vocal cord paralysis

37
qwertyuiopasdfghjklzxcvbnmqw ertyuiopasdfghjklzxcvbnmqwert yuiopasdfghjklzxcvbnmqwertyui opasdfghjklzxcvbnmqwertyuiopa sdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghj klzxcvbnmqwertyuiopasdfghjklz xcvbnmqwertyuiopasdfghjklzxcv bnmqwertyuiopasdfghjklzxcvbn mqwert yuiopasd fghjklzxcvbnmqwertyuiopasdfgh jklzxcvbnmqwertyuiopasdfghjkl zxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvb nmqwertyuiopasdfghjklzxcvbnm Vocal cord paralysis Current management trends 7/18/2010 Dr. T. Balasubramanian

Upload: dr-t-balasubramanian

Post on 10-Apr-2015

2.296 views

Category:

Documents


8 download

DESCRIPTION

This e book discusses vocal cord paralysis and its management

TRANSCRIPT

Page 1: Vocal Cord Paralysis

qwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbn

mqwert yuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnmqwertyuiopasdfghjklzxcvbnm

Vocal cord paralysis

Current management trends

7/18/2010

Dr. T. Balasubramanian

Page 2: Vocal Cord Paralysis

1

Otolaryngology online

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 ambiguous

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.

Page 3: Vocal Cord Paralysis

2

Otolaryngology online

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.

Page 4: Vocal Cord Paralysis

3

Otolaryngology online

The axons of the recurrent laryngeal nerve are situated anteriorly in the vagus as it

exits from the brain stem. In the cervical segment of the vagus nerve the recurrent

laryngeal nerve axons congregate on its ventro medial aspect.

On the right side of the neck the vagus nerve passes over the subclavian artery. In

this region the right recurrent laryngeal nerve branches from the main trunk of

vagus and loops around the subclavian artery from anterior to posterior and travels

upwards in the neck towards the larynx. In rare instances (less than 1% of cases)

the inferior laryngeal nerve branches out of the vagus nerve directly and enters the

larynx at the level of the cricoid cartilage. This non recurrent inferior laryngeal

nerve crosses posterior to the common carotid artery and enters the larynx

posterior to the cricothyroid joint. This non recurrent laryngeal nerve is prone to

injuries if the surgeon is not aware of its possibility. This aberrant course of the

recurrent laryngeal nerve can be explained embryologically. Normally the

recurrent laryngeal nerves are pulled upwards in the neck around the 6th

arches of

aorta on both sides. On the left side the 6th

arch remains as ductus arteriosis and

later becomes the ligamentum arteriosum. On the right side the 6th

aortic arch

normally resorbs during the embroyonic development causing the recurrent

laryngeal nerve to pass under the subclavian arch. In very rare instances this 4th

arch also get resorbed during embryonic development. This causes the right

subclavian artery to arise directly from the descending aorta and the right inferior

laryngeal nerve branches from the vagus and directly enters the larynx without

looping around any vascular structure.

Figure showing non recurrent laryngeal nerve.

Page 5: Vocal Cord Paralysis

4

Otolaryngology online

The recurrent laryngeal nerve as it ascends the neck courses from lateral to medial

till it reaches the tracheo oesphageal groove and then it enters the larynx. In a

quarter of patients this nerve may lie antero lateral to the tracheo oesophageal

groove where it could be endangered during thyroid surgeries. The left recurrent

laryngeal nerve arises from the main vagal trunk at the level of aortic arch where it

lies anterior to the bifurcation of left common carotid and subclavian arteries. It

then loops beneath the aorta lateral to the ligamentum arteriosum (which is a 6th

arch derivative) and ascends upwards and medially towards the larynx. In majority

of patients the recurrent laryngeal nerve courses via the mediastinum as a single

trunk one on either side till it reaches the cricoid cartilage. On rare occasions there

may be more than one main trunk on either side of the neck.

The following are the contributions made by the recurrent laryngeal nerve:

1. It supplies trachea and oesophagus with sensory and motor branches.

2. It supplies the deep cardiac plexus

3. It supplies cricopharyngeus muscle before entering into larynx

4. It supplies motor fibers to the intrinsic musculature of larynx but for

cricothyroid muscle.

