Updated: Sep 9, 2008
Bilateral vocal fold (vocal cord) immobility (BVFI) is a broad term that refers to all forms of reduced or absent movement of the vocal folds. Bilateral vocal fold (cord) paralysis (BVFP) refers to the neurologic causes of bilateral vocal fold immobility (BVFI) and specifically refers to the reduced or absent function of the vagus nerve or its distal branch, the recurrent laryngeal nerve (RLN). Vocal fold immobility may also result from mechanical derangement of the laryngeal structures, such as the cricoarytenoid (CA) joint.
Although a small number of conditions account for most cases of vocal cord immobility, this article presents a comprehensive differential diagnosis, followed by the clinical presentations, diagnostic workup, and treatment options. The goal of the article is to provide the clinician with a basic understanding of the rare entity of bilateral vocal fold immobility (BVFI).
The history of the procedures used to treat vocal cord immobility begins in 1855 with Garcia's work on mirror laryngoscopy. In the 1860s, Turk and Knight first described vocal cord paralysis. In 1922, Chevalier Jackson performed the first surgical procedure for bilateral vocal fold immobility (BVFP) when he endoscopically resected a vocal cord. He provided an airway at the expense of voice and airway protection. This dilemma continues to plague present surgeons. Since 1922, pioneers in laryngology have described arytenoidectomy, described vocal cord lateralization, and introduced the use of laser.
According to Benninger's findings in a series of 117 cases BVFI can be attributed to the following causes: surgical trauma (44%), malignancies (17%), endotracheal intubation (15%), neurologic disease (12%), and idiopathic causes (12%).1
In adults, conditions that mimic vocal fold immobility include paradoxical vocal fold motion and functional disorder.
Causes of vocal fold fixation differ in adults and in children. In adults, these include mechanical causes, inflammatory processes (affecting the CA or larynx), malignancy, surgery, neurologic causes, radiation injury, metabolic causes, and toxins. Mechanical derangement of the posterior glottis may also be referred to as posterior glottic stenosis (PGS). Bogdasarian and Olson classified PGS into the following 4 grades:2
Inflammatory processes that affect the larynx
Malignancy
Surgery
Neurologic causes
Radiation injury
Metabolic causes
Toxins
In children, causes of bilateral vocal fold immobility (BVFI) include central neurologic abnormalities, idiopathic causes, and iatrogenic causes.
Central neurologic abnormalities
Central neurologic abnormalities account for most cases of childhood bilateral vocal fold paralysis (BVFP). Arnold-Chiari deformity with meningomyelocele and hydrocephalus is the most common abnormality. Other CNS insults (eg, infarct, craniotomy, asphyxia) account for some cases, according to the findings in a study by Rosin et al.6
Idiopathic causes
Idiopathic causes are the second most common causes of childhood bilateral vocal fold paralysis (BVFP). Some researchers postulate that the etiology in some children with bilateral vocal fold paralysis (BVFI) is an imbalance between the adductors and abductors of the larynx that results in adducted vocal folds. With time, a balance is restored and symptoms abate as children mature. Although conjectural, this explanation fits with the clinical course of most children with bilateral vocal fold paralysis (BVFI) who spontaneously improve with time. Gacek hypothesized that fewer abductor fibers exist; therefore, injury to the nerve is more likely to cause abductor dysfunction.7 He also conjectured that, since abductor fibers are phylogenetically younger than adductor fibers, they may be more fragile.
Iatrogenic causes
Iatrogenic causes, including mediastinal procedures, cervical procedures, prolonged intubation, and birthing trauma, account for the remaining cases.
Although a comprehensive discussion of each of the causes is beyond the scope of this article, some principles should be emphasized. With the first episode of bilateral vocal fold paralysis (BVFP), patients may have dysphonia because the vocal cords are too far apart. Over time, however, the vocal cords can move to a medial position, and the patient may have a good voice and cough despite stridor and bilateral vocal fold paralysis (BVFP). As the vocal cords migrate toward the midline, the voice (and cough) improves, while the airway worsens. Clinicians should not mistake a good voice and cough as signs of a functioning larynx, especially in a patient with stridor. Aspiration and dysphagia may or may not be present in patients with vocal cord paralysis.
