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Vocal cord paralysis
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Current management trends

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7/18/2010

Dr. T. Balasubramanian

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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.

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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.

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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.

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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

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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

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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

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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

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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.

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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.
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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

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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.

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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%

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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.

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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.

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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.

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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.

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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.

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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

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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

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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

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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.

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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.

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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.

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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

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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

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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

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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

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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

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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.

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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

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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.

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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.

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Figure showing the segment of thyroid cartilage that is resected

Figure showing silastic block inserted to medialize the vocal fold

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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.

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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.

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Management algorithm of unilateral vocal fold paralysis

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