatory view (2 of 8)

Also at D3 (147 Hz), but while producing voice. Note that the vibratory blur occurs only in the posterior membranous vocal cord.
closed phase at D3

"Closed" phase (4 of 8)

At D3 again, now closed phase, which is not closed except posteriorly, explaining the lack of vibratory blur anteriorly in photo 2. Some vibratory cycles are chaotic, too, explaining the gravelly, rough quality of the voice.
open phase of vibration

B3, open phase (5 of 8)

At B3 (247 Hz), open phase of vibration, the anteroposterior stretch required to produce higher pitch, also somewhat reduces the tissue flaccidity. Vibratory amplitude (lateral excursion) is diminished as well.
open phase of vibration at D3

D3, open phase (3 of 8)

Under strobe light, open phase of vibration at D3 (147 Hz), note that the amplitude of vibration is enormous, as the air stream easily throws flaccid vocal cords very far laterally.
Reduced closure anteriorly is typical for flaccid vocal cords

B3, closed phase (6 of 8)

At B3 again, closed phase of vibration is not really closed, yet is more successful than at the lower pitch in photos 3 and 4. Reduced closure anteriorly is typical for flaccid vocal cords.
Open phase of vibration at B-flat 4

Bb4, open phase (7 of 8)

Open phase of vibration at B-flat 4 (466 Hz). Added antero-posterior stretch subtly reduces vibratory amplitude further, especially anteriorly.
excess lateral amplitude anteriorly is no longer seen

Bb4, closed phase (8 of 8)

Closed phase at same pitch as photo 7, is not closed, but the excess lateral amplitude anteriorly is no longer seen.

Four views of vocal cord bowing in the same person

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bowed vocal cords at medium range in partial abduction

Bowed vocal cords (1 of 8)

An older man has a foggy voice, worsening with use. At medium range in partial abduction, note the bowed vocal cord margins.
large oval gap between the cords

Prephonatory view (2 of 8)

At a greater distance but at the prephonatory instant, there is a large oval gap between the cords.
lateral excursions of the cords are huge due to the flaccidity of the cords

Open phase (3 of 8)

Now under strobe light, at C3 (131 Hz). The lateral excursions of the cords are huge due to the flaccidity of the cords. Compare with photos 5 and 7.
closed phase of vibration is not fully closed

Gravel voice (4 of 8)

At the same pitch, the closed phase of vibration is not fully closed, and the anterior segment that remains open is often unstable and flutters or vibrates as an independent segment, causing ‘gravel.’
vocal cords must lengthen to produce this higher pitch of F#3

Reduced flaccidity (5 of 8)

The vocal cords must lengthen to produce this higher pitch of F#3 (185 Hz). Lengthening also reduces flaccidity, explaining reduced amplitude (lateral travel) of vibration. Compare with photo 3 and 7.
completely closed phase of vibration at F#3

Closed phase (6 of 8)

The closed phase of vibration, also at F#3, is completely closed, and the voice is more stable at this pitch. Compare with photo 4 and 8.
cords are stretched and thinned at B-flat 5

Falsetto, open phase (7 of 8)

Now at B-flat 5 (932 Hz), the cords are stretched and thinned. Amplitude is quite large, because falsetto tends to de-activate tension within the thyroarytenoid muscles. Compare with photos 3 and 5.
Closed phase of vibration at the same pitch in falsetto

Falsetto, closed phase (8 of 8)

Closed phase of vibration at the same pitch in falsetto is not closed at all for the same reasons described in the caption for photo 7. Compare with photos 4 and 6.

Red herring capillary ectasia and mucosal injuries

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Ectatic capillary (1 of 4)

This young performer has a sense of a weakened voice and loss of vocal stamina. Here, we see an ectatic capillary of the left vocal cord (right of photo). Is the problem intermittent vocal hemorrhage from this vulnerable capillary? Is there increased susceptibility to edema due to this margin capillary?

Ectatic capillary, narrow band light (2 of 4)

Under narrow band light, the capillary is even more evident. The additional network of prominent capillaries prompt the same questions as in caption 1.

Margin swelling (3 of 4)

Under strobe light at B-flat 4 (494 Hz), we see subtle margin swelling (arrows), here of only “indicator lesion” magnitude.

Bowing, atrophy, and flaccidity (4 of 4)

The large amplitude of the open phase of vibration at the same pitch, along with the lack of closure in photo 3, reveals the actual problem to be bowing, atrophy, and flaccidity. These findings fit with the “bowing” symptom complex: loss of edge to voice quality and the tendency of voice quality and strength to “fade” as the day progresses.

Glottic furrow—not just bowing and not glottic sulcus

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Bowing vocal cords with furrows

Bowing vocal cords with furrows (1 of 4)

This middle-aged man's voice has become increasingly husky and weak across many years. In retrospect, it was never a "strong" voice. The cords are bowed, and the furrows seen here (arrows) become more visible in subsequent photos.
Closed phase

Closed phase (2 of 4)

Under strobe light at B-flat 2 (117 Hz), this is the "closed" phase of vibration, perhaps better defined in this instance as the "most closed" phase.
Open phase

Open phase (3 of 4)

The open phase at the same pitch, shows a linear groove just below the margin of each cord. Some might call these glottic sulci, but "furrow" would be the better definition, as seen in the next photo.
Lower pitch reveals furrow

Lower pitch reveals furrow (4 of 4)

At lower pitch, the amplitude of vibration is larger and the right cord (left of photo) reveals more clearly that the the linear depression is a wide furrow, not a slit-like sulcus.