5. It supplies sensory fibers to glottis, subglottis and trachea.

According to Katz about 40% of recurrent laryngeal nerves divided before entering

the larynx. During surgery in order to avoid damaging this vital nerve a surgeon

should always safely assume that there are more than one branch of this nerve close

to the larynx.

Relationship of the recurrent laryngeal nerve to inferior thyroid artery:

Historically much importance has been given to the relationship of the recurrent

laryngeal nerve with that of inferior thyroid artery. Some authors go to the extent

of identifying this nerve by identifying the inferior thyroid artery. It should be

stressed that this relationship is purely conjectural and does not lend itself to broad

generalizations. The left recurrent laryngeal nerve has been described to course

deep to the inferior thyroid artery in majority of cases while the right has been

shown to pass deep to, superficial to or between the branches of recurrent laryngeal

nerves in equal proportions.

The proximity of recurrent laryngeal nerve to inferior thyroid artery has

physiological significance. This artery provides blood supply to the recurrent

Page 6: Vocal Cord Paralysis

5

Otolaryngology online

laryngeal nerve. This close relationship with that of inferior thyroid artery places

the nerve at great risk during surgery if there is bleeding from this area.

Retrothyroid segment of recurrent laryngeal nerve:

This segment of nerve is important because it is prone to injuries during thyroid

surgeries. As the nerve courses towards the larynx it travels posterior to the thyroid

gland. It may even penetrate thyroid tissue also, in which case it becomes more

prone to injury during surgery.

This nerve has also been shown to have varying relationship to that of Berry's

ligament. It may course lateral, medial or through this ligament.

The presence of tubercle of Zukerkandl, which is a postero lateral protuberance of

thyroid tissue seen in more than 50% of individuals. This tubercle represents the

embryological fusion of ultimobranchial body with that of the principal median

thyroid process. This tubercle is usually located just caudal to the superior

parathyroid gland. If this tubercle is more than 1 cm then the recurrent laryngeal

nerve courses medial to this tubercle in a narrow fissure between this tubercle and

main thyroid parenchyma.

The only reliable landmark of recurrent laryngeal nerve close to thyroid is the

cricothyroid articulation. The recurrent laryngeal nerve passes posterior to this

joint to enter the larynx.

Intralaryngeally the anatomy of recurrent laryngeal nerve is more predictable. On

entering the larynx the recurrent laryngeal nerve divides into anterior (adductor

division) and posterior (abductor division). The abductor portion supplies the

posterior cricoarytenoid muscle while the adductor division supplies the

interarytenoid muscle, lateral cricoarytenoid muscle, and thyroarytenoid muscle. In

addition to these motor fibers it also supplies sensory fibers to the interior of the

larynx.

Communication between the recurrent laryngeal nerve and superior laryngeal

nerve:

Communication between the recurrent laryngeal nerve and superior laryngeal

nerve has been documented since the days of Galen (1st century A.D.). Neuronal

studies have shown that there are more than one site of these anastomosis

exchanging motor impulses between these branches.

These areas of anastomosis include:

1. Galen's anastomosis

2. Deep arytenoid plexus

Page 7: Vocal Cord Paralysis

6

Otolaryngology online

3. Superficial arytenoid plexus

4. Cricoid anastomosis

5. Thyroarytenoid anatomosis

6. Thyroid foramen

7. Cricothyroid anastomosis

Figure showing the various anastomotic points between the superior and recurrent

laryngeal nerves.

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

Page 8: Vocal Cord Paralysis

7

Otolaryngology online

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 structures) and intrinsic groups.

The intrinsic muscles of the larynx govern the movements of the vocal cords. These

muscles are innervated by the recurrent laryngeal nerve. The intrinsic muscles of

larynx have both their origin and insertion on the cricoid, thyroid or arytenoid

cartilages. These muscles act together to fulfill their functions i.e. respiration,

protection of larynx and vocalization. Studies have shown that each laryngeal

muscle is not a single entity but an assembly of anatomically distinct compartments

potentially adapted to serve different functions. These individual compartments

receive nerve supply from separate branches of recurrent laryngeal nerve.