In terms of the pathophysiology of CA fixation, inflammatory or fibrotic changes can paralyze or reduce the mobility of the joint. Various disorders can cause these changes.
History
The importance of a complete history cannot be overstated. The history should include the following:
In children, obtaining a history of birth trauma, central nervous system abnormality, intubations, or surgeries is important.
Physical examination
The physical examination should include listening to the voice and airway as the patient relays his or her history.
The standard head and neck examination should include careful evaluation of the larynx. Evaluate the following:
Adults
Only the patients with severe bilateral vocal fold (cord) immobility (BVFI) require surgical intervention. Patients with medical conditions (eg, rheumatoid arthritis, Wegener granulomatosis, gout) or neurologic conditions (eg, amyotrophic lateral sclerosis [ALS], Parkinsonism, stroke) rarely require surgical intervention because treatment of the underlying condition often improves airway compromise.
For patients with bilateral vocal fold paralysis (BVFP) due to iatrogenic injury in which the recurrent laryngeal nerve (RLN) or vagus nerve is injured (neurapraxia) but not severed, permanent surgical treatment should be postponed for at least 9 months after injury to allow spontaneous recovery. Laryngeal electromyographic (EMG) monitoring can be helpful in obtaining an index of potential recovery. Obtaining a baseline EMG 30-40 days after injury and second EMG 1 month later can help in evaluating the recovery status of the vocal cords (Munin).8 On the basis of the surgeon's clinical judgment, tracheostomy for patients with quickly deteriorating airways should be initiated quickly.
For adult patients with bilateral vocal fold (cord) paralysis (BVFP), the literature supports use of an endoscopic approach, with either posterior cordectomy or limited arytenoidectomy as the initial procedure of choice. Suture lateralization may play an adjunctive role. All of these are static permanent procedures; therefore, they should be undertaken only after spontaneous improvement has failed to occur or if EMG findings suggest permanent injury.
For patients with bilateral vocal fold immobility (BVFI) caused by PGS, serial endoscopic approaches with scar lysis or microflap trapdoor reconstruction of the interarytenoid (IA) region can be attempted before the static procedures are used.
Airway obstruction refractory to the above measures is particularly vexing. Treatment options include laryngofissure with arytenoidectomy, IA reconstruction, posterior cricoidotomy with stent placement, or posterior cricoidotomy with grafting. The literature is less clear concerning the indications for each of these approaches than those of other procedures.
Children
Surgical intervention is indicated when respiratory effects are significant. Cordopexy or arytenoidopexy, along with partial or complete arytenoidectomy, can help solve the airway problem during the ensuing months or years as one waits for possible recovery of the contralateral cord. Children with bilateral vocal fold paralysis (BVFP) require tracheostomy only when o the airway fails to improve with other measures. Findings of a literature review suggest that the airway can be managed expectantly, without a tracheostomy. Endoscopic management plays a limited role in children and is useful only for mild fixed stenosis and for revisional procedures in children who have undergone open procedures.
A review of vagus nerve and RLN anatomy is necessary to understand potential injuries that can cause vocal cord paralysis. The vagus nerve originates in the nucleus ambiguus of the medulla oblongata. At that point, it is composed of cells that receive neural input from the Broca area via decussating corticobulbar tracts; thus it provides input to both the right and left nuclei. Neural input from the cerebellum and extrapyramidal centers, as well as from visceral afferents, provides proprioceptive input that modulates the motor function of the vagus nerve at this site.
The motor fibers or visceral efferents that affect the larynx and pharynx occupy 2 specific sites within the nucleus ambiguus. One site becomes the superior laryngeal nerve (SLN); the other, the RLN. The vagus nerve leaves the medulla and enters the jugular foramen, along with the accessory nerve and jugular vein. Within the jugular foramen, the vagus nerve widens to form the superior ganglion, where the cell bodies of the sensory component of the nerve reside (somatic sensory). They provide sensation to the ear canal skin (Arnold nerve). As the vagus nerve exits the jugular foramen, it widens again to form the nodose ganglion, in which nerve cell bodies containing the sensory or visceral afferents from the larynx and pharynx reside.