Voice Building:

Voice Building (shorter version):

 



Vocal Cord Bruising

The rupture of one or more capillaries in the vocal cords, so that blood leaks into the tissue. This vocal cord bruising occurs as a result of excessively vigorous mucosal oscillation, usually during extensive or vigorous voice use, aggressive coughing, or even a very loud sneeze, and it can make the voice hoarse or otherwise limited.

If the ruptured capillary is extremely superficial, like the capillaries seen on the white of the eye, then a “thin suffusion” kind of bruise occurs, and there is no deformity of the vocal cord margin; within a few days, the voice recovers. If the vessel is a few cell layers deeper into the cord, then a small “puddle” of blood like a micro-hematoma may collect and create a kind of “blood blister.” Although a superficial bruise resolves quickly and doesn’t seem to cause permanent damage, the “blood blister” type can become a hemorrhagic polyp and require surgery; with state-of-the-art surgery, however, the voice can virtually always be restored to its original capabilities.


Photos:

Vocal Cord Bruise / Hemorrhage, Before and After Rest and Surgery

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Vocal cord bruise / hemorrhage (1 of 4)

Bruise, right vocal cord (left of image), estimated one week old, in combination with large polypoid vocal nodules. Note the yellowish discoloration, indicating partial breakdown of the hemoglobin (source of red color of blood) into hemosiderin as bruise is beginning to be cleared away.

Vocal cord bruise / hemorrhage (2 of 4)

Same patient, during phonation.

Vocal cord bruise / hemorrhage, after rest and surgery (3 of 4)

Bruise was allowed to resolve, and then patient underwent vocal cord microsurgery one week prior to this examination.

Vocal cord bruise / hemorrhage, after rest and surgery (4 of 4)

Same patient, during phonation. Note the patient’s tendency to phonate with a gap between the cords, as though the vocal cords “remember” the early contact that used to require separation during voicing. This gap can be lessened through expert speech (voice) therapy.

Vocal Cord Bruise / Hemorrhage

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Vocal cord bruise / hemorrhage (1 of 2)

Bruise, left vocal cord (right of image), estimated three weeks old, in combination with vocal nodules, capillary ectasia. There is likely an ectatic capillary also on the same side, within the nodule, that is the source of the leaking of blood into the tissues. When the bruise first occurred, it would have been most evident in the area of the nodule. As time passes, the central part of the bruise typically resolves first, with the last area to disappear anterior and posterior, as shown here. Note also the faint yellowish discoloration of the left cord, indicating residual hemosiderin (breakdown products of blood in tissue).

Vocal cord bruise / hemorrhage (2 of 2)

Same patient during phonation under standard light.

Vocal Cord Bruise / Hemorrhage, Before and After Rest

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Vocal cord bruise / hemorrhage (1 of 6)

Breathing position, standard light. Notice a superficial bruise of the left cord (right of image), still very bright red. The source vessel cannot be identified with certainty here, but would be expected to be in the mid-cord, where the bruising is least evident. This is because mucosal oscillation tends to "massage" the bruise anteriorly and posteriorly, when the bruise is a thin-suffusion "wet pavement" type rather than a pocket or "puddle" of blood.

Vocal cord bruise / hemorrhage (2 of 6)

Prephonatory instant, standard light, shows that the margin of the left cord (right of image) is relatively straight. This suggests that the bruising is a very thin layer, and not a pocket of blood (as mentioned in photo 1).

Vocal cord bruise / hemorrhage (3 of 6)

Closer phonatory view, strobe light, also shows subtle elevation of the right cord (left of image), and a tiny ectatic capillary (small arrow), both of which can suggest that this person has been using the voice a lot. Left cord shows a darker linear bruise (larger arrow). After the bruising clears, perhaps it will become evident that this is in fact the ectatic capillary.

Vocal cord bruise / hemorrhage: after 2 weeks of rest (4 of 6)

After two weeks of relative voice rest, standard light. Notice the yellowish discoloration, which represents the breakdown products of hemoglobin. No obvious culprit capillary is seen. The last blood to resorb is always at the periphery from the point of origin.

After 2 weeks of rest (5 of 6)

Strobe light, open phase of vibration. No obvious ectatic vessel is seen, except for the vessel on the non-bruised side (at arrow) that was seen in photo 3.

After 2 weeks of rest (6 of 6)

Strobe light, closed phase, shows small margin swellings, greater on the left cord (right of image) than on the right cord. This swelling is being addressed by ongoing mild voice conservation, “on the fly” – i.e., while the person carries on with her work.

Bruise Caused by Cough

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Closer view of bruise (2 of 2)

A person with violent sensory neuropathic coughing may injure the vocal cords, as illustrated by this bruise, right vocal cord (left of photo).

Bruise caused by violent coughing (1 of 2)

Closer view of bruise, with small collection of white mucus in the middle.

Bruising from Sensory Neuropathic Cough

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Bruising from SNC (1 of 1)

This individual occasionally coughs to the point of hoarseness. Particularly noteworthy is the subglottic bruise (arrow, dotted line) caused by profound Valsalva-retching kind of coughing. The rest of the right cord (left of photo) is also bruised.

Vocal Cord Bruising From Coughing

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Bruise from coughing (1 of 3)

This man had an episode of aggressive coughing a week earlier. Note the bruising over the vocal processes, which receive the major collisional force during coughing.

