Vocal fold immobility is a broad term that can be used to describe the abnormal movement of the true vocal folds. It can be unilateral, where only one true vocal fold is affected, or bilateral, in which both true vocal folds are affected. The abnormal movement can be characterized as being paretic, meaning some movement is present, albeit reduced or paralyzed, with complete cessation of vocal fold movement. If a true vocal fold is paralyzed, it can be described as being paralyzed in a midline, paramedian, or lateral position. This review will focus specifically on unilateral vocal fold paralysis.
It is imperative to understand the neuroanatomy of the true vocal folds to understand vocal fold paralysis. The vagus nerve innervates the larynx and its associated muscles. The vagus nerve is comprised of nerve fibers that arise from the nucleus ambiguus in the medulla portion of the brainstem. Upper-motor cortico-bulbar neurons originate from the cerebral cortex and descend to synapse onto these lower-motor vagal nerve fibers, which originate from the nucleus ambiguus.
After arising from the brainstem, the vagus nerve then exits the skull base at the jugular foramen and descends into the neck to give off three main branches (the pharyngeal branch, the superior laryngeal nerve [SLN], and the recurrent laryngeal nerve [RLN]). The SLN supplies sensation to the larynx above the glottis and innervates the cricothyroid muscle. The RLN descends further into the neck, loops around the subclavian artery (on the right) or the aortic arch (on the left), and ascends back up into the neck in the tracheoesophageal groove, where it enters the larynx posteriorly, near the cricothyroid joint. The RLN innervates all remaining intrinsic muscles of the larynx including the posterior cricoarytenoid, interarytenoid, lateral cricoarytenoid, and thyroarytenoid muscles.
When identified, unilateral vocal fold paralysis must be thoroughly evaluated, as there are a number of possible causes. Any pathology along any point of the neuromuscular pathway from the brainstem to the laryngeal muscles can cause paralysis. In the past, iatrogenic injury to the RLN during thyroid surgery was noted to be the most common cause of UVFP. However, given improvements in techniques, rates of iatrogenic injury have decreased. More recently, non-laryngeal primary malignancies (such as lung) have been reported to be the most common cause. Idiopathic UVFP, which some postulate to be a post-viral syndrome, is also a common cause. Central causes, such as previous cerebral vascular accidents, brain stem or high skull-base tumors, as well as peripheral neurologic etiologies, must be entertained in the differential. Lastly, a mechanical issue such as cricoarytenoid joint dislocation must be considered, especially in the setting of recent laryngeal trauma.
In 1991, Stanford University conducted a study and reviewed the literature regarding cases of UVFP from 1970 through 1991. Their review identified 1019 patients with UVFP. The most common etiology was neoplasm (35.5%), of which 54.8% were of lung origin. The second most common cause of UVFP in this group was post-surgical (24.6%), of which thyroid surgery was the cause in 55.4% of these cases. An idiopathic cause was the next most common, with a total of 14.3% of cases, while 13.3% were related to medical/inflammatory causes, 6% were related to traumatic events, and 6% were related to central causes. Because these are all known causes of UVFP, guided differential diagnosis and workup can be performed.
The true incidence of unilateral vocal fold paralysis is not known. However, it is known to be relatively uncommon. The reason for the difficulty in determining the true incidence is two-fold. First, making a confirmed diagnosis is a difficulty, as it requires a visual evaluation of the larynx, which requires indirect laryngoscopy or direct laryngoscopy with use of an endoscope. Second, a myriad of other pathologies can cause dysphonia, including acid reflux, laryngitis, muscle tension dysphonia, etc. Therefore, if symptoms like dysphonia are being used to make a presumed diagnosis, the true incidence would be drastically underestimated, as dysphonia due to unilateral vocal fold paralysis would often be attributed to other, more common causes.
Stanford University reviewed their experience with vocal fold paralysis from 1983 through 1991. They identified 187 charts that listed vocal fold paralysis as a diagnosis. One hundred and thirteen (113) of these charts met their inclusion criteria to be reviewed. Their data demonstrated 84 patients (74.3%) diagnosed with unilateral vocal fold paralysis and 29 patients (25.7%) with bilateral vocal fold paralysis. Among the unilateral vocal fold paralysis group, 45 (53.6%) were men, and 39 (46.4%) were women. The mean age was 58. In 57 patients (67.9%), the left cord was affected, whereas the right cord was affected in 27 patients (32.1%).
