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:
SLAD-R: Series of 4 photos
Six years post SLAD-R (1 of 4)
Six years after SLAD-R performed elsewhere. Note that re-innervation appears greater for left (right of photo) than right (left of photo) thyroarytenoid (TA) muscle. Signs of continuing atrophy of the TA muscle within the right cord (left of photo) include capacious ventricle ('V'); absence of “conus” ('C') bulk below the free margin (see contrast between /--/ on both sides); slight concavity or bowing of the free margin; and narrower band of the vocal cord itself that we sometimes refer to as the “spaghetti-linguini” larynx.
TA + LCA muscles (2 of 4)
While TA is more recovered on the left (right of photo) as seen in photo 1, here we see that the lateral cricoarytenoid (LCA) muscle has recovered more on the right (left of photo). At the prephonatory instant, the failure of the left (right of photo) vocal process to turn to the midline indicates continuing weakness of the LCA muscle.
Greater amplitude of right cord (3 of 4)
Under strobe illumination, open phase of vibration shows greater amplitude of right cord (left of photo), consistent with the atrophy of the permanently somewhat weak TA muscle seen in photo 1.
Patient has returned to Botox (4 of 4)
Closed phase of vibration. A few years after SLAD-R, this man’s spasms recurred sufficiently that he has resumed Botox injections.
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, seen with pharynx contraction: Series of 2 photos
Pharyngeal paralysis (1 of 2)
View of the laryngopharynx. This patient has pharyngeal paralysis on one side, which is already slightly evident because the posterior pharyngeal wall's midline (dotted line) is deviating here slightly to one side, even at rest.
Pharyngeal paralysis, more obvious with pharynx contraction (2 of 2)
The pharynx is contracted, and the posterior pharyngeal wall (midline again at dotted line) now deviates dramatically toward the non-paralyzed side of the pharynx. This pharynx contraction was elicited via extremely high-pitched voicing.
Pharyngeal paralysis: Series of 1 photo
Pharyngeal paralysis (1 of 1)
Panorama of the laryngopharynx. Note the capacious left pyriform sinus (right of photo), one strong indicator of paralysis of the pharynx on that side.
Pharyngeal paralysis: Series of 1 photo
Pharyngeal paralysis (1 of 1)
Blue-stained water swallowed by the patient has preferentially pooled in the left pyriform sinus (right of image), due to weakness of the left inferior pharyngeal constrictors.
IA-only paresis refers to weakness or paralysis of the larynx’s interarytenoid (IA) muscle—an unpaired muscle spanning between the bodies of both arytenoid cartilages—but 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.
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: Series of 4 photos
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?: Series of 8 photos
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.
Bowing (2 of 8)
The abducted vocal cords for breathing show vocal cord bowing but otherwise nothing particularly noteworthy.
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.
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?
Posterior commissure (5 of 8)
Deep inside the posterior commissure during phonation. The large chink persists.
TA function (6 of 8)
Closed phase of vibration at B3 (247 Hz) shows good thyroarytenoid (TA) function.
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.
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: Series of 5 photos
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 (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.)
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 (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.)
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.
Voice change that accompanies Parkinson’s disease (PD) typically has two components. One component is a change to the “inner engine” of the voice. It is as if the inner motivation or vitality of communication or voice is damped down; think of the “motor” being limited mostly to “idle” rather than “first, second, third, and fourth” gears. When coaxed or even goaded to produce more vigorous voice, a person with advanced PD may find it hard to impossible (depending upon severity) to increase loudness. If the average person can “choose” vocal loudness settings of 1 through 5, it is as though levels 2 through 5 become inaccessible to the person with PD.
A second component of PD-related voice change is that the larynx becomes weak and atrophied. This is not surprising, since any body part will tend to atrophy if it is never used in a vigorous way. The phenomenology of PD-related voice change is that the voice is overly quiet and soft-edged, and though speech does not tend to become slurred, it can lose its crispness of articulation, and the pace of speech may diminish.
Photos:
Parkinson’s-related voice change: Series of 3 photos
Parkinson’s-related voice change (1 of 3)
Larynx of person with severe Parkinson’s disease; breathing position. Note the remarkable atrophy of the vocal cords, manifested in particular by the capacious ventricles (green dotted lines), the margin bowing (arrows), loss of “conus” bulk, and increased visibility of the contours of the vocal processes (blue dotted lines).
Parkinson’s-related voice change (2 of 3)
Phonatory (voicing) position. In addition to the bowing of the vocal cords, especially the left cord (right of image), note the slight scissoring of the left vocal process to overlap the right vocal process, as indicated by the arrows.
Parkinson’s-related voice change (3 of 3)
Cords coming into phonatory position, magnified view. Here can be seen even more clearly that, due to Parkinson’s-related atrophy, the contours of the vocal processes are more visible (blue dotted lines), like an emaciated person’s ribs. Note also that the LCA muscles have contracted slightly before the IA: the “toes” (T’s) of the arytenoid cartilages are in contact before the “heels” (H’s).
