Many previous laboratory investigations of phonation involving physical models, excised larynges, and in vivo canine larynges have failed to fully specify the subglottal system. Many of these same studies have reported a variety of nonlinear phenomena, including bifurcations (e.g., various classes of phonation onset and offset, register changes, frequency jumps), subharmonics, and chaos, and attributed such phenomena to the biomechanical properties of the larynx. However, such nonlinear phenomena may also be indicative of strong coupling between the voice source and the subglottal tract. Consequently, in such studies, it has not been clear whether the underlying mechanisms of such nonlinear phenomena were acoustical, biomechanical, or a coupling of the acoustical and biomechanical systems. Using a physical model of vocal fold vibration, and tracheal tube lengths which have been commonly reported in the literature, it is hypothesized and subsequently shown that such nonlinear phenomena may be replicated solely on the basis of laryngeal interactions with the acoustical resonances of the subglottal system. Recommendations are given for ruling out acoustical resonances as the source of nonlinear phenomena in future laboratory studies of phonation.

The laryngeal neuromuscular mechanisms for modulating glottal posture and fundamental frequency are of interest in understanding normal laryngeal physiology and treating vocal pathology. The intrinsic laryngeal muscles in an in vivo canine model were electrically activated in a graded fashion to investigate their effects on onset frequency, phonation onset pressure, vocal fold strain, and glottal distance at the vocal processes. Muscle activation plots for these laryngeal parameters were evaluated for the interaction of following pairs of muscle activation conditions: (1) cricothyroid (CT) versus all laryngeal adductors (TA/LCA/IA), (2) CT versus LCA/IA, (3) CT versus thyroarytenoid (TA) and, (4) TA versus LCA/IA (LCA: lateral cricoarytenoid muscle, IA: interarytenoid). Increases in onset frequency and strain were primarily affected by CT activation. Onset pressure correlated with activation of all adductors in activation condition 1, but primarily with CT activation in conditions 2 and 3. TA and CT were antagonistic for strain. LCA/IA activation primarily closed the cartilaginous glottis while TA activation closed the mid-membranous glottis.

Objectives-To assess accuracy of the indentation method for stiffness measurements and to estimate the Young's modulus of the vocal fold using this technique. Study Design-Basic science.Methods-Indentation tests were performed using a range of indenter diameters and indentation depths on single and double layer silicone rubber models with a range of cover layer thicknesses with known geometry and Young's moduli. Measurements were repeated on intact vocal folds and isolated muscle and cover layer samples from three cadaveric human larynges.Results-Indentation on single-layer rubber models yielded Young's moduli with acceptable accuracy when the indentation depth was equal to or smaller than the indenter diameter, and both were smaller than the physical dimensions of the material sample. On two-layer models the stiffness estimation was similarly influenced by indenter diameter and indentation depth, and acceptable accuracy was reached when indentation depth was much smaller than the height of the top cover layer. Measurements on mid-membranous vocal fold tissue revealed location-dependent Young's moduli (in kPa) as follows: intact hemilarynx 8.6 (range 5.3 -13.1), isolated inferior medial surface cover 7.5 (range 7 -7.9), isolated medial surface cover 4.8 (range 3.9-5.7), isolated superior surface cover 2.9 (range 2.7 -3.2), and isolated thyroarytenoid muscle 2.0 (range 1.3 -2.7).Conclusions-Indenter diameter, indentation depth, and material thickness are important parameters in measurement of vocal fold stiffness using the indentation technique. Measurements on human larynges showed location-dependent differences in stiffness. The stiffness of the vocal folds was also found to be higher when the vocal fold structure was still attached to the laryngeal framework as compared to when the vocal fold was separated from the framework.

In an investigation of phonation onset, a linear stability analysis was performed on a two-dimensional, aeroelastic, continuum model of phonation. The model consisted of a vocal fold-shaped constriction situated in a rigid pipe coupled to a potential flow which separated at the superior edge of the vocal fold. The vocal fold constriction was modeled as a plane-strain linear elastic layer. The dominant eigenvalues and eigenmodes of the fluid-structure-interaction system were investigated as a function of glottal airflow. To investigate specific aerodynamic mechanisms of phonation onset, individual components of the glottal airflow (e.g., flow-induced stiffness, inertia, and damping) were systematically added to the driving force. The investigations suggested that flow-induced stiffness was the primary mechanism of phonation onset, involving the synchronization of two structural eigenmodes. Only under conditions of negligible structural damping and a restricted set of vocal fold geometries did flow-induced damping become the primary mechanism of phonation onset. However, for moderate to high structural damping and a more generalized set of vocal fold geometries, flow-induced stiffness remained the primary mechanism of phonation onset.

In a single-layered, isotropic, physical model of the vocal folds, distinct phonation types were identified based on the medial surface dynamics of the vocal fold. For acoustically driven phonation, a single, in-phase, x-10 like eigenmode captured the essential dynamics, and coupled with one of the acoustic resonances of the subglottal tract. Thus, the fundamental frequency appeared to be determined primarily by a subglottal acoustic resonance. In contrast, aerodynamically driven phonation did not naturally appear in the single-layered model, but was facilitated by the introduction of a vertical constraint. For this phonation type, fundamental frequency was relatively independent of the acoustic resonances, and two eigenmodes were required to capture the essential dynamics of the vocal fold, including an out-of-phase x-11 like eigenmode and an in-phase x-10 like eigenmode, as described in earlier theoretical work. The two eigenmodes entrained to the same frequency, and were decoupled from subglottal acoustic resonances. With this independence from the acoustic resonances, vocal fold dynamics appeared to be determined primarily by near-field, fluid-structure interactions.