The intrinsic muscles of the larynx are involved in a range of movements of

laryngeal cartilages which include:

1. Ballistic behavior as in cough reflexes

2. Fine tuned movements of speech

3. Smooth movements during respiration

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. Horizontal division of posterior

cricoarytenoid muscle has a greater percentage of slow twitch type I fibers

than the vertical or oblique compartments. These slow twitch muscle fibers

are usually located deep inside the muscle mass close to the underlying bone

or cartilage. In the case of axial muscles they tend to be located closer to the

midline. The fast twitch type II fibers are located towards the periphery in

order to gain better mechanical advantage and also to ensure better blood

supply which is necessary for normal functioning of these fibers. The

Page 9: Vocal Cord Paralysis

8

Otolaryngology online

vertical and oblique compartments of this muscle is composed of fast twitch

type II muscle fibers. The horizontal division and vertical divisions receive

separate innervations from different recurrent laryngeal nerve branches.

Studies have shown that fast type muscle fibers are responsible for gag reflex

and slow type muscle fibers for vocalization.

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. This

portion comprises of specialized slow twitch multiple innervated slow twitch

muscle fibers which helps in the process of vocalization.

b. Thyroarytenoidus externus - This muscle is a major adductor of

vocal fold

c. Thyroepiglotticus: This muscle shortens the vocal ligaments

The cricothyroid 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.

Page 10: Vocal Cord Paralysis

9

Otolaryngology online

Figure displaying 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.

Page 11: Vocal Cord Paralysis

10

Otolaryngology online

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.

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. In the beginning of this

century lot of importance was accorded to the position assumed by the paralyzed

cord as this was suspected to have topognostic significance. Median position of the

cord was suspected to be caused by pure recurrent laryngeal nerve paralysis and

lateral positions were considered to be due to combined paralysis of recurrent and

superior laryngeal nerves. Woodson believes that the position assumed by the

paralyzed cord depends on the degree of re innervation and synkinesis.

Various theories have been proposed to explain the various positions assumed by a

paralyzed 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

Page 12: Vocal Cord Paralysis

11

Otolaryngology online

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.

Recent studies pertaining to laryngeal innervation has shown that the superior and

recurrent laryngeal nerves have more interconnections then the oft repeated Galen's

anastomosis. Anatomical studies have demonstrated that superior laryngeal nerve

contributes motor fibers to intrinsic laryngeal muscles other than cricothyroid.

Some of the intrinsic muscles of larynx have more than one belly with differing

nerve supplies.

Page 13: Vocal Cord Paralysis

12

Otolaryngology online

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.

Peripheral 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

associated anomaly in these patients is the presence of hydrocephalus. The

mechanism of vocal cord palsy in these children is 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%

Page 14: Vocal Cord Paralysis

13

Otolaryngology online

Malignant disease: One third of all vocal cord paralysis is 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.

The following are the surgeries known to cause recurrent laryngeal nerve paralysis:

1. Cervical surgeries : This includes Thyroidectomy, parathyroidectomy,

anterior approach to cervical spine, carotid endarterectomy, cricopharyngeal

myotomy, repair of zenker's diverticulum

2. Thoracic surgeries: Pneumonectomy, lobectomy, repair of aortic aneurysm,

aortic valve replacement, oesophageal surgery, mediastinoscopy,

thymectomy, ligation of PDA, cardiac & pulmonary transplant.

3. Other surgeries / procedures: Skull base surgery, brain stem surgery, central

venous catheterization and endotracheal intubation.

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, and 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 laryngeal 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.