Pre-phonatory instant (2 of 3)

The vocal processes are approaching the point of touching (contact would occur gently with onset of talking and more aggressively with coughing).

Phonation (3 of 3)

Vocal cords are now in full contact. Note the unrelated moderately-severe vocal cord bowing.

The Evolution of Vocal Cord Bruising and Emergence of a Vulnerable Capillary

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Margin swelling and bruising (1 of 2)

This professional woman is extraordinarily dynamic and intense, and must talk all day to do her work. Here, the right vocal cord (left of photo) is bruised due to vibratory trauma. The margin swelling on the right causes her hoarseness more than the bruising, however.

Six weeks later (2 of 2)

Six weeks later, the bruise is mostly resolved. The capillary that “leaked” blood to form the bruise is now seen more clearly (long arrow). This ectatic capillary can be seen easily now when looking back at photo 1. The short arrows indicate the residual “smudges” of discoloration caused by breakdown products of the bruise. The last evidence of widespread vocal cord bruising is always in these two locations.

Videos:

Nodules and Other Vocal Cord Injuries: How They Occur and Can Be Treated
This video explains how nodules and other vocal cord injuries occur: by excessive vibration of the vocal cords, which happens with vocal overuse. Having laid that foundational understanding, the video goes on to explore the roles of treatment options like voice therapy and vocal cord microsurgery.


Vocal cord dysfunction (VCD)

Vocal cord dysfunction (VCD). We refer to this disorder as nonorganic breathing disorder, laryngeal (see that entry for a fuller definition), which should be distinguished from nonorganic breathing disorder, tracheal.


Photos:

Nonorganic Breathing Disorder, Laryngeal

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Nonorganic breathing disorder, laryngeal (1 of 4)

Normal quiet breathing with vocal cords widely abducted.

Nonorganic breathing disorder, laryngeal (2 of 4)

Typical posture of vocal cord dysfunction, with vocal cords only slightly abducted.

Breathing (3 of 4)

If air is drawn into the lungs in this posture, the vocal cords are brought into vibration and make inspiratory phonation (see blurring of the margins).

Nonorganic breathing disorder, laryngeal (4 of 4)

For comparison, same patient, normal (expiratory) phonation.

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Nonorganic breathing disorder, laryngeal (1 of 3)

Nonorganic breathing disorder in a patient who makes loud inspiratory noise with athletic exertion. Images shows functional partial closure during inspiration as a nonorganic phenomenon.

Nonorganic breathing disorder, laryngeal (2 of 3)

Normal abduction of vocal cords with elicited sniffing.

Nonorganic breathing disorder, laryngeal (3 of 3)

Note the convexity and vibratory blurring of the free margins, correlating with inspiratory phonation.



Vocal Cord Paralysis, Bilateral

A neurological disorder in which the nerve supply to both vocal cords is absent. This may be as the result of injury through external trauma, thyroid surgery, or blunt or penetrating trauma to the neck. Sometimes vocal cord immobility due to scarring—from an endotracheal tube, for instance—is mistaken for vocal cord paralysis, though the distinction is usually easy to determine, provided that an appropriately intense and directed workup is done. In particular, this workup must include topical anesthesia to the larynx so as to enable an extremely close visualization of the posterior commissure and subglottis, which may uncover evidence of scarring.

See also: intubation injury, stenosis, vocal cord synechia, and vocal cord paralysis, unilateral.


Photos:

Bilateral Vocal Cord Paralysis

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Maximum space between cords (1 of 2)

After thyroidectomy many years earlier, the patient’s exercise tolerance became minimal without becoming short of breath and making loud inspiratory vocal sounds. Eventually, she underwent tracheotomy, which she has continued to wear for more than ten years. This view shows the maximum space between her vocal cords, which paradoxically occurs when she exhales.

View during inhalation (2 of 2)

When asked to inhale with tracheotomy tube momentarily plugged, the passing air causes the vocal cords to indraw slightly and come into vibration, creating “involuntary inspiratory phonation.” Note the faint convexity and grey blur where the mucosa is vibrating.

Mucosal Indrawing with Inspiration

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Paralyzed vocal cord (1 of 2)

Paralyzed right vocal cord, with bowing and atrophy. Here, the left vocal cord is maximally but incompletely abducted. Subtle markings are for reference with photo 2.

Indrawing with inspiration (2 of 2)

With elicited inspiration, the mucosa of the undersurface of both vocal cords indraws due to Bernouilli effect/ micro-vortices and further narrows the airway. At the same time, the patient involuntarily makes inspiratory voice.


Vocal Cord Paralysis, Unilateral

Neurogenic inability of one vocal cord to move. Unilateral vocal cord paralysis is associated with weak voice of a degree that can vary between individuals. Symptoms may include one or more of the following: weak, air-wasting dysphonia; inability to be heard in noisy locations; a tendency of the voice to be somewhat stronger in the morning but to “fade” with use; and a tendency to cough when drinking thin liquids.

See also: vocal cord paralysis, bilateral.


