Vocal cord paralysis

By

Dr. T. Balasubramanian M.S. D.L.O.

Definition:  Vocal cord paralysis is caused by paralysis of intrinsic muscles of larynx.  This is a symptom of an underlying disorder and not a disease by itself.  The intrinsic muscles of the vocal cord are supplied by the vagus nerve.  The term vagus means "wanderer" which is the apt term to describe this nerve becuase of its long anatomical course.

Unilateral vocal fold paralysis occurs due to dysfunction of recurrent laryngeal or vagus nerve causes a breathy voice.  The breathiness of voice is caused by glottic chink which allows air to escape when the patient attempts to speak.  Normal voice production is dependent on proper glottal closure resulting from bilateral adduction of the vocal cords.  This adduction of vocal folds combined with subglottic air pressure causes the vocal folds to vibrate causing phonation.

Anatomy of vagus nerve:

The vagus nerve arises from three nuclei located in the medulla of brain.  They are:

1. Nucleus ambiguus

2. Nucleus dorsalis

3. Nucleus of tractus solitarius

Nucleus ambiguus:  Is the motor nucleus of the vagus nerve.  It lies within the medulla and is approximately 2 cm long in reticular formation of medulla. Superior portion of the nucleus projects fibers to the 9th cranial nerve, while the middle portion to the 10th nerve, and the inferior portion to the cranial part of the 11th cranial nerve.   The efferent fibers of the dorsal  nucleus innervates the involuntary muscles of bronchi, esophagus, heart,  stomach, small intestine, and part of the large intestine.  The efferent fibers of the nucleus of the tract of solitarius carry sensory fibers from the pharynx, larynx, and esophagus.



































Diagram showing nucleus ambiguus


The vagus nerve (wanderer) takes a tortuous path after emerging from the jugular foramen.  It has two ganglions.  The smaller superior ganglion and a larger inferior or nodose ganglion.  In the neck the vagus nerve runs behind the jugular vein and  carotid artery.  It supplies the muscles of the pharynx and most of the muscles of soft palate.  It gives rise to the superior laryngeal branch.  The right vagus nerve is 32 cm long, while the left nerve is 43 cm long.  Due to these variations in the length of vagus nerve, there could be a discernible lag in the movement of left vocal cord in comparison with the right cord.  To minimize this lag the left recurrent laryngeal nerve is supposed to contain more larger and fast conducting nerve fibers.   


Superior laryngeal nerve: This nerve gives rise to two branches 1. Internal and 2. external laryngeal branches.  The internal laryngeal branch of superior laryngeal nerve pierces the thyrohyoid membrane and supplies sensation to the larynx above the level of glottis.  The external laryngeal branch of superior laryngeal nerve innervates the cricothyroid muscle, which is the only laryngeal muscle not to be innervated by the recurrent laryngeal nerve. 

The right vagus nerve passes anterior to the subclavian artery and gives off the right recurrent laryngeal nerve.  This nerve loops around the subclavian artery to reach the tracheo oesophageal groove.  It accompanies the inferior thyroid artery for some distance before entering the larynx behind  the cricothryoid joint. 
The left vagus does not give off the recurrent laryngeal branch until it reaches the thorax.  The left recurrent laryngeal nerve winds around the aorta posterior to the ligamentum arteriosum.  It ascends back towards the larynx in the tracheo oesophageal groove. 

Laryngeal musculature:

The muscles of  larynx may be divided into extrinsic (muscles that attach the larynx to neighboring sructures) and intrinsic groups.

The intrinsic muscles of the larynx governs the movements of the vocal cords.  These muscles are innervated by the recurrent laryngeal nerve. 

1. Posterior cricoarytenoid muscle: This is the only abductor of the vocal folds.  It opens the glottis by rotatory motion on the arytenoid cartilages.  It also tenses the cord during phonation.

2. Lateral cricoarytenoid: Closes the glottis by rotating the arytenoids medially

3. Transverse arytenoid: Is the only unpaired intrinsic laryngeal muscle.  By approximating the bodies of arytenoids it closes the posterior aspect of the glottis.

