Chapter 32. Vocal Cord Paralysis

True vocal cord paralysis signifies loss of active movement of the “true” vocal cord, or vocal fold, secondary to disruption of the motor innervation of the larynx. Disruption of innervation may occur along the length of the recurrent laryngeal nerves and the vagi and may include damage to the motor nuclei of the vagus. It should be differentiated from fixation of the vocal cord secondary to direct infiltration of the vocal fold, larynx, or laryngeal muscles. It should also be distinguished from fixation at the cricoarytenoid joint, encountered with rheumatoid arthritis or following traumatic intubation.

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

Table 32–1 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 symptoms.

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 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 32–2 provides a summary of the relevant laryngeal musculature and their innervation.

To understand the causes of vocal cord paralysis, it is important to understand the pathways of the vagus and 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 8–10 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. Most 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 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 superficially 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.

The initial evaluation of any patient presenting with dysphonia must include a systemic voice assessment (see Chapter 29). 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 (see Chapter 29) 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 may be helpful in distinguishing between denervation of the intrinsic muscles and vocal cord fixation. It may also estimate the prognosis relative to reinnervation.

Unilateral Recurrent Laryngeal Paralysis

Essentials of Diagnosis

• Dysphonia.
• “Bovine” cough.
• Unilateral paramedian vocal fold paralysis.
• Voice may tire with use.

General Considerations

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 are found below the origin of the superior laryngeal nerve. The paralyzed vocal cord is found in the paramedian position owing to the unopposed action of the cricothyroid muscle (Figure 32–1). 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. The right vocal cord is involved in 3–30% of cases.

Most unilateral vocal cord paralyses are secondary to surgery; therefore, the relative 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 left atrial dilation (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. It is important to question patients regarding respiratory symptoms such as cough, hemoptysis, and dyspnea, particularly in patients who smoke as these symptoms may indicate an underlying malignant chest neoplasm. Signs suggestive of underlying chest malignancy 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, accurate imaging of the neck and chest must be performed; the first sign of a malignant chest neoplasm may be recurrent laryngeal nerve palsy. A chest CT should identify an intrathoracic cause. If negative, an MRI of the neck and posterior fossa should be performed (as in practice it is often difficult to distinguish between vagal and recurrent laryngeal nerve palsy). If still negative, an endoscopy including bronchoscopy should be considered.

Treatment

Nonsurgical Measures

Expectant treatment is recommended when there is no underlying malignant growth. Most unilateral cord palsies compensate within 6–18 months. Patient age, occupation, and preference as to how aggressively the vocal cord paralysis should be treated should all influence the treatment plan.

Surgical Measures

A range of surgical measures is available the aim of which is to allow contact with the opposite cord during phonation and swallowing and to improve the patients' ability to cough. Procedures may be static or dynamic. Dynamic procedures consist of re-innervation or laryngeal pacing with an implantable device; they are performed in relatively few centers worldwide and will not be discussed further. The two principal static measures are injection laryngoplasty and laryngeal framework surgery.

Injection Laryngoplasty

It involves injecting a material laterally into the vocal fold to displace it medially. An ideal injectable material would lack an antigenic response, have similar viscoelastic properties to the vocal fold, be resistant to resorption or migration, and be easy to prepare and inject with precise control. Substances commonly used include collagen, Vox, calcium hydroxyapatite, polyacrylamide gel, and fat.

Laryngeal Framework Surgery

Laryngeal framework surgery (in the form of medialization thyroplasty) involves the placement of a Silastic implant or Gore-tex lateral to the vocal fold via a window cut in the thyroid cartilage. The Silastic displaces the vocal fold 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 brainstem, or the cerebrum. Because of the inevitable loss of superior laryngeal nerve function, there is a decreased sensation of the larynx above the vocal cords on the affected side and a loss of cricothyroid muscle function. This loss of vagal nerve function leads to the paralyzed cord lying more laterally in the intermediate, or cadaveric, position (Figure 32–2).

Etiology

The origins of unilateral complete vagal paralysis include (1) iatrogenic causes (eg, skull base surgery), (2) neurologic causes (eg, multiple sclerosis, syringomyelia, and encephalitis), (3) a brainstem infarction (eg, Wallenberg syndrome), (4) a malignant growth (primary or secondary), and (5) inflammation (eg, skull base osteomyelitis).

Clinical Findings

Symptoms and Signs

Disruption of the vagus nerve at the skull base or at the motor nucleus of the vagus inevitably results in the loss of unilateral supraglottic sensation; a history of aspiration may therefore be obtained. Compensation of the contralateral vocal cord is often inadequate, and consequently the patient's voice remains weak and breathy.

Lesions of the skull base or brainstem may involve other cranial nerves (eg, the hypoglossal or glossopharyngeal nerves). Unilateral brainstem involvement is uncommon.

Laboratory Findings

Depending on the history and pattern of cranial nerve involvement, it may be worthwhile to obtain inflammatory markers such as a C-reactive protein or erythrocyte sedimentation rate (ESR), particularly if the patient has no history of surgery.

Imaging Studies

Imaging studies should adequately identify lesions of the skull base. MRI is the imaging modality of choice for the skull base because inflammatory changes on CT scans tend to present late and CT scanning does not image the brainstem satisfactorily.

Isotope bone scans may have use in patients who present with jugular foramen syndrome secondary to skull base osteomyelitis.

Treatment

Injection laryngoplasty is often unsuccessful in cases of complete vagal nerve paralysis because the relatively abducted position of the vocal cord leads to failure of injected materials 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.

Bilateral Recurrent Laryngeal Nerve Paralysis

Essentials of Diagnosis

• Often presents with stridor.
• Voice may be normal.
• Usually a history of thyroid surgery.
• Vocal cords fixed in median to paramedian position.

General Considerations

The patient may have a recent history of thyroid surgery—usually 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 because of the close approximation of the vocal cords (Figure 32–3).

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 after 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, since 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 is suitable in most cases.

Stitch lateralization of the vocal cord is an effective option during the recovery of nerve function because it prevents 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, though improving the airway, they carry the risk of increasing vocal impairment and aspiration.

Bilateral Complete Vagal Nerve Paralysis

Essentials of Diagnosis

• Weak voice.
• History of aspiration and choking.
• Vocal cords in intermediate position.
• Satisfactory glottic aperture at rest.

General Considerations

Bilateral, high vagal, or brainstem 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 brainstem infarction, multiple sclerosis, and motor neuron disease (eg, amyotrophic lateral sclerosis [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 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 32–4). There may be passive glottic closure on forced inspiration; therefore, it is important to correlate cord movement with the phase of respiration.

Imaging Studies

Brainstem 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 also helps 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.

We would like to acknowledge Rupert Obholzer, MRCS and R Gareth Rowlands FRCS(ORL-HNS) for their contribution to this chapter in the previous editions of CDT.