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.
The pharynx (loosely “throat”) has a “foodway” function to convey food and liquid from the mouth to the esophagus. It also serves as part of the “airway,” also from mouth into the larynx and trachea. These foodway/airway functions are kept separate so food and liquid do not enter the airway towards the lungs. At the moment of swallowing, vocal cords clamp firmly together and epiglottis drops over the entrance of the larynx to divert food and liquid into the esophagus. During each swallow, lasting perhaps a second, breathing is briefly suspended. Once the food/liquid has gone by, the larynx re-opens and breathing resumes.
A thin sheet of muscle surrounds the pharynx, and squeezes to narrow the pharynx and help to propel swallowed material. That contraction lasts for approximately one second, each time the person swallows. The muscle is innervated bilaterally by the pharyngeal branch of the vagus nerve and so one side or both sides can be paralyzed by tumor, fracture at the base of the skull, viral injury, etc.
This diagnosis is often overlooked, because clinicians may not be clear on how to make the diagnosis. The best way is to obtain a clear panoramic view of the laryngopharynx as seen in the photo series below, and ask the patient to produce a very high pitch. This maneuver “recruits” contraction of the pharynx outside of the act of swallowing and allows the examiner to see clearly the difference in the contraction of the two sides. The paralyzed side is pulled to the non-paralyzed side, again as seen below.
Some with unilateral pharynx paralysis can compensate and continue to swallow (with limitations). Others are completely unable to surmount the impediment of this kind of paralysis.
Pharyngeal Paralysis, Seen with Pharynx Contraction
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.
Photos of IA-only paresis:
Interarytenoid (IA) Weakness
Another Interarytenoid (IA) Muscle Paresis or Is It Avulsion?
Watch the Progression of A Rare Laryngeal Paresis Scenario Including Interarytenoid (IA) Muscle
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.
Parkinson’s-related Voice Change
Voice Building (shorter version):
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 room1. 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.
Adductory Spasmodic Dysphonia
Abductor Spasms, Worsened by Cognitive Loading
Laryngology 401: PCA-only Paresis, but the Actual Voice Problem Is Spasmodic Dysphonia
Remarkable Task-Specificity of Spasmodic Dysphonia
Assessment of Vocal Phenomenology Protects from Visual Red Herrings
Ludlow CL. Treatment for spasmodic dysphonia: limitations of current approaches. Curr Opin Otolaryngol Head Neck Surg. 2009; 17(3): 160–165. ↩
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:
- Vocal cord paresis, TA + LCA
- Vocal cord paresis, TA-only
- Vocal cord paresis, LCA-only
- Vocal cord paresis, PCA-only
- Vocal cord paresis, IA-only
Photos of TA + LCA vocal cord paresis:
Photos of TA-only vocal cord paresis:
Photos of LCA-only vocal cord paresis:
Photos of PCA-only vocal cord paresis:
Photos of IA-only vocal cord paresis:
Weakness or paralysis of the vocal cord’s posterior cricoarytenoid (PCA) muscle, but with normal function of the vocal cord’s other muscles. The PCA muscle abducts (lateralizes) the vocal cord for breathing. The following are indicators of PCA-only paresis:
- Movement: The vocal cord closes normally for voicing, but it does not abduct for breathing. It remains motionless at the midline.
- Position and appearance: Position is normal during phonation, but the vocal cord does not open (lateralize) for breathing. Because the cord does not appear to move (it adducts or closes normally, but from an already-adducted position), PCA-only paresis is often mistaken for complete vocal cord paralysis—TA (thyroarytenoid), LCA (lateral cricoarytenoid), and PCA. Key points of difference between PCA-only paresis and complete paralysis are that, in the former case, the tip of the vocal process is in a normal medial position and the vocal cord has normal bulk and tone.
- Appearance during voicing (under strobe lighting): Completely normal, because the adductors of the cord (TA and LCA muscles) are intact. Hence, as with a normal cord, there is no flaccidity or asymmetry of vibration.
- Voice quality: Entirely normal. Many individuals are told this is due to “compensation” of the opposite cord, but actually it is because the muscles used for voicing (TA + LCA) are intact.
PCA-only Paresis Years after Thyroid Lobectomy
Left PCA-only Paresis
Sharp Observation Required to Sort out this PCA-only Paresis and Cancer Scar Combo
Classic Findings Again of PCA-only Paresis
A Mediocre Examination for Paresis
Laryngology 401: PCA-only Paresis, but the Actual Voice Problem Is Spasmodic Dysphonia
Test your Mastery of Visual Nuances of Paresis with this Case
PCA-only Paresis of Right Vocal Cord and Normal Voice
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).
Photos of TA-only paresis:
Paresis, TA-only: before and after an Implant
TA-only Paresis before and after Voice Gel Injection
Just Bowing? No, TA-only Paresis
TA-only Paresis, before and after Recovery
Another TA-only Paresis
Arytenoid Mismatch Makes for Gravelly Voice Quality Is Hard to Fix in Some Cases of Vocal Cord Paralysis
One could medialize more aggressively posteriorly on the left, hoping to raise the level of the cord, but often attempts to compensate for arytenoid mismatch such as that seen here are only modestly successful. Arytenoid superstructure is not useful for assessment of match; instead, the examiner should judge match at the vocal processes.