The combination of both abductor (AB) and adductor (AD) vocal cord spasms in a person who has spasmodic dysphonia (SD). Most individuals with SD have a predominance of one spasm type or the other—AB or AD—such that we classify the person as having either “AB-SD” or “AD-SD.” Some individuals, however, have a significant amount of both types of spasms. That is, a person experiences phonatory arrests or squeezedowns caused by AD spasms, followed suddenly by dropouts to a whisper caused by AB spasms. This kind of person is described as having “mixed AB-AD spasmodic dysphonia.”
Treatment for SD usually involves two-muscle Botox injections: for AD-SD, injecting into both of the thyroarytenoid muscles; for AB-SD, into both of the posterior cricoarytenoid muscles. Treatment for mixed AB-AD SD usually begins with the two muscles causing spasms of which the patient is most aware; if the results are not satisfactory (often because the untreated kind of spasms come to the fore without competition from the other kind of spasms), some of these patients are then eventually treated with four-muscle injections.
The ability to relate to one’s voice and to hear and experience it insightfully. Vocal self-rapport includes being self-aware of pitch, effort level, quality, loudness, etc. Accomplished singers may have exquisite vocal self-rapport, being able to match pitch and be aware of vowel color, larynx position in the neck, and other kinesthetic feedback. At the other end of the spectrum, a small percentage of individuals have remarkably limited vocal self-rapport. Such individuals may not be able to match pitch. In addition, they may not even perceive the difference between an upward and downward vocal siren.
For a clinician, assessing the vocal capabilities of a patient without vocal self-rapport can be difficult, because such a patient may not be able to respond correctly to elicited vocal tasks which could otherwise reveal vocal limitations or aberrations. Furthermore, it can be difficult for a speech/voice therapist to shape or modify inappropriate voice production because, though the patient’s hearing may be normal, he or she may yet struggle to “hear” with any insight. That is, the patient can struggle to understand what is being asked of them during speech therapy, or to identify whether or not changes he or she makes to voice production are on target.
A non-life-threatening neurological disorder in which the muscles of the larynx involuntarily spasm and interfere with the voice. Spasmodic dysphonia (SD) is a focal dystonia, in this case involving the larynx—i.e., laryngeal dystonia. Laryngeal dystonia typically affects the voice, but can occasionally also affect breathing (respiratory dystonia). The term spasmodic dysphonia refers specifically to voice-affecting laryngeal dystonia.
Adductor vs. abductor:
There are two main variants of spasmodic dysphonia (SD). In the first variant, adductor SD (AD-SD), the vocal cords are pressed together excessively, intermittently cutting off words or giving the voice a constant strangled quality; this variant comprises 90% of the cases of SD. In the second variant, abductor SD (AB-SD), the vocal cords are abruptly and momentarily pulled apart while talking, causing the voice to drop out completely or down to a whispery, breathy sound. There are some cases in which a person has both of these variants: this is called mixed AB-AD SD.
Classic vs. tonic:
Another distinction that can be made is between classic variant and tonic variant cases of SD. In classic variant SD, the spasms cause phonatory arrests—that is, while the person is speaking, intermittent words or syllables are choked off (with AD-SD) or drop out (with AB-SD). In tonic variant SD, the spasms are more continuously sustained, so that the voice continuously sounds either strained (with AD-SD) or breathy (with AB-SD), but without any actual phonatory arrests. Because the presence of phonatory arrests is the symptom most often associated with SD, tonic variant SD goes undiagnosed or misdiagnosed far more frequently than does classic variant SD.
Treatment for spasmodic dysphonia:
There is no definitive “cure” for SD, but for most patients, periodic injections of Botox™ into the muscles of the larynx help a great deal, if there is optimal dosage and placement. These injections relax the malfunctioning muscles of the larynx, thereby minimizing the spasms and their impact on the voice. The effect of an injection typically lasts a few months, and then another injection is needed. For those having difficulty getting good results with Botox™ therapy, see our video below “Spasmodic Dysphonia: When Botox Disappoints.”
The leading surgical treatment currently offered for SD, Selective Laryngeal Adductor Denervation-Reinnervation, can be an option for individuals with the AD-SD variant. However, no treatment for SD works satisfactorily for all. The history of each of the several surgical treatments for SD always includes some failures.
Speech therapy is another treatment sometimes suggested for SD. While there are strong and even passionate individual proponents of speech therapy, the consensus view is that speech therapy is not expected to substantially improve the voice’s capabilities or reduce spasms other than perhaps in the therapy room ((Ludlow CL. Treatment for spasmodic dysphonia: limitations of current approaches.Curr Opin Otolaryngol Head Neck Surg. 2009; 17(3): 160–165.)). A brief course of speech therapy can be very helpful for patient education and perhaps a search for sensory tricks. Much confusion surrounds this subject, because individuals who have a nonorganic voice disorder can be mistakenly diagnosed with SD, and nonorganic voice disorders are routinely “cured” with speech therapy alone.
