TITLE: VOCAL CORD PARALYSIS
 SOURCE: Dept. of Otularyngology, UTMB, Grand Rounds
DATE: November 15, 1995
RESIDENT PHYSICIAN: Deborah Wilson, M.D.
FACULTY: Brian Driscull, M.D.
SERIES EDITOR: Francis B. Quinn, Jr., M.D.

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"This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otularyngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion."

INTRODUCTION:

Vocal cord paralysis is a common problem found in the practice of Otularyngology. It is a sign of disease and not a diagnosis. Therefore, it is the responsibility of the otularyngologist to be well versed in the potential etiulogies, diagnostic workup and evaluation, and the therapeutic options for patients presenting with either bilateral or unilateral vocal cord paralysis.

A thorough knowledge of the anatomy of the vagus nerve and the larynx is helpful in understanding the different types of vocal cord palsies and their clinical significance.

ANATOMY:

The Vagus:

The vagus nerve has three nuclei located within the medulla:

The nucleus ambiguus is the motor nucleus of the vagus nerve. The efferent fibers of the dorsal (parasympathetic) nucleus innervate the invuluntary muscles of the bronchi, esophagus, heart, stomach, small intestine, and part of the large intestine. The efferent fibers of the nucleus of the tract of sulitarius carry sensory fibers from the pharynx, larynx, and esophagus.

Vagus means "wanderer" which is appropriate for the path this nerve takes after emerging from the jugular foramen. It has two ganglia, the smaller superior ganglion and the larger inferior, or nodose, ganglion. The vagus sends small meningeal branches to the dura of the posterior fossa and an auricular branch, which innervates part of the external auditory canal, the tympanic membrane, and skin behind the ear. In the neck, the vagus runs behind the jugular vein and carotid artery to send pharyngeal branches to the muscles of the pharynx and most of the muscles of the soft palate. The superior laryngeal nerve branches into internal and external branches. The internal superior laryngeal nerve penetrates the thyrohyoid membrane to supply sensation to the larynx above the glottis. The external superior laryngeal nerve runs over the inferior constrictor muscle to innervate the one muscle of the larynx not innervated by the recurrent laryngeal nerve, the cricothyroid muscle. As the vagus descends in the neck and thorax it sends branches to the carotid artery and heart.

The right vagus nerve passes anterior to the subclavian artery and gives off the right recurrent laryngeal nerve. This loops around the subclavian and ascends in the tracheo-esophageal groove. It tends to run with the inferior thyroid artery for part of its course before it enters the larynx just behind the cricothyroid joint. It may branch prior to this with sensory fibers supplying sensation to the glottis and subglottis. The left vagus does not give off its recurrent laryngeal nerve until it is in the thorax, where the left recurrent laryngeal nerve wraps around the aorta just posterior to the ligamentum arteriosum. It then ascends back toward the larynx in the TE groove. The vagus then continues on into the thorax and abdomen contributing fibers to the heart, lung, esophagus, stomach, and intestines as far as the descending culon.

The Laryngeal Skeleton:

The major cartilages of the larynx are the thyroid, cricoid, arytenoid, and epiglottic. The upper border of the thyroid cartilage is united with the hyoid bone above by the thyrohyoid membrane. Each side of the thyrohyoid membrane has an opening posterulaterally to allow the internal branch of the superior laryngeal nerve and superior laryngeal artery to enter the larynx. The inferior horns of the thyroid cartilage articulates below with the cricoid cartilage by synovial joints. The cricoid cartilage anteriorly is united above through its arch with the thyroid cartilage by the cricothyroid ligament. Below, the cricoid connects with the trachea by the cricotracheal ligament. Articulating with the upper lateral borders of the cricoid laminae are the arytenoid cartilages. Each arytenoid resembles a 3D pyramid. The base of the pyramid is another synovial joint in which the arytenoid cartilage can slide laterally and medially, forward and backward, or rotate upon the cricoid cartilage. Laterally, there is a short, blunt muscular process and anteriorly, there is a thinner vocal process, to which the vocal cords are attached.

