Modeling the Pathophysiology of Phonotraumatic Vocal Hyperfunction With a Triangular Glottal Model of the Vocal Folds

Abstract

Purpose: Our goal was to test prevailing assumptions about the underlying biomechanical and aeroacoustic mechanisms associated with phonotraumatic lesions of the vocal folds using a numerical lumped-element model of voice production.

Method: A numerical model with a triangular glottis, posterior glottal opening, and arytenoid posturing is proposed. Normal voice is altered by introducing various prephonatory configurations. Potential compensatory mechanisms (increased subglottal pressure, muscle activation, and supraglottal constriction) are adjusted to restore an acoustic target output through a control loop that mimics a simplified version of auditory feedback.

Results: The degree of incomplete glottal closure in both the membranous and posterior portions of the folds consistently leads to a reduction in sound pressure level, fundamental frequency, harmonic richness, and harmonics-to-noise ratio. The compensatory mechanisms lead to significantly increased vocal-fold collision forces, maximum flow-declination rate, and amplitude of unsteady flow, without significantly altering the acoustic output.

Conclusion: Modeling provided potentially important insights into the pathophysiology of phonotraumatic vocal hyperfunction by demonstrating that compensatory mechanisms can counteract deterioration in the voice acoustic signal due to incomplete glottal closure, but this also leads to high vocal-fold collision forces (reflected in aerodynamic measures), which significantly increases the risk of developing phonotrauma.

Figure 1.

Contrast between body-cover model (solid red line) and triangular body-cover model (dotted blue line) for (a) glottal air flow, (b) vocal-fold contact area, and (c) vocal-fold contact force due to the collision spring.

Figure 2.

Effect of the model inputs on selected normalized vocal measures. Model inputs: (a) subglottal pressure, (b) posterior glottal displacement (PGD), (c) cricothyroid muscle activation, and (d) supraglottal constriction. Model outputs represented as: blue crosses: harmonics-to-noise ratio; red circles: sound pressure level; green asterisks: fundamental frequency.

Figure 3.

Combined effect of the compensatory mechanisms in terms of their normalized variation as a function of the posterior glottal displacement (PGD). Model inputs represented as: blue crosses: subglottal pressure; red circles: cricothyroid muscle activation; green asterisks: thyroarytenoid muscle activation; black diamonds: supraglottal constriction.

Figure 4.

Selected output measures under increasing incomplete glottal closure as a function of the posterior glottal displacement (PGD). (a) Flow range (AC-Flow), (b) Maximum flow-declination rate (MFDR), (c) maximum contact pressure (MCP), (d) net energy transfer (NET). Blue circles: noncompensated case; red asterisks: compensated case; solid red line: linear fit with R ² values of AC-Flow = .9808, MFDR = .8630, MCP = .8758, NET = .7226.

Figure 5.

Regressed z score versus sound pressure level (SPL) for (a) flow range (AC-Flow) and (b) maximum flow-declination rate (MFDR). Blue circles: noncompensated case; red asterisks: compensated case; solid black line: z-score mean; dashed black line: z-score double standard deviation.

Figure A1.

Triangular body-cover model. PGO = posterior glottal opening.

Figure A2.

Arytenoid posturing and its equivalent on the proposed model. PGO = posterior glottal opening; MGO = membranous glottal opening; PGD = posterior glottal displacement; a_r ^d = arytenoid displacement; a_r ^o = arytenoid rotation; L_a = arytenoid face.