Arytenoid Adduction and Abduction

The position of the arytenoid cartilage can be surgically altered to control the position of the vocal process, and hence the glottic aperture, in patients with laryngeal paralysis. Arytenoid adduction (AAd) mimics the action of the lateral cricoarytenoid muscle (LCA) to place the paralyzed vocal fold near the midline, where it can be approximated by the contralateral mobile vocal fold during speech and swallowing. Arytenoid abduction (AAb) mimics the action of the posterior cricoarytenoid muscle (PCA) to displace the vocal process laterally and rostrally. This increases the glottic airway in patients with airway obstruction due to bilateral laryngeal paralysis. An AAb suture is also useful in some patients with unilateral paralysis, when the arytenoid prolapses into the airway, displacing the vocal process inferiorly. The abduction suture pulls the vocal process superiorly, without negating the medial displacement achieved by the adduction sutures to pull it superiorly. Occasionally, anterior prolapse of the arytenoid in unilateral paralysis causes airway obstruction, which can be relieved by arytenoid abduction.

Arytenoid adduction is accomplished by placing a suture in the muscular process of the arytenoid, which is the origin of the LCA; this suture is passed anteriorly through the paraglottic space and is secured to the inferior cornu of the thyroid ala. This anterior traction pulls the muscular process forward and internally rotates the arytenoid ( Fig. 63.1 ). The vocal process, which is orthogonal to the muscular process, is displaced medially, dragging the membranous vocal fold with it. Arytenoid adduction can be performed in conjunction with type I thyroplasty. Arytenoid abduction mimics the action of the PCA (see Fig. 63.1 ). It also uses a suture placed in the muscular process of the arytenoid cartilage; however, traction is applied differently, pulling posteriorly and inferiorly. The PCA inserts on the posterior surface of the cricoid, a site that is very difficult to access. However, research in cadaver larynges indicates that anchoring the abduction suture near the inferior cornu of the thyroid cartilage achieves very similar anatomic results ( Fig. 63.2 ). The cricoarytenoid joint is a multiaxial ball-and-socket joint ; therefore, the force vector of the PCA does not preclude medial displacement of the vocal process by adductor muscles. This has two implications: First, the posterior support of an abduction suture does not prevent an arytenoid adduction suture from medializing the vocal process. Second, in a patient with bilateral abductor laryngeal paralysis, an abduction suture does not abolish any residual adductor muscle activity during phonation. In fact, an abduction suture can unmask latent adductor activity.

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Arytenoid adduction and abduction procedures.

Anterior traction on the muscular process internally rotates the arytenoid so that the vocal process moves medially. Posterior traction externally rotates the arytenoid and moves the vocal process laterally.

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Posterior view of the larynx demonstrates the sites of attachment for the posterior suspension suture: the muscular process of the arytenoid cartilage, where the fibers of the PCA muscle converge, and the inferior cornu of the thyroid cartilage.

Arytenoid adduction is not the first-choice surgical option for most patients with unilateral laryngeal paralysis. Injection laryngoplasty or medialization laryngoplasty are simpler procedures that are very effective when the vocal process of the paralyzed vocal fold lies near the midline. But when the vocal process is significantly laterally displaced, thyroplasty or injection laryngoplasty is inadequate to achieve glottic closure. Research in animal models indicates that in flaccid laryngeal paralysis, the acoustic and aerodynamic results of arytenoid adduction plus thyroplasty are superior to the results of thyroplasty alone. Arytenoid adduction has been reported to carry somewhat greater surgical risks and is a more involved procedure than thyroplasty. But arytenoid adduction is a valuable component of the therapeutic armamentarium and the risk-to-benefit ratio is favorable in patients with significant glottal incompetence.

The clinical impact of laryngeal paralysis varies greatly. Some patients with unilateral paralysis are completely asymptomatic. At the other end of the spectrum, some patients are aphonic and have severe problems with aspiration during swallowing. Two key factors that influence glottal closure in patients with laryngeal paralysis are the configuration of the paralyzed vocal fold and the compensatory function of the contralateral fold.

It is now generally accepted that a medial vocal fold position results from residual or regenerated innervation of laryngeal muscles. When innervation of the adductor muscles is significant, the paralyzed fold is located near the midline, and compensatory activity of the normal side of the larynx can often close the glottis during phonation. In such cases, aspiration is rare, and hoarseness or breathiness responds well to surgical medialization of the membranous vocal fold performed by injection or thyroplasty. On the other hand, complete flaccid paralysis results in a cadaveric position of the vocal fold with a laterally displaced vocal process. This position results in severe glottal incompetence, often referred to as a posterior gap .

