Vocal cord paralysis refers to the immobility of the vocal cord, while vocal cord paresis refers to the impaired mobility of the vocal cord. Both can be due to processes intrinsically affecting the vocal cord itself (scarring, tumor, etc.), due to cranial neuropathies of the nerves providing vocal cord mobility [the vagus nerve, the recurrent laryngeal nerve (RLN), and the superior laryngeal nerve (SLN)], central neurologic problems [stroke, tumor, multiple sclerosis (MS), etc.], or systemic disease [amyotrophic lateral sclerosis (ALS), Guillain-Barre syndrome, etc.]. Vocal cord paralysis is most commonly unilateral, and this is discussed in detail in another StatPearls article. Here we will concentrate on the rarer bilateral vocal cord paralysis.
The vocal cords serve two functions: production of voice (phonation) and protection of the lower airways via glottic competence. The presentation and symptoms will depend upon the underlying etiology of the bilateral paralysis and the resultant position of the vocal cords. If the cords are paralyzed in a more median position, stridor and breathing symptoms may predominate (or the patient may be asymptomatic) while the voice may be normal, and no aspiration events will occur. If the vocal cords are paralyzed in a more lateral position, the airway will be widely patent and unable to close. This may present with significant voice complaints of breathiness and potential aspiration or choking, but with far fewer breathing or stridor complaints. Management will similarly depend on the underlying etiology and vocal cord position, as well as the overall prognosis of the patient.
Bilateral vocal cord paresis may be the presenting finding of a pathology that will then progress to true bilateral vocal cord paralysis, but it can also be an entity in its own right and non-progressive. This depends on the underlying etiology.
Causes of bilateral vocal cord paresis:
Causes of bilateral vocal cord paralysis:
Benninger et al estimated that bilateral vocal cord paralysis can be attributed to surgical trauma in 44% of cases, malignancies in 17%, secondary to endotracheal intubation in 15% of cases, due to neurologic disease in 12% of patients and idiopathic causes in 12% of cases. Following thyroid or other surgery, a bilateral vocal cord paralysis can result in acute respiratory distress necessitating urgent airway intervention. Damage to the RLN adversely affects both abduction and adduction of the vocal cords due to laryngeal muscle denervation. Since the adductor muscle fibers are four times greater than abductor muscle fibers, the vocal cords assume a static paramedian position following injury. Direct stimulation of the vocal cords by an ETT and cuff during intubation and extubation may lead to vocal cord edema. Case reports have also described injury by direct surgical trauma, nerve division or ligature, pressure-induced neuropraxia, and postoperative edema.
In infants and children with bilateral vocal cord paralysis who primarily present with stridor Arnold-Chiari malformation II associated with hydrocephalus and myelomeningocele is the most common neurologic finding in infants with bilateral vocal cord paralysis, diagnosed following an MRI scan with cerebellar ectopia below the foramen magnum. Extension of the cerebellar tonsils, brainstem, and medulla through the foramen magnum into the spinal canal leads to vagal nerve compression and bilateral vocal cord dysfunction. Birth related trauma due to vertex or breech delivery and the use of forceps can also lead to RLN injury, though less commonly a bilateral injury. In infants, cardiovascular surgery, including patent ductus arteriosus ligation and repair of a tracheoesophageal fistula, are common causes of bilateral vocal cord paralysis.
A palsy of the superior laryngeal nerve (SLN) causes pitch changes in a patient’s voice secondary to paralysis of the cricothyroid muscle. Bilateral SLN palsy leads to hoarseness and abduction of the vocal cords, increasing aspiration risk. Although uncommon, vocal cord palsy can also occur in stroke patients with damage to the cerebral cortex or brainstem supplying the vagus, and hence the RLN. Laryngeal dysfunction is secondary to injury of the nucleus ambiguous and nucleus solitarius. In addition, compression secondary to a tumor can cause bilateral RLN palsy, leaving the vocal cords in the paramedian position.
Another extremely rare cause of bilateral RLN paralysis is Guillain Barre syndrome (GBS), the most common acquired demyelinating neuropathy. Although GBS classically presents as loss of deep tendon reflexes with ascending muscular paralysis, cranial nerves can be affected in addition to peripheral nerves. GBS can also manifest with respiratory distress necessitating mechanical ventilation, development of cardiac arrhythmias, and hemodynamic instability.
As the primary cause of bilateral vocal cord paralysis is post-surgical nerve injury, it is predominantly seen in adults with a history of thyroid or other bilateral neck surgery. Idiopathic causes may show a slight female predominance, but there is no high-quality data published on this subject at this time.