Photos:
Adductory spasmodic dysphonia: Series of 2 photos
AD-SD (1 of 2)
Sustained, clear phonation, standard light. Note vibratory blur of the vocal cord margins. The false vocal cords (lines) are in normal relation to the true vocal cords.
AD-SD (2 of 2)
Involuntary adductory spasm. Note that the false vocal cords suddenly over-close (arrows) as a result of the adductory spasm, and voice momentarily stops (along with vibratory blur).
Abductor spasmodic dysphonia: Series of 4 photos
AB-SD (1 of 4)
Prephonatory instant, with arytenoid cartilages involuntarily positioned apart. Mostly tonic position giving voice relatively constant breathiness.
AB-SD (2 of 4)
Phonatory blur, standard light. Again note the separation of the arytenoid cartilages posteriorly (upper end of the photo), and broad vibratory blur, both consistent with breathy voice.
AB-SD (3 of 4)
Occasionally, patient is able to bring posterior cords together for an instant of normal-sounding voice.
AB-SD (4 of 4)
An instant later, the vocal cords involuntarily separate due to an abductory spasm, dropping the voice again to a whispery quality.
Abductor spasms, worsened by cognitive loading: Series of 4 photos
Abductor spasmodic dysphonia patient (1 of 4)
Vocal cords in normal breathing position, in a person with abductor spasmodic dysphonia (SD). The next three photos show how the vocal cord spasms seen with SD can get worse when the person performs more cognitively loaded or involved tasks (that is, the person has to think more). This pattern is related to the widespread understanding that SD's symptoms can be task-specific.
Limited abductor spasms (2 of 4)
When making voice with guttural vocal fry or sustained creaky falsetto, this person is able to keep the vocal cords together, at least part of the time.
Increased abductor spasms (3 of 4)
When the person tries to sustain a sung tone (slightly more cognitively loaded), the vocal cords involuntarily separate, producing a very breathy voice.
Even greater abductor spasms (4 of 4)
When the person speaks (even more cognitively loaded), the vocal cords separate even further, and the voice's breathiness is pronounced.
Adductory spasm: Series of 2 photos
Adductory spasm (1 of 2)
Continuous phonation, standard light. Note the position of the false cords in relation to each other, and also the distance between the anterior face of the arytenoids and the petiole of the epiglottis.
Adductory spasm (2 of 2)
A moment later, an adductory spasm occurs. The spasm may momentarily stop the voice (phonatory arrest). Note the inward squeezing of the entire supraglottis (false cords, arytenoids, and petiole).
Laryngology 401: PCA-only paresis, but the actual voice problem is spasmodic dysphonia: Series of 3 photos
Sense of instability (1 of 3)
This person had a major voice change after thyroidectomy for a large goiter. Within 2 months, voice recovered fully--except for a sense of instability. The PCA-only paresis is not the explanation because voice-making muscles (TA + LCA) are intact. And in fact vocal capability testing shows that both yell and projected voice are normal. The visual finding here of vocal cord bowing and capacious ventricle do not count as a breathing position finding with PCA-only paresis due to the unopposed action of LCA muscle, combined with an uncontracted TA muscle, both of which cause pseudo-bowing.
Vibratory amplitude (2 of 3)
During phonation under strobe light, with TA tensing, "bowing" disappears. Furthermore the vibratory "blur" at the margin of the left fold (right of photo) is equal to the right (left of photo), telling us that vibratory amplitude is approximately the same on both sides.
Spasm (3 of 3)
An audible/ visible spasm occurs when the right vocal cord jerks laterally for 4 frames (~ 1/8th of a second). The problem isn't PCA weakness on the left (right of photo), but instead an abductory spasm on the right (left of photo), fully mobile cord!
Remarkable task-specificity of spasmodic dysphonia: Series of 4 photos
Young singer (1 of 4)
This young soprano has had to put singing to the side due to a peculiar instability at a very specific part of her singing range: approximately G4 to B4. Speaking voice is completely normal. Above and below G4 to B4 the voice works well. Here, during somewhat distant view during breathing, no mucosal abnormality is seen.
Phonation (2 of 4)
During phonation at high pitch designed to reveal margin swelling, there is a slight gap of “physiologic bowing” but arytenoids seem to approximate well.
Closed phase (3 of 4)
Closed phase of vibration at G4 (392 Hz). Nothing significant is seen in this admittedly somewhat distant view.
Sudden spasm (4 of 4)
Ten frames, a fraction of a second-later, a sudden spasm is seen (arrows) and heard. This adductory spasm happens consistently and repeatedly with numerous elicitations, but only in the narrow pitch range already noted in caption 1.
Assessment of vocal phenomenology protects from visual red herrings: Series of 2 photos
Swelling? (1 of 2)
The vocal cords of a physical education teacher with mild, intermittent ‘hoarseness’ and cracking of voice. Given her occupation, the mind goes to “voice abuse” and the margin swelling seen here might play into the diagnosis of “vocal overdoer with mucosal injury.” However, the vocal capability battery (voice testing) protects from a misdiagnosis.