Immediately distal to the nodose ganglion, the SLN exits the vagus nerve and courses along the carotid artery to the larynx, where it enters the larynx through the thyrohyoid membrane, dividing into internal and external branches. The internal branch provides sensory function (visceral afferent), and the external branch provides motor function to the cricothyroid muscle (visceral efferent). The vagus nerve then descends in the neck immediately lateral to the carotid artery.
The right RLN fibers exit from the vagus nerve as the nerve crosses anteriorly over the subclavian artery. The RLN loops posteriorly around the subclavian artery to enter the larynx through the Killian-Jamieson area or superior to the fibers of the cricopharyngeal muscle entering the larynx at the cricothyroid space.
The left RLN divides much further in the mediastinum, exiting the vagus nerve as it crosses anterior to the aorta and lateral to the ligamentum arteriosum (ie, remnant of the patent ductus arteriosum between the aorta and the pulmonary vein). It then extends superiorly to enter the larynx opposite the right RLN. The RLN branches into the posterior sensory branch and the motor anterior branch to the posterior cricoarytenoid (PCA), IA, lateral cricoarytenoid (LCA), and thyroarytenoid (TA) muscles. The IA muscle is the only motor branch that receives bilateral innervation, which allows some movement of both vocal folds when one RLN is nonfunctional.
In adults, any definitive procedure to address vocal cord paralysis, whether unilateral or bilateral, must not be undertaken while a possibility for recovery exists. Recovery can occur as long as 12 months after injury. Every attempt must be made to determine if function is likely to return. This determination should include video direct laryngoscopy, during which the vocal fold can be palpated to assess mobility and bronchoscopy. In addition, laryngeal EMG can be used to evaluate normal action potentials (normal nerve), the absence of potentials (nonfunctioning nerve), defibrillating potentials (worsening nerve), or polyphasic potentials (regenerating nerve). The 12-month wait for return of function can be shortened by obtaining 2 laryngeal EMGs several months apart and by looking for evidence of improved function or stabilized function.8
As many as 70% of children with bilateral vocal fold (cord) paralysis (BVFP) require a tracheostomy. However, spontaneous recovery occurs in half of the patients, sometimes in those as old as11 years. If the condition spontaneously resolves, it typically does so 24-36 months after diagnosis. Therefore, destructive static procedures should be delayed for approximately 3 years because of this potential for recovery. Delaying surgery in children with bilateral vocal fold (cord) immobility (BVFI) caused by PGS is not beneficial; consequently, bilateral vocal fold immobility (BVFI) must be diagnosed correctly in these children to prevent restriction from surgical repair.
Medical management of the inflammatory conditions of the cricoarytenoid (CA) joint (eg, gout) and the laryngeal mucosa (eg, syphilis, tuberculosis) that result in mechanical fixation may improve the patient's airway. Corticosteroids may be effective in several conditions (eg, Wegener granulomatosis, sarcoidosis, polychondritis). Glucose management may help neuropathy due to diabetes mellitus. Reflux management may be helpful in patients with bilateral vocal fold (cord) immobility (BVFI) due to laryngopharyngeal reflux.
Procedures for bilateral vocal fold immobility (BVFI) due to IA scarring with or without CA ankylosis
Procedures for bilateral vocal fold (cord) paralysis (BVFP)
Procedures for BVFI
This discussion does not specifically address surgical management of glottic fixation other than to warn of the difficulty in differentiating between fixation and paralysis in some patients.
Procedures for BVFP -General algorithmA general algorithm for the treatment of patients with BVFP is the following: If the patient does not require a tracheotomy for a significantly compromised airway, the first procedure can be unilateral posterior cordotomy. The patient is told that this may not provide a sufficient airway, but it has the least adverse effects on his or her voice. The results may need to be revised, or a medial arytenoidectomy may be considered as the next step. Total arytenoidectomy can be performed if necessary.