Page 15: Vocal Cord Paralysis

14

Otolaryngology online

Superior laryngeal nerve: This branch from the vagus supplies the main sensory

innervation of larynx in the glottic and supraglottic regions with some minimum

contribution to posterior subglottic area. It branches out of the vagus nerve just

below the nodose ganglion. It is branched from the medial aspect of the vagus

nerve. It lies superficial to the superior cervical ganglion form which it receives

sympathetic supply. This nerve also supplies the carotid body. Its motor

innervation supplies the cricothyroid muscle. Traditional belief is that paralysis of

superior laryngeal nerve causes bowing and flaccidity of true vocal cords with

decreased vocal range and laryngeal rotation. According to Sulica this premise is

not entirely accurate. In human larynx the superior laryngeal nerve has complex

functional inter relationship with the recurrent laryngeal nerve. Hence the degree

of compensation of these two nerves following injury is not entirely straight

forward.

Figure showing the anatomy of superior laryngeal nerve.

Page 16: Vocal Cord Paralysis

15

Otolaryngology online

The average length of superior laryngeal nerve is about 2 cm in males and 1.5 cms

in females. It divides into an internal and external laryngeal branches.

Internal laryngeal nerve branch: is predominantly sensory in nature. This nerve

runs parallel and medial to the superior laryngeal artery. At the level of greater

cornu of hyoid bone it turns medially, passing deep to thyrohyoid muscle. This

nerve enters the larynx through the thryohyoid membrane just above the superior

border of inferior pharyngeal constrictor muscle. After entering into the larynx this

nerve divides into three branches i.e. superior, middle and inferior. The superior

division divides into two / three branches supplying sensations to the lingual surface

of epiglottis, lateral aspect of glosso epiglottic fold. The middle division innervates

the aryepiglottic fold, vocal folds, vestibular folds and the posterior aspect of

arytenoid. The inferior division is the largest of the branches of superior laryngeal

nerve. It lies along the medial aspect of pyriform fossa. It is this nerve which is

blocked when pyriform fossa block is given for endolaryngeal surgical procedures.

This branch supplies the interarytenoid muscle. This nerve gives out a branch that

communicates with the recurrent laryngeal nerve (Galen's loop).

External branch of superior laryngeal nerve is smaller in caliber when compared to

the internal branch. It supplies motor fibers to the cricothyroid muscle. It may

provide occasional supply to the thyroarytenoid muscle. Rarely it may also provide

sensation to the glottis. This nerve arises from the superior laryngeal nerve at the

level of greater cornu of hyoid bone. At this level it lies just posterior to the superior

thyroid artery.

Kierner classified the superior laryngeal nerve into 4 types depending on the

relationship of its external branch to the superior pole of thyroid gland.

Type I nerve: In this type the external branch of superior laryngeal nerve cross the

superior thyroid artery about 1cm above the superior pole of thyroid gland.

Type II nerve: In this type the external branch of superior laryngeal nerve crosses

the superior thyroid artery within 1 cm of the superior pole of thyroid gland.

Type III nerve: In this type the external branch of superior laryngeal nerve crosses

the superior thyroid artery under cover of the superior pole of thyroid gland.

Type IV nerve: In this type the external branch of superior laryngeal nerve

descends dorsal to the superior thyroid artery and crosses its branches just superior

to the upper pole of thyroid gland.

Page 17: Vocal Cord Paralysis

16

Otolaryngology online

Awareness of these anatomical variations will help the surgeon in preserving this

branch during head and neck surgeries.

The external branch of the superior laryngeal nerve divides into two branches and

supplies the oblique and rectus bellies of cricothyroid muscle. It should be borne in

mind that this nerve pierces the inferior constrictor of pharynx before supplying the

cricothyroid muscle.

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.

Fibreoptic laryngoscopic examination: This is the ideal procedure to assess the

dynamic functions of the vocal folds. This is so because holding the tongue during

indirect / direct laryngoscopic examination alters the biomechanics of the larynx

thereby affecting the findings. In fibreoptic laryngoscopic examination the tongue is

not held and the larynx is examined under physiologic conditions. While examining

the larynx the patient is asked to perform the “e-sniff maneuver”. In this maneuver

the patient alternates between phonating the vowel “e” and sniffing. This causes

alternating abduction and adduction movement of the vocal folds helping the

examiner to assess the mobility of the cords with reasonable degree of accuracy. It

is always better to focus on the movement of the vocal folds rather than that of

arytenoids. Overhanging arytenoids obscuring the visualization of vocal folds

should arouse suspicion of dislocation of arytenoids in patients with history of

trauma.