Spasmodic dysphonia (2 of 2)
During the vocal capability testing (part 2 of the Integrative Diagnostic Model), one hears no significant mucosal swelling phenomenology (during application of vocal cord swelling checks), but instead a quivery, jittery instability. The actual diagnosis? Spasmodic dysphonia.
Spasmodic Dysphonia: A Peculiar Voice Disorder
Dr. Robert Bastian reviews the various types and subtypes of spasmodic dysphonia (SD). Numerous voice examples are included, along with video of the vocal folds. SD is a rare neurological disorder caused by laryngeal dystonia, and it interferes with the smooth functioning of the voice. Tiny spasms of the vocal folds may cause the voice to catch or cut out, strain or squeeze away, and sometimes to drop momentarily to a whisper.
Spasmodic Dysphonia: When Botox Disappoints
In this video, Dr. Bastian discusses common problems with Botox treatment for spasmodic dysphonia (SD) and offers clear, practical advice to increase the effectiveness of these treatments.
2014 NSDA 25th Anniversary Symposium
In this video, Dr. Bastian leads a panel discussion on Spasmodic Dysphonia.
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:
Paresis, TA + LCA, before and after placement of an implant: Series of 6 photos
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.
Paresis, TA + LCA, before and after injection of voice gel: Series of 8 photos
Paresis, TA + LCA (1 of 8)
Panorama shows normally functioning PCA muscle (supplied by posterior branch), indicated by abduction of both vocal cords to a fully lateralized position.
Paresis, TA + LCA (2 of 8)
As vocal cords just begin to move to adducted, phonatory position, note that the left cord (right of image) leads medially with the tip of the vocal process, while right vocal process remains turned laterally due to paralysis of the LCA muscle.
Paresis, TA + LCA (3 of 8)
Close-up of posterior commissure during phonation shows continuing lateral pointing of the right vocal process (left of image), again due to a paralyzed LCA muscle.
Paresis, TA + LCA (4 of 8)
Panoramic view during phonation shows lateral buckling due to flaccidity of paralyzed TA muscle, left vocal cord (right of image).
Paresis, TA + LCA: voice gel injection (5 of 8)
A needle is being inserted into the TA muscle to inject voice gel as a temporary implant to plump up the cord so that the left cord (right of image) will be able to "reach" it during phonation—and also, to counteract the flaccidity seen in photo 4 above.
Paresis, TA + LCA: after voice gel injection (6 of 8)
After plumping of the right vocal cord (left of image) with voice gel is completed.
Paresis, TA + LCA: after voice gel injection (7 of 8)
Phonation after voice gel injection, standard light. Note better closure of the cords.
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.
Paresis, TA + LCA, before and after injection of voice gel: Series of 5 photos
Paresis, TA + LCA (1 of 5)
Right vocal cord paresis (left of image). Note marked atrophy as compared with the left cord. Highly lateralized position denotes some persistent action of the right posterior cricoarytenoid muscle.
Paresis, TA + LCA (2 of 5)
Initiation of phonation. Note medical turning of left vocal process of arytenoid (right of image), and absent movement of the right vocal cord. Neither thyroarytenoid nor lateral cricoarytenoid muscles are innervated.
Paresis, TA + LCA: voice gel injection (3 of 5)
Immediately following injection of right vocal cord (left of image) with voice gel, with patient in videoendoscopy room chair, under topical anesthesia. Note bulging of right vocal cord.
Paresis, TA + LCA: 1 month after voice gel injection (4 of 5)
A month later, showing plumping up of the right vocal cord (left of image) with voice gel. Vocal cord continues to abduct fully, due to functioning posterior branch of recurrent nerve, which innervates the posterior cricoarytenoid muscle.
Paresis, TA + LCA: 1 month after voice gel injection (5 of 5)
Phonation. There is some movement to the midline due to the bilaterally innervated interarytenoid muscle. The lateral cricoarytenoid muscle is paralyzed, as seen in lateral turning of the vocal process. Voice is dramatically improved as compared with pre-injection. The voice gel will be expected to gradually absorb over three to nine months, during which time the anterior branch of the recurrent nerve may recover its function.
Paresis, TA + LCA, with recovery: Series of 4 photos
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.
Vocal cord paresis: Series of 2 photos
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.
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.
Paresis, TA + LCA, before and after medialization: Series of 7 photos
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.
Telescope panoramic views are routinely not adequate for assessing paresis!: Series of 4 photos
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.
Forcing the larynx to give up its (paresis and intubation injury) secrets: Series of 4 photos
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:
Paresis, TA-only: Series of 3 photos
Paresis, TA-only (1 of 3)
Panoramic view of the larynx with the cords in full abduction. Note the asymmetry — particularly the bowed free margin on left (right of image), and capacious ventricle.
Paresis, TA-only (2 of 3)
Close-up at near-closure for phonation. Equal bilateral adduction and matching angles of medial line of aytenoid cartilages demonstrates that LCA muscles are working bilaterally. This appears to be a paresis of TA muscle alone.
Paresis, TA-only (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.