Suture lateralization is a newer procedure, and its role has yet to be defined. Laryngofissure with arytenoidectomy is reserved for major reconstructive surgery in patients with a severely compromised airway. Decisions of the appropriate surgical procedure must be based on individual clinical parameters. Four techniques are discussed in further detail: posterior cordotomy or cordectomy, endoscopic limited or complete arytenoidectomy, suture lateralization (Ejnell procedure), and laryngofissure with arytenoidectomy.
Posterior cordotomy or cordectomy
Kashima and Dennis proposed these procedures in 1989.9 Complications are rare. The procedures are effective and easily repeatable in cases of recurrence. Laccourreye recently reported a 92% decannulation rate with this approach in 25 patients.10 The procedure is performed as follows:
Endoscopic limited or complete arytenoidectomy
Ossoff et al first described complete arytenoidectomy via an endoscopic approach in 1984.11 Subsequent findings from both dog models and patient series suggest that a complete arytenoidectomy is unnecessary to achieve a high decannulation rate. Eckel et al, however, compared arytenoidectomy with posterior cordectomy and found no difference in effectiveness, but the chance for subclinical aspiration in patients who underwent complete arytenoidectomy was increased.12 The procedure is performed as follows:
Suture lateralization (Ejnell procedure)
This technique may be performed alone or with posterior cordectomy, limited arytenoidectomy, or submucosal partial cordectomy. The suture may be placed with the needle inserted from the skin into larynx. This technique is a technically demanding and requires appropriate positioning of the needles and passage of the suture through the needles. The Lichtenberger needle greatly facilitates this approach. This technique may be a reasonable for revision in cases in which additional lateralization of the TVF is desired. The procedure is performed as follows:
Laryngofissure with arytenoidectomy
A surgical procedure is warranted for patients in whom vocal fold paralysis persists for several years and who are tracheostomy dependent. Bower et al showed that an external arytenoidectomy via a laryngofissure (originally described by Helmus and later by Singer et al in adults13,14 ) provides a superior decannulation rate (84%) compared with that of endoscopic laser arytenoidectomy (56%).15 The procedure is performed as follows:
Adults
The use of systemic corticosteroids and systemic antibiotics generally are recommended in each of the described endoscopic procedures. Topical fibrin glue may decrease scarring and hasten improved healing at the surgical site.
Children
After a laryngofissure is created with arytenoidectomy, perform periodic endoscopy to determine the need for decannulation or downsizing the tracheostomy tube.
The goal of all the described procedures is to restore a glottic airway despite compromised abductor and adductor function. Altered vocal quality and loss of airway protection resulting in poor cough and aspiration are possible consequences of each of these static procedures. All voice parameters are negatively affected as the airway is improved. Once the voice is affected, returning it to its previous condition often is impossible.
These complications develop with varying probabilities based on the degree of airway opening achieved with a specific technique, amount of residual abductor and adductor function, and laryngeal sensation.
Specific complications of posterior cordotomy and endoscopic partial or complete arytenoidectomy include granuloma formation, chondritis of arytenoids, carbon dioxide laser–related fire, IA scar formation, possible aspiration, and a breathy voice.
Spontaneous recovery can be expected in 55% of patients; almost half of patients who recover do so within the first year. Recovery may occur as late as 11 years after initial diagnosis.
All 6 patients treated by Dennis and Kashima with a posterior cordotomy achieved a functional airway without a tracheostomy.9 In 10 of 11 patients in Ossoff et al, a functional airway without tracheostomy was created after complete arytenoidectomy with an endoscopic carbon dioxide laser.11 Remacle et al had the same result in 40 of 41 patients with endoscopic partial arytenoidectomy.16 Eckel et al compared the results of patients treated with posterior cordotomy with those of a group of patients treated with complete arytenoidectomy.12 Both techniques were equally effective for achieving a functional airway, but patients treated with complete arytenoidectomy had more subclinical aspiration.
The plethora of etiologies in bilateral vocal fold (cord) paralysis (BVFP) and the multiple interventions do not allow easy comparison of techniques. Most series involving surgical techniques are small, and the findings generally support the authors' biases. Nonetheless, creative surgeons have a number of options that eventually should allow creation of a decannulated and safe airway in most patients.
