76 Vocal Fold Paralysis Flashcards
Describe the anatomy of the vocal folds as part of the larynx.
Describe the anatomy of the vocal folds as part of the larynx.
The larynx is divided into the supraglottis, glottis, and subglottis (Figure 76-2A). The glottis is comprised of the paired true vocal folds (TVF). The supraglottis encompasses all the tissue of the larynx above the TVFs. The laryngeal ventricles extend laterally and superiorly, under the false vocal folds, and end blindly in the laryngeal saccule. The subglottis begins approximately 1 cm below the rima glottis (the area where the TVFs meet during phonation), extending to the inferior border of the cricoid cartilage. The TVFs are involved in phonation, whereas the false vocal folds are typically not. The false vocal folds are formed of mucosa overlying the superior aspect of the thyroarytenoid muscle and other connective tissue. The TVFs are covered by stratified squamous epithelium, differentiating them from the ciliated pseudostratified columnar epithelium of the remainder of the respiratory tract. Deep to the squamous epithelium of the TVFs is the superficial lamina propria (Reinke’s space), which together comprise the vocal cover that affords vibration during phonation. Deeper are the intermediate and deep lamina propria, making the vocal ligament. The vocal ligament sits on top of the vocalis muscle (the medial portion of the thyroarytenoid muscle) and is the superior extent of the conus elasticus, a fibrous tissue condensation extending up from the cricoid cartilage.
Other than phonation, what are the functions of the vocal folds?
Other than phonation, what are the functions of the vocal folds?
Although phonation is an important function, it is not the primary role of the true and false vocal folds. Protection of the lower airway during swallowing is the most crucial function of the larynx, and the vocal folds are imperative to this. In addition, the TVFs provide the ability to cough and clear the airway and allow increased intra-abdominal pressure to build during a Valsalva maneuver. A Valsalva affords the ability to equalize middle ear pressure, lift weight, and bear down for bowel movements and child birth.
Describe the innervation of the larynx.
Describe the innervation of the larynx.
The larynx is innervated by various sensory and motor branches of the vagus nerve (CN X). After the vagus exits the skull base it gives off a branch, the superior laryngeal nerve (SLN). The SLN then divides into internal and external branches. The internal branch carries sensory information from the laryngeal mucosa above the TVFs. The external branch innervates the cricothyroid muscle, which contracts to bring the thyroid cartilage closer to the cricoid cartilage, thus lengthening the TVFs and allowing pitch elevation of the voice. After giving off the superior laryngeal nerve, the vagus descends into the neck within the carotid sheath, along with the internal carotid artery and internal jugular vein (posterolateral to the internal carotid artery and posteromedial to the internal jugular vein). As the vagus enters into the thoracic cavity, it sends a branch cephalad, which is the recurrent laryngeal nerve (RLN). The right RLN splits from the right vagus nerve at the cervicothoracic junction, passing posterior to the right subclavian artery, and ascending posterior to the common carotid along the tracheoesophageal groove. One percent of right RLNs arise at the level of the thyroid gland and can be more readily injured during thyroidectomy. The left RLN takes off from the vagus nerve at the aortic arch, wrapping posteriorly underneath the ligamentum arteriosum and ascending cephalad in the tracheoesophageal groove. The RLNs enter the larynx near the cricothyroid joint and then split into anterior and posterior branches. The RLN innervates all the intrinsic muscles of the larynx (thyroarytenoid (TA), lateral cricoarytenoid (LCA), interarytenoid (IA) and posterior cricoarytenoid (PCA)), except the cricothyroid muscle. It also supplies sensory innervation to the mucosa of the TVFs and below.
If innervation to the larynx is injured, what can happen?
If innervation to the larynx is injured, what can happen?
It should be understood that the innervation to the larynx is more complex than described above. There are anastamoses of the motor and sensory system as well as between the right and left sides. When the RLN and/or SLN sustains an injury, repair and reinnervation is often incomplete and variable among the smaller, terminal branches. Because the RLN carries adductor (TA, LCA, and IA) and abductor (PCA) fibers, damage to the nerve severe enough to cause Wallerian degeneration results in “cross-wiring” or synkinetic reinnervation and lack of purposeful motion to the affected muscles. Synkinetic TVFs will have good tone and often a normal interference pattern on LEMG whereas completely denervated TVFs will atrophy.
Describe the embryology pertinent to the RLN.
Describe the embryology pertinent to the RLN.
The larynx develops from the branchial arch system. The supraglottis and superior laryngeal nerve arise from the fourth arch. The cricoid cartilage and recurrent laryngeal nerve arise from the sixth arch. On the right the sixth segmental artery disappears completely, and the fourth arch artery remains as the subclavian artery. This explains why the right recurrent laryngeal nerve passes under only the right subclavian vessels and has a shorter distance to travel back to the larynx. In contrast, on the left side, the sixth arch artery persists as the ductus arteriosus, which later fibroses to become the ligamentum arteriosum. This remnant necessitates a longer course for the left recurrent laryngeal nerve, forcing it to descend into the chest before returning to the larynx. The effect of this embryologic development on the course of the RLN explains why intrathoracic processes can result in unilateral vocal fold paralysis (Table 76-2).
