Vocal hyperfunction is a prevalent voice disorder with significant impacts on the daily lives of patients, but has poorly understood causes. At its root, vocal hyperfunction is neurological, involving excessive muscular activation due to compensation for some underlying issue. In order to improve understanding of the causes of this disorder and ultimately improve its treatment, this thesis uses computational models to investigate mechanical aspects in the development of vocal fold nodules in phonotraumatic vocal hyperfunction (a specific class of vocal hyperfunction), specifically: whether biomechanical differences in stiffness of the vocal folds can lead to inefficient speech production that predisposes one to developing these nodule, and whether swelling can establish an amplifying feedback loop, a so-called "vicious cycle", wherein swelling leads to compensatory adjustments that incur further swelling and ultimately lead to nodule. To address these questions a two-dimensional finite-element vocal fold model coupled with a simplified one-dimensional flow model was developed with modifications to this basic model made to study the phenomena of interest. Towards modelling swelling, a computationally efficient approach to model the epithelium layer of the vocal folds is also developed and validated.
To investigate the first research question, the aforementioned model was adapted to study phonation onset pressure, a measure of effort required to produce speech, as a function of vocal fold stiffness. The results show that onset pressure is primarily dependent on just three stiffness distributions: smooth distributions with body-cover stiffness differences and smooth distributions with inferior-superior stiffness differences minimize onset pressure while a uniform stiffness increase increases onset pressure. Since a uniform stiffness increase increases the natural frequency of the vocal folds, this increase in onset pressure is roughly associated with increases in frequency. This suggests that for a given average stiffness (onset frequency) deviations from an optimal body-cover and inferior-superior-like distribution lead to increases in phonatory effort that could increase susceptibility to vocal hyperfunction.
To investigate the second research question, the finite element model was augmented with a model of swelling, as well as an epithelium using a membrane model. Results showed that swelling has negligible impact on loudness of speech but significantly influences frequency, and that furthermore, swelling increases measures of phonotrauma. These results suggest that swelling could incur a vicious cycle. Specifically, a decrease in fundamental frequency initiates compensatory adjustments through increased muscle tension and subglottal pressure, which tends to increase phonotrauma in the folds, and increased swelling with phonotrauma does not tend to limit further swelling. This result demonstrates how swelling can potentially lead to the formation of nodule