Several techniques and approaches for the restoration of glottic competence in patients with bilateral vocal fold (cord) immobility (BVFI) are experimental but are promising. They include PCA muscle reinnervation, electrical stimulation of the laryngeal muscles, and use of the Cummings mechanical device.
PCA muscle reinnervation
Most efforts at laryngeal reinnervation have been focused on patients with unilateral vocal fold paralysis (UVFP). Chhetri et al has recently reported results with a combined procedure in which arytenoid adduction was performed with ansa cervicalis anastomosis to the RLN in a group of patients with UVFP.17 The reinnervation group had no benefit.
A group in the Netherlands selectively reinnervated the feline PCA muscle by using the phrenic nerve.18 Reinnervation was confirmed in 10 of 11 cats, but significant abductor function was restored in only 4 of 11. The authors' explanation was gradual ankylosis of the cricoarytenoid (CA) joint that limited the effects of improved abductor muscle function. This approach might be useful in patients with bilateral vocal fold (cord) paralysis (BVFP) and significant airway obstruction. The role of reinnervation in patients with BVFP remains undefined.
Electrical stimulation of the laryngeal muscles
Electrical muscle stimulation has been studied for more than 20 years. Current technology permits the creation of implanted laryngeal stimulators. Laryngeal stimulators send a stimulus that can be administered as a continuous current, an intermittent current, or a triggered (preferably by respiratory effort) pacing current. MedTronic has manufactured a number of prototype devices for this purpose, and they are still being researched.
In patients with BVFP, laryngeal pacing involves the use of an external apparatus that senses inspiration and reanimates the paralyzed larynx of the patient. Stimuli are delivered through a needle electrode to locate and pace the abductor muscle and through an electrode implanted in the PCA muscle or RLN branch that extends to the PCA muscle. Challenges include imprecise and excessive electrical stimulation, scar formation, bulky power sources, muscle fatigue with continuous stimulation, and difficulty in synchronizing the pacing with the respiratory effort in a convenient way. Researchers express optimism, but technical problems with the electrodes at the muscle site prevent widespread adoption of this technology.
Use of the Cummings mechanical device
Cummings has reported the use of an implantable device placed into the larynx through a thyroplasty window. This device engages the soft tissues of the larynx (including the TA muscle) with a screw. The screw then is rotated to pull the tissue laterally. Cummings et al conducted the investigation in sheep, with favorable results. Human studies are pending.
Benninger MS, Gillen JB, Altman JS. Changing etiology of vocal fold immobility. Laryngoscope. Sep 1998;108(9):1346-50. [Medline].
Bogdasarian RS, Olson NR. Posterior glottic laryngeal stenosis. Otolaryngol Head Neck Surg. Nov-Dec 1980;88(6):765-72. [Medline].
Gellad ZF, Hampton D, Tebbit CL, et al. Bilateral vocal cord paralysis following stent placement for proximal esophageal stricture. Endoscopy. Jul 16 2008;[Medline].
Jung A, Schramm J, Lehnerdt K, et al. Recurrent laryngeal nerve palsy during anterior cervical spine surgery: a prospective study. J Neurosurg Spine. Feb 2005;2(2):123-7. [Medline].
Jin YH, Jeong TO, Lee JB. Isolated bilateral vocal cord paralysis with intermediate syndrome after organophosphate poisoning. Clin Toxicol (Phila). Jun 2008;46(5):482-4. [Medline].
Rosin DF, Handler SD, Potsic WP, et al. Vocal cord paralysis in children. Laryngoscope. Nov 1990;100(11):1174-9. [Medline].
Gacek RR. Hereditary abductor vocal cord paralysis. Ann Otol Rhinol Laryngol. Jan-Feb 1976;85(1 Pt 1):90-3. [Medline].
Munin MC, Murry T, Rosen CA. Laryngeal electromyography: diagnostic and prognostic applications. Otolaryngol Clin North Am. Aug 2000;33(4):759-70. [Medline].
