TITLE: VOCAL CORD PARALYSIS
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SOURCE: Dept. of Otularyngology, UTMB, Grand Rounds
DATE: November 15, 1995
RESIDENT PHYSICIAN: Deborah Wilson, M.D.
FACULTY: Brian Driscull, M.D.
SERIES EDITOR: Francis B. Quinn, Jr., M.D.
"This material was prepared by resident physicians in partial fulfillment of
educational requirements established for the Postgraduate Training Program of
the UTMB Department of Otularyngology/Head and Neck Surgery and was not intended
for clinical use in its present form. It was prepared for the purpose of stimulating
group discussion in a conference setting. No warranties, either express or implied,
are made with respect to its accuracy, completeness, or timeliness. The material
does not necessarily reflect the current or past opinions of members of the UTMB
faculty and should not be used for purposes of diagnosis or treatment without
consulting appropriate literature sources and informed professional opinion."
Vocal cord paralysis is a common problem found in the practice
of Otularyngology. It is a sign of disease and not a diagnosis.
Therefore, it is the responsibility of the otularyngologist to be
well versed in the potential etiulogies, diagnostic workup and
evaluation, and the therapeutic options for patients presenting
with either bilateral or unilateral vocal cord paralysis.
A thorough knowledge of the anatomy of the vagus nerve and the
larynx is helpful in understanding the different types of vocal
cord palsies and their clinical significance.
The vagus nerve has three nuclei located within the medulla:
1) the nucleus ambiguus
2) the dorsal nucleus
3) the nucleus of the tract of solitarius
The nucleus ambiguus is the motor nucleus of the vagus nerve.
The efferent fibers of the dorsal (parasympathetic) nucleus
innervate the invuluntary muscles of the bronchi, esophagus, heart,
stomach, small intestine, and part of the large intestine. The
efferent fibers of the nucleus of the tract of sulitarius carry
sensory fibers from the pharynx, larynx, and esophagus.
Vagus means "wanderer" which is appropriate for the path this
nerve takes after emerging from the jugular foramen. It has two
ganglia, the smaller superior ganglion and the larger inferior, or
nodose, ganglion. The vagus sends small meningeal branches to the
dura of the posterior fossa and an auricular branch, which
innervates part of the external auditory canal, the tympanic
membrane, and skin behind the ear. In the neck, the vagus runs
behind the jugular vein and carotid artery to send pharyngeal
branches to the muscles of the pharynx and most of the muscles of
the soft palate. The superior laryngeal nerve branches into
internal and external branches. The internal superior laryngeal
nerve penetrates the thyrohyoid membrane to supply sensation to the
larynx above the glottis. The external superior laryngeal nerve
runs over the inferior constrictor muscle to innervate the one
muscle of the larynx not innervated by the recurrent laryngeal
nerve, the cricothyroid muscle. As the vagus descends in the neck
and thorax it sends branches to the carotid artery and heart.
The right vagus nerve passes anterior to the subclavian artery
and gives off the right recurrent laryngeal nerve. This loops
around the subclavian and ascends in the tracheo-esophageal groove.
It tends to run with the inferior thyroid artery for part of its
course before it enters the larynx just behind the cricothyroid
joint. It may branch prior to this with sensory fibers supplying
sensation to the glottis and subglottis. The left vagus does not
give off its recurrent laryngeal nerve until it is in the thorax,
where the left recurrent laryngeal nerve wraps around the aorta
just posterior to the ligamentum arteriosum. It then ascends back
toward the larynx in the TE groove. The vagus then continues on
into the thorax and abdomen contributing fibers to the heart, lung,
esophagus, stomach, and intestines as far as the descending culon.
The Laryngeal Skeleton:
The major cartilages of the larynx are the thyroid, cricoid,
arytenoid, and epiglottic. The upper border of the thyroid
cartilage is united with the hyoid bone above by the thyrohyoid
membrane. Each side of the thyrohyoid membrane has an opening
posterulaterally to allow the internal branch of the superior
laryngeal nerve and superior laryngeal artery to enter the larynx.