What is the difference between vocal fold immobility, vocal fold paralysis, and vocal fold paresis?
What is the difference between vocal fold immobility, vocal fold paralysis, and vocal fold paresis?
It is important to use the correct terminology when evaluating vocal folds that do not move, as it refers to the etiology of their dysfunction. Immobility is a general term that does not indicate a cause; it refers to the lack of movement of the vocal folds from any cause, neurologic or mechanical. In addition, any nonmobile vocal fold that has yet to be designated as one with permanent motion impairment is called immobile rather than paralyzed. In contrast, paralysis of the vocal folds specifically refers to lack of movement (or immobility) from a permanent neurologic cause. If a vocal fold has a partial motion abnormality that is yet to be designated as permanent (i.e., a patient who presents with a new onset partial vocal TVF motion abnormality) it is called hypomobile; it is only given the diagnosis of a TVF paresis when it is 6 months or older with no other mechanical explanation, and is therefore from a permanent neurologic cause.
Describe the findings on laryngoscopy and stroboscopy seen in vocal fold paralysis.
Describe the findings on laryngoscopy and stroboscopy seen in vocal fold paralysis.
In a complete unilateral paralysis, the fold will neither abduct nor adduct and will sit in a neutral position somewhere between adducted and abducted. The position of the immobile or paralyzed TVF does not necessarily distinguish between vagus and RLN injury. As reinnervation occurs in RLN injury, not all minor branches of the nerve may recover, and the position of the affected vocal fold often changes over time. The healthy, opposite vocal fold will have full abduction and adduction capability, and will try to cross the midline to meet the paralyzed fold (Figure 76-1). The arytenoid cartilage on the side of denervation most often falls anteriorly into the airway, but the appearance of the arytenoid does not give any definitive information on the neurologic status of the affected RLN. On stroboscopy one may see a transglottic gap without significant vibration or a complete (but dominantly open) closure pattern with asymmetry depending on the position of the immobile TVF. Denervation atrophy after a few weeks or months may lead to greater vibratory amplitude. There is typically supraglottic hyperfunction (secondary muscle tension) due to the compensatory effort by the surrounding intrinsic laryngeal muscles, which may even cause pain/discomfort.
In bilateral vocal fold paralysis, it is important to differentiate between those patients with bilateral midline TVFs and those with TVFs that remain paramedian with a glottic gap. When the folds are immobile in the midline, patients typically experience a normal voice but significant airway compromise and respiratory distress. On the contrary, when the TVFs lie in a paramedian position, the patient will not routinely have airway compromise but the voice will be severely affected with a transglottic gap on stroboscopy.
What is a glottic gap/glottic insufficiency?
What is a glottic gap/glottic insufficiency?
A glottic gap refers to a pathologic space between the true vocal folds during phonation. It is possible to see this grossly in the setting of severe atrophy or vocal fold paralysis/immobility. Often, laryngovideostroboscopy (flexible laryngoscopy modality that uses a strobe light to give better visualization of the movement and closure pattern of the vocal folds) is needed to identify a more subtle glottic gap due to small benign lesions, paresis/hypomobility, early atrophy or scar. Glottic insufficiency is the pathologic and excess loss of air from the vocal folds due to a glottic gap. Glottic insufficiency typically is the cause of secondary muscle tension dysphonia that presents on exam as hyperfunctional behaviors of the supraglottic structures that are attempting to compensate for the glottic insufficiency. In females, a posterior glottic gap is often physiologic and normal.
What is the role of laryngeal electromyography in evaluating vocal fold paralysis?
What is the role of laryngeal electromyography in evaluating vocal fold paralysis?
Laryngeal electromyography (LEMG) is a test to help characterize the innervation status of an immobile vocal fold. It uses the body’s own electricity to demonstrate whether or not the RLN is sending signals to the muscle’s motor units or if the muscle is just firing on its own without any input. LEMG can determine if an immobile TVF is from a neurologic cause or a mechanical cause, such as cricoarytenoid joint dislocation, with the latter demonstrating normal LEMG activity. If the muscle is normally innervated, multiple action potentials from many motor units will overlap into a normal interference pattern and there is no spontaneous/random electrical activity. Alternatively, if the muscle is denervated, fibrillation potentials and positive waves are spontaneously seen. During the time when reinnervation is occurring or after incomplete reinnervation, polyphasic motor units are present. LEMG may indicate the potential for return of neuromuscular activity months before a clinical exam shows vocal fold motion. Synkinesis or other poor prognostic findings such as persistent positive waves/fibrillation potentials after serial LEMGs a few months apart help the physician recommend early permanent augmentation.
Which other tests should be included in the workup of unexplained unilateral TVF immobility or paralysis?
