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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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3 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 Otolaryngology online

5 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 Otolaryngology online

6 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 Otolaryngology online

7 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 Otolaryngology online

8 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. Otolaryngology online

10 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 Otolaryngology online

11 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 Malignant disease Surgical trauma Idiopathic Non surgical trauma Inflammatory Neurologic Miscellaneous Percentage 31% 29% 24% 7% 4% 1% 4%

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13 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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14 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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16 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. Otolaryngology online

17 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. 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

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19 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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20 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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23 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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24 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 Otolaryngology online

25 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.


Speech symptoms


Short breath groups, Decreased loudness of speech, Reduced precision of articulation and Diminished intelligibility.


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. 2. 3. Changes in posture and muscle tone. Increased supraglottal constriction Increased expiratory drive

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26 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 Otolaryngology online

27 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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28 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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29 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. Otolaryngology online

30 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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31 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 neckcrease 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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32 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. 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.

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Management algorithm of unilateral vocal fold paralysis

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