Arytenoid abduction for bilateral vocal fold immobility.Curr Opin Otolaryngol Head Neck Surg. 2011 Dec; 19(6):428-33.CO
PURPOSE OF REVIEW
The pathophysiology of bilateral vocal fold immobility includes two broad categories: mechanical fixation and neurogenic paralysis. A mobile arytenoid can be surgically abducted, and this procedure has been reported as a treatment for patients with bilateral neurogenic laryngeal paralysis. This article reviews the theoretical basis and clinical outcomes of this procedure.
Two concepts form the theoretical basis for arytenoid abduction. First, in most cases of neurogenic paralysis, laryngeal muscles are not denervated; there is considerable residual or regenerated function of adductor muscles. The vocal fold lies near the midline, because there is inadequate force to abduct the vocal fold. Second, the cricoarytenoid joint is multiaxial. The posterior cricoarytenoid (PCA) muscle rotates the arytenoid about an oblique axis to pull the vocal process laterally and superiorly, while the axis of adduction is nearly vertical. Thus, surgical abduction of the arytenoid, by simulating contraction of the PCA muscle, should not preclude active adduction during phonation or swallow. Surgical arytenoid abduction has been reported to improve the airway in many patients with bilateral laryngeal paralysis, with little or no impairment of vocal function. It is less successful in patients with inspiratory adductor muscle activity, long-term immobility, or previous procedures to statically enlarge the glottis.
Arytenoid abduction is a promising treatment for selected patients with bilateral neurogenic laryngeal paralysis.