Treatment of Vocal Fold Paralysis

Treatment of Vocal Fold Paralysis

VyVy N. Young

Blake C. Simpson

Vocal fold paralysis (VFP) can have a profound impact on a patient’s quality of life. Bilateral vocal fold paralysis (BVFP) is life threatening because of airway compromise, and occasionally, unilateral vocal fold paralysis (UVFP) is potentially life threatening, if poor airway protection leads to aspiration pneumonia. In the case of UVFP in a professional voice user, severe dysphonia or aphonia can lead to loss of income or unemployment. For these reasons, prompt and sometimes aggressive treatment of VFP is frequently indicated. The surgical armamentarium available to treat UVFP and BVFP continues to expand, and otolaryngologists should be aware of the myriad treatment options available to the patient. This chapter outlines the many changes that have occurred in the diagnosis and treatment of VFP during the past few years, highlighting the armamentarium that is available to the treating otolaryngologist.

For the purpose of clarity, this chapter deals primarily with adult VFP and is divided into two distinct topics: UVFP and BVFP.



The etiology of UVFP involves dysfunction of either the brainstem nuclei, the vagus nerve, or the recurrent laryngeal nerve (RLN) supplying the involved side of the larynx (Fig. 69.1). Corticobulbar fibers from the cerebral cortex descend through the internal capsule and synapse on the motor neurons in the nucleus ambiguus. The nucleus ambiguus is the area within the brainstem (medulla) from which arise the fibers that will contribute to the vagus nerve. Lower motor neurons leave the nucleus ambiguus and travel laterally, exiting the medulla between the olive and the pyramid as a series of eight to ten rootlets. These rootlets coalesce into a single nerve root, known as the vagus nerve, which then exits the skull base via the jugular foramen. The vagus nerve descends in the carotid sheath, giving off three major branches: the pharyngeal branch, the superior laryngeal nerve, and the RLN. The SLN supplies sensation to the glottic and supraglottic larynx, as well as motor input to the cricothyroid (CT) muscle, which controls vocal fold lengthening and pitch. The RLN arises from the vagus nerve in the upper chest and loops under the aortic arch (left) or subclavian artery (right) and ascends back into the neck, traveling in the tracheoesophageal groove. The nerve enters the larynx posteriorly, adjacent to the CT joint. The RLN innervates the ipsilateral posterior cricoarytenoid (PCA), interarytenoid (IA) (an unpaired muscle), lateral cricoarytenoid (LCA), and thyroarytenoid (TA) muscles. Thus, the RLN supplies all of the intrinsic laryngeal muscles with the exception of the CT muscle. Ipsilateral RLN transection results in nearcomplete vocal fold immobility. (The ipsilateral CT muscle does not contribute to vocal fold adduction or abduction). It is important to remember, however, that the IA muscle is unpaired, and contralateral RLN input to the IA can lead to some adduction of the vocal fold on the paralyzed side (Fig. 69.2) (1).

The causes of unilateral VFP are myriad, but can be broken down into categories to highlight the relevant pathophysiology (2). These are shown in (Table 69.1).

In the past, nonlaryngeal malignancy was generally cited as the most common cause of UVFP, while iatrogenic nerve injury likely represented the most common cause for otolaryngologic referral. Recently, a large retrospective study over 20 years demonstrated a reversal of this trend, such that iatrogenic surgical trauma has now become the most common etiology for unilateral vocal fold immobility (3).

Traditionally, thyroidectomy was often thought to account for most of these iatrogenic cases. However, more recent data have shown that nonthyroid surgeries such as carotid endarterectomies and anterior cervical spine

surgery are the causative etiology approximately twice as often as thyroidectomy, 31% versus 16% of all causes, respectively (3). Merati et al. (4) also reported a 47.6% rate of iatrogenic injury in 84 patients with acute vocal fold motion impairment, including 27.5% following cervical spine procedures and 15% after thyroidectomy. While iatrogenic VFP caused by anterior cervical spine surgery is clearly on the rise, it is unclear whether this increase is caused by a change in surgical technique or by a rise in the overall number of these surgeries being performed. The overall incidence of this complication has previously been reported to be around 1% but more recent studies have found a higher rate (11%) of early persistent RLN palsy (5). Netterville et al. (6) has noted that the complication is almost exclusively right-sided and is probably caused by a stretch injury of the RLN by the Cloward retractor. The shorter, more oblique course of the right RLN seems to predispose it to injury (6). Other common iatrogenic surgical causes of UVFP include esophagectomy, thymectomy, neck dissection, mediastinoscopy, and cardiothoracic surgery, including aortic surgery, coronary artery bypass grafting, and pulmonary lobar resection (2,7,8). Endotracheal intubation (9), prolonged nasogastric tube placement, and even esophageal stethoscope placement have been implicated as occasional causes of VFP (Table 69.2).