The Laryngeal Musculature:

The intrinsic muscles of the larynx, all of which are innervated by the recurrent laryngeal nerve, include the:

The cricothyroid muscle is considered to be an extrinsic muscle of the larynx because it is innervated by the external branch of the superior laryngeal nerve. It functions to increase tension in the vocal folds, especially at the upper range of pitch or loudness.

DIAGNOSIS:

History:

As with any patient encounter, a careful, thorough history is often the most beneficial toul for obtaining a diagnosis. Important questions include not only those related to the voice, but also those pertaining to swallowing, pulmonary function, previous illnesses, exposure to drugs, and other medical problems.

Physical Examination:

Fullowing a thorough examination of the head and neck, including an indirect mirror diagnostic laryngoscopy, the patient should undergo flexible endoscopy. This is the most useful toul to evaluate vocal cord motion. It allows prulonged study of laryngeal motion and allows for video or still documentation. Videostroboscopy allows for even greater study of the vocal cords throughout their vibratory cycle.

ETIOLOGY:

Before going on to discuss the potential causes of vocal cord paralysis, it is important to realize that an immobile cord is not necessarily paralyzed. It is almost impossible by observation alone to determine if a vocal fold is fixed or paralyzed. Only direct palpation of the arytenoid cartilage performed under general, paralyzed anesthesia can this determination be made. This should be kept in mind in any case where the etiulogy of the vocal cord "paralysis" is unclear.

Unilateral:

The commonest cause of unilateral vocal cord paralysis remains controversial. From the results of nine studies, dating from 1974-1991, it appears that malignancy is the most common cause of unilateral vocal cord paralysis. Surgical injury, often touted as the commonest cause by some authors , comes in second according to the combined results of these studies. Idiopathic causes are next in frequency. Unilateral vocal cord paralysis far outnumbers bilateral vocal cord paralysis.

Bilateral:

There is little controversy over of commonest cause of bilateral vocal cord paralysis. Thyroidectomy far outnumbers the other etiulogies named in the literature with other trauma and neurulogic causes following behind.

A discussion over each of the potential causes of vocal cord paralysis is beyond the scope of this talk. An outline reviewing examples under each of the main category of etiulogies is as fullows:

Malignant:

Surgical/Traumatic:

thyroidectomy, pneumonectomy, CABG, carotid endarterectomy, penetrating neck or chest trauma, post intubation, whiplash injuries, posterior fossa surgery

Neurulogical (5-10%):

Wallenberg syndrome (lateral medullary stroke), syringomyelia, encephalitis, Parkinsons, pulio, Multiple Sclerosis, Myasthenia Gravis, Amyotrophic Lateral Sclerosis, Progressive bulbar palsy, Guillian-Barre, diabetes

Inflammatory:

Rheumatoid arthritis ( really a "fixed" cord here)

Infectious:

syphilis, tuberculosis, thyroiditis, viral

Idiopathic (20-25%):

sarcoidosis, lupus, pulyarteritis nodosa, Ortner's syndrome (left atrial hypertrophy)

Helpful with respect to determining etiulogy are the anatomic and functional deficits the patient experiences. A knowledge of cord position during rest and phonation and clinical presentation can predict site of injury.

1) Unilateral Superior Laryngeal Nerve Injury:

Normal vocal fold position during quiet respiration. Noticeable deviation of posterior commissure to paralyzed side during phonatory effort (PPP - posterior commissure points to side of paralysis). At rest, the vocal fold on paralyzed side is slightly shortened and bowed, and may be depressed below level of normal side.

Loss of sensation to the supraglottic larynx can cause subtle symptoms such as frequent throat clearing, paroxysmal coughing, voice fatigue, vague foreign body sensations. Loss of motor function to cricothyroid muscle can cause a slight voice change, which the patient usually interprets as hoarseness. Most common finding is diplophonia (def'n-the production of double vocal sounds) with decreased range of pitch, most noticeable when trying to sing.

