Fariborz Alipour1, Michael Karnell2. 1. Department of Communication Sciences and Disorders, The University of Iowa, Iowa City, Iowa. Electronic address: alipour@iowa.uiowa.edu. 2. Department of Otolaryngology Head Neck Surgery, University of Iowa Healthcare, Iowa City, Iowa.
Abstract
PURPOSE: Supraglottic compression is frequently observed in individuals with dysphonia. It is commonly interpreted as an indication of excessive circumlaryngeal muscular tension and ventricular medialization. The purpose of this study was to describe the aerodynamic and acoustic impact of varying ventricular medialization in a canine model. METHODS: Subglottal air pressure, glottal airflow, electroglottograph, acoustic signals, and high-speed video images were recorded in seven excised canine larynges mounted in vitro for laryngeal vibratory experimentation. The degree of gap between the ventricular folds was adjusted and measured using sutures and weights. Data were recorded during phonation when the ventricular gap was narrow, neutral, and large. Glottal resistance was estimated by measures of subglottal pressure and glottal flow. RESULTS: Glottal resistance increased systematically as ventricular gap became smaller. Wide ventricular gaps were associated with increases in fundamental frequency and decreases in glottal resistance. Sound pressure level did not appear to be impacted by the adjustments in ventricular gap used in this research. CONCLUSIONS: Increases in supraglottic compression and associated reduced ventricular width may be observed in a variety of disorders that affect voice quality. Ventricular compression may interact with true vocal fold posture and vibration resulting in predictable changes in aerodynamic, physiological, acoustic, and perceptual measures of phonation. The data from this report supports the theory that narrow ventricular gaps may be associated with disordered phonation. In vitro and in vivo human data are needed to further test this association.
PURPOSE: Supraglottic compression is frequently observed in individuals with dysphonia. It is commonly interpreted as an indication of excessive circumlaryngeal muscular tension and ventricular medialization. The purpose of this study was to describe the aerodynamic and acoustic impact of varying ventricular medialization in a canine model. METHODS: Subglottal air pressure, glottal airflow, electroglottograph, acoustic signals, and high-speed video images were recorded in seven excised canine larynges mounted in vitro for laryngeal vibratory experimentation. The degree of gap between the ventricular folds was adjusted and measured using sutures and weights. Data were recorded during phonation when the ventricular gap was narrow, neutral, and large. Glottal resistance was estimated by measures of subglottal pressure and glottal flow. RESULTS: Glottal resistance increased systematically as ventricular gap became smaller. Wide ventricular gaps were associated with increases in fundamental frequency and decreases in glottal resistance. Sound pressure level did not appear to be impacted by the adjustments in ventricular gap used in this research. CONCLUSIONS: Increases in supraglottic compression and associated reduced ventricular width may be observed in a variety of disorders that affect voice quality. Ventricular compression may interact with true vocal fold posture and vibration resulting in predictable changes in aerodynamic, physiological, acoustic, and perceptual measures of phonation. The data from this report supports the theory that narrow ventricular gaps may be associated with disordered phonation. In vitro and in vivo human data are needed to further test this association.