Page 18: Vocal Cord Paralysis

17

Otolaryngology online

In some patients with unilateral vocal fold paralysis associated compensatory

mechanisms like supraglottic contraction (dysphonia plica ventricularis) kicks in.

Vocal fold mobility may not be visible in these patients. Koufmann technique

should be used to study vocal fold mobility in these patients. The patient is asked to

sigh or hum through the nose while the larynx is being examined. This removes

unwanted supraglottic compensatory mechanisms enabling better visualization of

the vocal folds.

Pointers that indicate to the possibility of arytenoid dislocation are:

1. Arytenoid oedema

2. Difference in the level of vocal folds

3. Absence of “Jostle sign”. This is brief lateral movement of arytenoid on the

immobile side during glottic closure due to contact from the mobile

arytenoid.

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. Sometimes mild abduction of

the involved cord could be seen. This could be accounted for by the fact that

interarytenoid muscle has bilateral innervation. 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.

Page 19: Vocal Cord Paralysis

18

Otolaryngology online

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.

Examination of neck is a must in all these patients. Neck should be examined for

the presence of thyroid mass, cervical adenitis.

Examination of palatal movement is very important in these patients. Its movement

should be observed while the patient is phonating “a”. If there is asymmetry on the

side of recurrent laryngeal nerve paralysis (the palate retracts towards the normal

side) then high vagal lesion should be suspected as the palate is also involved.

Complete cranial nerve examination is not out of place in these patients as

concurrent involvement of lower four cranial nerves indicates lesion at the level of

jugular foramen.

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.

Videostroboscopy: Plays an important role in examining the vocal folds for mobility

disorders. This brings out the loss of mucosal wave pattern which is the earliest sign

of vocal fold disorder. It also shows incomplete closure with large glottic chinks in

patients with unilateral vocal fold paralysis. Paralyzed vocal folds show increased

amplitude of vibrations due to atrophied vocalis muscle. In cases of mild paralysis

of vocal folds the increased amplitude as seen in Videostroboscopy could be the only

Page 20: Vocal Cord Paralysis

19

Otolaryngology online

positive sign. This examination also helps in assessment of vocal fold height

differences and status of vocal process during phonation.

Maximal phonation time: Is a simple bedside test to assess the vocal cord status of a

patient. The patient is asked to take a deep breath and asked to phonate vowel “ee”

for as long as possible. Normal healthy adult can do it for 25 seconds. In patients

with vocal fold paralysis they may not be able to maintain it for more than 10

seconds because of phonatory waste.

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.

Electromyography: The technique of electromyography is 100 years old. This

technique is used to study the electrical activities of muscles. It is used not only to

diagnose paralysis of vocal folds but also to predict the chances of spontaneous

recovery. This test should always be viewed in conjunction with other clinical

features. Ideally laryngeal electromyography is performed when active intervention

is considered or when there is a need for reassuring the patient. It should be borne

in mind that laryngeal electromyography will detect recovery only at the time of

testing; it does not predict later recovery. The damaged recurrent laryngeal nerve

regenerates at the rate of 1mm / day and hence theoretically it could take at least a

year for the recovery to be complete.

If laryngeal electromyography shows no signs of muscle recovery then it is

prudent to undertake corrective surgical measures with the hope of later recovery.

If polyphasic potentials are present then a delay in active intervention of use of

cordal injections will help.

Laryngeal electromyography is vital before attempting to reduce dislocated

arytenoid cartilage. If there is evidence of paralysis of vocal cord then reduction of

dislocated arytenoid is deferred.

Laryngeal electromyography uses three testing techniques.

1. Diagnostic needle testing

2. Fine wire electromyography

3. Repetitive stimulation

Page 21: Vocal Cord Paralysis

20

Otolaryngology online

Diagnostic needle testing looks for the type of electrical activity both at rest

and during voluntary recruitment.