4. Oblique arytenoid: This muscle along with transverse arytenoid closes the laryngeal inlet during the act of swallowing.

5. Thyroarytenoid: This muscle is very broad and is divided into three portions:

         a. Thyroarytenoidus internus - Also known as the vocalis muscle tenses the vocal cord and thus plays an important role   during phonation
         b. Thyroarytenoidus externus - This muscle is a major adductor of vocal fold

         c.  Thyroepiglotticus: This muscle shortens the vocal ligaments


The cricothryoid muscle is considered to be an extrinsic muscle of larynx since it is innervated by the external branch of superior laryngeal nerve.  It basically functions by increasing the tension on the vocal folds especially during high pitch and loud voice production.


































Figure displaying the intrinsic muscles of larynx



Functionally larynx can be divided into three successive physiologic sphincters at different anatomical levels.  These sphincters in cephalo caudal order are:

1. Aryepiglottic folds

2. Vestibular folds

3. Vocal folds

The muscles controlling these sphincters are derived from the intrinsic muscles of larynx.  These sphincters can contract together or independently.  All these sphincteric components act in unison during the act of swallowing thus preventing effectively any aspiration of food into the airway. 
The vestibular and vocal folds may oppose without closure of the aryepiglottic sphincter.  This can be observed during direct laryngoscopic examination.

The vestibular folds cannot be closed independently of the vocal folds, on the contrary the vocal folds adduct without closure of the other two sphincters during phonation.

















Direct laryngoscopic view of vocal cord




Pathophysiology of vocal cord paralysis:

     The physiologic function of larynx is adversely affected by vocal fold paralysis.  Interference with the protection of the tracheobronchial tree and respiration are more serious and life threatening than interference with voice production.  In recurrent laryngeal nerve paralysis the vocal folds may assume a number of positions.  Six positions have been described.  They are median, paramedian, cadaveric (intermediate), gentle abduction and full abduction.  The various positions of the vocal cords cannot be recorded precisely. 


Various theories have been proposed to explain the various positions assumed by a paralysed vocal cord. 

Semon's law:  This theory proposed by Rosenbach and Semon in 1881, depends on the concept that abductor fibres in the recurrent laryngeal nerves are more susceptible to pressure than the adductor fibers.  After a number of amendments this law is stated as " In the course of a gradually progressing organic lesion involving the recurrent laryngeal nerve three stages can be observed.  In the first stage only the abductor fibers are damaged, the vocal folds approximate in the midline and adduction is still possible.  In the second stage the additional contracture of adductors occur so that the vocal folds are immobilized in the median position.  In the third stage the adductors become paralysed and the vocal folds assume a cadaveric position".

This theory is fraught with clinical and experimental inconsistencies.   It was assumed that the nerve fibers supplying the abductors of the vocal folds lie in the periphery of the recurrent laryngeal nerve and any progressive lesion involves these fibers first before involving the deeper fibers that supply the adductors.   It was even suggested that adductors being phylogentically older are more resistant to insults than the newer abductors.  According to this theory in all progressive lesions involving the recurrent laryngeal nerve the abductors paralyze first followed by the adductors.  When  recovery takes place the first muscle group to recover will be the adductors before the abductors could recover. 

Differential innervation theory:  This theory was based on the anatomic fact that the recurrent laryngeal nerve often branched outside the larynx.  Injury to individual branches could cause paralysis of specific groups of muscles accounting for the varying positions assumed by the paralysed cord. 

Changes in the cricoarytenoid joint and paralysed muscles:  These changes have been proposed to explain the position of the cord in vocal fold paralysis.  This theory of progressive fibrosis of muscles has no anatomical proof.

Interarytenoid muscle contraction:  In this theory the paramedian position of a paralysed vocal cord is attributed to contraction of interarytenoid muscle which is supposed to receive bilateral innervation.  In reality this is not true as the interarytenoid muscle just helps to close the posterior glottic chink.

Disturbance of autonomic supply:  This theory has no experimental evidence.  It suggests that the vocal cord position is determined by the laryngeal muscle tone due to autonomic innervation.