Paresis, TA-only: before and after an implant: Series of 5 photos
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:
LCA weakness: Series of 2 photos
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 (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:
Paresis, PCA-only: Series of 4 photos
Paresis, PCA-only (1 of 4)
PCA muscle of the right vocal cord (left of image) is not working. TA and LCA are perceived as intact, based on the combination of: 1) normal voice; 2) the right cord is not bowed; 3) ability to medially turn or at least keep in line the right vocal process (see also photo 2); and 4) the right cord is not atrophied, nor is the right ventricle unusually capacious.
Paresis, PCA-only (2 of 4)
During phonation, there is no sign of lateral turning of the right vocal process, which would indicate LCA weakness. Furthermore, vibratory blurring (in this standard-light view) appears to be fairly equal on each side, suggesting there is no flaccidity of the right cord, contrary to what one would expect were the TA weak on that side.
Paresis, PCA-only (3 of 4)
Strobe light, closed phase of vibration, again showing that there is no lateral turning of the vocal process.
Paresis, PCA-only (4 of 4)
Strobe light, open phase of vibration. The amplitude of vibration for each cord appears to be equal, just as it did (based on blurring) in photo 2. This finding confirms that the TA is not weak, as such weakness would make the right cord flaccid and increase its amplitude of vibration.
PCA-only paresis years after thyroid lobectomy: Series of 6 photos
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.
Photos of IA-only vocal cord paresis:
IA-only paresis: Series of 5 photos
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.
Another interarytenoid (IA) muscle paresis or is it avulsion?: Series of 8 photos
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.
Bowing (2 of 8)
The abducted vocal cords for breathing show vocal cord bowing but otherwise nothing particularly noteworthy.
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.
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?
Posterior commissure (5 of 8)
Deep inside the posterior commissure during phonation. The large chink persists.
TA function (6 of 8)
Closed phase of vibration at B3 (247 Hz) shows good thyroarytenoid (TA) function.
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.
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: Series of 5 photos
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 (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.)
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 (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.)
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.
Videos:
Injection Medialization for Vocal Cord Paresis
See an example of one variant of vocal cord paresis and how it limits the voice. Then watch a medialization procedure in which voice gel is injected into the vocal cord affected by paresis, and hear how the voice thereafter improves.
Weakness or paralysis of the vocal cord’s posterior cricoarytenoid (PCA) muscle, but with normal function of the vocal cord’s other muscles. The PCA muscle abducts (lateralizes) the vocal cord for breathing. The following are indicators of PCA-only paresis:
Movement: The vocal cord closes normally for voicing, but it does not abduct for breathing. It remains motionless at the midline.
Position and appearance: Position is normal during phonation, but the vocal cord does not open (lateralize) for breathing. Because the cord does not appear to move (it adducts or closes normally, but from an already-adducted position), PCA-only paresis is often mistaken for complete vocal cord paralysis—TA (thyroarytenoid), LCA (lateral cricoarytenoid), and PCA. Key points of difference between PCA-only paresis and complete paralysis are that, in the former case, the tip of the vocal process is in a normal medial position and the vocal cord has normal bulk and tone.
Appearance during voicing (under strobe lighting): Completely normal, because the adductors of the cord (TA and LCA muscles) are intact. Hence, as with a normal cord, there is no flaccidity or asymmetry of vibration.
Voice quality: Entirely normal. Many individuals are told this is due to “compensation” of the opposite cord, but actually it is because the muscles used for voicing (TA + LCA) are intact.
Paresis, PCA-only (1 of 4)
PCA muscle of the right vocal cord (left of image) is not working. TA and LCA are perceived as intact, based on the combination of: 1) normal voice; 2) the right cord is not bowed; 3) ability to medially turn or at least keep in line the right vocal process (see also photo 2); and 4) the right cord is not atrophied, nor is the right ventricle unusually capacious.
Paresis, PCA-only (2 of 4)
During phonation, there is no sign of lateral turning of the right vocal process, which would indicate LCA weakness. Furthermore, vibratory blurring (in this standard-light view) appears to be fairly equal on each side, suggesting there is no flaccidity of the right cord, contrary to what one would expect were the TA weak on that side.
Paresis, PCA-only (3 of 4)
Strobe light, closed phase of vibration, again showing that there is no lateral turning of the vocal process.
Paresis, PCA-only (4 of 4)
Strobe light, open phase of vibration. The amplitude of vibration for each cord appears to be equal, just as it did (based on blurring) in photo 2. This finding confirms that the TA is not weak, as such weakness would make the right cord flaccid and increase its amplitude of vibration.
PCA-only paresis years after thyroid lobectomy: Series of 6 photos
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.
Left PCA-only paresis: Series of 4 photos
Abducted breathing position (1 of 4)
As the patient is taking a breath, only the right cord (left of photo) abducts (though not yet fully in this photo). Left cord (right of photo) remains at midline and vocal process remains in line with the membranous cord, suggesting that the LCA muscle on the left (right of photo) is working.
Full approximation of cords, TA is intact (2 of 4)
Full approximation of the cords, and furthermore there is no enlargement of the ventricle (at 'X') and this also suggests left TA muscle is also intact.