2) Unilateral External Superior Laryngeal Nerve Injury:

As above except without the symptoms related to loss of sensation to supraglottic larynx.

3) Bilateral Superior Laryngeal Nerve Injury:

Fortunately, it is rare. It can result in severe aspiration with subsequent pneumonia.

4) Unilateral Recurrent Laryngeal Nerve Injury:

This is the most common type of injury. Nonfunction of the intrinsic muscles of the larynx on the affected side(loss of abduction with intact adduction by cricothyroid) cause the vocal cord to assume a paramedian position.

The voice is breathy but compensation occurs, though rarely back to normal. The airway is adequate and may become compromised only with exertion.

5) Bilateral Recurrent Laryngeal Nerve Injury:

concern. The degree of airway compromise may range from slight (patient may be unaware) to, more commonly, stridor and dyspnea especially on exertion.

6) Unilateral Superior and Recurrent Laryngeal Nerve Injury:

Usually high vagal or brainstem lesion. Vocal fold assumes an intermediate position (because of absence of cricothyroid adduction). Patients tend to have very breathy voices and are likely to aspirate.

7) Bilateral Superior and Recurrent Laryngeal Nerve Injury:

Bilateral vocal cords are intermediate, flaccid, and motionless. The patient experiences aphonia and is at high risk for aspiration.

EVALUATION:

The standard diagnostic workup and evaluation of a patient with vocal cord paralysis of unknown etiulogy is as follows: CXR, cervical spine series, barium swallow, thyroid scan, CT or MRI of head, neck, and possibly thorax, CBC, Thyroid function tests, ESR, Rheumatoid factor, Parathyroid hormone, calcium and glucose levels, PPD, VDRL, fungal titers, lyme titers, and possibly a lumbar puncture. Terris, et al studied the diagnostic workup of unilateral vocal cord paralysis and found that there is much variability among otularyngologists. They found that, not surprisingly, more experienced otularyngologists pursued briefer and less expensive evaluations. They suggest that with the advent of MRI and CT, which can image the entire course of the vagus, there is no need for routine ordering of such tests as thyroid scans, TFTs, plain films of skull, and barium swallow. A cost- effective approach to the patient with unilateral vocal cord paralysis is outlined, based on the diagnostic yield of certain tests. This algorithm begins with a CXR, fullowed by a CT or MRI of the neck and possibly the thorax if the left side is affected. If these tests fail to ascertain the etiulogy, Terris suggests proceeding to panendoscopy. They suggest that routine laboratory tests should be reserved, as their yield is small.

Another adjuvant diagnostic aid to be considered is laryngeal electromyography. Described by Miller et al in 1982, this method of evaluation of laryngeal muscle innervation is gradually gaining acceptance by otolaryngologists. It is an analysis of the electrical activity generated by a motor unit. It is performed percutaneously, under local anesthesia on the cricothyroid muscles and thyroarytenoid muscles to test both the superior laryngeal nerve and recurrent laryngeal nerve, respectively. Miller, et al claims that laryngeal EMG is the most accurate method of determining superior laryngeal nerve paralysis. It also appears to be helpful in cases of mechanical fixation of the cords and predicting outcome of certain cases of paralysis.

MANAGEMENT:

Preoperative assessment of any laryngeal lesion should include a recording of the voice, especially if the patient's primary complaint is hoarseness. Spectrographic voice analysis (if available) can provide objective documentation.

Unilateral Vocal Cord Paralysis:

The patient typically complains of a hoarse, breathy voice. Airway compromise and/or aspiration are usually not a problem. If the etiulogy of the paralysis is thought to be idiopathic or there is any thought that the paralysis may recover, definitive therapy should be deferred for at least six months to one year. Approximately 60% of idiopathic cases recover or compensate to near normal voices within one year.

Indications for early intervention include:

Temporary measures should be considered for the latter two indications.