It has long been recognized that vocal fold injection cannot restore glottal competence when the glottal gap is large. This has been known since the early days of injection laryngoplasty, when the injectate of choice was polytetrafluoroethylene (Teflon). The efficacy of Isshiki type I thyroplasty in closing a posterior gap is controversial, and it has been contended, based on clinical observation, that a posterior extension of the thyroplasty implant can close a posterior gap. However, the biomechanics of the cricoarytenoid joint dictate that the arytenoid does not glide medially in response to a medially directed force. Instead, pressure on the lateral surface of the arytenoid results in external rotation of that cartilage, so that the vocal process is abducted. Arytenoid adduction is much more effective than thyroplasty in closing the posterior glottis.

The term “posterior gap” is not entirely accurate, because the maximal glottic opening is between the vocal processes, not at the posteriormost extent of the glottis. The open glottis actually converges posterior to the vocal processes. Lateral displacement of the vocal process involves external rotation of the arytenoid cartilage, not lateral displacement of the body of the arytenoids. In other words, the angle between the membranous vocal fold and its posterior cartilaginous portion decreases as the vocal fold abducts. Thus, the posterior portion of the cartilaginous vocal fold is medial to the vocal process in abduction, and it prevents glottic closure even with vigorous hyperadduction of the normal vocal fold ( Fig. 63.3 ). Procedures that medialize the membranous vocal fold may achieve some medial displacement of the vocal process; however, the force vectors created by such procedures are inadequate to effect significant external rotation of the arytenoid cartilage.

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(A) Vocal fold paralysis in a lateral, abducted position. Note anterior prolapse of the arytenoid, which blocks view of the vocal process. (B) Phonation in same patient. Note compensatory shortening and hyperadduction of the mobile vocal fold. Despite approximation of the bodies of the arytenoid, there is a large glottal gap due to lateral displacement of vocal process of the paralyzed vocal fold.

Vocal fold injection and type I thyroplasty do not address differences in the level of vocal folds. The paralyzed vocal fold often lies in a plane different from that of the mobile vocal fold. Although both folds are firmly attached to the anterior commissure, the vocal process may sag on the paralyzed side, or it may lie above the glottic plane, as it does in physiologic abduction. Thus, the vertical gap between the edges of the vocal folds can be significant, even when they appear to be touching when viewed from above in a two-dimensional image. The paralyzed fold can lie either above or below the glottal plane. In cadaver specimens from subjects who had chronic vocal fold paralysis, the vocal fold has been reported to be caudally displaced with a wide ventricle and shift of the conus elasticus to a horizontal plane. Other reports describe superior displacement of the paralyzed vocal fold, essentially the same position assumed by an actively abducted vocal fold.

A difference in the level of the vocal folds can often be appreciated with indirect mirror laryngoscopy, which permits binocular vision. In 1932, noting observations with mirror laryngoscopy, New and Childrey stated, “In the absence of any innervation from the recurrent nerve fibers, the cord is somewhat relaxed or bowed; it is, therefore, shortened, somewhat narrowed and depressed, lying at a lower level than normal.” In a two-dimensional video image, a level difference is not apparent; however, what can be perceived is a difference in the apparent length of the vocal folds. As noted by Brewer and colleagues, a paralyzed vocal fold often appears shorter than its mobile mate. During phonation, the mobile vocal fold appears to shorten to nearly the same length as its paralyzed mate (see Fig. 63.3 ). Cadaver studies indicate that foreshortening of the paralyzed fold is usually an optical illusion. A lateralized vocal fold appears shorter when it is not in the same visual plane as the normal one, with the vocal process at a higher level, or sometimes a lower level. Thus, accommodation for a paralyzed vocal fold involves not only hyperadduction by the other side, but also elevation of the vocal process. Arytenoid adduction corrects the position of a superiorly displaced vocal process and appears to lengthen the vocal fold because it moves the vocal process caudally. This vertical component of motion is endoscopically perceived as a length change. The visual image shortens because of rotation of the vocal fold out of the optical plane. In arytenoid adduction, the arytenoid rotates about an oblique, nearly vertical helical axis; as the vocal process moves medially, it is displaced caudally as well. The axis of arytenoid abduction is quite different; it is nearly horizontal and in the axial plane it differs from the adduction axis by around 60 degrees ( Fig. 63.4 ). Hence, AAb moves the vocal process laterally and rostrally, pulling it up out of the airway. An abducted vocal fold appears shorter when viewed from above, but the length does not actually change. The vocal fold merely appears shorter because it is tilted out of the visual plane. As AAd moves the vocal process back down to the physiologic position of glottic closure, the vocal fold is parallel to the image plane, and the vocal fold appears longer.