Dennis DP, Kashima H. Carbon dioxide laser posterior cordectomy for treatment of bilateral vocal cord paralysis. Ann Otol Rhinol Laryngol. Dec 1989;98(12 Pt 1):930-4. [Medline].
Laccourreye O, Paz Escovar MI, Gerhardt J, et al. CO2 laser endoscopic posterior partial transverse cordotomy for bilateral paralysis of the vocal fold. Laryngoscope. Mar 1999;109(3):415-8. [Medline].
Ossoff RH, Sisson GA, Duncavage JA, et al. Endoscopic laser arytenoidectomy for the treatment of bilateral vocal cord paralysis. Laryngoscope. Oct 1984;94(10):1293-7. [Medline].
Eckel HE, Thumfart M, Wassermann K, et al. Cordectomy versus arytenoidectomy in the management of bilateral vocal cord paralysis. Ann Otol Rhinol Laryngol. Nov 1994;103(11):852-7. [Medline].
Helmus C. Microsurgical thyrotomy and arytenoidectomy for bilateral recurrent laryngeal nerve paralysis. Laryngoscope. Mar 1972;82(3):491-503. [Medline].
Singer MI, Hamaker RC, Miller SM. Restoration of the airway following bilateral recurrent laryngeal nerve paralysis. Laryngoscope. Oct 1985;95(10):1204-7. [Medline].
Bower CM, Choi SS, Cotton RT. Arytenoidectomy in children. Ann Otol Rhinol Laryngol. Apr 1994;103(4 Pt 1):271-8. [Medline].
Remacle M, Lawson G, Mayne A, et al. Subtotal carbon dioxide laser arytenoidectomy by endoscopic approach for treatment of bilateral cord immobility in adduction. Ann Otol Rhinol Laryngol. Jun 1996;105(6):438-45. [Medline].
Chhetri DK, Gerratt BR, Kreiman J, et al. Combined arytenoid adduction and laryngeal reinnervation in the treatment of vocal fold paralysis. Laryngoscope. Dec 1999;109(12):1928-36. [Medline].
van Lith-Bijl JT, Stolk RJ, Tonnaer JA, et al. Laryngeal abductor reinnervation with a phrenic nerve transfer after a 9-month delay. Arch Otolaryngol Head Neck Surg. Apr 1998;124(4):393-8. [Medline].
Bower CM, Choi SS, Cotton RT. Arytenoidectomy in children. Ann Otol Rhinol Laryngol. Apr 1994;103(4 Pt 1):271-8. [Medline].
Cavo JW Jr. True vocal cord paralysis following intubation. Laryngoscope. Nov 1985;95(11):1352-9. [Medline].
Coffey CS, Vallejo SL, Farrar EK, et al. Sarcoidosis Presenting as Bilateral Vocal Cord Paralysis From Bilateral Compression of the Recurrent Laryngeal Nerves From Thoracic Adenopathy. J Voice. May 9 2008;[Medline].
Cohen SR. Pseudolaryngeal paralysis: a postintubation complications. Ann Otol Rhinol Laryngol. Sep-Oct 1981;90(5 Pt 1):483-8. [Medline].
Correa AJ, Reinisch L, Sanders DL, et al. Inhibition of subglottic stenosis with mitomycin-C in the canine model. Ann Otol Rhinol Laryngol. Nov 1999;108(11 Pt 1):1053-60. [Medline].
Cummings CW, Redd EE, Westra WH, et al. Minimally invasive device to effect vocal fold lateralization. Ann Otol Rhinol Laryngol. Sep 1999;108(9):833-6. [Medline].
Daya H, Hosni A, Bejar-Solar I, et al. Pediatric vocal fold paralysis: a long-term retrospective study. Arch Otolaryngol Head Neck Surg. Jan 2000;126(1):21-5. [Medline].
Dedo DD, Dedo HH. Vocal Cord Paralysis. Otolaryngology. 1980;3:2489-2503.
Dedo HH, Sooy CD. Endoscopic laser repair of posterior glottic, subglottic and tracheal stenosis by division or micro-trapdoor flap. Laryngoscope. Apr 1984;94(4):445-50. [Medline].