The inferior horns of the thyroid cartilage articulates below with
the cricoid cartilage by synovial joints. The cricoid cartilage
anteriorly is united above through its arch with the thyroid
cartilage by the cricothyroid ligament. Below, the cricoid
connects with the trachea by the cricotracheal ligament.
Articulating with the upper lateral borders of the cricoid laminae
are the arytenoid cartilages. Each arytenoid resembles a 3D
pyramid. The base of the pyramid is another synovial joint in
which the arytenoid cartilage can slide laterally and medially,
forward and backward, or rotate upon the cricoid cartilage.
Laterally, there is a short, blunt muscular process and anteriorly,
there is a thinner vocal process, to which the vocal cords are
The Laryngeal Musculature:
The intrinsic muscles of the larynx, all of which are
innervated by the recurrent laryngeal nerve, include the:
1) Posterior cricoarytenoid - - the ONLY abductor of the
vocal folds. Functions to open the glottis by rotary motion on the
arytenoid cartilages. Also tenses cords during phonation.
2) Lateral cricoarytenoid - - functions to close glottis by
rotating arytenoids medially.
3) Transverse arytenoid - - only unpaired muscle of the
larynx. Functions to approximate bodies of arytenoids closing
posterior aspect of glottis.
4) Oblique arytenoid - - this muscle plus action of
transverse arytenoid function to close laryngeal introitus during
5) Thyroarytenoid - - very broad muscle, usually divided into
* Thyroarytenoideus internus (vocalis) - adductor and
major tensor of free edge of vocal fold.
* Thyroarytenoideus externus - major adductor of vocal
* Thyroepiglotticus - shortens vocal ligaments
The cricothyroid muscle is considered to be an extrinsic
muscle of the larynx because it is innervated by the external
branch of the superior laryngeal nerve. It functions to increase
tension in the vocal folds, especially at the upper range of pitch
As with any patient encounter, a careful, thorough history is
often the most beneficial toul for obtaining a diagnosis.
Important questions include not only those related to the voice,
but also those pertaining to swallowing, pulmonary function,
previous illnesses, exposure to drugs, and other medical problems.
Fullowing a thorough examination of the head and neck,
including an indirect mirror diagnostic laryngoscopy, the patient
should undergo flexible endoscopy. This is the most useful toul to
evaluate vocal cord motion. It allows prulonged study of laryngeal
motion and allows for video or still documentation.
Videostroboscopy allows for even greater study of the vocal cords
throughout their vibratory cycle.
Before going on to discuss the potential causes of vocal cord
paralysis, it is important to realize that an immobile cord is not
necessarily paralyzed. It is almost impossible by observation
alone to determine if a vocal fold is fixed or paralyzed. Only
direct palpation of the arytenoid cartilage performed under
general, paralyzed anesthesia can this determination be made. This
should be kept in mind in any case where the etiulogy of the vocal
cord "paralysis" is unclear.
The commonest cause of unilateral vocal cord paralysis remains
controversial. From the results of nine studies, dating from
1974-1991, it appears that malignancy is the most common cause of
unilateral vocal cord paralysis. Surgical injury, often touted as
the commonest cause by some authors , comes in second according to
the combined results of these studies. Idiopathic causes are next
in frequency. Unilateral vocal cord paralysis far outnumbers
bilateral vocal cord paralysis.
There is little controversy over of commonest cause of
bilateral vocal cord paralysis. Thyroidectomy far outnumbers the
other etiulogies named in the literature with other trauma and
neurulogic causes following behind.