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Axes of rotation in arytenoid adduction and abduction as determined in three-dimensional motion analysis of simulated LCA contraction (AAd) and PCA contraction (AAb) in cadaver larynges.

The cricoarytenoid joint is a shallow, multiaxial ball-and-socket joint. Vocal folds do not open and close along a fixed “track,” and the rostrocaudal level of the vocal process is not completely dictated by internal and external rotation. Cadaver studies of simulated muscle contraction demonstrate that the axis of rotation for the PCA is quite different from that for the LCA (see Fig. 63.4 ). This means that varying the force of individual muscles enables the rostrocaudal position of the vocal process to be varied independent of its mediolateral position. Patients who are compensating for unilateral vocal fold paralysis seem to foreshorten the mobile vocal fold during phonation, and this can be attributed to depression of the active vocal process to oppose the displaced immobile vocal process.

Because of the multiaxial nature of the cricoarytenoid joint, the vocal process of a paralyzed vocal fold is not necessarily located along the path of physiologic motion. In a normal larynx, the vocal process moves upward as the vocal fold is adducted. This motion is dictated by the vectors of force applied by the muscles to the cricoarytenoid joint. But in flaccid paralysis, the pull of the PCA is lost, so that the arytenoid may “tip” forward (see Fig. 63.3A ). The vector of the pull in the arytenoid adduction procedure is similar to that of the LCA, anteriorly and slightly inferiorly. Thus, the procedure cannot correct, and may even exacerbate, the anterior tilt of the arytenoid, which places the vocal process caudal to the phonatory position. One approach to correcting such a “sagging” arytenoid is to apply posterior suspension using an arytenoid abduction suture, pulling posteriorly and inferiorly on the vocal process to “rock” the arytenoid into a position that is more favorable for phonation (see Fig. 63.2 ). Another approach to the sagging arytenoid is adduction arytenoidopexy, which fixes the arytenoid to the cricoid posteriorly.

The membranous vocal fold is dragged medially by arytenoid adduction. However, if the thyroarytenoid muscle is atrophic, which is frequently the case in cadaveric paralysis, a glottal gap is still evident anterior to the vocal process. This is because much of the mass of the vocal fold is composed of muscle; with muscle atrophy, the vocal fold shrinks and becomes thin and concave. This loss of bulk can be addressed by concomitant or subsequent medialization by injection or type I thyroplasty.

Surgery to reposition the arytenoid is less effective in patients with long-standing laryngeal paralysis. This limitation does not appear to be due to joint fixation. In most patients who undergo arytenoid adduction for long-standing unilateral laryngeal paralysis, the cricoarytenoid muscle and the arytenoid can be successfully rotated. But the apparent length of the arytenoid, and presumably its vertical position, is not improved, so compensatory hyperfunction is still required for speech. It is possible that contracture and fibrosis of soft tissues, such as muscle and mucosa, prevent correction of the vertical position of the vocal fold. The outcome of the arytenoid adduction procedure is also less favorable in patients with paralysis as a result of central neural lesions, such as tumor or stroke, because of associated sensory, reflex, and/or cognitive deficits.

Dysphagia can be a significant problem when laryngeal paralysis is the result of a vagus nerve injury. This is a common problem in patients with vagus nerve paralysis after skull base surgery; AAd can be performed very soon after such surgery. Pharyngeal propulsion is impaired owing to ipsilateral paralysis of constrictor muscles but the cricopharyngeal muscle retains tone because it is a continuous muscular sling that receives bilateral innervation. Pharyngeal pressure is inadequate to push the bolus into the esophagus, which results in stasis of secretions and ingested food in the hypopharynx. In such cases, a cricopharyngeal myotomy can be effective in improving swallowing and reducing aspiration. Cricopharyngeal myotomy is easily performed in conjunction with the arytenoid adduction procedure.

Arytenoid abduction (AAb) is effective in relieving airway obstruction in selected patients with bilateral vocal fold immobility. The voice is often near normal in patients with bilateral paralysis because the larynx is not totally denervated. Adductor muscles have residual or regenerated innervation, holding the vocal folds at or near midline, while abductor function is inadequate to open the glottis. AAb externally rotates the arytenoid and pulls it up out of the airway to widen the glottis. Unlike endoscopic arytenoidectomy, it does not create an open wound in the larynx that can subsequently contract and negate the airway improvement. Moreover, because of the biomechanics of the cricoarytenoid joint, arytenoid abduction does not abolish any residual adductor function; thus, arytenoid abduction can significantly improve the airway without impairing the voice.

Sometimes patients with laryngeal paralysis have inappropriate adductor activity during inspiration, which is attributable to synkinetic reinnervation of adductor muscles. Such activity opposes the action of the arytenoid abduction suture and limits the efficacy of the surgery.