Wagner and Grossman theory:  This is the most popular and widely accepted theory which could account for the varying positions assumed by a paralysed vocal cord.  This theory was first proposed by Wagner and Grossman (1897).  This theory states that in complete paralysis of recurrent laryngeal nerve the cord lies in the paramedian position because the intact cricothyroid muscle adducts the cord.  (Because the superior laryngeal nerve is intact).  If the superior laryngeal nerve is also paralysed the cord will assume an intermediate position because of the loss of adductive force.  This theory has been confirmed by electro myological studies. 
According to this theory, chest lesions should cause recurrent laryngeal nerve paralysis alone, but in many patients with lung cancer the cord assumes a intermediate position.  This has been attributed to the phenomenon of retrograde atrophy of the vagus nerve up to the level of nucleus ambiguus.
Paralysed vocal cords may demonstrate some movement due to the action of interarytenoid muscle which gets bilaterally innervated.

Pathogenesis of vocal cord paralysis:

Vocal cord paralysis is a sign of disease and is not a diagnosis.  It may be due to a lesion anywhere from the cerebral cortex to the neuromuscular junction.  Because of the large size of the nucleus ambiguus, small lesions in it may produce isolated laryngeal and pharyngeal motor losses.  Lesions involving the nucleus ambiguus may cause bilateral paralysis more often than unilateral palsy.
Peripehral damage to the laryngeal innervation may be of three types:

1. Damage to the vagus trunk above the nodose ganglion, the origin of superior laryngeal nerve

2. Damage to the vagus nerve below the level or to the recurrent laryngeal nerve

3. Damage to the superior laryngeal nerve alone.

Vocal cord paralysis may be congenital or acquired.

Congenital vocal cord palsy:  Many infants with stridor may have congenital paralysis of vocal cords.  This could occur with or without other associated abnormalities (i.e. neurologic, laryngeal and cardiac defects).  The most commonly assoicated anamoly in these patients is the presence of hydrocephalus.  The mechanism of vocal cord palsy in these children are still not clear.  It could be due to stretching of the vagus nerve, due to complicated delivery etc.

Acquired causes of vocal cord palsy:


Table showing the probable acquired causes of vocal cord palsy along with their incidences:

Causes of vocal cord palsy	Percentage
Malignant disease	31%
Surgical trauma	29%
Idiopathic	24%
Non surgical trauma	7%
Inflammatory	4%
Neurologic	1%
Miscellaneous	4%

Malignant disease:  One third of all vocal cord paralysis are caused by malignancies like lung cancer, oesophageal cancer and thyroid malignancies.  Other rare causes could include temporal lobe malignancies, posterior fossa tumors, paragangliomas etc.

Surgical trauma: is the second commonest cause of vocal cord paralysis.  Thyroid surgeries are the commonest.  Mediastinal surgeries, oesophageal surgeries can also cause vocal cord palsy.

Nonsurgical trauma:  Injuries to neck caused by automobile accidents and penetrating neck injuries can cause vocal cord palsy.

Inflammatory causes:  By far the most common cause is tuberculosis.  This could be due to apical scarring of the mediastinum or enlargement of hilar nodes. Other rare causes include jugular vein thrombophlebitis following csom, subacute thryoiditis,  meningitis both viral and bacterial.

Neurologic causes:  Include brain stem ischemia, multiple sclerosis and head injuries.

Miscellaneous causes: include hemolytic anemia, thrombosis of subclavian vein, syphilis, collagen disorders, lead and arsenic poisoning.

Idiopathic causes: A major chunk of the recurrent laryngeal nerve paralysis fall under this group where in no demonstrable abnormality could be attributed to recurrent larygneal nerve paralysis.  Left vocal cord is commonly involved in these patients.   Many of the idiopathic recurrent laryngeal nerve paralysis is caused by viral infections (subclinical).  Recovery is common in these patients.

Clinical features:

Unilateral superior laryngeal nerve injury:

These patients have very slight voice change.  Patients may even complain of hoarseness of voice.  Singers find it difficult to maintain the pitch.  Diplophonia is common in these patients (defect in the production of double vocal sounds).  The pitch range is decreased in these patients.  This is due to the fact that cricothryoid muscle is very important in maintenance of vocal cord tension and this muscle is supplied by the superior laryngeal nerve. 