Photos:

Injection Laryngoplasty with Temporary Gel

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Laryngoplasty

Laryngoplasty (1 of 4)

This person awakened with a weak, whispery voice after emergency abdominal surgery. Now 3+ months later, voice is returning by degrees but is still very weak. In this photo, the patient is breathing quietly. The weak left vocal cord is more bowed than the right.
whispery air-wasting voice

Reason for air-wasting (2 of 4)

When she tries to produce voice, the left vocal cord comes only part of the way to the midline, leaving a large gap, and explaining her whispery air-wasting voice quality.
Voice gel injected into vocal cord

Voice gel injected into vocal cord (3 of 4)

On the same day, due to pressing patient need, the left vocal cord was “plumped” with voice gel. That material typically provides temporary benefit of 6 to 12 weeks, gradually absorbing during that time.
Vocal cords close completely

Vocal cords close completely (4 of 4)

Voice is dramatically improved, now that her vocal cords can more fully close to reduce the air-wasting and transform the voice from whispery to strong. Compare with photo 2.

Vocal Cord Paralysis

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Vocal cord paralysis (1 of 2)

Paralysis of left vocal cord (right of image), breathing position. Note that the left cord is bowed and atrophied as compared with the right.

Vocal cord paralysis (2 of 2)

Same patient during phonation, showing that the cords do not approximate; this correlates with a weak, breathy, air-wasting voice quality.

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Vocal cord paralysis (1 of 5)

This person has an extremely weak and air-wasting voice. Here, with the vocal cords in breathing position, the cause of this voice problem is not yet evident.

Phonation (2 of 5)

The cause of the problem is still not evident.

Closer view (3 of 5)

The explanation becomes more apparent. As will ultimately be seen, this patient has paralysis of the left vocal cord (right of image); that is, the TA, LCA, and PCA muscles on that side are all affected. Best seen here is evidence of TA weakness (bowing of free margin, loss of left cord bulk especially in the area of the “conus”, and enlarged ventricle). The cord is paramedian, suggesting that the PCA muscle is not working, too. The LCA muscle is hard to evaluate in this view, however.

Evidence of LCA weakness (4 of 5)

Phonation in the low chest register (note the wide zone of blurring of the vocal cord's free margin). Here, the vocal process is clearly seen to turn laterally ( arrow), indicating LCA weakness, in addition to the TA and PCA weakness seen in photo 3.

Phonation at very high pitch (5 of 5)

Phonation at very high pitch (thus, the vibratory blur narrows). The antero-posterior lengthening of the left cord at this high pitch turns the left vocal process back towards the midline (compare with photo 2), masking the LCA weakness. This low voice/high voice difference in the posterior commissure is routinely but not universally seen with LCA weakness.

Vocal Cord Paralysis, Before and After Medialization

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Vocal cord paralysis: before medialization (1 of 12)

A classic example of “spaghetti-linguine” vocal cords, here in breathing position. The “linguine” cord (left of image) is normal; the “spaghetti” cord (right of image) is paralyzed, likely since birth. On the paralyzed side, notice the deep and broad ventricle, mild bowing of the margin of the cord, and reduced width of the upper surface of the cord (“spaghetti”-like), as compared with the non-paralyzed side.

Vocal cord paralysis: before medialization (2 of 12)

Phonation, more distant view, under standard light. Notice the considerable gap between the vocal cords. This gap correlates with the patient’s weak and air-wasting voice quality.

Vocal cord paralysis: before medialization (3 of 12)

Open phase of vibration, under strobe light. The paralyzed cord (right of image) has a much increased amplitude (lateral or outward excursion) and exaggerated bowing, due to its flaccidity.

Vocal cord paralysis: before medialization (4 of 12)

“Closed” phase of vibration, which is of course not closed at all, because the paralyzed cord (right of image) cannot come fully to the midline.

Vocal cord paralysis: 1 week after medialization (5 of 12)

One week after surgical medialization of the paralyzed cord (right of image), using a silastic implant buried deeply within the cord. Notice that the ventricle is no longer capacious, and the free margin is no longer bowed. Furthermore, in contrast with photo 1 of this series, the “spaghetti-linguine” description of these vocal cords is no longer apt.

Vocal cord paralysis: 1 week after medialization (6 of 12)

Phonation, under standard light. The gap between the cords is no longer seen (compare with photo 2), and the patient's spontaneous speaking voice sounds normal. She can recruit loudness effectively without any luffing or observable weakness.

Vocal cord paralysis: 1 week after medialization (7 of 12)

Open phase of vibration, under strobe light. The lateral or outward excursion of the paralyzed cord (right of image) is now similar to that of the non-paralyzed cord. Compare with photo 3.

Vocal cord paralysis: 1 week after medialization (8 of 12)

The closed phase of vibration is much more closed than preoperatively. Compare with photo 4.

Vocal cord paralysis: 5 months after medialization (9 of 12)

Five months after medialization. Compare this partially abducted position with photos 1 and 5 of this series.

Vocal cord paralysis: 5 months after medialization (10 of 12)

Phonation, under standard light, showing vibratory blur. Compare with photos 2 and 6 of this series.

Vocal cord paralysis: 5 months after medialization (11 of 12)

Open phase of vibration, under strobe light. As in photo 7 of this series, and in contrast to photo 3, the implant does not permit the paralyzed cord (right of image) to “buckle” laterally, or outward. If anything, the vibratory excursion of the non-paralyzed (and un-implanted) cord is greater than that of the paralyzed, implanted cord.

Vocal cord paralysis: 5 months after medialization (12 of 12

The closed phase of vibration is now virtually normal, similar to photo 8 and in contrast with photo 4.

Extrusion of Vocal Cord Implant

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Extrusion of vocal cord implant (1 of 3)

Patient with a paralyzed left vocal cord (right of image), who several years ago had successful medialization of that cord with a silastic wedge. More recently, several months ago, she noticed pain and swelling during some intense aerobic activity and then a persistently roughened voice quality. This view shows that the left cord is inflamed.