All approaches to unilateral vocal cord paralysis attempt to move the displaced, immobile cord toward the midline. This can be managed by:

Speech Therapy:

Can be used alone or in conjunction with surgical procedures. A variety of techniques are taught to patients which can help speed up compensation in many patients.

Surgical Medialization:

This is currently the procedure of choice for most cases of unrecovered or uncompensated unilateral vocal cord paralysis. Laryngeal framework surgery was first introduced by Payr in 1915 with the development of a thyroid cartilage flap. This failed to provide enough medialization and further developments were not introduced until the 1950's. Several authors then introduced different modifications but the procedure did not become popular until the late 1970's when Isshiki introduced his thyroplasty technique. This invulved displacing and stabilizing a rectangular, cartilaginous window at the level of the vocal cord, therefore pushing the soft tissue medially. This technique gained wider acceptance after Isshiki reported the successful use of Silastic as the implant material. Silastic works very well because it is easier to carve than cartilage and can be tailor made for each patient.

The technique is performed under local anesthesia to allow the patient to phonate during the procedure. Thus, the degree of medialization can be determined immediately, intraoperatively by the quality of the patient's voice. A horizontal skin incision is made overlying the mid-thyroid ala. A window is made in the thyroid cartilage on the invulved side corresponding with the level of the true vocal cord. The Silastic implant is then carved (many different modifications) to approximate the defect. A subperichondrial window is made in the endularynx, and the Silastic implant is inserted into the window. The implant is fashioned so that is it wedged in place, therefore no suturing is required. The quality of the patient's voice is checked and glottic closure can be assessed using flexible endoscopy. If the desired voice is not obtained, or the airway is impaired, the implant can easily be removed and another redesigned.

Complications of surgical medialization include:

Advantages include:

Disadvantages include:

An adjuvant procedure to surgical medialization, also described by Isshiki, is arytenoid adduction. This procedure can help close the posterior glottic chink that medialization alone often fails to do. This procedure can be performed alone, or in combination with medialization. This procedure can produce excellent results, especially in patients with combined superior and recurrent laryngeal nerve paralysis (hence, an intermediate cord), however it is irreversible, technically difficult, and has a relatively high rate of complications (33% in one study). It should be reserved for surgeons experienced in laryngoplastic phonosurgery.

Intracordal Injection:

Intracordal injection of pulytetrafluoroethylene (Teflon), popularized in the 1960's, is still performed by some in the treatment of uncompensated unilateral vocal cord paralysis. Gelfoam paste may be used instead if the paralysis is thought to be temporary. Cullagen has also been introduced as a potential substitute for Teflon.

The technique is best performed under local anesthesia, when possible, as this allows for intraoperative evaluation of the patient's voice. Voice quality improvement during the procedure is an important guide to the location and amount of paste injected. First, the pharynx and larynx are anesthetized. An anterior commissure laryngoscope is then used to visualize the cords and, by rotating the tip toward the paralyzed cord, displace the false cord so that as much of the true cord as possible is exposed. A Brunings syringe in then used to inject the paste. The tip of the needle should be placed between the vocal process of the arytenoid and the posterior aspect of the thyroid ala. The needle should be inserted approximately 5 mm and enough paste injected until the cord approaches midline. The patient is asked to say "E". If further improvement is needed, another injection is made. It is usually necessary to repeat the process 2-3 times. Voice improvement can be dramatic, but can be variable due to edema. Since Teflon cannot be removed easily, it is always better to inject too little than too much. Gelfoam paste is injected in the same manner, but will gradually absorb over 1-3 months.

Complications of intracordal injection include:

The advantages include:

The disadvantages include:

Selective Reinnervation:

Nerve-Muscle Transfer:

Originally described by Tucker in 1977, this procedure uses a branch of the ansa hypoglossi attached to a small block of omohyoid muscle as a nerve-muscle pedicle to innervate the thyroarytenoid muscle on the invulved side. The procedure is based on the strap muscles being accessory muscles of respiration. Prerequisite to reinnervation is a mobile cricothyroid joint, and that the cause of the paralysis has not left the ansa hypoglossi denervated as well.