On indirect laryngoscopy examination the vocal folds appear normal during quiet respiration.  There could be seen a deviation of the posterior commissure to the paralysed side.  The posterior commissure points towards the side of the paralysis.  At rest the paralysed vocal fold is slightly shortened and bowed and may lie at a lower level than the opposite cord. 

There is also associated loss of sensation in the supraglottic area causing subtle symptoms like frequent throat clearing, paroxysmal coughing, voice fatigue and foreign body sensation in the throat.


Bilateral superior laryngeal nerve injury:  Fortunately this condition is very rare.  It could result in fatal aspiration and pneumonia.  This condition is infact difficult to diagnose as there is no asymmetry between the vocal folds.

Unilateral recurrent laryngeal nerve injury: Is the most common situation encountered.  Left cord is affected commonly than the right as the left vagus nerve takes a more tortuous course.  To start with the voice is breathy, but the normal vocal cord starts to compensate soon.  The air way is adequate and there is no stridor in these patients.  On indirect laryngoscopic examination the affected cord could assume any of the 6 positions described above.  The cord may appear not to move, while the opposite cord will compensate for the lack of mobility.  When right vocal cord is paralysed then tuberculosis or bronchial malignancies should be considered to be a possibility.  Left vocal cord is involved in oesophageal malignancies, and in viral infections.

Unilateral superior and recurrent laryngeal nerve injury: This occurs usually in high vagal or brain stem lesions.  Vocal folds are in intermediate position and the patient tends to have a breathy voice.  There is also a tendency to aspirate.

Bilateral recurrent laryngeal nerve palsy:  In this condition both cords assume a paramedian position compromising the airway.  This commonly occurs following total thyroidectomy or in thyroid malignancies.  The patient will commonly manifest with stridor.  The voice will be near normal.

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 etiology 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.   
   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.

Imaging has a very important role to play in the evaluation of causes for vocal cord palsy.  CT scan and MRI imaging of neck and thorax to rule out lesions that could involve the recurrent laryngeal nerves in these areas must be performed.

Management:

The voice of the patient should be recorded, since the major complaint is going to be hoarseness of voice. 

Indications of early intervention include:

1. Life threatening aspiration

2. A known etiology which leaves no chance of recovery

3. Psychological and professional factors (relevant in singers)

Ideally speaking a wait and watch approach is useful in patients with unilateral idiopathic paralysis of vocal cords.  Spontaneous recovery is the order of the day in these patients.  The wait period may last up to 6 months in some patients. 

Treatment for unilateral paralysis of vocal cord include:

1. Speech therapy

2. Surgical medialisation of the paralysed cord

3. Intracordal injections

4. Selective reinnervation


Speech therapy: Can be used alone or in conjunction with other surgical modalities of management. 

Surgical medialisation:

Is currently the accepted modality of management for all cases of refractory unilateral paralysis of vocal cords.
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 involved 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 involved 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 endolarynx, 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:

1. Airway compromise
2. Wound infection
3. Hematoma
4. Extrusion of the implant
5. Laryngocutaneous fistula formation

Advantages of surgical medialisation procedure:

1. Reversible
2. Can be effective even with fixed cord
3. The patient has immediate benefit

Disadvantages:

1. Skin incision

2. Edema can distort glottic defect

3. Results variable

4. Posterior commissure closure is not adequate

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 injections:

Intracordal injection of polytetrafluoroethylene (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.  Collagen 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:

1. Airway edema

2. Granuloma formation

3. Results not predictable

Advantages:

1. No skin incision required

2. Out patient procedure

3. Results satisfactory in majority of cases




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 involved 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.

Advantages:

1. The vocal fold is medialised without resorting to any implants

2. Better pitch control

3. Other methods can be attempted even if this fails

Disadvantages:

1. Skin incision

2. Prolonged wound healing


Management of bilateral vocal cord palsy:

The initial aim is to secure the airway as these patients will manifest withs stridor.  A tracheostomy should be performed on an immediate basis. 


Vocal cord lateralisation procedures:


     This involves 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 involves 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 involves 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:

     Involves 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 involves 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.