Abstract

Superior laryngeal nerve (SLN) paralysis results in abnormalities in voice, but it is not clear what occurs at the level of the vocal fold. One theory is that SLN paralysis leads to vocal fold height asymmetry, with the paralyzed vocal fold at a higher vertical position than the normal fold. We examined vocal fold height asymmetry to determine whether this could explain symptoms experienced by patients with SLN paralysis. It was hypothesized that the height asymmetry of the cords contributes to the breathiness, hoarseness, and vocal fatigue that appear in SLN paralysis because the vocal cord mismatch causes an incomplete glottal closure. This allows for air to escape and thus results in decreased vocal efficiency. Using an excised larynx model with induced cord height asymmetry, the team measured changes in vocal fold open quotient, glottal midline, vibratory behavior, and subglottic pressure and flow at phonation onset. Arytenoid adduction sutures allowed for glottic approximation, and sutures placed on the vocal processes created the height asymmetry. A high-speed camera was used to record images. Height asymmetry was found to cause an increased vocal fold open quotient, higher phonation-onset subglottic pressure and flow, vocal fold desynchronization, a shifting glottal midline, and complex vibratory behavior with numerous modes of vibration. Individuals with SLN paralysis may have to exert more pressure and airflow because of these factors, causing fatigue and hoarseness, and may also have less closure of their vocal cords, as indicated by the increased open quotient, contributing to breathiness. This suggests that vocal fold height asymmetry can potentially explain the symptoms of SLN paralysis.

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