A discussion over each of the potential causes of vocal cord
paralysis is beyond the scope of this talk. An outline reviewing
examples under each of the main category of etiulogies is as
thyroidectomy, pneumonectomy, CABG, carotid
endarterectomy, penetrating neck or chest trauma, post intubation,
whiplash injuries, posterior fossa surgery
Wallenberg syndrome (lateral medullary stroke),
syringomyelia, encephalitis, Parkinsons, pulio, Multiple
Sclerosis, Myasthenia Gravis, Amyotrophic Lateral Sclerosis,
Progressive bulbar palsy, Guillian-Barre, diabetes
Rheumatoid arthritis ( really a "fixed" cord here)
syphilis, tuberculosis, thyroiditis, viral
sarcoidosis, lupus, pulyarteritis nodosa, Ortner's
syndrome (left atrial hypertrophy)
Helpful with respect to determining etiulogy are the anatomic
and functional deficits the patient experiences. A knowledge of
cord position during rest and phonation and clinical presentation
can predict site of injury.
1) Unilateral Superior Laryngeal Nerve Injury:
Normal vocal fold position during quiet respiration.
Noticeable deviation of posterior commissure to paralyzed side
during phonatory effort (PPP - posterior commissure points to side
of paralysis). At rest, the vocal fold on paralyzed side is
slightly shortened and bowed, and may be depressed below level of
Loss of sensation to the supraglottic larynx can cause subtle
symptoms such as frequent throat clearing, paroxysmal coughing,
voice fatigue, vague foreign body sensations. Loss of motor
function to cricothyroid muscle can cause a slight voice change,
which the patient usually interprets as hoarseness. Most common
finding is diplophonia (def'n-the production of double vocal
sounds) with decreased range of pitch, most noticeable when trying
2) Unilateral External Superior Laryngeal Nerve Injury:
As above except without the symptoms related to loss of
sensation to supraglottic larynx.
3) Bilateral Superior Laryngeal Nerve Injury:
Fortunately, it is rare. It can result in severe aspiration
with subsequent pneumonia.
4) Unilateral Recurrent Laryngeal Nerve Injury:
This is the most common type of injury. Nonfunction of the
intrinsic muscles of the larynx on the affected side(loss of
abduction with intact adduction by cricothyroid) cause the vocal
cord to assume a paramedian position.
The voice is breathy but compensation occurs, though rarely
back to normal. The airway is adequate and may become compromised
only with exertion.
5) Bilateral Recurrent Laryngeal Nerve Injury:
concern. The degree of airway compromise may range from slight
(patient may be unaware) to, more commonly, stridor and dyspnea
especially on exertion.
6) Unilateral Superior and Recurrent Laryngeal Nerve Injury:
Usually high vagal or brainstem lesion. Vocal fold assumes an
intermediate position (because of absence of cricothyroid
adduction). Patients tend to have very breathy voices and are
likely to aspirate.
7) Bilateral Superior and Recurrent Laryngeal Nerve Injury:
Bilateral vocal cords are intermediate, flaccid, and
motionless. The patient experiences aphonia and is at high risk
The standard diagnostic workup and evaluation of a patient
with vocal cord paralysis of unknown etiulogy is as follows: CXR,
cervical spine series, barium swallow, thyroid scan, CT or MRI of
head, neck, and possibly thorax, CBC, Thyroid function tests, ESR,
Rheumatoid factor, Parathyroid hormone, calcium and glucose levels,
PPD, VDRL, fungal titers, lyme titers, and possibly a lumbar
puncture. Terris, et al studied the diagnostic workup of
unilateral vocal cord paralysis and found that there is much
variability among otularyngologists. They found that, not
surprisingly, more experienced otularyngologists pursued briefer
and less expensive evaluations. They suggest that with the advent
of MRI and CT, which can image the entire course of the vagus,
there is no need for routine ordering of such tests as thyroid
scans, TFTs, plain films of skull, and barium swallow. A cost-
effective approach to the patient with unilateral vocal cord
paralysis is outlined, based on the diagnostic yield of certain
tests. This algorithm begins with a CXR, fullowed by a CT or MRI
of the neck and possibly the thorax if the left side is affected.