Although uncommon, vocal cord paralysis is a well-known cause of stridor in neonates, most congenital cases are unilateral. Murty et al. estimate the incidence of bilateral vocal cord paralysis to be 0.75 cases per million births per year. Neonatal bilateral vocal cord paralysis rarely occurs in isolation; factors such as prematurity and bronchopulmonary dysplasia often coexist, in addition to neurologic abnormalities that can lead to worse outcomes in infants. Congenital vocal cord paralysis should be part of the differential diagnosis for an infant with respiratory distress. Following laryngomalacia, vocal cord paralysis is the second most common congenital laryngeal abnormality in the pediatric population (with the vast majority being unilateral paralysis), likely due to improved survival of premature infants and infants with complex congenital abnormalities. In up to 48% to 62% of all-aged children with bilateral vocal cord paralysis, spontaneous recovery of vocal cord function can occur, but the prognosis rests with the overall health of the child and any concomitant medical problems.
The pathophysiology of the intrinsic vocal cord or arytenoid scarring and damage is relatively straightforward: it is a replacement of normally mobile tissues with fibrosis and scar that creates a mechanical tethering of these mobile tissues, preventing normal movement.
As RLN damage is the most common cause of bilateral vocal cord paralysis, we will review this pathophysiology in more detail. Vagal motor efferent fibers originate in the medulla oblongata. The nucleus ambiguous contains cell bodies of nerves that innervate the soft palate, pharynx, and larynx, while the dorsal nucleus contains visceral efferent fibers to the abdomen and thorax. The vagus nerve exits the cranium through the jugular foramen. The accessory nerve joins the vagus as it exits the jugular foramen.
The superior laryngeal nerve (SLN) branches off the vagus as it passes between the common carotid artery and internal jugular vein. Subsequently, the SLN divides into the external and internal branches. The internal branch of the superior laryngeal nerve provides sensory innervation to the mucosa above the true vocal cords. The external branch innervates the cricothyroid muscle (essential in changing the pitch of the voice). The right vagus nerve travels anterior to the subclavian artery into the abdomen, while the right RLN branches off and loops around the subclavian artery, ascending back into the neck to reach the larynx. The right RLN enters the larynx and provides sensory innervation to the laryngeal mucosa below the vocal folds and motor innervation to all the laryngeal muscles except the cricothyroid. The left vagus nerve takes a similar course into the abdomen, posterior to the aorta near the take-off of the ductus arteriosus, with the left RLN branching off and wrapping around the aorta before ascending into the neck and traveling in the tracheoesophageal groove to reach the larynx. The left RLN is more prone to injury due to its longer course.
Bilateral vocal cord paralysis can be caused by injury to the vagus nerve from its cerebral origins to its branches in the thorax and abdomen, and due to some redundancy, the position of the vocal cords (especially in bilateral paralysis) does not always reliably predict the site of the lesion. Injury to the RLN is most common, classically leaving the vocal cords in a paramedian position when unilateral or in a median position when bilateral. Injury to the SLN will lower the pitch of the voice and can lead to a bowing deformity of the vocal cords due to a loss of tensile tone from the denervated cricothyroid muscles. A high vagal injury can leave the cord in a nearly fully abducted (also called "cadaveric") position.
The primary presenting complaints of a patient with bilateral vocal cord paralysis are voice changes (hoarseness, pitch changes, vocal fatigue, etc.) and breathing difficulties (stridor, increased work of breathing, aspiration/pneumonia, etc.). A history of the onset and duration of symptoms should be obtained, as well as whether they are progressing or stable. Any antecedent events should be documented, including prior URI, any neck surgery or trauma, malignancy, radiation therapy, and a thorough past medical history should be obtained. Of specific interest is any systemic rheumatologic or connective tissue disease, as well as any immunosuppression. A thorough physical exam is required, with an emphasis on the head & neck and lung examination. Breathing and voice at rest should be noted, as well as with effort. After a patient has been speaking for a few minutes, the inspiratory stridor may become evident or worsen. Diagnosis is made clinically based on flexible fiberoptic laryngoscopy, where the vocal cords are observed to be immobile, and their position can be noted. If the diagnosis is still incertain, video stroboscopy and bronchoscopy can provide additional information about the fluid-wave of the vocal cord vibrations and rule out subglottic and tracheal pathology, such as subglottic stenosis or tracheomalacia.
