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Vocal Fold Paralysis
Key Points
- 1.
Understand the embryology and anatomy of the recurrent and superior laryngeal nerves (RLN and SLN). Unilateral or bilateral injury to one or both of these nerves can lead to a range of dysfunctions in voice, swallowing, and the ability to cough.
- 2.
A comprehensive history focusing on recent surgeries, intubations, or viral illnesses is critical in determining the etiology of vocal fold paralysis. A complete head and neck examination to evaluate other cranial neuropathies or masses is also required. In the setting of unexplained unilateral vocal fold paralysis, a computed tomography (CT) scan of the neck from the skull base through the aortic arch with contrast is typically obtained to evaluate the entire course of the RLN ( Box 78.1 ).
- 3.
In adults, unilateral vocal fold paralysis typically presents with hoarseness, dysphagia, and dyspnea with speaking but not dyspnea with exercise. Bilateral vocal fold paralysis typically presents with dyspnea on exertion and inspiratory stridor. Voice and swallowing may be normal in patients with bilateral paralysis. Bilateral RLN paralysis can be life-threatening and may present as an acute airway emergency ( Table 78.1 ).
- 4.
It is rare for a vocal fold paresis to recover after 6 months from the date of insult. Laryngeal electromyography (LEMG) is often helpful in determining the prognosis for recovery before 6 months have passed from the date of injury. Temporary vocal fold augmentation is used to bridge the gap before paralysis is deemed permanent by time or LEMG criteria.
- 5.
Treatment for unilateral vocal fold paralysis augments and medializes the immobile vocal fold to allow the mobile, opposite vocal fold to meet it and restore glottic competence. Treatment for bilateral vocal fold paralysis is aimed at enlarging the airway, often at the expense of voice, by removing normal vocal fold tissue or lateralizing one of the paralyzed folds.
Pearls
- 1.
The position of the affected true vocal fold (TVF) does not correlate with the level or extent of injury to the vagus nerve or RLN branch. Not all branches of the nerve may recover and the position of the paralyzed or immobile vocal fold may vary over time.
- 2.
Laryngeal EMG is a tool used to measure motor unit recruitment. When the muscle is denervated, fibrillation potentials and positive waves are seen, whereas polyphasic motor units are seen when reinnervation occurs.
- 3.
Augmenting unilateral TVF immobility does not eliminate the risk of aspiration when there is also a sensory deficit from an affected SLN. However, improving the patient’s ability to cough more effectively may be sufficient to protect the lungs and tolerate aspiration.
- 4.
Early augmentation with temporary injection in symptomatic patients with unilateral TVF immobility offers better long-term outcomes and a decreased need for permanent augmentation.
- 5.
In bilateral complete vocal fold immobility, tracheostomy may initially be required, but many of these patients can later be decannulated after surgery to enlarge the glottic airway.
Box 78.1
Key Historical Questions in a Patient Presenting With Vocal Fold Paralysis
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Symptom frequency, associations, relieving/exacerbating factors, onset, duration
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Avoiding communication because of the effort required?
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Decreased ability to complete everyday tasks/work?
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Decreased participation in strenuous sports/activities?
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Conversion to a relatively sedentary lifestyle? (more common in bilateral paralysis)
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History of aspiration pneumonia/swallowing difficulty?
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Previous neurologic, head and neck, carotid, or cardiothoracic surgery?
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History of alcohol and tobacco use?
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Is it difficult to project the voice?
-
History of endotracheal intubation?
Table 78.1
Signs and Symptoms of Vocal Fold Paralysis
| Unilateral |
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| Bilateral |
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Questions
1
Describe the anatomy of the vocal folds as part of the larynx.
The larynx is divided into the supraglottis, glottis, and subglottis ( Fig. 78.2A ). The glottis comprises paired true vocal folds (TVFs). The supraglottis encompasses all tissues 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 centimeter below the rima glottis (the area where the TVFs meet during phonation), extending to the inferior border of the cricoid cartilage. TVFs are involved in phonation, whereas 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 tissues. The TVFs are covered by stratified squamous epithelium, differentiating them from the ciliated pseudostratified columnar epithelium of the remainder of the respiratory tract. The superficial lamina propria (Reinke’s space) is deep to the squamous epithelium of the TVFs, which together comprise the vocal cover that affords vibration during phonation. The intermediate and deep lamina propria are deeper, forming 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.
2
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 intraabdominal pressure to build during a Valsalva maneuver.
3
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 nerve exits the skull base, it gives off branches, including the superior laryngeal nerve (SLN). The SLN divides into the 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 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 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 extends 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 the anterior and posterior branches. The RLN innervates all of the intrinsic muscles of the larynx (thyroarytenoid [TA], lateral cricoarytenoid [LCA], interarytenoid [IA], and posterior cricoarytenoid [PCA]), except for the cricothyroid muscle. It also supplies sensory innervation to the mucosa of the TVFs and below.
4
If innervation to the larynx is injured, what can happen?
It should be understood that innervation of the larynx is more complex than described above. There are anastomoses of the motor and sensory system, as well as between the right and left sides. When the RLN and/or SLN sustain an injury, repair and reinnervation are 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.
5
Describe the embryology pertinent to the RLN.
The larynx develops from the branchial arch. 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 78.2 ).
Table 78.2
Causes of Vocal Fold Paralysis/Immobility
| Idiopathic (postviral neuropathy) Thyroid or parathyroid surgery Skull base surgery Vagal neoplasm Anterior cervical fusion surgery Carotid surgery Traumatic intubation/extubation Arytenoid dislocation Cricothyroid joint fixation Rheumatoid arthritis Osteomyelitis of skull base Tuberculosis Chronic alcohol abuse Fibrosis from radiation to head and neck Endotracheal tube cuff injury to RLN Thoracic surgery Surgery of/near aortic arch Tumors of the head and neck Laryngeal ventricle or piriform sinus mass Intrathoracic, mediastinal neoplasm Thoracic/cervical trauma Aortic aneurysm Left atrial dilation (“Ortner syndrome”) Brainstem infarction (bulbar palsy) (rare) Wallenberg syndrome Multiple sclerosis ALS Poliomyelitis Lupus Granulomatous disease (e.g., sarcoidosis) Diabetic polyneuropathy Polyarteritis nodosum |
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