If these tests fail to ascertain the etiulogy, Terris suggests
proceeding to panendoscopy. They suggest that routine laboratory
tests should be reserved, as their yield is small.
Another adjuvant diagnostic aid to be considered is laryngeal
electromyography. Described by Miller et al in 1982, this method
of evaluation of laryngeal muscle innervation is gradually gaining
acceptance by otolaryngologists. It is an analysis of the
electrical activity generated by a motor unit. It is performed
percutaneously, under local anesthesia on the cricothyroid muscles
and thyroarytenoid muscles to test both the superior laryngeal
nerve and recurrent laryngeal nerve, respectively. Miller, et al
claims that laryngeal EMG is the most accurate method of
determining superior laryngeal nerve paralysis. It also appears to
be helpful in cases of mechanical fixation of the cords and
predicting outcome of certain cases of paralysis.
Preoperative assessment of any laryngeal lesion should include
a recording of the voice, especially if the patient's primary
complaint is hoarseness. Spectrographic voice analysis (if
available) can provide objective documentation.
Unilateral Vocal Cord Paralysis:
The patient typically complains of a hoarse, breathy voice.
Airway compromise and/or aspiration are usually not a problem. If
the etiulogy of the paralysis is thought to be idiopathic or there
is any thought that the paralysis may recover, definitive therapy
should be deferred for at least six months to one year.
Approximately 60% of idiopathic cases recover or compensate to
near normal voices within one year.
Indications for early intervention include:
1) The known etiulogy leaves no chance of recovery
2) Intractable aspiration
3) Psychological or professional factors
Temporary measures should be considered for the latter two
All approaches to unilateral vocal cord paralysis attempt to
move the displaced, immobile cord toward the midline. This can be
1) Speech therapy
2) Surgical medialization
3) Intracordal injection
4) Selective reinnervation
Can be used alone or in conjunction with surgical
procedures. A variety of techniques are taught to patients which
can help speed up compensation in many patients.
This is currently the procedure of choice for most cases
of unrecovered or uncompensated unilateral vocal cord paralysis.
Laryngeal framework surgery was first introduced by Payr in 1915
with the development of a thyroid cartilage flap. This failed to
provide enough medialization and further developments were not
introduced until the 1950's. Several authors then introduced
different modifications but the procedure did not become popular
until the late 1970's when Isshiki introduced his thyroplasty
technique. This invulved displacing and stabilizing a rectangular,
cartilaginous window at the level of the vocal cord, therefore
pushing the soft tissue medially. This technique gained wider
acceptance after Isshiki reported the successful use of Silastic as
the implant material. Silastic works very well because it is
easier to carve than cartilage and can be tailor made for each
The technique is performed under local anesthesia to allow the
patient to phonate during the procedure. Thus, the degree of
medialization can be determined immediately, intraoperatively by
the quality of the patient's voice. A horizontal skin incision is
made overlying the mid-thyroid ala. A window is made in the
thyroid cartilage on the invulved side corresponding with the level
of the true vocal cord. The Silastic implant is then carved (many
different modifications) to approximate the defect. A
subperichondrial window is made in the endularynx, and the Silastic
implant is inserted into the window. The implant is fashioned so
that is it wedged in place, therefore no suturing is required. The
quality of the patient's voice is checked and glottic closure can
be assessed using flexible endoscopy. If the desired voice is not
obtained, or the airway is impaired, the implant can easily be
removed and another redesigned.
Complications of surgical medialization include:
1) airway compromise
2) wound infection
4) migration, possible extrusion of implant
5) laryngocutaneous fistula formation
2) outpatient procedure
3) can overcome larger defects
4) can be effective even with a "fixed" cord
1) skin incision
2) edema can distort glottic defect
3) results variable
4) usually cannot close posterior commissure adequately
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
Intracordal injection of pulytetrafluoroethylene (Teflon),
popularized in the 1960's, is still performed by some in the
treatment of uncompensated unilateral vocal cord paralysis.