Fine wire electromyography uses multiple fixed fine wire electrodes. This

technique is used to examine patients with suspected synkinesis or laryngeal

dystonia.

Repetitive stimulation records the compound action potential of a muscle as

the nerve is stimulated. This test supersedes voluntary control of muscle

fibers and is used to test the integrity of the nerve. The major use of this test

is assessing patients with myasthenia gravis.

Types of wave forms recorded by laryngeal electromyography:

1. Normal wave form

2. Injury wave form

3. Recovery wave form

4. Evidence of old injury

Nerve injury leaves the muscle without innervation. The muscle fibers become

hypersensitive to acetylcholine causing them to discharge spontaneously. This is

evident when the muscle fibers are stimulated as in the case of insertion of needle

when laryngeal electromyography is being performed. Two primary wave forms

are generated. The first one is the positive sharp waves and the next one being

waves caused due to muscle fibrillation. The presence of these two waves indicates

that the muscle has lost its innervation, and is yet to be contacted by the

regenerating nerve sprout. It also indicates the muscle has not undergone fibrosis

due to lack of innervation. A fibrosed muscle due to lack of innervation is

prognostically bad.

When the muscle fibers are contacted by the sprouting nerve the nerve starts to

contract voluntarily under the influence of the regenerating nerve. Since these

newer sprouts have slow conduction rates the muscle fibers will be slightly delayed

in their action

Page 22: Vocal Cord Paralysis

21

Otolaryngology online

Image shows recordings from normally contracting thyroarytenoid muscle. The

amplitude of these waves is 700 mV and the duration is 7 ms.

Image showing polyphasic potentials.

Page 23: Vocal Cord Paralysis

22

Otolaryngology online

Figure showing normal recruitment pattern seen during phonation (eee)

Image showing recordings of fibrillating muscle spindles following denervation

The combination of normal firing potentials of normally innervated muscle spindles

and the slow firing of denervated spindles which come into contact with the

sprouting new nerve causes a complex long duration wave form known as

polyphasic potentials. The presence of these polyphasic potentials indicate nerve

regeneration and thus carries good prognosis.

Large amplitude potentials recorded after vocal fold paralysis indicates that the

injury is old and stable.

Page 24: Vocal Cord Paralysis

23

Otolaryngology online

Diagnostic laryngeal electromyography also indicates the number of normal

neuromuscular units firing. A large number of units firing fast indicates normally

innervated vocal fold while the presence of few motor units firing fast indicate

peripheral nerve injury. The presence of large number of motor units firing slowly

indicates that the central nervous system could be impaired.

Diagnostic laryngeal electromyography is usually performed one year after vocal

fold paralysis. The findings of the first year may be considered to be final for most

clinical purposes. These findings can be grouped under 4 categories for the sake of

convenience.

1. Dense peripheral nerve injury with no recruitment

2. A severe peripheral injury with few motor units firing fast

3. A moderate peripheral injury with many motor units firing fast

with very little recruitment

4. Normal recruitment

Laryngeal electromyography not only helps in making a decision of treatment

modality, it also helps in the understanding the exact pathophysiology of the vocal

fold paralysis.

Management:

Decisions regarding the management of vocal cord paralysis are made on the basis

of the laryngeal function that is compromised due to the paralysis. In patients with

unilateral paralysis of vocal cords the voice is breathy and the patient faces risk of

aspiration due to compromised adduction of the vocal folds. In bilateral paralysis of

vocal folds the gravest cause for concern is total loss of abduction of both vocal folds

compromising the airway causing stridor. These patients usually have near normal

and functional voice. Some patients with unilateral recurrent laryngeal nerve

paralysis complain of shortness of breath while speaking. This should not be

confused with airway compromise. This is due to the fact that excess air leaks out of

the lungs while the patient speaks due to improper laryngeal seal. In order to

overcome this air leak some patients increase their respiratory effort and laryngeal

muscular activity causing increased strain to the vocal folds.

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

hoarseness of voice.