Phonation, LCA is intact (3 of 4)
The posterior commissure during phonation. Note that there is no lateral turning of the vocal process, validating that the left LCA muscle (right of photo) is intact.
Phonation under strobe light, PCA-only paresis (4 of 4)
During phonation, strobe light, open phase of vibration. Left TA (right of photo) function again validated in that the amplitude of vibration on the left (right of photo) is not greater than on the right (left of photo). If the left TA muscle were paralyzed, then the amplitude on the left (right) would be greater than on the right (left).
Sharp observation required to sort out this PCA-only paresis and cancer scar combo: Series of 4 photos
Unequal lateralization (1 of 4)
The vocal cords appear equally lateralized, but are not. The right one (left of photo) is paramedian and does not abduct, and the left (right of photo) is abducted, and moves to the midline with phonation, as seen in photos 3 and 4.
PCA not working (2 of 4)
Shifting the view posteriorly, it is easier to see that the right PCA muscle does not work, and without its lateralizing pull, the unopposed LCA muscle turns the vocal process sharply medially (arrow). Right TA is intact despite pseudobowing, caused here by exaggerated LCA action.
Phonation, closed phase (3 of 4)
Under strobe light. The vocal cords push against each other equally, and IA muscle pulls the “heels” of both arytenoid cartilages together, causing the right vocal process (left of photo) to point anteriorly, just like on the left (right of photo).
Phonation, open phase (4 of 4)
Open phase of vibration. Amplitude of vibration is greater on the right (left of photo) but not due to TA muscle atrophy, but instead as a result of mucosal stiffness on the left (right of photo) The explanation: superficial laser cordectomy performed years earlier for early cancer. Medial-to-lateral capillary reorientation is the visual clue of mucosal regeneration/ scarring.
Classic findings again of PCA-only paresis: Series of 4 photos
Post thyroidectomy (1 of 4)
After thyroidectomy, this individual’s voice was breathy for several months postoperatively, but then recovered fully. Yet, her right vocal cord appears to be paralyzed, rather than paretic. Here note that PCA on the left (right of photo) pulls that (normal) cord fully laterally, while the right cord (left of photo) remains midline and with slight medial turning of the vocal process to suggest right LCA muscle is intact.
Phonatory view (2 of 4)
Making voice under standard light, the cords appear to close at the midline, consistent with intact IA and bilaterally intact LCA muscles. Equal vibratory blur between the two sides suggests that the both TA muscles are also intact.
LCA and TA muscles working (3 of 4)
Under strobe light, closed phase of vibration: Medial compression appears equal and the vocal processes (indicated by lines) point straight anteriorly, again confirming that both LCA muscles are working, and suggesting that both TA’s are also working.
PCA-only paresis (4 of 4)
Open phase with equal amplitude (lateral excursion) of vibration of both cords, indicating that the TA muscle is not atrophic or flaccid. Put all of the above findings together, and this is classic PCA-only paresis of the right vocal cord.
A mediocre examination for paresis: Series of 3 photos
PCA not working, TA is weak (1 of 3)
The patient reported a voice quality of about "50%" after neck surgery a few months earlier and has (so far) recovered to "75%." The patient's difficulty tolerating the examination despite extensive topical anesthesia results in incomplete (though sufficient) information. Here it appears that PCA is not working on the right (left of photo), as the vocal cord position is paramedian rather than fully lateralized. Right TA muscle (left of photo) appears weak, too, as indicated by "spaghetti-linguini" bulk asymmetry (brackets), mild vocal cord bowing (dotted line) and capacious right ventricle (left of photo). This view does not permit evaluation of conus for atrophy, nor of LCA function.
LCA recovered (2 of 3)
Visual finding of full closure during phonation in this distant view, along with good ability to increase loudness at low pitch without audible luffing both suggest but do not prove that LCA is likely recovered, and also that there is some tone in the atrophied TA muscle.
TA partially recovered (3 of 3)
A sub-optimal view of open phase of vibration also suggests that the TA muscle is partially recovered. In all, this is a barely-adequate examination but when an examiner can invest deeply in subtle and even distant findings, an examination such as this that does not meet an examiner's standard of quality, can yet suffice for diagnosis and treatment planning.
Laryngology 401: PCA-only paresis, but the actual voice problem is spasmodic dysphonia: Series of 3 photos
Sense of instability (1 of 3)
This person had a major voice change after thyroidectomy for a large goiter. Within 2 months, voice recovered fully--except for a sense of instability. The PCA-only paresis is not the explanation because voice-making muscles (TA + LCA) are intact. And in fact vocal capability testing shows that both yell and projected voice are normal. The visual finding here of vocal cord bowing and capacious ventricle do not count as a breathing position finding with PCA-only paresis due to the unopposed action of LCA muscle, combined with an uncontracted TA muscle, both of which cause pseudo-bowing.
