Vocal Cord Paralysis



Vocal Cord Paralysis: Introduction





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.







Table 32–1. Etiology of Vocal Cord Paralysis in Adults. 






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 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.







Table 32–2. Summary of Innervation of the Vocal Cord. 






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.






Patient Evaluation





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.








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


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


Sulica L, Blitzer A. Electromyography and the immobile vocal fold. Otolaryngol Clin North Am. 2004;3759. ISSN: 0030-6665.






Unilateral Vocal Cord Paralysis





Unilateral Recurrent Laryngeal Paralysis



Essentials of Diagnosis




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



General Considerations

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Jun 5, 2016 | Posted by in HEAD AND NECK SURGERY | Comments Off on Vocal Cord Paralysis

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