Page 25: Vocal Cord Paralysis

24

Otolaryngology online

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)

4. Dysphagia associated with vocal cord paralysis. Laryngeal anesthesia following

superior laryngeal nerve injury is the reason for continued dysphagia. These

patients in addition to arytenoid adduction also need cricopharyngeal myotomy.

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

5. Electrical stimulation of posterior cricoarytenoid muscle

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

of management. Behavioral voice therapy is very helpful in rehabilitating a weak

and breathy voice. Voice therapy may be used as a standalone treatment of with

other medical modalities of treatment.

Before beginning speech therapy the pitch, loudness and quality of voice should

be evaluated. Breathiness, reduced loudness and a weak cough have been associated

with leakage of air through glottis.

Indications for voice therapy:

1. A period of voice therapy must be considered for patients with

unilateral vocal fold paralysis without dysphagia. These

patients should have no aspiration and a good cough.

2. Voice therapy is always recommended prior to any restorative

surgery

Page 26: Vocal Cord Paralysis

25

Otolaryngology online

3. Speech and behavioral therapy is useful in managing unilateral

vocal fold paralysis in pediatric age group.

Various causes of speech breakdown should be assessed before starting voice

therapy. These causes can be broadly classified as Respiration, phonation,

resonation and articulation.

Causes Speech symptoms

Respiration Short breath groups, Decreased loudness

of speech, Reduced precision of

articulation and Diminished

intelligibility.

Phonation Altered pitch, Decreased loudness of

speech, Abnormal quality, Phonation

breaks and Diminished intelligibility

Resonation and articulation Changes in nasality, Reduced precision

of articulation, Altered rhythm of

speech, and Diminished intelligibility

The various compensatory mechanisms which are evident in patients with vocal

cord palsy should be considered. Patients may use these maneuvers to help voice

but they place strain on the voice mechanism inadvertently.

These changes include:

1. Changes in posture and muscle tone.

2. Increased supraglottal constriction

3. Increased expiratory drive

Page 27: Vocal Cord Paralysis

26

Otolaryngology online

Posture changes, reduction of muscle tone will go a long way in improving the

therapeutic result.

Two dominant patterns of voice symptoms have emerged. They are

1. Hypo functional voice symptom – These include

symptoms related to vocal fold paralysis

2. Hyper functional voice symptom – These symptoms are

related to the compensatory mechanisms and are

associated with voice strain and fatigue.

Voice therapy procedures can be divided into:

Direct procedures

Indirect procedures

Indirect procedures: Include counseling, education, vocal hygiene and maximizing

posture.

Direct procedures: These include normalization of expiratory drive, decreasing

transglottic pressure and optimizing medial compression of the vocal folds.

The best way to decrease expiratory drive is to encourage the patient to speak in a

quiet and confident tone. When a patient is speaking in a quiet and confident voice

the air pressure and air flow match the resistance of vocal folds.

Glottic closure can be manipulated by manipulating the sounds in a syllable.

Surgical medialisation:

Is currently the accepted modality of management for all cases of refractory

unilateral paralysis of vocal cords. This procedure is purely static in nature and

hence ignores the long term effects of vocal cord palsy like atrophy which could

cause deterioration of voice some years after surgery.

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

Page 28: Vocal Cord Paralysis

27

Otolaryngology online

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

Page 29: Vocal Cord Paralysis

28

Otolaryngology online

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:

Injection augmentation of vocal folds date back to 1911 when Brunings injected

paraffin via indirect laryngoscopy to medialize the immobile vocal fold.

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

Page 30: Vocal Cord Paralysis

29

Otolaryngology online

Advantages:

1. No skin incision required

2. Out patient procedure

3. Results satisfactory in majority of cases

Autologous fat injections:

Vocal fold injection for global augmentation of vocal fold is a successful way to treat

glottic closure insufficiency. Autologous fat is an excellent material for this purpose.

Advantages of fat:

1. Since autologous it is readily available.

2. Does not cause any unwanted reactions

3. It has excellent biomechanical properties

4. Bilateral vocal fold injections can also be performed

Disadvantages of autologous fat injection:

1. Variable survival of transplanted fat. Hence

over injection is required.