Downey WC, Keenan WG. Laryngofissure approach for bilateral abductor paralysis. Arch Otolaryngol. 1968;88:513-17.
Dray TG, Robinson LR, Hillel AD. Idiopathic bilateral vocal fold weakness. Laryngoscope. Jun 1999;109(6):995-1002. [Medline].
Endo K, Okabe Y, Maruyama Y, et al. Bilateral vocal cord paralysis caused by laryngeal mask airway. Am J Otolaryngol. Mar-Apr 2007;28(2):126-9. [Medline].
Fukuda H, Kitani M, Imaoka K. [A case of hereditary motor and sensory neuropathy with vocal cords palsy and diaphragmatic weakness]. Rinsho Shinkeigaku. Feb 1993;33(2):175-81. [Medline].
Gardner GM. Posterior glottic stenosis and bilateral vocal fold immobility: diagnosis and treatment. Otolaryngol Clin North Am. Aug 2000;33(4):855-78. [Medline].
Goodwin WJ Jr, Isaacson G, Kirchner JC, et al. Vocal cord mobilization by posterior laryngoplasty. Laryngoscope. Aug 1988;98(8 Pt 1):846-8. [Medline].
Grahne B, Poppius H, Viljanen AA, et al. Surgical treatment of chronic laryngeal stenosis secondary to vocal cord paralysis: pre and postoperative evaluation of ventilatory function. Laryngoscope. Feb 1983;93(2):163-7. [Medline].
Gray SD, Kelly SM, Dove H. Arytenoid separation for impaired pediatric vocal fold mobility. Ann Otol Rhinol Laryngol. Jul 1994;103(7):510-5. [Medline].
Hartl DM, Brasnu D. [Recurrent laryngeal nerve paralysis: current knowledge and treatment]. Ann Otolaryngol Chir Cervicofac. Mar 2000;117(2):60-84. [Medline].
Hillel AD, Benninger M, Blitzer A, et al. Evaluation and management of bilateral vocal cord immobility. Otolaryngol Head Neck Surg. Dec 1999;121(6):760-5. [Medline].
Holinger LD, Holinger PC, Holinger PH. Etiology of bilateral abductor vocal cord paralysis: a review of 389 cases. Ann Otol Rhinol Laryngol. Jul-Aug 1976;85(4 Pt 1):428-36. [Medline].
Inomata S, Nishikawa T, Suga A, et al. Transient bilateral vocal cord paralysis after insertion of a laryngeal mask airway. Anesthesiology. Mar 1995;82(3):787-8. [Medline].
Isaacson G, Moya F. Hereditary congenital laryngeal abductor paralysis. Ann Otol Rhinol Laryngol. Nov-Dec 1987;96(6):701-4. [Medline].
Jackson C. Ventriculocordectomy. Arch Surg. 1922;4:257-74.
Kashima HK. Bilateral vocal fold motion impairment: pathophysiology and management by transverse cordotomy. Ann Otol Rhinol Laryngol. Sep 1991;100(9 Pt 1):717-21. [Medline].
Lacy PD, Hartley BE, Rutter MJ, et al. Familial bilateral vocal cord paralysis and Charcot-Marie-tooth disease type II-C. Arch Otolaryngol Head Neck Surg. Mar 2001;127(3):322-4. [Medline].
Lichtenberger G, Toohill RJ. Technique of endo-extralaryngeal suture lateralization for bilateral abductor vocal cord paralysis. Laryngoscope. Sep 1997;107(9):1281-3. [Medline].
Neuschaefer-Rube C, Haase G, Angerstein W, et al. [Unilateral recurrent nerve paralysis in suspected Lyme borreliosis]. HNO. Mar 1995;43(3):188-90. [Medline].
Rahbar R, Valdez TA, Shapshay SM. Preliminary results of intraoperative mitomycin-C in the treatment and prevention of glottic and subglottic stenosis. J Voice. Jun 2000;14(2):282-6. [Medline].
Reker U, Rudert H. [Modified posterior Dennis and Kashima cordectomy in treatment of bilateral recurrent nerve paralysis]. Laryngorhinootologie. Apr 1998;77(4):213-8. [Medline].
