Current Otolaryngology > VIII. Larynx and Hypopharynx > Chapter 30.

Vocal Cord Paralysis >

INTRODUCTION: VOCAL CORD PARALYSIS

True vocal cord paralysis signifies immobility of the "true" vocal cord, or vocal fold,
secondary to disruption of the relevant motor innervation of the larynx. Disruption of
innervation may occur along the length of either recurrent laryngeal nerve and the vagi,
and it may involve damage to the motor nuclei of the vagus. It should be differentiated
from fixation of the vocal cord secondary to direct pathological infiltration of the vocal
fold, the larynx, or laryngeal muscles. It should also be distinguished from fixation of the
vocal cord secondary to cricoarytenoid joint fixation, which is encountered with
rheumatoid patients or following traumatic intubation.

The site of disruption of the nerve supply leads to a characteristic pattern in the position
of the vocal cords and is an important component in the diagnosis of the underlying
pathology. However, distinguishing between recurrent laryngeal nerve paralysis and vocal
cord paralysis secondary to disruption of the vagus nerve can be difficult.

Table 301 summarizes the main causes of vocal cord paralysis in adults. Once the cause
of the vocal cord paralysis is ascertained, the next stage is to consider the rehabilitation
and treatment of the patient depending on his or her overriding symptoms.

Table 301. Etiology of Vocal Cord Paralysis in Adults.

Type of paralysis Etiology

Unilateral Recurrent Neoplasia

Laryngeal Iatrogenic causes

Trauma

Aneurysms

Idiopathic causes

Bilateral Recurrent Post-thyroid surgery

Laryngeal Thyroid neoplasia

Unilateral Vagal Iatrogenic causes

Neoplasia

Neurological causes

Brain stem infarction

Skull base

Osteomyelitis

Idiopathic causes
Type of paralysis Etiology
Bilateral Vagal Neurological causes

ANATOMY
The relevant anatomy of the larynx is best understood in terms of the muscles producing
abduction and adduction of the vocal cords and their nerve supply. All of the intrinsic
laryngeal muscles, except the cricothyroid muscle, which is supplied by the external
branch of the superior laryngeal nerve, are supplied by the recurrent laryngeal nerve. The
sole abductor of the vocal cords is the posterior cricoarytenoid muscle. Table 302
provides a summary of the relevant laryngeal musculature and their innervation.

Table 302. Summary of Innervation of the Vocal Cord.

Muscle Nerve
Adductors (lateral cricoarytenoid, thyroarytenoid, Recurrent laryngeal (adductor
interarytenoids) branch)

Posterior cricoarytenoid Recurrent laryngeal (abductor

branch)

Cricothyroid External laryngeal

In order to understand the potential causes of vocal cord paralysis, it is important to

understand the pathways of the vagus and the recurrent laryngeal nerves. The course of
the vagi in both sides of the head and neck are identical, but the recurrent laryngeal
nerves differ significantly in their course once they leave the vagus.

The nuclei lie in the upper medulla and give rise to 810 rootlets that lie between the
glossopharyngeal nerve superiorly and the spinal root of the accessory nerve inferiorly.
The muscles of the pharynx, upper esophagus, larynx, and palate are all supplied by
motor fibers originating in the nucleus ambiguus. The majority of these fibers join the
vagus at the inferior cervical ganglion below the jugular foramen, from the cranial root of
the accessory nerve.

The vagus leaves the cranial cavity via the jugular foramen together with the
glossopharyngeal and hypoglossal nerves. It then descends vertically in the neck within
the carotid sheath, adherent to the internal carotid artery, lying deep between the internal
jugular vein and the artery itself.

The right vagus enters the thorax crossing superficial to the right subclavian artery. The
right recurrent laryngeal nerve then leaves the vagus, curling underneath the artery to
run superiorly in the tracheoesophageal groove and pass under the inferior constrictor of
the pharynx, into the larynx.

The left vagus enters the thorax deep to the left brachiocephalic vein, between the carotid
and subclavian arteries. The left recurrent laryngeal nerve leaves the vagus as it crosses
the aortic arch, and then passes under the ligamentum arteriosum before taking a similar
course to the right recurrent laryngeal nerve.