2. Effort involved in harvesting fat

3. Patients may have temporary dysphonia

Indications for autologous fat injection:

Autologous fat injection is indicated only to close small / medium sized glottal gap.

This procedure is not useful in patients with more than 4 mm glottal gap or with

shortened / slackened vocal folds. Similarly this procedure is contraindicated in

patients with contralateral poor abduction of vocal cord.

Page 31: Vocal Cord Paralysis

30

Otolaryngology online

These patients should have adequate subcutaneous fat tissue for harvesting.

Fat harvesting:

This is usually done either by open method or by liposuction. Now a day’s

liposuction is the most preferred approach of fat harvesting method as it is less

invasive. Open method is suitable for patients with modest amounts of

subcutaneous fat. Most common area from where fat is harvested is from the infra

umbilical region.

Lipoinjection is usually performed using 18 or 19 gauge needle. Since the fat that is

to be injected is highly viscous pressurized injection devise like Brunning’s syringe

is preferred.

Complications of autologous fat injection:

1. Lipid granuloma

2. Sub optimal voice improvement

3. Persistent post-operative dysphonia

Collagen injection of paralyzed vocal fold:

This was first used in 1980’s. These injections just increase the bulk of the vocal

fold and in no way improves the mobility of the vocal fold. The main role of these

injections is to reduce the phonatory waste.

Originally Bovine collagen is used for these injections. Main advantage of collagen

over fat injection is the ease with which collagen can be injected. Major problem

with bovine collagen is the risk of graft rejection because it is a xenograft.

Now autologous collagen can be harvested from the skin of individuals and used to

inject the paralyzed cord.

Use of micronized acellular dermis to be injected into the paralyzed vocal fold:

This material is available since the year 2000. It is a product of human organ

donation. The dermis is harvested from the torso and legs of cadavers following the

Page 32: Vocal Cord Paralysis

31

Otolaryngology online

protocol of organ donation. The material harvested should be checked for HIV and

Hepatitis infections.

Human acellular dermis provides a scaffold on injection. Growth of tissue and

neovascularization occurs over this scaffold.

Other materials that can be injected to increase the bulk of the paralysed cord

include:

1. Calcium hydroxyapatite

2. Hyaluronan

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 its 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.

Page 33: Vocal Cord Paralysis

32

Otolaryngology online

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

Medialization thyroplasty:

Payr in 1915 first described this procedure. He created an anterior based cartilage

flap overlying vocal folds and pushed it medially. Medialization thyroplasty is

performed commonly these days for unilateral vocal fold paralysis with a large

glottic chink.

Indications:

1. Symptomatic dysphonia, aspiration, glottic insufficiency

2. Vocal fold atrophy including age related ones

Gortex / silastic block can be used to hold the medialized cartilage flap.

Page 34: Vocal Cord Paralysis

33

Otolaryngology online

Figure showing the segment of thyroid cartilage that is resected

Figure showing silastic block inserted to medialize the vocal fold

Page 35: Vocal Cord Paralysis

34

Otolaryngology online

Management of bilateral vocal cord palsy:

The initial aim is to secure the airway as these patients will manifest with stridor. A

tracheostomy should be performed on an immediate basis.

Vocal cord lateralization 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.

Page 36: Vocal Cord Paralysis

35

Otolaryngology online

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.

Anastomosis between the phrenic nerve and the damaged recurrent laryngeal nerve

has been attempted in patients with bilateral recurrent laryngeal nerve paralysis

with varying results.

Electrical stimulation of posterior cricoarytenoid muscle:

This method is apparently more physiologic and dynamic in nature. This method is

rather useful in treating patients with bilateral abductor paralysis. Paced

stimulation of posterior cricoarytenoid muscle is performed using an implantable

stimulator. Care should be taken to ensure that the frequency of stimulation /

pacing should sync with the process of respiration.

Page 37: Vocal Cord Paralysis

36

Otolaryngology online

Management algorithm of unilateral vocal fold paralysis