A detailed family and birth histories (including prolonged or protracted delivery, assistive devices used during delivery, concurrent congenital medical problems, and length of any NICU stay should be inquired. The remaining pertinent points of history are the same as in adult patients. Bilateral vocal cord paralysis often presents with stridor and feeding difficulties, and children with congenital bilateral vocal cord paralysis are more likely to exhibit severe manifestations such as cyanosis and apnea. Children with bilateral vocal cord paralysis often present with a normal voice because the vocal cords remain in the paramedian position with abductor paralysis, but can have marked inspiratory stridor and accessory muscle use with inspiration. Diagnosis is usually made via awake fiberoptic laryngoscopy, which is possible even in very small children, though more challenging than in adults. This will also rule out laryngomalacia, which is far more common than bilateral vocal cord paralysis but can have similar presenting symptoms. If the diagnosis is still uncertain, direct laryngoscopy and bronchoscopy under anesthesia may be required. This is done with the patient spontaneously breathing so the motion of the vocal cords can be assessed intraoperatively. This also allows lower airway examination to rule out concurrent or alternate pathology such as subglottic stenosis and tracheo- or bronchomalacia.
The investigations that aid in diagnosis are as follows:
Flexible fiberoptic laryngoscopy: Is an essential part of the initial physical examination and is performed with the patient awake in the office to assess spontaneous and volitional vocal cord movement.
Direct laryngoscopy and bronchoscopy: If there is any question as to the status of the vocal cords or of the lower airway, this examination is indicated. This also allows palpation of the arytenoid joints to rule out fixation.
Laryngeal electromyography: This is performed with the patient awake in the office to determine the innervation status of the laryngeal muscles, which can elucidate the duration of the paralysis and recovery potential after a neurologic injury. For details of EMG interpretation, please see the StatPearls article entitled "electromyography."
Imaging of the recurrent laryngeal nerve: In a patient with new-onset, idiopathic bilateral vocal cord paralysis, the entire course of the RLNs must be imaged to rule out a tumor or CNS pathology. CT is the most commonly employed modality, though MRI can also be used. The area to be imaged is from the high brainstem (nuclei of the vagus nerve) to the aorta (inferior-most course of the left RLN as it loops around the aortic arch).
Lab tests: There is no single lab test in bilateral vocal cord paralysis, and which investigations to consider will be guided by each patient's history and overall medical picture. Potassium, calcium, glucose, antineutrophil cytoplasmic antibody test, thyroid function tests, lyme disease titers, tuberculosis skin tests, uric acid levels, rheumatoid factor test, antinuclear antibody tests, and erythrocyte sedimentation rate can all be considered.
Although surgical intervention is commonly indicated in patients with bilateral vocal cord paralysis, medical management of inflammatory and infectious conditions such as syphilis, tuberculosis, gout, and relapsing polychondritis is essential. Corticosteroids are effective in conditions such as sarcoidosis, polychondritis, and Wegener’s granulomatosis. Glucose management is imperative to aid neuropathy in patients with diabetes mellitus. Management of reflux is often recommended during the recovery period in an effort to minimize untoward stimulation of the larynx. Greater than 50% of children will undergo spontaneous symptom resolution in the first 12 months of life, though the prognosis is much more guarded for bilateral vocal cord paralysis when compared to unilateral. This fact must be taken into consideration prior to any invasive intervention that can impact a patient’s ability to phonate or swallow. In adults, the prognosis will depend much more on the etiology, and additional studies such as EMG can have predictive value in post-surgical cases to ascertain the likelihood of recovery. If the patient is having increased work of breathing or significant stridor, some sort of surgical intervention to improve the airway will be required, even if spontaneous recovery can be expected. If the prognosis for recovery is favorable, a reversible procedure such as botulinum toxin injection or tracheostomy should be performed. If minimal or no recovery is expected, then laryngeal surgery can be considered in an attempt to decannulate the patient.
In the past, tracheostomy was the most common procedure performed in patients with bilateral vocal cord to establish a secure airway. It provides the greatest airway diameter and maintains the laryngeal structure, so it is potentially reversible without long-term sequelae. Although tracheostomy remains the standard in settings of glottic obstruction, it is associated with significant chronic care burden, cost, psychosocial impairment, and increased mortality. Patients experienced a reduced quality of life and must undergo continuous management of their tracheostomies, which can be particularly undesirable in children. In a national series of 885 infants undergoing tracheostomy, the in-hospital mortality was 14%.Endoscopic techniques have been shown to be more cost-effective as compared to tracheostomy in the management of permanent bilateral vocal cord paralysis.  Although several alternative procedures have been developed to manage bilateral vocal cord paralysis, they all have the ability to produce permanent changes of the larynx that may predispose patients to lifelong aspiration and dysphonia postoperatively.
Produced by Clostridium botulinum, botulinum toxin is a neurotoxin that prevents the release of acetylcholine from pre-synaptic axon terminals, leading to flaccid paralysis of the target muscle. For patients with vocal cord paralysis, toxin injection is utilized to block aberrant reinnervation of adductor muscles by inspiratory motor neurons. This enables abductor inspiratory motor neurons to become more effective and enable glottic opening. This technique only affects a transient improvement in symptoms for approximately three to six months at a time, requiring repeated injections for longer-lasting relief. This is a viable option in idiopathic spasmodic vocal cord dysfunction, or in cases where complete recovery of function is expected but at a protracted rate.