PATIENT EVALUATION
The initial evaluation of any patient presenting with dysphonia must include a systemic
voice assessment (see Chapter 28: Benign Laryngeal Lesions). A thorough history must
be taken, noting the onset and duration of the dysphonia. A detailed medical and surgical
history is particularly important. The examination must include a full ear, nose, and throat
examination as well as a detailed inspection of the vocal cords and larynx using the three
methods of indirect and direct diagnostic laryngeal endoscopy (see Chapter 28: Benign
Laryngeal Lesions).

Once the diagnosis of unilateral or bilateral vocal cord palsy has been established, flexible
nasolaryngoscopy or rigid laryngoscopy should be performed to rule out an associated
infiltrating lesion. This lesion can produce fixation of the vocal fold, which may be missed
with a mirror examination. Although difficult to distinguish clinically, if unilateral or
bilateral vocal cord paralysis secondary to high disruption of the vagus nerve can be
ascertained after inspecting the vocal cords, a full examination of the other cranial nerves
should be instituted.

Laryngeal electromyography is a useful adjunct in establishing that vocal cord immobility

is due to denervation of the intrinsic muscles and not secondary to vocal cord fixation. It
can also be used to estimate the prognosis relative to reinnervation.

Koufman JA, Postma GW, Whang CS et al. Diagnostic laryngeal electromyography: the
wake forest experience 1995-1999. Otolaryngol Head Neck Surg. 2001;124:603.
(Evaluation of laryngeal electromyography in the management of vocal cord paralysis.)
[PMID: 11391248]

Rosen CA, Murray T. Diagnostic laryngeal endoscopy. Otolaryngol Clin North Am.
2000;33:751. (Techniques used in evaluation of the larynx.) [PMID: 10918658]

Simpson CB, Fleming DJ. Medical and vocal history in the evaluation of dysphonia.
Otolaryngol Clin North Am. 2000;33:719. (Review of history taking in voice disorders.)
[PMID: 10918656]

UNILATERAL VOCAL CORD PARALYSIS

UNILATERAL RECURRENT LARYNGEAL PARALYSIS
Essentials of Diagnosis
Dysphonia.

"Bovine" cough.

Unilateral paramedian vocal fold paralysis.

 If a vocal cord is compensated for, voice may tire with use.

General Considerations
The site of disruption of the nerve supply to the vocal cord can be ascertained depending
on the final position of the cords and the side that is paralyzed. The initial stage in
evaluating a unilateral vocal cord paralysis is to establish whether the paralysis is
secondary to a recurrent laryngeal nerve injury or to disruption of the vagus nerve.
Lesions producing the characteristic paramedian vocal cord palsy will be found below the
origin of the superior laryngeal nerve. The paralyzed vocal cord is found in the
paramedian position due to the unopposed action of the cricothyroid muscle (Figure 30
1). Left vocal cord paralysis is more common than paralysis of the right vocal cord
because of the longer and more convoluted course of the left recurrent laryngeal nerve
within the thorax. The right vocal cord is involved in 330% of cases.

Figure 301.

Right recurrent laryngeal nerve paralysis (dotted line = midline): (A) at rest, the paralyzed
cord takes up a paramedian position; (B) on phonation.

The patient history is important and as most causes of unilateral vocal cord paralysis are
secondary to surgery, the timing of the onset of the dysphonia to any relevant surgery is
crucial.

Etiology
The causes of unilateral recurrent laryngeal paralysis can be iatrogenic (eg, following
thyroid, esophageal, cervical spine, and thoracic surgery). It can also be caused by a
primary and secondary lung carcinoma or a malignant tumor of the esophagus or thyroid.
Aneurysms of the aorta or great vessels (eg, Ortner syndrome) and trauma may also
contribute to the development of this palsy. The etiology may also be idiopathic.