Extrusion of vocal cord implant (2 of 3)

Strobe lighting. Note the convex shape of the left cord’s anterior end (the lower end, in this photo). This convexity is not caused by over-medialization, but instead by the inflammatory reaction.

Extrusion of vocal cord implant (3 of 3)

Closer view shows that the problem is exposure of the silastic implant. The actual silastic is bare at the arrow. Whitish exudate covers the remaining exposed implant. This is a rare event after medialization with a silastic implant.

Voice Gel for Immediate Help

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Paralysis of left vocal cord (1 of 4)

An older man with left vocal cord paralysis (right of photo) after chest surgery involving the upper mediastinum. This is maximum adduction at the prephonatory instant showing bowing and atrophy of the left cord (right of photo). Voice is exceedingly weak and air-wasting.

Vocal gel injection (2 of 4)

At the beginning of voice gel injection in a voice lab, with the patient sitting in an examination chair. The trajectory of the 27-gauge needle is indicated with the dotted line. A second bolus of gel will be injected farther posteriorly.

Cord closer to midline (3 of 4)

At the conclusion of the injection, the left cord has been plumped up and also shifted towards the midline.

Complete adduction of cords (4 of 4)

The vocal cords can close completely now for voice production. Voice is dramatically stronger and the patient can say many more words on a breath before running out of air.

TA + PCA-only Paresis

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Breathing position (1 of 5)

Abducted (breathing) position, shows the bowed contour of the left cord (right of photo), and loss of mass due to wasting of muscle within the cord. The left vocal process points medially ( see arrow), suggesting that the LCA muscle is still active.

Phonatory position (2 of 5)

During attempted phonation, note the gap (see arrows) that remains between the cords, accounting for her breathiness. In this view, vocal processes are reasonably antero-posterior in orientation, again suggesting good LCA function. In addition, note the lateral buckling of the left cord (right of photo), due to its flaccidity.

Voice gel injection (3 of 5)

At the moment just before voice gel injection into this flaccid cord. Blood is due to the cricothyroid membrane puncture moments before, for the purpose of providing topical anesthesia.

Plumped vocal cord (4 of 5)

Needle hub pulls the false cord laterally and true vocal cord is noticeably plumped up by the gel.

After voice gel injection (5 of 5)

Phonation, immediately after voice gel injection. Notice that the vocal cords come into much better contact. Voice is correspondingly dramatically improved.

55 Years of Paralysis with Every Classic Finding

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Breathing position, bowed left cord (1 of 4)

Drastically weak voice since age 21 in a man now in his upper seventies. Breathing position. The normal right cord (left of photo) is fully lateralized, has a relatively straight margin (see line) and conus muscle bulge (pinker undersurface of cord marked by “C”) is fairly full. The abnormal left cord (right of photo) is paramedian (slightly lateral to midline), bowed (see line), and its conus muscle bulge practically nonexistent (marked by "C").

Approaching voicing position (2 of 4)

Approaching voicing position under standard light. Right cord (left of photo) has come almost to midline. Vocal process points slightly medially (arrow). Left cord (right of photo) shows lateral pointing of vocal process (arrow), bowed margin (see line), and its ventricle is capacious. Ventricle extends laterally from dotted line on each cord.

Vocal cord closure, large gap (3 of 4)

Voicing under strobe light, at maximum vibratory closure. Large gap explains major air-wasting dysphonia. Note directionality of vocal processes that appear to indicate LCA is working on the right (left of photo), and is not on the left (right of photo); note also the bowing of the left cord (right of photo).

Open phase of vibration, flaccidity of right cord (4 of 4)

Open phase of vibration shows what appears to be flaccidity (very large lateral excursion) of the right (neurologically intact) cord (left of photo). Flaccidity in working cord is often seen: the question is whether that is functionally “necessary” to allow vibration. I.E. would a normally tensed cord fail to oscillate with so little “grip” of the airstream? Or is it flaccid due to age and lack of a working partner to help keep it strong?

Medialization Laryngoplasty Typically Doesn’t Fix the LCA “Finding.”

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Left vocal cord paralysis (1 of 4)

Many years after treatment for lung cancer, this man's voice has abruptly weakened. Here we see left vocal cord paralysis (right of photo). The most striking finding (of several) in this view is the margin bowing of the left cord (compare dotted lines, right of photo).

Bowing during phonation (2 of 4)

During phonation, the right vocal process (left of photo) turns medially due to intact LCA; on the left (right of photo), with LCA paralyzed, the vocal process turns laterally (compare posterior arrows).

After medialization (3 of 4)

A few months after medialization (an implant placed deep inside the left vocal cord), the left vocal cord margin is now straight rather than bowed (compare with photo 1).

Lateral turning remains unchanged (4 of 4)

During phonation, a striking change is the diminished gap between the cords, and this explains his much stronger voice. The lateral turning of the left vocal process (right of photo) is still seen, however. Medialization tends to “fix” the flaccidity and lateralization of the paralyzed vocal cord, and to reduce the gap between the cord. Compare with photo 2. As seen here, the lateral turning of the vocal process is still seen to some degree. If the voice were not so good and satisfying to the patient, this visual finding would be an argument for arytenoid adduction.

Voice Gel Injection for Vocal Cord Paralysis

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Left vocal cord paralysis (1 of 4)

This photo shows left vocal cord paralysis in the breathing position. Note the margin bowing, “spaghetti-linguini” difference in bulk, and capacious ventricle. Note: the * is for comparison with photo 3.