Vibratory amplitude (2 of 3)
During phonation under strobe light, with TA tensing, "bowing" disappears. Furthermore the vibratory "blur" at the margin of the left fold (right of photo) is equal to the right (left of photo), telling us that vibratory amplitude is approximately the same on both sides.
Spasm (3 of 3)
An audible/ visible spasm occurs when the right vocal cord jerks laterally for 4 frames (~ 1/8th of a second). The problem isn't PCA weakness on the left (right of photo), but instead an abductory spasm on the right (left of photo), fully mobile cord!
Test your mastery of visual nuances of paresis with this case: Series of 4 photos
LCA working, TA partially working (1 of 4)
Many years earlier, this man had thoracic surgery for patent ductus arteriosis repair. Immediately postoperatively, voice was down to “20%.” Within several months it had recovered to about “50%” where it has remained for 30 years. Two notable findings: bowing of left vocal cord (right of photo) along with subtle twitching, but without a significant “spaghetti” sign of atrophy as compared with the right, and medial turning of the left vocal process (right of photo). The conclusion: LCA appears to be working, and TA is working at least partially.
Closer view (2 of 4)
Close visualization of the posterior commissure during “sniff” confirms that PCA is not working on the left (right of photo); LCA action is confirmed with exaggerated medial turning of the vocal process.
Closed phase (3 of 4)
Under strobe light, showing closed phase at low pitch. Posterior folds close completely, confirming LCA function. The left vocal cord (right of photo) looks to be at a slightly lower level, confirming at least some level of atrophy.
Open phase (4 of 4)
Open phase of vibration shows larger amplitude of vibration of left vocal cord (right of photo). Putting all of these findings together in big picture terms: LCA is working “fully,” TA partially, and PCA not at all.
PCA-only paresis of right vocal cord and normal voice: Series of 3 photos
(1 of 3)
After neck surgery, this person's voice was grossly abnormal (weak, whispery) for several months. Now voice is normal, and the patient is being seen only for laryngopasm. In this view, the right vocal cord (left of photo) is midline, because the PCA muscle on that side is not working to lateralize it. This suggests that the posterior branch of the recurrent laryngeal nerve has not recovered.
(2 of 3)
Closed phase of vibration under strobe light shows that the cords close fully, suggesting that the right sided TA and LCA muscles necessary for normal voice (served by anterior branch of the recurrent laryngeal nerve) have recovered fully. The open phase of vibration (next photo) will verify (or disprove) this speculation.
(3 of 3)
In fact, the lateral excursions of the vocal cords are the same (compare the lateral "distance" from the midline (indicated by the dotted line).. This verifies that there is no weakness (flaccidity) of the right TA muscle. The lack of lateral turning of the vocal process verifies that the LCA muscle is also working on that side. Hence, PCA-only paresis.
Weakness or paralysis of the vocal cord’s thyroarytenoid (TA) muscle, but with normal function of the vocal cord’s other muscles. The TA muscle “inhabits” the vocal cord and normally provides bulk and internal tone to the cord. The following are indicators of TA-only paresis:
Movement: The vocal cord opens normally for breathing and closes normally for voicing.
Position and appearance: Position is normal. Typically, the margin of the cord is slightly concave, the ventricle is capacious, and the conus area below the free margin is lacking in bulk.
Appearance during voicing (under strobe lighting): Closure at the posterior commissure is complete and symmetrical bilaterally. Under strobe light, one sees flaccidity as indicated by increased amplitude of vibration; the lateral excursions become exaggerated and the mucosal wave increases. One may also see chaotic fluttering.
Voice quality: Weak and air-wasting and often indistinguishable from a case of complete vocal cord paralysis—TA, LCA (lateral cricoarytenoid), and PCA (posterior cricoarytenoid).
Paresis, TA-only (1 of 3)
Panoramic view of the larynx with the cords in full abduction. Note the asymmetry — particularly the bowed free margin on left (right of image), and capacious ventricle.
Paresis, TA-only (2 of 3)
Close-up at near-closure for phonation. Equal bilateral adduction and matching angles of medial line of aytenoid cartilages demonstrates that LCA muscles are working bilaterally. This appears to be a paresis of TA muscle alone.
Paresis, TA-only (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.
Paresis, TA-only: before and after an implant: Series of 5 photos
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.
TA-only paresis before and after voice gel injection: Series of 5 photos
TA weakness, intact LCA + PCA (1 of 5)
TA weakness indicated by bowed margin and “spaghetti-linguini” difference between the cords. Medial turning of vocal process (arrow) suggests intact LCA; abducted position suggests intact PCA function. Blood is from cricothyroid membrane puncture to instill topical anesthesia.
Prephonatory instant (2 of 5)
Before voice gel injection at prephonatory instant. Wasting of left cord (right of photo), and capacious ventricle on the left (right of photo) clearly evident.
Gel injection (3 of 5)
At beginning of voice gel injection (needle at white arrow).
Straight vocal cord margin (4 of 5)
At conclusion of voice gel, note straight left cord margin (right of photo). Compare with photos 1 and 3.
Phonation (5 of 5)
Phonation after injection complete. Voice dramatically strengthened. Compare with photo 2.