Rimell FL, Dohar JE. Endoscopic management of pediatric posterior glottic stenosis. Ann Otol Rhinol Laryngol. Apr 1998;107(4):285-90. [Medline].
Sanders I. Electrical stimulation of laryngeal muscle. Otolaryngol Clin North Am. Oct 1991;24(5):1253-74. [Medline].
Sofferman RA, Haisch CE, Kirchner JA, et al. The nasogastric tube syndrome. Laryngoscope. Sep 1990;100(9):962-8. [Medline].
Sommer DD, Freeman JL. Bilateral vocal cord paralysis associated with diabetes mellitus: case reports. J Otolaryngol. Jun 1994;23(3):169-71. [Medline].
Strong MS, Healy GB, Vaughan CW, et al. Endoscopic management of laryngeal stenosis. Otolaryngol Clin North Am. Nov 1979;12(4):797-805. [Medline].
Terris DJ, Arnstein DP, Nguyen HH. Contemporary evaluation of unilateral vocal cord paralysis. Otolaryngol Head Neck Surg. Jul 1992;107(1):84-90. [Medline].
Wani MK, Yarber R, Hengesteg A, et al. Endoscopic laser medial arytenoidectomy versus total arytenoidectomy in the management of bilateral vocal fold paralysis. Ann Otol Rhinol Laryngol. Nov 1996;105(11):857-62. [Medline].
Whited RE. Posterior commissure stenosis post long-term intubation. Laryngoscope. Oct 1983;93(10):1314-8. [Medline].
Woodson BT, McFadden EA, Toohill RJ. Clinical experience with the Lichtenberger endo-extralaryngeal needle carrier. Laryngoscope. Sep 1991;101(9):1019-23. [Medline].
Zalzal GH. Posterior glottic fixation in children. Ann Otol Rhinol Laryngol. Sep 1993;102(9):680-6. [Medline].
Zeitels SM. The evolution of the assessment and treatment of paralytic dysphonia. Otolaryngol Clin North Am. Aug 2000;33(4):803-16. [Medline].
vocal, vocal fold paralysis, vocal cords, vocal cord, bilateral vocal fold paralysis, bilateral vocal cord paralysis, bilateral vocal cord immobility, vocal cord paralysis, bilateral vocal fold immobility, BVFP, BVFI, recurrent laryngeal nerve, cricoarytenoid joint, bilateral vocal fold
Joel A Ernster, MD, Active Staff, Penrose-St Francis Healthcare System; Active Staff, Memorial Health System; Clinical Instructor, University of Colorado Health Sciences Center
Joel A Ernster, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Head and Neck Society, American Rhinologic Society, Colorado Medical Society, and Triological Society
Disclosure: Nothing to disclose.
Arturo Avila Chavez, MD, Assistant Professor, Department of Otolaryngology and Head and Neck Surgery, Instituto Nacional De Enfermedades Respiratorias of Mexico City
Disclosure: Nothing to disclose.
Douglas Skarada, MD, Consulting Staff, Department of Otolaryngology, Salem Hospital
Disclosure: Nothing to disclose.
Clark A Rosen, MD, Director, University of Pittsburgh Voice Center; Associate Professor, Department of Otolaryngology and Communication Science and Disorders, University of Pittsburgh School of Medicine
Clark A Rosen, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, and Pennsylvania Medical Society
Disclosure: Bioform Medical Consulting fee Consulting
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Robert M Kellman, MD, Professor and Chair, Department of Otolaryngology and Communication Sciences, State University of New York, Upstate Medical University
Robert M Kellman, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, American Neurotology Society, American Rhinologic Society, American Society for Head and Neck Surgery, Medical Society of the State of New York, and Triological Society
Disclosure: GE Healthcare Honoraria Review panel membership
Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association
Disclosure: Nothing to disclose.
Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society
Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation unstricted gift unknown; Axis Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board membership; Syndicom Ownership interest Consulting; Oxlo Consulting; Medvoy Ownership interest Management position
© 1994-
by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)