Voice-making position (2 of 4)

Here the paralysis is shown in the voice-making position. Note the lateral buckling of the left vocal cord (right of photo). This flaccidity and the gap between the vocal cords explain the patient’s breathy (air-wasting) voice quality.

Voice gel injection (3 of 4)

This is the same patient at the beginning of voice gel injection. Needle at arrow coming from subglottis upwards and laterally. At * one can see the beginning of bulging in the posterior ventricle. The vocal cord also looks slightly shifted towards the midline. Compare with photo 1.

After voice gel injection (4 of 4)

Voice-making position after voice gel injection is complete and bulge in ventricle at * is more evident. Closure is much better; the voice is dramatically stronger and the air-wasting quality much less. Compare with photo 2.

Posterior Commissure Synechiae

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Tethered vocal cords (1 of 5)

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

Before laser removal (3 of 5)

The thulium laser fiber (F) is touching the synechiae, with laser energy about to be delivered.

Immediately after laser (4 of 5)

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

One month post-op (5 of 5)

A month later, no residue of the synechiae is seen, and the vocal cords can spring farther apart than in photo 1.

Injection Medialization for Vocal Fold Paresis
See an example of one variant of vocal fold paresis and how it limits the voice. Then watch a medialization procedure in which voice gel is injected into the vocal fold affected by paresis, and hear how the voice thereafter improves.


Vocal Cord Paresis

Vocal cord paresis is the partial loss of voluntary motion for one or more of the muscles that move the vocal cords. Paresis is to be distinguished from paralysis, which refers to a complete loss of motion. Sometimes, however, the terms “paralysis” or “paralyzed” are used less precisely to encompass any kind of loss of motion, partial or complete. But we prefer the term “paresis” whenever it applies, and below we suggest a way to use this term when describing more complicated cases of vocal cords with reduced or no mobility.

Paresis or paralysis of a muscle or muscle group is caused by damage to its nerve supply. In other words, the underlying cause of a paretic or paralyzed muscle’s immobility is not a disorder of that muscle per se, but a disorder of the nerve supplying that muscle. Perhaps for this reason, it is common to speak of paralysis according to the nerve involved, rather than the muscle or muscles; in the world of laryngology, for example, we speak of “paralysis of the recurrent nerve.” However, it seems more logical to describe paralysis or paresis according to what is actually immobilized: the muscles. For example: if in a given case only the posterior cricoarytenoid (PCA) muscle is immobilized, then instead of calling that “paralysis of the recurrent nerve,” we would call it “PCA-only vocal cord paresis.”

In that example, though, some might wonder if it would be better for us to say “paralysis” instead of “paresis.” In other words, should we describe the nature of the immobility of the PCA muscle alone (so that, if the PCA is totally immobile, we would say “PCA-only vocal cord paralysis”) or that of the vocal cord’s entire set of muscles (which as a group is only partially immobile, so we would stick with “PCA-only vocal cord paresis”)? We think that, in general, it is more helpful to do the latter. To illustrate, here is an imaginary conversation: “Is this vocal cord paralyzed or paretic?” “Paretic.” “Which kind of paresis is it?” “PCA-only.”

It is surprisingly easy to diagnose the different variants of vocal cord paresis with a straightforward visual examination. Click on a particular variant to learn more:


Photos of TA + LCA vocal cord paresis:

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Paresis, TA + LCA (1 of 6)

Distant view shows lesser normal-appearing abduction left cord (right of image) during breathing, suggesting that the left posterior cricoarytenoid muscle is working. Note the lesser bulk of the left vocal cord as compared with the right, although this is subtle at this viewing distance.

Paresis, TA + LCA (2 of 6)

At closer range, still in breathing position, one can see more easily the “linguine” of the right vocal cord (left of image) compared with the “spaghetti” and slight bowing of the left. These findings correlate with left thyroarytenoid (TA) muscle weakness and atrophy.

Paresis, TA + LCA (3 of 6)

In phonatory position under strobe light, the bowing of the left cord (right of image) is more evident, as is the lateral turning of the left vocal process, consistent with weakness of the left lateral cricoarytenoid (LCA) muscle. Lines denote the direction each vocal process is pointing.

Paresis, TA + LCA: 1 week after implant is placed (4 of 6)

One week after placement of a large silastic implant into the left vocal cord (right of image). Notice the temporary eversion of the left ventricle, almost simulating a large polyp.

Paresis, TA + LCA: 3 months after implant is placed (5 of 6)

A few months later, fullness of left vocal cord (right of image) remains, but eversion / edema of ventricular mucosa has resolved. Compare with image 1.

Paresis, TA + LCA: 3 months after implant is placed (6 of 6)

During phonation, much better closure (with markedly improved voice) but still slightly lateral turning of the left vocal process (right of image). Compare with image 3.
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Panorama shows normally functioning PCA muscle (supplied by posterior branch), indicated by abduction of both vocal cords to a fully lateralized position.

Paresis, TA + LCA (2 of 8)

As vocal cords just begin to move to adducted, phonatory position, note that the left cord (right of image) leads medially with the tip of the vocal process, while right vocal process remains turned laterally due to paralysis of the LCA muscle.

Paresis, TA + LCA (3 of 8)

Close-up of posterior commissure during phonation shows continuing lateral pointing of the right vocal process (left of image), again due to a paralyzed LCA muscle.