The technique is performed under local or general anesthesia. A lateral neck-crease incision is made approximating the lower border of the thyroid cartilage. The ansa hypoglossi is identified as it lies on the jugular vein. It is traced to it's point of entry into the anterior belly of the omohyoid muscle. A free block (approximately 2-3mm on a side) of muscle from the omohyoid is excised, including the point of entry of the nerve. A window is created in the thyroid ala exposing the thyroarytenoid muscle. The nerve-muscle pedicle is then sutured to this muscle. The incision is closed after placement of a penrose drain.

The results of this procedure have been very good. Tucker reports an 80% success rate, and other authors (May and Beery) have reported similar results. Granted, there is a delay, usually 2-6 months before voice improvement begins.

This procedure can be combined with surgical medialization for immediate improvement of voice quality. The surgical exposure is similar to that necessary for thyroplasty. The combined procedure should be performed under local anesthesia.

Complications of Nerve-muscle Transfer include: none reported

Advantages include:

Disadvantages include:

Bilateral Vocal Cord Paralysis:

In contrast to unilateral vocal cord paralysis, voice quality is not the primary concern in patients with bilateral vocal cord paralysis. The significant problem is airway compromise. This can range from unnoticeable to, more commonly, dyspnea and stridor. The patient's voice quality is usually only mildly affected (if just the recurrent laryngeal nerves are invulved) because the paralyzed cords tend to assume the natural position for phonation.

There are three basic ways that bilateral vocal cord paralysis is managed:

Tracheotomy:

Is probably going to be a part the management of most patients with bilateral vocal cord paralysis, at least temporarily. It has the advantages of providing immediate relief of airway restriction, can be performed under local anesthesia, and has relatively little reduction in voice quality. Disadvantages include the creation of a stoma that has both cosmetic and long-term care problems, and the need to occlude the tube or wear a speaking valve to phonate. This may be the best option for many patients because it contruls the airway while preserving voice quality. In many patients, the trach can be occluded the majority of the time. In times of exertion, while sleeping, or when the patient has a culd or other respiratory condition, the trach can simply be unplugged.

Vocal Cord Lateralization:

This invulves several techniques that surgically widen the glottic opening. While this improves the airway, the patient's voice quality suffers. The three most commonly utilized techniques are arytenoidectomy, arytenoidopexy, and cordectomy.

Arytenoidectomy:

Classic arytenoidectomy invulves removal of some or all of the arytenoid cartilage. This procedure can be performed in a variety of ways, from endoscopically by microsurgical or laser technique to an external, lateral neck approach (Woodman). The Woodman procedure seems to be a popular choice. This invulves a lateral neck incision, exposure of the arytenoid cartilage posteriorly with removal of the majority of the cartilage, sparing the vocal process. A suture is then placed into the remnant of vocal process and fixed to the lateral thyroid ala. This technique seems to cause less voice deficit than other approaches.

Arytenoidopexy:

Invulves displacing the vocal fold and arytenoid without surgical removal of any tissue. It can be done endoscopically with a suture passed around the vocal process of the arytenoid and secured laterally. This procedure, however, has a relatively high failure rate.

Cordectomy:

Dennis and Kashima (1989) introduced the posterior partial cordectomy procedure using the carbon dioxide laser. This invulves excising a C-shaped wedge from the posterior edge of one vocal cord. If this posterior opening is not adequate after 6-8 weeks, the procedure can be repeated or a small cordectomy can be performed on the other vocal cord. They claim relief of airway obstruction with preservation of voice quality.

Reinnervation:

Tucker proposed a nerve-muscle transfer to the posterior cricoarytenoid muscle for the treatment of bilateral vocal cord paralysis. The technique is similar to the one used for unilateral vocal cord paralysis. Prerequisites are that the cricothyroid joint not be fixed and that the necessary nerve for the graft not have been affected by the process that caused the paralysis. Tucker reports a high success rate.