Figure 69.1 Illustration of the neural pathway for the nerves controlling laryngeal function, beginning in the central nervous system (CNS), and terminating with the RLN in the endolarynx. From Academy of Otolaryngology-Head and Neck Surgery: Patient of the Month Program, Volume 31, Number 7. Simpson CB: Breathy dysphonia. Hamilton, Ontario: BC Decker Inc., 2002, with permission.

Figure 69.2 Intrinsic laryngeal musculature and innervation schematic. Note the bilateral innervation of the IA muscle by the RLN. From Rosen CA, Simpson CB. Operative techniques in laryngology. New York, NY: Springer, 2008, with permission.




Iatrogenic (surgical trauma)
















Nonsurgical trauma






Adapted from Rosenthal LHS, Benninger MS, Deeb RH. Vocal fold immobility: a longitudinal analysis of etiology over 20 years. Laryngoscope 2007;117:1864-1870, with permission.


Surgery or Procedure

Mechanism of Nerve Injury or Relevant Anatomy

Anterior cervical spine

Retraction; stretch injury of RLN (right more common) (6)


RLN injury in tracheoesophageal groove

Carotid endarterectomy

Vagal injury during dissection


RLN injury, usually left

Coronary artery bypass grafting

1. Retraction or direct injury to vagus or RLN during internal mammary artery harvest for grafting (8)

2. Hypothermic nerve injury from ice cardioplegia (7)

Pulmonary resection

Usually left upper lobe or RLN injury

Endotracheal intubation

Possible pressure neuropraxia from compression of anterior rami of RLN caused by a high-riding endotracheal cuff in the subglottis (9)

RLN, recurrent laryngeal nerve.

Nonlaryngeal malignancies are another common cause of unilateral VFP. The most common scenario involves bronchiogenic carcinoma of the lung associated with a left RLN paralysis. The cause in these cases is usually mediastinal spread of the malignancy into the aortopulmonary window. These paralyses rarely resolve spontaneously, and deserve early intervention. Other nonlaryngeal malignancies include thyroid, esophageal, and skull base (i.e., paraganglioma) tumors. Because of the common association of nonlaryngeal malignancies with VFP, it is imperative that all unexplained VFP cases be evaluated by means of an appropriate imaging study that looks at the full course of the cervicothoracic vagus and RLN (1).

The neurologic event most commonly associated with unilateral VFP is stroke, usually of the brainstem. In these patients, however, other neurologic symptoms (e.g., paraplegia) or additional cranial nerve (CN) involvement are the rule, and isolated unilateral VFP in this setting is highly unlikely (1). Many of these patients have severe dysphagia and aspiration caused by ipsilateral laryngopharyngeal sensory and motor deficits. Such patients can be challenging to treat, and may fail to improve despite adequate medialization surgery of the paralyzed vocal fold.

Uncommon neurologic causes of VFP include Arnold-Chiari malformation, amyotrophic lateral sclerosis (ALS), Guillain-Barré syndrome, Eaton-Lambert syndrome,
Parkinson disease, Shy-Drager syndrome, progressive bulbar palsy, myasthenia gravis, multiple sclerosis, and postpolio syndrome. Almost all of these disorders will have other obvious signs of progressive neurologic disease in addition to unilateral VFP and, in many cases, the neurologic condition has already been diagnosed before the patient presents with voice complaints. Most of these progressive neurologic conditions present with much more complicated (yet often subtle) findings on head and neck examination, such as a bowed vocal fold or vocal fold atrophy (Parkinson, ALS, postpolio syndrome), unexplained vocal fatigue with subtle reduced vocal fold mobility (myasthenia gravis in particular), vocal spasms (ALS), tongue fasciculations (ALS), and dysarthria (ALS, bulbar palsy). It is important to obtain a neurology consultation when a progressive neurologic disease is suspected.

Idiopathic and miscellaneous causes of unilateral VFP are also seen frequently. A few case reports suggest that “idiopathic” UVFP may be caused by herpes simplex infection (HSV1) of the vagus nerve or its branches. The injury is presumed to be an inflammatory neuropathy, similar to the cranial neuritis observed with Bell palsy (10). Although this theory is widely regarded as true, little scientific data have been published to demonstrate that HSV neuritis is the causative agent in “idiopathic” UVFP.

In addition, no studies exist that evaluate the benefit of corticosteroids or antiviral medications in the treatment of this condition. Limited data are available to document the natural history of this “idiopathic” UVFP, although Blau and Kapadia (11) reported spontaneous recovery in approximately 50%. Dworkin and Treadway (12) also described spontaneous recovery in 25% of patients with more than 3-month follow-up. It is apparent that additional study is needed to evaluate the cause and treatment of “idiopathic” UVFP. Lastly, it is important to remember that idiopathic UVFP is a diagnosis of exclusion, once a detailed history and appropriate imaging studies fail to demonstrate a cause.