Unilateral vocal fold paralysis may manifest itself in a myriad of ways. However, most commonly, hoarseness is the primary complaint. The severity of dysphonia may relate to the position of the paralyzed vocal fold. If the vocal fold is paralyzed in a lateral position, patients will likely complain of a breathy voice, due to air escaping through the glottis because the paralyzed vocal fold can not make contact with the contralateral side. However, if the vocal fold is paralyzed in the midline position, the dysphonia may not be as severe. Dysphagia is another common complaint, due to the inability to entirely close the glottis, which impairs the swallowing mechanism. If severe, this may lead to an inability to protect the airway during the swallow, which may lead to recurrent aspiration pneumonia. Other symptoms may include a breathlessness or shortness of breath, stridor or globus sensation.
A physical exam is usually performed using either indirect laryngoscopy by mirror exam or by using a flexible nasolaryngoscope. At this point, it should be determined if the vocal fold paralysis is bilateral or unilateral. Furthermore, the position in which the paralyzed true vocal fold sits is a key factor that must be determined.
Appropriate workup of a patient with UVFP begins with a complete history and physical examination. And evaluation with a flexible nasolaryngoscope should be performed to assess the functional status of the vocal folds. If a patient presents with UVFP immediately following thyroid or other neck surgery (with known or suspected injury), a formal workup may not be warranted. However, if the cause of UVFP is unknown, imaging is mandated. Due to the high incidence of malignancy, imaging of the skull base, neck, and chest is needed to evaluate the entire course of the RLN on both the right and left sides. Preference on imaging techniques vary depending on Otolaryngologist preference but may include chest x-rays, CT scans or MRI scans. If there is evidence of other cranial nerve involvement and concern for a high-vagal injury (such as palatal weakness), an MRI of the skull-base may be recommended to evaluate further.
One modality that may be used to help guide diagnostic and treatment decisions is laryngeal electromyography (LEMG). This can be used to help narrow the differential and help rule out cricoarytenoid (CA) joint dislocation as a cause of UVFP. CA joint dislocation would present with normal LEMG findings, indicating the neuromuscular junction is intact, but rather the immobility of the true vocal fold is due to joint dislocation. LEMG is most useful at 1 to 6 months following the injury/onset of paralysis. Findings on LEMG may include normal motor unit potentials, which indicate an intact neuromuscular junction, fibrillation potentials, which indicate denervation injury to the muscle, or poly-phasic action potentials, which indicate re-innervation of the muscle. Depending on the clinical scenario, these findings may be useful to help direct treatment options.
Treatment should be directed at treating the underlying etiology of the UVFP (if applicable), preventing aspiration and improving dysphonia. Multiple factors must be taken into account regarding the specific treatment provided and decisions must be tailored to each clinical scenario.
Idiopathic unilateral vocal fold paralysis and its prognosis are topics that deserve special mention. Although not well defined in the literature, idiopathic vocal fold paralysis is often believed to be secondary to a post-viral or post-infectious insult. Just as idiopathic facial nerve paralysis can occur affecting cranial nerve seven or idiopathic sudden sensor-neural hearing loss can occur affecting cranial nerve eight, the vagus nerve is also susceptible to such insult manifesting as idiopathic vocal fold paralysis. In 2008, Sulica reviewed twenty reports in the literature in an effort to delineate the prognosis and likelihood of recovery in patients affected by idiopathic vocal fold paralysis.
In this study, a total of 717 cases of idiopathic unilateral vocal fold paralysis were reviewed. In total, complete return of mobility occurred in 36% +/- 22% of patients, while some motion returned in 39% +/- 20% of patients. In 52% +/- 17% of patients, complete recovery of voice was obtained. This discrepancy in improvement in voice and mobility emphasize that resolution of dysphonia can occur without full recovery of vocal fold mobility, and thus highlights the importance of vocal therapy. In this review, most cases recovered within well under a year after initial onset. However, rare cases were noted to improve and recover well after this one-year mark. This information may prove helpful in deciding whether or not a period of observation may be reasonable before proceeding with surgical treatment in cases of idiopathic UVFP.