Clinical Findings
SYMPTOMS AND SIGNS
The presenting symptoms associated with the dysphonia as well as the position of the
vocal cords are the key to the underlying diagnosis. Patients present with dysphonia; their
voices may become weak with use. The dysphonia may be of sudden onset with no
associated features or there may be a preceding history of other illness (eg, respiratory
illness). It is important to question patients regarding respiratory symptoms such as
cough, hemoptysis, and dyspnea, particularly in patients who smoke as any of these
symptoms may indicate an underlying malignant chest neoplasm. The signs suggesting an
underlying malignant chest tumor are significant for the physician to note. These signs
may include evidence of clubbing, which is seen in patients with bronchogenic carcinoma;
Horner syndrome; and a pleural effusion.

Vocal cord paralysis secondary to recurrent laryngeal nerve paralysis classically produces
an immobile vocal cord in the paramedian position. Depending on the time of patient
presentation after the development of dysphonia, the other vocal fold may compensate
for the immobile one, thus limiting the degree of hoarseness experienced.
IMAGING STUDIES
For patients with recurrent laryngeal nerve palsy, an accurate imaging of the neck and
chest must be performed; the first sign of a malignant chest neoplasm may be the
development of recurrent laryngeal nerve palsy. An initial chest x-ray should be followed
by computed tomography (CT) scans from the skull base to the diaphragm for left vocal
cord paralysis and by a CT scan from the skull base to at least the thoracic inlet for right
vocal cord paralysis.

Treatment
NONSURGICAL MEASURES
Expectant treatment is recommended when there is no underlying malignant growth. The
majority of unilateral cord palsies will compensate within 618 months. Patient age,
occupation, and preference as to how aggressively the vocal cord paralysis should be
treated should all factor into the treatment plan.
SURGICAL MEASURES
Among the surgical treatments available, the two primary surgical measures are injection
laryngoplasty and laryngeal framework surgery.
Injection Laryngoplasty
Injection laryngoplasty utilizes polytef (PTFE, commonly known as Teflon), absorbable
gelatin paste (ie, Gelfoam paste), or fat. The selected substance is injected laterally into
the vocal fold, as far as is possible, in order to displace it medially. Teflon is a permanent
material and does have some complications (eg, granuloma formation); therefore, it is
most suitable for patients with incurable neoplasms, who have advanced medical illness,
and in situations where subtle improvements in voice changes are not required. Gelfoam
paste is useful in restoring vocal function in patients whose recovery is expected and who
use their voices on a professional basis. Gelfoam injection can be repeated, if necessary.
Fat is a useful alternative to Gelfoam and can also be repeated.
Laryngeal Framework Surgery
Laryngeal framework surgery (in the form of thyroplasty) involves the placement of a
Silastic implant lateral to the vocal fold via a window cut in the thyroid cartilage. The
Silastic causes the vocal fold to be displaced medially, ensuring adequate glottic closure.

UNILATERAL COMPLETE VAGAL PARALYSIS

Essentials of Diagnosis
Weak, breathy hoarseness.

Possible history of aspiration.

Site of injury above the origin of the superior laryngeal nerve.

Vocal cord in lateralized intermediate position.

General Considerations
During the evaluation of a unilateral high vagal palsy, it is important to establish whether
the site of damage to the nerve is at the skull base, the brain stem, or the cerebrum.
Because of the inevitable loss of superior laryngeal nerve function, there will be a
decreased sensation of the larynx above the vocal cords on the affected side, and a loss
of cricothyroid function. This loss of vagal nerve function leads to the paralyzed cord
taking up an intermediate, or cadaveric, position (Figure 302).

Figure 302.

Right vagal nerve paralysis: (A) at rest, the paralyzed cord takes up an intermediate position;
(B) on phonation.

Etiology
The origins of unilateral complete vagal paralysis include: (1) iatrogenic causes (eg, skull
base surgery), (2) neurological causes (eg, multiple sclerosis, syringomyelia, and
encephalitis), (3) a brain stem infarction (eg, Wallenberg syndrome), (4) a malignant
growth (primary or secondary), and (5) inflammation (eg, skull base osteomyelitis). The
nerve paralysis may also be idiopathic.