Rarely, medications can cause VFP. The most notorious substances are the Vinca alkaloids (vincristine and vinblastine), which are known to cause neurotoxicity. The VFP in this case is dose related and usually resolves over a 4- to 6-week period after stopping or adjusting the dose of the medication. Both unilateral and bilateral VFP have been reported (13). Cisplatinum, also a potential source of neurotoxicity, has been implicated as a cause of reversible bilateral VFP (14,15).

Systemic diseases can (also rarely) cause vocal fold immobility, because of either paralysis or joint fixation. Such diseases include gout, sarcoidosis, tuberculosis, rheumatoid arthritis, and hypothyroidism (only in cases of myxedema) (16). Again, these systemic diseases would be expected to have myriad symptoms in addition to unilateral vocal fold immobility, and these conditions should not be suspected in cases of isolated VFP.

In the case of endotracheal intubation leading to unilateral vocal fold mobility, it is important to rule out the possibility of arytenoid cartilage dislocation or subluxation as the true cause of an immobile vocal fold. This is best done with laryngeal electromyography (LEMG) (see below and also Chapter 70.) Other traumatic causes of VFP include blunt or penetrating injuries to the neck.


Vocal Quality and Swallowing

The evaluation of UVFP begins with a thorough history and physical examination. The symptoms of UVFP are well known to all otolaryngologists. These symptoms are related to glottic insufficiency resulting from some degree of lateral displacement of the paralyzed vocal fold. The primary symptom of UVFP is dysphonia, or hoarseness. The voice can vary from simple vocal fatigue in mild or well-compensated cases, to almost complete aphonia in severe cases. Much of the quality of the voice is determined by the muscular tone and position of the affected vocal fold and each patient’s unique glottal compensatory strategy during phonation. An atrophic and poorly compensated VFP typically presents with a breathy, weak voice caused by air escape. The voice may also have a “watery” or “wet” quality to it if secretions are retained in the pyriform sinus, as is typical in high vagal injuries. With time, most patients eventually progress to a stronger but not normal voice using various compensatory strategies. Supraglottic hyperfunctional strategies are common. These patients constrict the supraglottic tract either laterally, apposing the false folds, or in an anterior posterior dimension, apposing the epiglottis to the arytenoids or the arytenoid cartilage to the contralateral false fold. This hyperfunctional muscular contraction leads to a characteristic rough, pitch-locked, low-frequency voice. This voice can sound similar to that of a patient with primary muscular tension dysphonia, and the diagnosis of VFP may not be suspected (17). “Unloading” of the voice, as described later in this chapter, is used to help analyze these patients. In contrast, other patients may develop an unnaturally high-pitched voice that is breathy in quality. This has been referred to as a “paralytic falsetto,” and is characterized by a mean increase in fundamental frequency 85 Hz above “natural” pitch. This condition is thought to be caused by compensatory contraction of the ipsilateral CT muscle, which remains innervated in isolated RLN paralysis (18).

Swallowing difficulties are often encountered, specifically aspiration of liquids, along with a weak and ineffective cough. Some dysphagia for solids may also be present, especially in brainstem or high vagal injuries, because of the concomitant denervation of the pharyngeal constrictors. Risk of aspiration is heightened in these instances as well, because of the loss of ipsilateral laryngeal sensation from SLN involvement.

Vocal Inventory

It is important to obtain a vocal inventory of the patient’s voice responsibilities (both work related and social). Vocal professionals rely on a serviceable voice for their livelihood, and these patients should be questioned regarding their upcoming work schedule to help determine the urgency of early surgical intervention (19). Most professional voice users will opt for temporizing vocal augmentation (e.g., Gelfoam, carboxymethylcellulose, and hyaluronic acid) so that they can return to work as soon as possible. Standardized patient-based voice handicap instruments are useful during the initial assessment and for documenting treatment progress (see Chapter 65).


A patient with UVFP can occasionally complain of being “short of breath”; however, careful history will show that the patient is not experiencing airway obstruction, as seen with BVFP. These patients are actually reporting a breathlessness that principally occurs during conversation and is caused by inefficient laryngeal closure. Poor glottal closure impairs the capacity to project the voice because of a “leaky” valve. Many patients increase respiratory effort and laryngeal muscle activity in an attempt to achieve glottal closure and produce a louder voice. These compensatory behaviors are mostly ineffective, placing undue strain on the paralaryngeal musculature, and resulting in vocal fatigue. This leaky laryngeal valve obviously requires increased respiratory drive to function, further contributing to the breathless feeling many patients report. In addition, exertional activity that requires lifting, pushing, and pulling can be difficult for patients with UVFP, because of the lack of an effective valsalva mechanism.



