Asymmetric triangular body-cover model of the vocal folds with bilateral intrinsic muscle activation.

Many voice disorders are linked to imbalanced muscle activity and known to exhibit asymmetric vocal fold vibration. However, the relation between imbalanced muscle activation and asymmetric vocal fold vibration is not well understood. This study introduces an asymmetric triangular body-cover model of the vocal folds, controlled by the activation of bilateral intrinsic laryngeal muscles, to investigate the effects of muscle imbalance on vocal fold oscillation. Various scenarios were considered, encompassing imbalance in individual muscles and muscle pairs, as well as accounting for asymmetry in lumped element parameters. Measurements of amplitude and phase asymmetries were employed to match the oscillatory behavior of two pathological cases: unilateral paralysis and muscle tension dysphonia. The resulting simulations exhibit muscle imbalance consistent with expectations in the composition of these voice disorders, yielding asymmetries exceeding 30% for paralysis and below 5% for dysphonia. This underscores the relevance of muscle imbalance in representing phonatory scenarios and its potential for characterizing asymmetry in vocal fold vibration.

Asymmetric triangular body-cover model of the VFs with bilateral intrinsic muscle activation.

Many voice disorders are linked to imbalanced muscle activity and known to exhibit asymmetric vocal fold vibration. However, the relation between imbalanced muscle activation and asymmetric vocal fold vibration is not well understood. This study introduces an asymmetric triangular body-cover model of the vocal folds, controlled by the activation of intrinsic laryngeal muscles, to investigate the effects of muscle imbalance on vocal fold oscillation. Various scenarios were considered, encompassing imbalance in individual muscles and muscle pairs, as well as accounting for asymmetry in lumped element parameters. The results highlight the antagonistic effect between the thyroarytenoid and cricothyroid muscles on the elastic and mass components of the vocal folds, as well as the impact on the vocal process from the imbalance in the lateral cricoarytenoid and interarytenoid adductor muscles. Measurements of amplitude and phase asymmetry were employed to emulate the oscillatory behavior of two pathological cases: unilateral paralysis and muscle tension dysphonia. The resulting simulations exhibit muscle imbalance consistent with expectations in the composition of these voice disorders, yielding asymmetries exceeding 30% for paralysis and below 5% for dysphonia. This underscores the versatility of muscle imbalance in representing phonatory scenarios and its potential for characterizing asymmetry in vocal fold vibration.

Triangular body-cover model of the vocal folds with coordinated activation of the five intrinsic laryngeal muscles.

Poor laryngeal muscle coordination that results in abnormal glottal posturing is believed to be a primary etiologic factor in common voice disorders such as non-phonotraumatic vocal hyperfunction. Abnormal activity of antagonistic laryngeal muscles is hypothesized to play a key role in the alteration of normal vocal fold biomechanics that results in the dysphonia associated with such disorders. Current low-order models of the vocal folds are unsatisfactory to test this hypothesis since they do not capture the co-contraction of antagonist laryngeal muscle pairs. To address this limitation, a self-sustained triangular body-cover model with full intrinsic muscle control is introduced. The proposed scheme shows good agreement with prior studies using finite element models, excised larynges, and clinical studies in sustained and time-varying vocal gestures. Simulations of vocal fold posturing obtained with distinct antagonistic muscle activation yield clear differences in kinematic, aerodynamic, and acoustic measures. The proposed tool is deemed sufficiently accurate and flexible for future comprehensive investigations of non-phonotraumatic vocal hyperfunction and other laryngeal motor control disorders.

Bayesian estimation of vocal function measures using laryngeal high-speed videoendoscopy and glottal airflow estimates: An in vivo case study.

This study introduces the in vivo application of a Bayesian framework to estimate subglottal pressure, laryngeal muscle activation, and vocal fold contact pressure from calibrated transnasal high-speed videoendoscopy and oral airflow data. A subject-specific, lumped-element vocal fold model is estimated using an extended Kalman filter and two observation models involving glottal area and glottal airflow. Model-based inferences using data from a vocally healthy male individual are compared with empirical estimates of subglottal pressure and reference values for muscle activation and contact pressure in the literature, thus providing baseline error metrics for future clinical investigations.

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

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.

Modeling the effects of a posterior glottal opening on vocal fold dynamics with implications for vocal hyperfunction.

Despite the frequent observation of a persistent opening in the posterior cartilaginous glottis in normal and pathological phonation, its influence on the self-sustained oscillations of the vocal folds is not well understood. The effects of a posterior gap on the vocal fold tissue dynamics and resulting acoustics were numerically investigated using a specially designed flow solver and a reduced-order model of human phonation. The inclusion of posterior gap areas of 0.03-0.1 cm(2) reduced the energy transfer from the fluid to the vocal folds by more than 42%-80% and the radiated sound pressure level by 6-14 dB, respectively. The model was used to simulate vocal hyperfucntion, i.e., patterns of vocal misuse/abuse associated with many of the most common voice disorders. In this first approximation, vocal hyperfunction was modeled by introducing a compensatory increase in lung air pressure to regain the vocal loudness level that was produced prior to introducing a large glottal gap. This resulted in a significant increase in maximum flow declination rate and amplitude of unsteady flow, thereby mimicking clinical studies. The amplitude of unsteady flow was found to be linearly correlated with collision forces, thus being an indicative measure of vocal hyperfunction.