Which other tests should be included in the workup of unexplained unilateral TVF immobility or paralysis?
In patients with new onset unilateral TVF paralysis that cannot be explained by a recent surgery, intubation, trauma or known pathology, it is important to consider extrinsic causes, specifically masses compressing the recurrent laryngeal nerve anywhere along its course. A CT scan with contrast from the skull base through the aortic arch is the initial test of choice as a chest X-ray is rarely helpful. If the CT is negative and the history and neurologic exam suggests multiple cranial neuropathies, an MRI of the brain and brainstem is indicated. If there is associated stridor that cannot be explained by laryngoscopy, tracheobronchoscopy should be performed.
What are the potential sequelae of unilateral true vocal fold immobility?
What are the potential sequelae of unilateral true vocal fold immobility?
Aspiration pneumonia is a potentially fatal sequela and early injection augmentation is offered preventatively in acute TVF immobility in an effort to improve “pulmonary toilet” (the ability to cough and clear secretions). Augmenting a unilateral TVF immobility by no means guarantees improvement in dysphagia or prevention of aspiration pneumonia, as it may be related to a sensory deficit from SLN dysfunction. However, improving the patient’s ability to cough more effectively may be enough to protect the lungs from small aspirations and will also improve voice.
What are the potential sequelae of bilateral true vocal fold paralysis?
What are the potential sequelae of bilateral true vocal fold paralysis?
Airway compromise is the primary concern in bilateral TVF paralysis. Most patients do not tolerate the insult if it occurs acutely. Patients who have long-standing bilateral paralysis (or who had a gradual onset) may have stridor at rest or with exercise but function to a satisfactory level when they are otherwise healthy. However, as in the setting of an acute upper respiratory infection, even a small amount of edema in an already narrow glottis can significantly decrease the cross-sectional area of the airway and lead to a life-threatening situation.
What are the treatment options for new onset unilateral vocal fold immobility?
What are the treatment options for new onset unilateral vocal fold immobility?
When underlying causes have been ruled out or are concurrently being treated, the first step to manage a unilateral TVF immobility in a symptomatic patient is temporary injection augmentation of the affected TVF. This can be performed in the office, at the bedside or in the operating room with a material that typically lasts 2 to 6 months. Early augmentation has been shown to improve long-term voice outcomes and decrease the need for permanent augmentation (the reason for this phenomenon is incompletely understood). LEMG is performed as early as 3 weeks from the time of injury and can be repeated 2 months later, affording prognostic information. Various factors such as patient age, occupation, comorbid conditions, and preferences all play a role in management. Watchful waiting is satisfactory in many who can swallow and communicate sufficiently.
What are the treatment options for a long-standing unilateral vocal fold paralysis?
What are the treatment options for a long-standing unilateral vocal fold paralysis?
Treatment options include injection laryngoplasty, medialization laryngoplasty with or without arytenoid adduction, and RLN reinnervation. Reinnervation procedures can be performed to re-establish tone to the intrinsic muscles of the larynx but these will not produce motion of the TVF and often require augmentation to improve voice during the period of nerve regrowth. No procedure to treat unilateral TVF paralysis will ever restore actual purposeful motion of the affected TVF.
Injection laryngoplasty, deep into the TA muscle, is accomplished via a percutaneous or peroral route in the office, or via suspension laryngoscopy in the operating room. The materials available for long-term (>6 months) augmentation include: calcium hydroxylapatite, micronized dermis, hyaluronic acid, and autologous fat (fat is considered the only permanent injectable by many and is only performed in the OR because of harvesting). Injection laryngoplasty can be very effective for a small glottic gap when the paralyzed vocal fold is midline or paramedian. For larger glottic gaps, injection is often less than satisfactory and medialization laryngoplasty is a more effective treatment (Figure - A, Coronal section of the larynx, demonstrating depth of needle placement and location deep in the thyroarytenoid muscle for injection laryngoplasty. B, Axial section glottis showing Gore-Tex® medialization).
Medialization laryngoplasty, or laryngeal framework surgery, involves the placement of a carved silastic block, Gore-Tex® strip, or prefabricated implant within the paraglottic space, pushing the affected TVF medially (see Figure 76-2B). An adjunctive treatment to medialization laryngoplasty includes arytenoid adduction with or without arytenopexy. The arytenoid cartilage is repositioned by anchoring sutures into a more physiologic position for phonation. This is employed when there is a large posterior glottic gap or mismatch of the height of the vocal processes of the arytenoid cartilages (Figure 76-2B).
What are the treatment options for acute bilateral vocal fold immobility?
What are the treatment options for acute bilateral vocal fold immobility?
Patients with bilateral incomplete paralysis can experience partial or even full recovery, and LEMG is employed in this setting to help with prognosis. Treatment options aim to both preserve and protect the patient’s airway, while awaiting one or both sides to recover motion. Suture lateralization of one vocal fold or tracheostomy is typically used to overcome the acute insult. Theoretically, both of these treatments are reversible.