Arytenoidectomy is an irreversible procedure referring to the endoscopic removal of the arytenoid cartilage (sometimes only the prolapsed cuneiform cartilages are removed) to expand the glottic inlet transversely, creating a greater diameter airway for inspiration. It is either performed on its own or in combination with vocal fold resection, referred to as arytenoid cordectomy. Resection of the mucosa and cuneiform cartilage over the arytenoid leads to a widening of the glottis. This technique has demonstrated positive results in terms of augmented ventilation in patients with bilateral vocal cord paralysis, particularly in pediatric patients. Further advancement of the procedure occurred with the utilization of a CO2 laser to aid in the precision of the procedure, achieving hemostasis and reducing postoperative edema. With an arytenoidectomy, some patients may experience worsening dysphonia postoperatively, which can be permanent. This procedure also leaves the patient vulnerable to scarring and granuloma formation, which can cause airway narrowing and require multiple surgical revisions. Fortunately, endoscopic laser resections do not require the patient to undergo tracheostomy placement. The utilization of an endoscopic plasma coblator, as opposed to the CO2 laser, resulting in less scar formation due to reduced heat damage to adjacent tissues in one study.
Cordotomy is another endoscopic surgical procedure to enlarge the glottic airway. A cordotomy is accomplished via an incision of the vocal fold, ligament, and the thyroarytenoid muscle posteriorly at the attachment to the arytenoid. Cordotomy, like arytenoidectomy, is susceptible to granuloma and scar formation. Revision cordotomy can be required in up to 30% of patients secondary to reduced glottic diameter from scarring or granulation tissue formation. The most common complication associated with cordotomy was altered voice quality due to vocal fold damage. Laser endoscopic cordotomy has become the favored therapeutic intervention for VCP as compared to an arytenoidectomy, as it is less invasive and reduces the incidence of aspiration. Voice quality can be impaired after resection, but overall voice outcomes are often superior to arytenoidectomy, particularly in adult patients.
The goal of reinnervation is to establish vocal cord abduction through the restoration of the activity of the posterior cricoarytenoid (PCA) muscle. While this procedure enables the return of spontaneous vocal cord abduction, it does not affect adduction. The anastomosis of the RLN is a complicated procedure due to the variability and complexity of its supply. The phrenic nerve has been utilized to reinnervate the PCA muscle; results in one study showed inspiratory vocal fold abduction was achieved in 93% of cases. Although patients suffered from hemidiaphragm paralysis, they had substantial recovery of diaphragmatic motion and respiratory function within 12 months. Marina et al. had previously shown that only a branch of the phrenic nerve could be utilized to minimize loss of diaphragmatic function and maintain respiratory parameters. A more modern technique is the use of a pedicled neuromuscular flap from the ansa cervicalis, avoiding the diaphragmatic complications of the phrenic nerve sacrifice. This procedure is technically very challenging and is most successful when performed by the few surgeons with significant experience in its use. All of these laryngeal reinnervation procedures are far more commonly used in unilateral vocal cord paralysis.
This remains in the pre-clinical phases but holds several promising avenues for treatment in the future. With this technique, gene delivery to injured or denervated muscles enhances the growth of damaged neurons to aid in rejuvenating damaged laryngeal muscles. These genes encode neurotrophic or growth factors that aid in the stimulation of muscle differentiation and proliferation. Either delivered directly into the laryngeal muscles or into the RLN, they are absorbed by neuronal cell bodies through retrograde axonal transport. Once appropriately transduced into target cells, they produce peptides that promote RLN growth, synaptic formation, and regeneration.
In adults, recovery of idiopathic vocal cord paralysis (or vocal cord paralysis due to non-transecting nerve injury) can occur as early as 12 months following injury. Although spontaneous recovery is expected in 55% of patients, full recovery can be very protracted. The prognosis for complete spontaneous recovery is far worse in bilateral vocal cord paralysis than unilateral. Recovery of glottic function is otherwise most dependent on the underlying etiology, and the overall prognosis of this root cause.
Vocal cord paralysis can lead to the following complications:
Bilateral vocal cord paralysis is a challenging and troublesome entity in the adult and pediatric population. Surgical interventions including tracheostomy, arytenoidectomy, cordotomy, and laryngeal reinnervation have all been employed to successfully manage this condition. Risks and benefits of intervention should be weighed with each surgical technique, as well as the delicate balance between a patient airway and preservation of voice and swallowing functions. Treatment strategies should be individualized based on the patient’s clinical presentation, the surgeon’s expertise, but most importantly on the expected likelihood of spontaneous recovery. Irreversible procedures should not be performed unless the chance of spontaneous recovery is low to nil.
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