Just bowing? No, TA-only paresis: Series of 4 photos
Prephonatory view (1 of 4)
As the cords approach voice-making position, in a man with weak voice symptoms. What details do you see?
Phonation (2 of 4)
Now closed for phonation, the right vocal cord margin (left of photo) is bowed as compared with the left (right of photo), more normal cord.
Bowing and Atrophy (3 of 4)
At closer range, not only bowing, but also absence of the "conus" bulge ("C") below the right cord (left of photo), indicates TA atrophy in a second way.
Open phase (4 of 4)
Under strobe light, at the open phase of vibration, the bowed margin of the right cord is seen even more clearly. Its greater lateral vibratory excursion adds flaccidity to previously-noted bowing and atrophy.
"Mostly-TA" paresis: Series of 4 photos
Atrophy (1 of 4)
After an upper respiratory infection, this man's voice was self-rated at "45%" of normal strength. After 3 weeks, it suddenly increased to "65%," and then very slowly improved over the next 5 months to "85%" at the time of this examination. Note subtle atrophy of the left fold (right of photo).
TA atrophy (2 of 4)
One finding of subtle TA atrophy is the smaller "conus" bulge on the left (right of photo). Compare the brackets on the two sides. Complete abduction suggests PCA function is intact.
LCA intact (3 of 4)
As the vocal cords are coming to midline for phonation, the bowed left vocal cord margin, indicating TA atrophy, is accentuated. Left vocal process is turning medially, suggesting preserved LCA function.
Closed phase (4 of 4)
An extremely subtle finding of flaccidity is the incomplete closure of the left anterior cord during the closed phase of vibration under strobe light. A highly speculative interpretation? Perhaps a complete left vocal paralysis, with early recovery of left LCA and some TA. Then more gradual recovery to this subtle TA-only paresis.
TA-only paresis, before and after recovery: Series of 4 photos
Bowing and atrophy (1 of 4)
Mediastinal lymphoma has just been discovered as the cause of this middle-aged man’s marked vocal weakness. He describes it as “50%” of normal. Note bowing of the right cord (left of photo) and atrophy (“spaghetti-linguini larynx”).
Dramatic flaccidity (2 of 4)
Under strobe light, showing dramatic flaccidity and increased lateral excursion of vibration of the right cord (left of photo) as compared with the left (right of photo). Vocal processes are fairly symmetrical suggesting LCA is at least mostly intact.
Bowing reduced (3 of 4)
After several cycles of chemotherapy, the patient feels well and voice had recovered to “100%” but is at this moment only “75%” due to an upper respiratory infection (see pinkness). Note as well that the right vocal cord (left of photo) has recovered much of its bulk, bowing is reduced, and the “spaghetti-linguini” appearance is virtually gone.
Equalized amplitude (4 of 4)
Under strobe light, the amplitude of vibration is equalized between the two sides and it almost looks like the lateral excursion is greater on the left (originally normal) vocal cord.
Another TA-only paresis: Series of 4 photos
Left vocal cord paralysis (1 of 4)
This person noted abrupt and severe voice change about six months earlier. Examination elsewhere at that time showed a “paralyzed left vocal cord.” The patient remembers seeing that one vocal cord did not move at all suggesting that perhaps TA + LCA + PCA were initially paralyzed. Voice is partially recovered by the time of this examination, but still moderately weak. Note that PCA muscles are working bilaterally. Left TA (right of photo) is clearly atrophied (spaghetti – linguini comparison), margin bowing, etc. We can’t yet decide about LCA function.
Working LCA muscles (2 of 4)
As the vocal cords approach each other just before phonation, the vocal processes turn medially on both sides, though perhaps a little better on the right than the left. Now we know that LCA muscles are both working.
Deficient TA muscle (3 of 4)
At the pre-phonatory instant, just before vibratory blurring, the normal right cord (left of photo) has a straight margin, while the left (right of photo) is bowed (TA is deficient). Both vocal processes are in a line—NOT pointing laterally on the left as would be the case if the LCA were not working. We see again that the only muscle not working is the left TA.
Open phase of vibration (4 of 4)
Here, under strobe light, at open phase of vibration, note that the lateral amplitude of the left vocal cord (right of photo) is greater, due to flaccidity of the atrophied left TA muscle.
Vocal cord atrophy goes away when nerve supply to the thyroarytenoid muscle returns: Series of 2 photos
(1 of 2)
After open-heart surgery, the left vocal cord is highly paretic. The evidence in the left vocal cord (right of photo) includes a) bowed vocal cord margin; b) capacious ventricle (V); and c) the "spaghetti" caliber of the left vocal cord as compared with the "linguini" caliber on the right (left of photo). Compare bracket length.
(2 of 2)
Notice after recovery of the nerve that the margin bowing on the left is no longer seen. The ventricle (V) is no longer capacious; and the "spaghetti-linguini" disparity between the caliber of the cords has become "linguini-linguini" due to recovery of normal bulk of the thyroarytenoid muscle within the left vocal cord.
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