NORMAL PHYSIOLOGY, PATHOPHYSIOLOGY, AND TREATMENT OF VOICE DISORDERS

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A biomechanical modeling study employing mathematical optimization demonstrated that the cricoarytenoid joint had a longitudinal axis along the cricoid joint with a rocking action. This is in contrast to the hypothesized rotation of a vertical axis. The rocking motion reduced variance in the distance between the two joint surfaces. The predicted trajectories followed the same paths as movement trajectories obtained from a normal speaker. A study of vocal fold trajectories in normal speakers during different voice onsets demonstrated displacement, velocity and timing differences. It found a uniform trajectory for vocal fold adduction before all three types of voicing. The only difference was the time between vocal fold closure and voice onset which suggests that the differences were in the degree of buildup of subglottal pressure prior to vibration onset. A study of brain stem c fos expression with electrical stimulation of the superior laryngeal nerve which elicits the adductor response, demonstrated that the probable laryngeal sensori-motor response pathway involves the nucleus tractus solitarius, the lateral tegmental field in the medullary reticular formation, to the nucleus ambiguous. A comparison of sensori-motor laryngeal response conditioning between patients with adductor spasmodic dysphonia and normal control subjects was completed. The R1 and contralateral R2 responses have less inhibition of the conditioned responses in the patients than in the control subjects. However, the patients had normal response latencies and frequencies of unconditioned responses suggesting that the brain stem mechanisms for these responses were unaffected. Rather, the results suggest that central modulation of the responses is altered in adductor spasmodic dysphonia.