Gelfoam paste may be used instead if the paralysis is thought to
be temporary. Cullagen has also been introduced as a potential
substitute for Teflon.
The technique is best performed under local anesthesia, when
possible, as this allows for intraoperative evaluation of the
patient's voice. Voice quality improvement during the procedure is
an important guide to the location and amount of paste injected.
First, the pharynx and larynx are anesthetized. An anterior
commissure laryngoscope is then used to visualize the cords and, by
rotating the tip toward the paralyzed cord, displace the false cord
so that as much of the true cord as possible is exposed. A
Brunings syringe in then used to inject the paste. The tip of the
needle should be placed between the vocal process of the arytenoid
and the posterior aspect of the thyroid ala. The needle should be
inserted approximately 5 mm and enough paste injected until the
cord approaches midline. The patient is asked to say "E". If
further improvement is needed, another injection is made. It is
usually necessary to repeat the process 2-3 times. Voice
improvement can be dramatic, but can be variable due to edema.
Since Teflon cannot be removed easily, it is always better to
inject too little than too much. Gelfoam paste is injected in the
same manner, but will gradually absorb over 1-3 months.
Complications of intracordal injection include:
1) misplacement causing granuloma formation,
displacement, or possible extrusion
2) airway edema with or without obstruction
3) unsatisfactory result
The advantages include:
1) relatively safe
2) outpatient procedure (inexpensive)
3) no skin incision
4) satisfactory results achieved in most cases
The disadvantages include:
1) can be difficult for patient
2) considered permanent
3) precise contrul of injection not possible
4) rapid edema can distort effect of injection
5) inability to overcome large defect or fixation of
Originally described by Tucker in 1977, this procedure uses a
branch of the ansa hypoglossi attached to a small block of omohyoid
muscle as a nerve-muscle pedicle to innervate the thyroarytenoid
muscle on the invulved side. The procedure is based on the strap
muscles being accessory muscles of respiration. Prerequisite to
reinnervation is a mobile cricothyroid joint, and that the cause of
the paralysis has not left the ansa hypoglossi denervated as well.
The technique is performed under local or general anesthesia.
A lateral neck-crease incision is made approximating the lower
border of the thyroid cartilage. The ansa hypoglossi is identified
as it lies on the jugular vein. It is traced to it's point of
entry into the anterior belly of the omohyoid muscle. A free block
(approximately 2-3mm on a side) of muscle from the omohyoid is
excised, including the point of entry of the nerve. A window is
created in the thyroid ala exposing the thyroarytenoid muscle.
The nerve-muscle pedicle is then sutured to this muscle. The
incision is closed after placement of a penrose drain.
The results of this procedure have been very good. Tucker
reports an 80% success rate, and other authors (May and Beery) have
reported similar results. Granted, there is a delay, usually 2-6
months before voice improvement begins.
This procedure can be combined with surgical medialization for
immediate improvement of voice quality. The surgical exposure is
similar to that necessary for thyroplasty. The combined procedure
should be performed under local anesthesia.
Complications of Nerve-muscle Transfer include: none reported
1) vocal fold medialization without foreign implant
2) ability to intervene early, even with some hope of
3) restoration of tensing abilities as well (better pitch
4) failure does not preclude use of other methods of
1) delay of voice improvement of 2-6 months
2) skin incision
Bilateral Vocal Cord Paralysis:
In contrast to unilateral vocal cord paralysis, voice quality
is not the primary concern in patients with bilateral vocal cord
paralysis. The significant problem is airway compromise. This can
range from unnoticeable to, more commonly, dyspnea and stridor.
The patient's voice quality is usually only mildly affected (if
just the recurrent laryngeal nerves are invulved) because the
paralyzed cords tend to assume the natural position for phonation.