Paresis, TA + LCA (4 of 8)

Panoramic view during phonation shows lateral buckling due to flaccidity of paralyzed TA muscle, left vocal cord (right of image).

Paresis, TA + LCA: voice gel injection (5 of 8)

A needle is being inserted into the TA muscle to inject voice gel as a temporary implant to plump up the cord so that the left cord (right of image) will be able to " reach" it during phonation—and also, to counteract the flaccidity seen in photo 4 above.

Paresis, TA + LCA: after voice gel injection (6 of 8)

After plumping of the right vocal cord (left of image) with voice gel is completed.

Paresis, TA + LCA: after voice gel injection (7 of 8)

Phonation after voice gel injection, standard light. Note better closure of the cords.

Paresis, TA + LCA: after voice gel injection (8 of 8)

Phonation under strobe light, open phase of vibration. This view shows that the voice gel has abolished the flaccidity seen above in photo 4.
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Paresis, TA + LCA (1 of 5)

Right vocal cord paresis (left of image). Note marked atrophy as compared with the left cord. Highly lateralized position denotes some persistent action of the right posterior cricoarytenoid muscle.

Paresis, TA + LCA (2 of 5)

Initiation of phonation. Note medical turning off left vocal process of arytenoid (right of image), and absent movement of the right vocal cord. Neither thyroarytenoid nor lateral cricoarytenoid muscles are innervated.

Paresis, TA + LCA: voice gel injection (3 of 5)

Immediately following injection of right vocal cord (left of image) with voice gel, with patient in videoendoscopy room chair, under topical anesthesia. Note bulging of right vocal cord.

Paresis, TA + LCA: 1 month after voice gel injection (4 of 5)

A month later, showing plumping up of the right vocal cord (left of image) with voice gel. Vocal cord continues to abduct fully, due to functioning posterior branch of recurrent nerve, which innervates the posterior cricoarytenoid muscle.

Paresis, TA + LCA: 1 month after voice gel injection (5 of 5)

Phonation. There is some movement to the midline due to the bilaterally innervated interarytenoid muscle. The lateral cricoarytenoid muscle is paralyzed, as seen in lateral turning of the vocal process. Voice is dramatically improved as compared with pre-injection. The voice gel will be expected to gradually absorb over three to nine months, during which time the anterior branch of the recurrent nerve may recover its function.
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Paresis, TA + LCA, with recovery (1 of 4)

Left vocal cord “paralysis” (TA, LCA, primarily, with suggestion of slight PCA activity). In breathing position, one can see the left cord (right of photo) bowing and the capacious ventricle, indicating TA weakness. Intermediate abducted position of left cord suggests some PCA function remains.

Paresis, TA + LCA, with recovery (2 of 4)

During phonation, lateral turning of the left vocal process (right of photo) indicates LCA weakness, as does the large phonatory gap.

Paresis, TA + LCA, with recovery (3 of 4)

Six weeks later, there is definite improvement of voice, though it remains abnormally weak. In this abducted (breathing) position, note that the left cord (right of photo) is less bowed and the ventricle is less capacious. This would be viewed as more than a “soft” finding, requiring skeptical, nuanced observation and some suspension. Compare with photo 1.

Paresis, TA + LCA, with recovery (4 of 4)

During phonation, one can see closer approximation. The vocal process on the left (right of photo) no longer turns laterally, even when using low pitch in an attempt to accentuate this finding.
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Paresis, right vocal cord

Vocal cord paresis (1 of 2)

Paresis, right vocal cord (left of image). Notice the slight loss of muscle bulk on the right cord as the upper surface dips subtly into the ventricle, whereas it remains a more flat upper surface farther laterally into the ventricle on the left.
ight vocal cord process turns slightly laterally due to LCA muscle weakness

Vocal cord paresis (2 of 2)

Phonation under strobe light: the right vocal cord process turns slightly laterally due to LCA muscle weakness. The membranous cord also buckles laterally due to its underlying TA muscle atrophy and flaccidity.
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Paresis, TA + LCA (1 of 7)

This patient has idiopathic right TA + LCA paresis. From a distant view, the unopposed pull of the right PCA (left of photo) can already be detected, but is better seen in the next photo.

Paresis, TA + LCA (2 of 7)

At closer range and in a breathing position, both PCA muscles work to fully lateralize the cords. The right (left of photo, in red) TA paralysis/atrophy is seen via a spaghetti-linguini difference in the cords and a larger, deeper right ventricle. Most notably, the right vocal process pulls laterally because the paralyzed LCA does not resist unopposed pull of the active PCA.

Paresis, TA + LCA (3 of 7)

Beginning to approach phonation position, the cords begin to move to the midline via function of the IA muscles, and the left cord (right of photo) reaches the midline via function of the left LCA muscle. Absent function of the right LCA and TA (left of photo) continues to be seen clearly in this view.

Paresis, TA + LCA (4 of 7)

During phonation, vibratory blur is seen under standard light, and lateral buckling of the flaccid right cord (left of photo).

Paresis, TA + LCA: after medialization (5 of 7)

Soon after a simple medialization of right cord (left of photo) with a silastic wedge, resulting in the plumpness of the right cord. Compare with photos 1 and 2.

Paresis, TA + LCA: after medialization (6 of 7)

Again beginning to approach phonation position. See again the plumpness of the right cord (left of photo). Compare with photo 3.