If no aspiration is evident and no ominous pathology is discovered on work-up, observation for a 6-12 month period in hopes of regaining vocal fold motion may be a reasonable option (as discussed previously). Referral to speech therapy for vocal and swallow therapy may also be recommended, especially prior to surgery if being considered. If the main complaint is dysphonia, vocal therapy can be an extremely affective strategy and can oftentimes negate the need for surgical intervention.
However, surgical interventions including temporary or permanent augmentation are also viable options that must be considered. Vocal fold augmentation is utilized to “augment” and medialize the paralyzed vocal fold into a more midline position to allow the contralateral true vocal fold to make improved contact during deglutination and phonation, ultimately helping to prevent aspiration and improve dysphonia. If aspiration is present, a more aggressive approach such as immediate injection augmentation may be indicated given the need to protect the airway.
Multiple considerations must be taken into account before proceeding with injection augmentation. There are a number of different materials that can be used for augmentation, all which have varying lengths of effects. If immediate or temporary injection augmentation is desired, it might be reasonable to choose a material with a known shorter half-life. This way, if there is the possibility of regaining vocal fold motion, only a temporary augmentation will persist. However, if an observational period has passed and there is a limited change of recovery, a more permanent augmentation may be useful, and a longer-acting material should be used.
Injection augmentation with Teflon was a material that was used popularly in the past, but is rarely used today given the risk and morbidity of the development of a Teflon granuloma. Gel-foam has been historically used, but is very short acting (~4-6 weeks), and given this extremely limited effect, is rarely used today. AlloDerm is a commonly employed material, and is known to have an effect that lasts approximately 2-4 months. Sodium carboxymethylcellulose is another material that is often used, and can be expected to have an effect ranging approximately 2-3 months. A longer lasting option, which can be expected to last approximately 18 months, is calcium hydroxlapatite Regardless of the material chosen, proper placement of injection should be deep to the superficial lamina propia, at the medial aspect of the thyroarytenoid muscle.
Injection augmentation can be performed under general anesthesia in the operating room under direct visualization with micro-suspension laryngoscopy, or alternatively, the procedure can be done percutaneously with direct visualization via nasolaryngoscopy in the office setting, with the patient awake. If a patient has multiple co-morbidities and there is a concern with general anesthesia, an office-based injection may serve as the better candidate. This yields the benefit of immediate feedback regarding improvement in dysphonia. However, the injection might not be as accurately placed or as easy as compared to performing augmentation under micro-suspension laryngoscopy in the operating room.
A more permanent surgical option is laryngeal framework surgery (medialization laryngoplasty), which is commonly used in cases of long-standing unilateral vocal fold paralysis. Surgical detail of this procedure is beyond the scope of this article, but in brief, a window is made in the thyroid cartilage, and an implant is placed to medialize the true vocal fold. A variety of materials have been used, but Gore-Tex strips and Silastic implants remain to be the favored materials commonly used today.
Another surgical procedure that deserves mention is arytenoid adduction. A suture is suspended from the muscular process of the arytenoid anteriorly to the thyroid cartilage, which mimics the action of the lateral cricoarytenoid muscle, causing vocal fold adduction. This procedure, although rarely used alone, may serve as a useful adjunct in the treatment of UVFP.
In summary, UVFP is a common disorder presented to the otolaryngologist and other medical practitioners. If identified, imaging from the skull-base superiorly to the aortic arch inferiorly is necessary to evaluate the full course of the RLN. Chest x-ray, CT scans, or MRI scans are often used. Treatment plans will vary depending on the patient and injury, but options are generally focused on airway protection and improving dysphonia. Techniques and surgical procedures that should be considered are speech and swallow therapy, injection augmentation, medialization laryngoplasty (laryngeal framework surgery), and arytenoid adduction.
The management of UVFP is multidisciplinary. The disorder is often encountered in clinical practice by both primary care providers and nurse practitioners. A consult with an otolaryngologist is highly recommended if UVFP is suspected. Besides imaging studies, laryngoscopy is often necessary.
Treatment plans will vary depending on the patient and injury, but options are generally focused on airway protection and improving dysphonia. Techniques and surgical procedures that should be considered are speech and swallow therapy, injection augmentation, medialization laryngoplasty (laryngeal framework surgery), and arytenoid adduction. The outlook for most patients with UVFP is good as long as the primary cause is benign and not associated with severe damage to the laryngeal nerve. (Level V)
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