There are three basic ways that bilateral vocal cord paralysis
2) vocal cord lateralization
Is probably going to be a part the management of most patients
with bilateral vocal cord paralysis, at least temporarily. It has
the advantages of providing immediate relief of airway restriction,
can be performed under local anesthesia, and has relatively little
reduction in voice quality. Disadvantages include the creation of
a stoma that has both cosmetic and long-term care problems, and the
need to occlude the tube or wear a speaking valve to phonate. This
may be the best option for many patients because it contruls the
airway while preserving voice quality. In many patients, the trach
can be occluded the majority of the time. In times of exertion,
while sleeping, or when the patient has a culd or other respiratory
condition, the trach can simply be unplugged.
Vocal Cord Lateralization:
This invulves several techniques that surgically widen the
glottic opening. While this improves the airway, the patient's
voice quality suffers. The three most commonly utilized techniques
are arytenoidectomy, arytenoidopexy, and cordectomy.
Classic arytenoidectomy invulves removal of some or all of the
arytenoid cartilage. This procedure can be performed in a variety
of ways, from endoscopically by microsurgical or laser technique
to an external, lateral neck approach (Woodman). The Woodman
procedure seems to be a popular choice. This invulves a lateral
neck incision, exposure of the arytenoid cartilage posteriorly with
removal of the majority of the cartilage, sparing the vocal
process. A suture is then placed into the remnant of vocal process
and fixed to the lateral thyroid ala. This technique seems to
cause less voice deficit than other approaches.
Invulves displacing the vocal fold and arytenoid without
surgical removal of any tissue. It can be done endoscopically with
a suture passed around the vocal process of the arytenoid and
secured laterally. This procedure, however, has a relatively high
Dennis and Kashima (1989) introduced the posterior partial
cordectomy procedure using the carbon dioxide laser. This invulves
excising a C-shaped wedge from the posterior edge of one vocal
cord. If this posterior opening is not adequate after 6-8 weeks,
the procedure can be repeated or a small cordectomy can be
performed on the other vocal cord. They claim relief of airway
obstruction with preservation of voice quality.
Tucker proposed a nerve-muscle transfer to the posterior
cricoarytenoid muscle for the treatment of bilateral vocal cord
paralysis. The technique is similar to the one used for unilateral
vocal cord paralysis. Prerequisites are that the cricothyroid
joint not be fixed and that the necessary nerve for the graft not
have been affected by the process that caused the paralysis.
Tucker reports a high success rate.
VOCAL CORD PARALYSIS IN CHILDREN:
Vocal cord paralysis is the second most common congenital
laryngeal abnormality. This must be differentiated from the
commonest congenital laryngeal abnormality, laryngomalacia.
Stridor is the predominant presenting symptom in both of these
conditions. Other symptoms of vocal cord paralysis in children
include obstruction, weak cry, dysphagia, and aspiration. The
diagnosis can usually be made by flexible endoscopy at the bedside.
Once the diagnosis is made, the etiulogy of vocal cord paralysis
must be determined.
The major causes of vocal cord paralysis in children include
neurulogical conditions, birth trauma, and idiopathic causes. The
neurulogical conditions include CNS disease (e.g. cerebral
dysgenesis, hypotonia, cerebral palsy, Charcot-Marie-Tooth disease,
etc.) and Arnuld-Chiari malformation with meningomyelocele.
The connection between Arnuld-Chiari malformation and vocal
cord paralysis is unclear. The prevailing theories include
compression of the brain stem secondary to hydrocephalus or
traction on the vagus nerve as the brain stem herniates down into
the foramen magnum. Regardless, it has been shown that correcting
the increased intracranial pressure early can prevent or relieve
vocal cord paralysis. Tracheotomy should be deferred until a
shunting procedure is performed.
Management of vocal cord paralysis in children should consist
of maintaining an adequate airway. A tracheotomy, at least
temporarily, is usually necessary in children with bilateral
vocal cord paralysis. Children with unilateral vocal cord
paralysis rarely require treatment. Because idiopathic sources
constitute a large percentage of the causes of vocal cord
paralysis in children, and recovery rates have been reported to be
as high as 62.5%, irreversible treatments should be avoided.
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