Paresis, TA + LCA: after medialization (7 of 7)

During phonation, there is much better contact between the cords, and the right cord (left of photo) is no longer flaccid. Compare with photo 4.
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TA weakness (1 of 4)

94 year-old with gradual weakening of voice across 2 years. Breathing (abducted) position shows left PCA muscle (right of photo) to be intact. In spite of distant view, spaghetti-linguini, capacious ventricle, and margin bowing are obvious indicators of TA weakness.

Prephonatory instant (2 of 4)

Prephonatory instant and distant view are inadequate to assess LCA, which preliminarily looks like it may be working; that is, the left vocal process (right of photo) initially looks to be pointing straight anteriorly.

LCA not working (3 of 4)

Prephonatory instant at closer range shows the classic lateral turning of vocal process showing LCA is in fact not working.

Phonatory blur (4 of 4)

During phonatory blur, one can see additional lateral buckling of the left cord (right of photo), due to TA flaccidity. The lesson: distal chip or fiberoptic scopes with topical anesthesia are required for best assessment of vocal cord paresis, despite the greater optical resolution of rigid telescopes.
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Intubation injury (1 of 4)

This young man was intubated for months at birth. For all of his life of more than 20 years, voice has been what he describes as “50%” of normal. Then after a recent URI, it descended to “20%. ” In this “breathing” position, one would say that abduction is normal, and evidence of intubation erosions is seen within dotted lines.

Forceful exhalation (2 of 4)

As he exhales forcefully, it appears that TA and LCA are normal on the left (right of photo). LCA cannot yet be evaluated on the right (left of photo). The medial dotted line indicates the free margin on each side, and the lateral one, the beginning of the ventricle. The posterior commissure divots are still seen (additional dotted lines).

Phonation begins (3 of 4)

As phonation begins, the flaccid right vocal cord (left of photo) buckles laterally. Posterior commissure visualization will add more information.

LCA (4 of 4)

The right vocal process (left arrow) turns laterally, suggesting that LCA is not working (along with previously-noted TA in photos 2 and 3). Left vocal process (right of photo) turns medially but the rest of the arytenoid more posteriorly appears to be eroded away as also seen in photos 1 and 2.

Photos of TA-only vocal cord paresis:

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Panoramic view of the larynx

Paresis, TA-only (1 of 3)

Panoramic view of the larynx with the cords in full abduction. Note the asymmetry — particularly the bowed free margin on left (right of image), and capacious ventricle.
paresis of TA muscle

Paresis, TA-only (2 of 3)

Close-up at near-closure for phonation. Equal bilateral adduction and matching angles of medial line of aytenoid cartilages demonstrates that LCA muscles are working bilaterally. This appears to be a paresis of TA muscle alone.
left cord bowing and capacious ventricle

Paresis, TA-only (3 of 3)

Close-up view, in abducted, breathing position. The "spaghetti" of the left cord (right of image) does not match the normal "linguini" of the right cord. Also, note the left cord bowing and capacious ventricle.
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Paresis, TA-only (1 of 5)

During abducted breathing position, note the atrophy of the left cord (right of image), mild margin convexity, and the capacious ventricle (at bottom-right), all of which indicate TA paresis. The cord abducts fully, demonstrating intact PCA fuction. LCA function cannot be determined in this view.

Paresis, TA-only (2 of 5)

Adducted position for phonation, with phonatory blurring as seen under standard light. LCA appears to be functioning, as indicated by the strict anterior-posterior direction of the left vocal process (right of image), just the same as for the right. This accounts for quite good approximation of the cords. The ventricle again appears capacious (dotted oval). Based upon these first two photos, we can surmise that this is a TA-only paresis.

Paresis, TA-only (3 of 5)

Under strobe light, showing increased amplitude of vibration of the left cord (right of image). This finding suggests in yet another way that the TA muscle is paralyzed.

Paresis, TA-only: after implant is placed (4 of 5)

After placement of an implant into the left cord (right of image). Note the bulging of that cord and straightening of the cord's margin, and also that the ventricle on that side no longer appears capacious. Compare with photo 1.

Paresis, TA-only: after implant is placed (5 of 5)

Under strobe illumination. Note that the lateral excursion of both cords is the same, since the left cord (right of image) is now less flaccid. Compare with photo 3

Photos of LCA-only vocal cord paresis:

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Phonation in the low chest register

LCA weakness, in a patient with vocal cord paralysis (1 of 2)

Phonation in the low chest register (note the wide zone of vibratory blurring). Here, the vocal process is clearly seen to turn laterally (arrow), a tell- tale indicator of LCA weakness. As other views of this particular patient would indicate, she actually also has weakness of the TA and PCA muscles, not just LCA-only paresis, but this view alone would correspond to a patient who had LCA-only paresis.
LCA weakness, masked by high pitch

LCA weakness, masked by high pitch (2 of 2)

Phonation at very high pitch (as expected, the vibratory blur narrows). The antero-posterior lengthening of the left cord (right of image) at this high pitch turns the vocal process on that side back towards the midline (compare with photo 1), masking the LCA weakness. This low voice/high voice difference in the posterior commissure is routinely but not universally seen with LCA weakness.

Photos of PCA-only vocal cord paresis:

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PCA muscle of the right vocal cord is not working

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

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.
no lateral turning of the vocal process

Paresis, PCA-only (3 of 4)

Strobe light, closed phase of vibration, again showing that there is no lateral turning of the vocal process.
The amplitude of vibration for each cord appears to be equal

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.
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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.