Unilateral Recurrent Laryngeal Paralysis
- “Bovine” cough.
- Unilateral paramedian vocal fold paralysis.
- Voice may tire with use.
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.
Right recurrent laryngeal nerve paralysis (dotted line = midline). (A) At rest, the paralyzed cord takes up a paramedian position. (B) On phonation.
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.
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.
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.
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.
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.
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.
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.
Hamilton DW et al. Bioplastique injection laryngoplasty: Voice performance outcome. J Laryngol Otol, 2007;121(5):427–435.
Rosen CA et al., Vocal fold augmentation with calcium hydroxyapatite: Twelve month report. Laryngoscope 2009;119(5):1033–1041.
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
- Weak, breathy hoarseness.
- Possible history of aspiration.
- Site of injury above the origin of the superior laryngeal nerve.
- Vocal cord in lateralized intermediate position.
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).
Right vagal nerve paralysis. (A) At rest, the paralyzed cord takes up an intermediate position. (B) On phonation.
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).
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.
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 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.
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.
Anderson TD, Mirza N. Immediate percutaneous medialization for acute vocal fold immobility with aspiration. Laryngoscope.
. (Efficacy of Gelfoam injection laryngoplasty.)
Carrau RL. Laryngeal framework surgery for the management of aspiration. Head Neck
. (Medialization laryngoplasty with silicone, with or without arytenoid adduction.)
Hughes CA. Unilateral true vocal cord paralysis: Cause of right-sided lesions. Otolaryngol Head Neck Surg
. (Etiology of right vocal cord palsy.)
Kriskovich MD. Vocal fold paralysis after anterior cervical spine surgery: Incidence, mechanism, and prevention of injury. Laryngoscope
. (Incidence of 2–6%; mechanism due to compression of the nerve during retraction.)
Lo CY. A prospective evaluation of recurrent laryngeal nerve paralysis during thyroidectomy. Arch Surg
. (0.9% of patients developed permanent unilateral vocal cord palsy.)
Ramadan HH. Outcome and changing cause of unilateral vocal cord paralysis. Otolaryngol Head Neck Surg.
. (Surgical and neoplastic causes underlying the majority of vocal cord paralyses.)
Zeitels SM. New procedures for paralytic dysphonia: Adduction arytenopexy, Gortex medialization laryngoplasty, and cricothyroid subluxation. Otolaryngol Clin North Am 2000;33(4):841–854.