The chaos mechanism of above-range phonation was examined in symmetrically modeled vocal folds by using the traditional two-mass model assumption. The Poincaré map technique was used to display chaotic attractors. This method provided an effective description of irregular vocal-fold movements. The power spectrum, Lyapunov exponent, and Kaplan–Yorke dimension were employed to describe chaotic vibrations in the vocal-fold model. These nonlinear dynamic analyses suggested that, for the positive Lyapunov exponent, chaotic attractors contribute to irregular vocal-fold vibrations. Descriptions of complicated irregular vibrations of the vocal fold yielded evidence of chaos. To investigate the effects of independent parameters such as subglottal pressure, coupling stiffness, and phonation neutral area, bifurcation diagrams based on the Poincaré map were discussed. The results confirmed that the dynamics of the two-mass model was strongly influenced by independent parameters. Nonlinear dynamic methods were expected to provide useful information for better understanding of irregular vocal-fold vibrations as well as of the dynamic mechanism of above-range phonation in excised larynx experimentation.

Four vocally untrained healthy adults, 2 men and 2 women, completed the study. A double-blind placebo-controlled approach was used to administer three treatments to each participant on separate days. Drugs treatments involved a single 60-mg dose of a diuretic, Lasix (LA), on one day, and a single 50-mg dose of an oral antihistamine, diphenhydramine hydrochloride (DH), on another day. A third day involved the administration of a placebo, sugar pills (SP). Critical posttreatment measures were weight (kg), which estimated systemic dehydration, saliva viscosity (centipoise), which estimated secretion dehydration, and phona-tion threshold pressure (PTP, in cm H ₂ O), at high pitches, which indicated pulmonary drive for phonation. The central experimental question was: Does systemic dehydration, or secretory dehydration, or both, mediate increases in PTP that are known to occur following dehydration treatments? The results showed that LA induced systemic dehydration, as shown by a decrease in total body mass of about 1%. Weight losses were seen during a 1- to 4-hour block following drug administration and persisted for at least 8 hours thereafter. PTPs also increased in that condition, about 23% relative to baseline, but only several hours after whole-body dehydration was initially seen (5–12 hours after drug administration). In contrast, no evidence was seen that DH accomplished either secretory dehydration or PTP shifts. The results indicate that systemic dehydration can mediate PTP increases. The influence of secretory dehydration on PTP is unclear.