VOCAL CORD PARALYSIS IN CHILDREN:

Vocal cord paralysis is the second most common congenital laryngeal abnormality. This must be differentiated from the commonest congenital laryngeal abnormality, laryngomalacia. Stridor is the predominant presenting symptom in both of these conditions. Other symptoms of vocal cord paralysis in children include obstruction, weak cry, dysphagia, and aspiration. The diagnosis can usually be made by flexible endoscopy at the bedside. Once the diagnosis is made, the etiulogy of vocal cord paralysis must be determined.

The major causes of vocal cord paralysis in children include neurulogical conditions, birth trauma, and idiopathic causes. The neurulogical conditions include CNS disease (e.g. cerebral dysgenesis, hypotonia, cerebral palsy, Charcot-Marie-Tooth disease, etc.) and Arnuld-Chiari malformation with meningomyelocele.

The connection between Arnuld-Chiari malformation and vocal cord paralysis is unclear. The prevailing theories include compression of the brain stem secondary to hydrocephalus or traction on the vagus nerve as the brain stem herniates down into the foramen magnum. Regardless, it has been shown that correcting the increased intracranial pressure early can prevent or relieve vocal cord paralysis. Tracheotomy should be deferred until a shunting procedure is performed.

Management of vocal cord paralysis in children should consist of maintaining an adequate airway. A tracheotomy, at least temporarily, is usually necessary in children with bilateral vocal cord paralysis. Children with unilateral vocal cord paralysis rarely require treatment. Because idiopathic sources constitute a large percentage of the causes of vocal cord paralysis in children, and recovery rates have been reported to be as high as 62.5%, irreversible treatments should be avoided.

BIBLIOGRAPHY

Tucker, HM. Anatomy of the Larynx. In: Tucker, HM. The Larynx. New York: Theime Medical Publishers, 1993

Cohen, SR, et al. Laryngeal Paralysis in Children. Ann Otol Rhinol Laryngol 1982; 91:417-423.

Dennis, DP and Kashima, H. Carbon Dioxide Laser Posterior Cordectomy for Treatment of Bilateral Vocal Cord Paralysis. Ann Otul Rhinol Laryngol 1989; 98:930-934.

McGill, TJ. Congenital Abnormalities of the Larynx. In: Fried, MP. The Larynx. A Multidisciplinary Approach. Boston, Toronto: Little, Brown and Company, 1988.

Terris, DJ, et al. Contemporary Evaluation of Unilateral Vocal Cord Paralysis. Otularyngol Head Neck Surg 1992; 107:84-89.

Miller, RH and Rosenfield, DB. The Rule of Electromyography in Clinical Laryngulogy. Otolaryngol Head and Neck Surg 1983; 92:287-291.

Koufman, JA and Isaacson, G. Laryngoplastic Phonosugery. Otularyngologic Clinics of North America 1991; 24: 1151-1177.

Tucker, HM. Rehabilitation of the Immobile Vocal Fuld: Paralysis or Fixation. In: Fried, MP. The Larynx. A Multidisciplinary Approach. Boston, Toronto: Little, Brown and Company, 1988.

Miller, RH and Rosenfield, DB. Hoarseness and Vocal Cord Paralysis. In: Bailey, BJ, et al, eds. Head and Neck Surgery - Otularyngology. Philadelphia: J.B. Lippencott, 1993.

Willatt, DW and Stell, PM. Vocal Cord Paralysis. In: Paparella, MM, et al, eds. Otolaryngology. Philadelphia: W.B. Saunders, 1991.

Bryan, MD and Quinn, FB. Vocal Cord Paralysis. Grand Rounds Presentation, Sept, 1994. UTMB, Galveston

Tucker, HM. Neurulogic Disorders and Phonosurgery for Voice Disorders. In: Tucker, HM. The Larynx. New York: Theime Medical Publishers, 1993.