There is little yield from ordering screening laboratory tests such as chemistry panel, complete blood count, urinalysis,
Venereal Disease Research Laboratory, or fluorescent treponemal antibody absorption test, thyroid function tests, autoimmune panels, or erythrocyte sedimentation rate. Terris et al. (27) studied 84 patients with UVFP in which serologic studies had 0% yield in determining the cause. If additional elements of the history and physical examination point toward a systemic process as the cause of UVFP, directed serology tests may be indicated. In general, however, a “shotgun” approach to the workup of uncomplicated UVFP is unnecessary and wasteful.

Imaging Studies

As screening tools, barium swallow and thyroid scans have virtually no yield in determining the cause of VFP and are not advocated in the diagnostic workup (28). In contrast, a modified barium swallow or functional endoscopic evaluation of swallowing to evaluate swallowing and aspiration risk (29) is frequently helpful in managing cases of dysphagia in the workup of VFP.

In cases where a clear-cut temporal relation exists between surgical iatrogenic trauma and VFP, no additional radiologic workup is necessary. In cases where no cause can be found for the VFP, imaging studies are essential. Some disagreement exists to what constitutes an “adequate” radiologic assessment for unexplained VFP. Most investigators agree that a CT scan (with contrast) or magnetic resonance imaging (MRI) encompassing the base of the skull through the upper chest is adequate. The radiologist should be informed that the entire course of the vagus down to the take-off point of the RLN in the thoracic cavity needs to be included in the study. Benninger et al. (1) have argued that CT or MRI of the neck combined with chest radiography constitutes an adequate workup. They noted that 100% of pulmonary or mediastinal malignancies associated with VFP were detected on routine chest radiography, and that imaging of the chest by CT was unnecessary. Others disagree with this approach. Glazer et al. (28) demonstrated that of 18 metastatic mediastinal masses seen on CT, only 5 were visualized on routine chest radiographic study. Koufman et al. (30) advocate the addition of MRI of the brainstem in cases of obvious “high vagal” lesion (palatal paralysis + VFP), because this is a difficult area to image and small lesions can be missed.

The utility of imaging studies in the setting of vocal fold paresis is less well defined, as the presence of partial vocal fold motion is considered by many to be indicative of a lower likelihood of a radiographically identifiable compressive lesion of the RLN. These authors do not routinely perform radiologic evaluation of patients with vocal fold paresis.

Laryngeal Electromyography

LEMG has an increasingly crucial role in the workup of unilateral vocal fold immobility. The findings of LEMG are important in determining prognosis, differentiating UVFP and CA joint pathology, diagnosing suspected vocal fold paresis, and directing treatment decision making (31,32,33,34,35,36).

Useful information from LEMG is obtained between 1 and 6 months after the onset of VFP. Evaluation outside of these parameters can render the information misleading (too early), or of limited usefulness (too late) (37). Munin et al. (37) have shown that serial LEMG provide better prognostic information in the determination of UVFP recovery.

Qualitative LEMG has been a long-time tool in the evaluation of VFP. More recent reports describe quantitative aspects of LEMG that provide additional information regarding prognosis (38,39). The term “spontaneous activity” refers to fibrillation potentials (spontaneous discharges during rest). This finding is consistent with active nerve denervation (Fig. 69.7B). “Recruitment” is the finding of increase in the number and rate of motor unit discharges as contraction is increased (as the patient increases the loudness of the vocalization); this can be reduced or absent with nerve injury. Normal motor unit potentials (MUP) are biphasic or triphasic, whereas polyphasic MUP indicate early reinnervation (Fig. 69.7C). Clear-cut cases of normal (class I) and grossly abnormal (class V) give good prognostic information. Statham et al. (38) have recently demonstrated that motor unit recruitment can be quantitatively measured within the TA muscle complex by a “turns analysis,” evaluating the number of “turns,” or peaks of the measured MUP signal. Their report evaluated both control and UVFP patients and revealed that a mean decrease in turns below 400 at maximal effort is reflective of a neurogenic lesion (Fig. 69.8).

Additionally, synkinesis reflects a misdirected reinnervation following RLN injury and/or reinnervation from nonnative nerves and is demonstrated by MUP in the TA muscle complex during vocal fold abduction tasks (such as a sniff) (Fig. 69.9A and B). The presence of synkinesis has been shown to be a poor prognostic indicator (34). Smith et al. (39) demonstrated that use of quantitative LEMG improves the ability to predict return of vocal fold motion, with 100% positive and 89.5% negative predictive values in their study utilizing this technique. Clearly, LEMG in general, and quantitative LEMG specifically, represent a clinically useful tool in the management of patients with VFP.