Clinical Findings
SYMPTOMS AND SIGNS
Disruption of the vagus nerve at the skull base or at the motor nucleus of the vagus on
one side will inevitably result in the loss of unilateral supraglottic sensation; a history of
aspiration may therefore be obtained. Compensation of the contralateral vocal cord is rare
and consequently the patient's voice remains weak and breathy.

If there are lesions of the skull base or brain stem, other cranial nerves (eg, the
hypoglossal or glossopharyngeal nerves) may be involved. Unilateral brain stem
involvement is uncommon.
LABORATORY FINDINGS
Depending on the history and pattern of cranial nerve involvement, it may be worthwhile
obtaining inflammatory markers such as a C-reactive protein or ESR (erythrocyte
sedimentation rate), particularly if there is no history of prior surgery.
IMAGING STUDIES
Imaging studies should adequately identify lesions of the skull base. MRI is the imaging
modality of choice for the skull base as inflammatory changes on CT scans tend to
present late and CT scanning is also not satisfactory in imaging the brain stem.

Isotope bone scans are the gold standard of investigation for those rare diabetic patients
who present with jugular foramen syndrome secondary to skull base osteomyelitis.

Treatment
Injection laryngoplasty is not often successful in cases of complete vagal nerve paralysis
because of the relatively abducted position of the vocal cord and the failure of injected
materials such as Teflon to adequately displace the cord medially.

Medialization laryngoplasty, using silicone implants, is the optimal treatment method.

Laryngoplasty may be combined with arytenoid adduction when the posterior glottic
aperture is still not satisfactorily approximated. Most procedures are performed both to
prevent aspiration and improve voice quality.

Anderson TD, Mirza N. Immediate percutaneous medialization for acute vocal fold
immobility with aspiration. Laryngoscope. 2001;111:1318. (Efficacy of Gelfoam injection
laryngoplasty.) [PMID: 11568562]

Carrau RL. Laryngeal framework surgery for the management of aspiration. Head Neck.
1999;21:139. (Medialization laryngoplasty with silicone, with or without arytenoid
adduction.) [PMID: 10091982]

Hughes CA. Unilateral true vocal cord paralysis: cause of right-sided lesions. Otolaryngol
Head Neck Surg. 2000;122:678. (Etiology of right vocal cord palsy.) [PMID: 10793345]

Kriskovich MD. Vocal fold paralysis after anterior cervical spine surgery: incidence,
mechanism, and prevention of injury. Laryngoscope. 2000;110:1467. (Incidence of 2
6%; mechanism due to compression of the nerve during retraction.) [PMID: 10983944]

Lo CY. A prospective evaluation of recurrent laryngeal nerve paralysis during

thyroidectomy. Arch Surg. 2000;135:204. (0.9% of patients developed permanent
unilateral vocal cord palsy.) [PMID: 10668882]

Msiung MW. Fat augmentation for glottic insufficiency. Laryngoscope. 2000;110:1026.

(Fat injection laryngoplasty as an alternative to Gelfoam.) [PMID: 10852525]

Ramadan HH. Outcome and changing cause of unilateral vocal cord paralysis. Otolaryngol
Head Neck Surg. 1998;118:199. (Surgical and neoplastic causes underlying the majority
of vocal cord paralyses.) [PMID: 9482553]

BILATERAL VOCAL CORD PARALYSIS

BILATERAL RECURRENT LARYNGEAL NERVE PARALYSIS
Essentials of Diagnosis
Often presents with stridor.

Voice may be normal.

Usually a patient history of thyroid surgery.

Vocal cords fixed in median to paramedian position.

General Considerations
The patient may have a recent history of thyroid surgeryusually total thyroidectomy.
Rarely, an advanced malignant thyroid tumor may be an underlying cause. If
unrecognized, presentation may be late as normal voice production is possible due to the
close approximation of the vocal cords (Figure 303).

Figure 303.

Bilateral recurrent laryngeal nerve paralysis (dotted line = midline): (A) at rest and (B) on
phonation.

Clinical Findings
A patient who presents with a bilateral recurrent laryngeal nerve palsy usually does so in
an emergency situation, following the development of stridor. The patient may have been
well previously, with an apparently normal voice, but developed airway decompensation
following an upper respiratory tract infection. Because the vocal folds are adducted,
minimal swelling may precipitate stridor.
Treatment
In an emergency situation, tracheostomy is often the only viable option. It is important to
discuss with the patient the possible options for long-term treatment if decannulation is to
be considered, as any operation to improve the airway may make the voice worse and
increase the risk of aspiration. Some patients are happy maintaining their tracheostomy
tube on a long-term basis and a fenestrated, cuffless tube will be suitable in most cases.

Stitch lateralization of the vocal cord is an effective option during the recovery of nerve
function as it avoids the need for a long-term tracheostomy. Partial or full recovery may
occur in more than 50% of patients. The main operative procedure currently in practice is
laser arytenoidectomy or unilateral or bilateral cordectomy.

Other lateralization procedures exist; however, while improving the airway, they all carry
the risk of increasing vocal impairment and aspiration.

BILATERAL COMPLETE VAGAL NERVE PARALYSIS

Essentials of Diagnosis
Weak voice.

History of aspiration and choking.

Bilateral immobile vocal cords in intermediate position.

Satisfactory glottic aperture.

General Considerations
Bilateral, high vagal, or brain stem involvement is unusual and often secondary to a
neurological cause. The complete loss of supraglottic sensation results in a significant risk
of aspiration. Vagal paralysis is often accompanied by the involvement of other cranial
nerves, typically the glossopharyngeal and hypoglossal nerves.

Etiology
Neurological causes of bilateral complete vagal nerve paralysis include brain stem
infarction, multiple sclerosis, and motor neurone disease (eg, amyotrophic lateral
sclerosis, or ALS).

Clinical Findings
SYMPTOMS AND SIGNS
Patients present with either an acute or progressive onset of a weak, breathy voice
associated with a history of choking and dysphagia. There may be a history of
nasopharyngeal regurgitation. Patients are short of breath on exertion and may develop
stridor in the presence of an upper respiratory tract infection. The patient may be
dysarthric and have signs of other cranial nerve involvement, such as paralysis of the
tongue and loss of a gag reflex. Bilateral vagal nerve paralysis produces immobile vocal
cords located in an intermediate position with a widened glottic aperture (Figure 304).

Figure 304.
Bilateral vagal nerve paralysis: (A) at rest and (B) on phonation.

IMAGING STUDIES
Brain stem disease is best visualized with the aid of MRI scans.

Treatment
Treatment is directed at preventing aspiration and ensuring adequate nutrition. If stridor
develops, which is often in the presence of an underlying pneumonia or upper respiratory
tract infection, then a tracheostomy is usually required. A cuffed tracheostomy tube will
also help to diminish aspiration. Long-term enteral nutrition via a percutaneous
gastrostomy tube is often necessary. If the vocal cord paralysis is stable, then
medialization techniques may be used.

Laccourreye O, Paz Escorar MI, Gerhardt J, Mans S, Biacate B, Brasner D. CO 2 laser

endoscopic posterior partial transverse cordotomy for bilateral paralysis of the vocal fold.
Laryngoscope. 1999;109:415. (Useful alternative treatment for bilateral vocal cord
paralysis.) [PMID: 10089968]

Rovo L, Jori J, Brzozha M, Caigner J. Airway complications after thyroid surgery: minimally
invasive management of bilateral recurrent nerve injury. Laryngoscope. 2000;110:140.
(Stitch lateralization as an alternative treatment for bilateral recurrent laryngeal nerve
palsy.) [PMID: 10646730]

Segas J, Stavroulakis P, Manolopoulos L, Yiotakis J, Adamopoulos G. Management of

bilateral vocal cord paralysis: experience at the University of Athens. Otolaryngol Head
Neck Surg. 2001;124:68 (Laser-assisted posterior cordectomy.) [PMID: 11228456]

Copyright 2006 The McGraw-Hill Companies. All rights reserved