Many common voice disorders are chronic or recurring conditions that are likely to result from faulty and/or abusive patterns of vocal behavior, referred to generically as vocal hyperfunction. An ongoing goal in clinical voice assessment is the development and use of noninvasively derived measures to quantify and track the daily status of vocal hyperfunction so that the diagnosis and treatment of such behaviorally based voice disorders can be improved. This paper reports on the development of a new, versatile, and cost-effective clinical tool for mobile voice monitoring that acquires the high-bandwidth signal from an accelerometer sensor placed on the neck skin above the collarbone. Using a smartphone as the data acquisition platform, the prototype device provides a user-friendly interface for voice use monitoring, daily sensor calibration, and periodic alert capabilities. Pilot data are reported from three vocally normal speakers and three subjects with voice disorders to demonstrate the potential of the device to yield standard measures of fundamental frequency and sound pressure level and model-based glottal airflow properties. The smartphone-based platform enables future clinical studies for the identification of the best set of measures for differentiating between normal and hyperfunctional patterns of voice use.

Different source-related factors can lead to vocal fold instabilities and bifurcations referred to as voice breaks. Nonlinear coupling in phonation suggests that changes in acoustic loading can also be responsible for this unstable behavior. However, no in vivo visualization of tissue motion during these acoustically induced instabilities has been reported. Simultaneous recordings of laryngeal high-speed videoendoscopy, acoustics, aerodynamics, electroglottography, and neck skin acceleration are obtained from a participant consistently exhibiting voice breaks during pitch glide maneuvers. Results suggest that acoustically induced and source-induced instabilities can be distinguished at the tissue level. Differences in vibratory patterns are described through kymography and phonovibrography; measures of glottal area, open/speed quotient, and amplitude/phase asymmetry; and empirical orthogonal function decomposition. Acoustically induced tissue instabilities appear abruptly and exhibit irregular vocal fold motion after the bifurcation point, whereas source-induced ones show a smoother transition. These observations are also reflected in the acoustic and acceleration signals. Added aperiodicity is observed after the acoustically induced break, and harmonic changes appear prior to the bifurcation for the source-induced break. Both types of breaks appear to be subcritical bifurcations due to the presence of hysteresis and amplitude changes after the frequency jumps. These results are consistent with previous studies and the nonlinear source-filter coupling theory.

Purpose: The purpose of this study was to determine the validity of preliminary reports showing that glottal aerodynamic measures can identify pathophysiological phonatory mechanisms for phonotraumatic and nonphonotraumatic vocal hyperfunction, which are each distinctly different from normal vocal function. Method: Glottal aerodynamic measures (estimates of subglottal air pressure, peak-to-peak airflow, maximum flow declination rate, and open quotient) were obtained noninvasively using a pneumotachograph mask with an intraoral pressure catheter in 16 women with organic vocal fold lesions, 16 women with muscle tension dysphonia, and 2 associated matched control groups with normal voices. Subjects produced /pae/ syllable strings from which glottal airflow was estimated using inverse filtering during /ae/ vowels, and subglottal pressure was estimated during /p/ closures. All measures were normalized for sound pressure level (SPL) and statistically tested for differences between patient and control groups. Results: All SPL-normalized measures were significantly lower in the phonotraumatic group as compared with measures in its control group. For the nonphonotraumatic group, only SPL-normalized subglottal pressure and open quotient were significantly lower than measures in its control group. Conclusions: Results of this study confirm previous hypotheses and preliminary results indicating that SPL-normalized estimates of glottal aerodynamic measures can be used to describe the different pathophysiological phonatory mechanisms associated with phonotraumatic and nonphonotraumatic 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 cm2 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.

Three-way interactions between sound waves in the subglottal and supraglottal tracts, the vibrations of the vocal folds, and laryngeal flow were investigated. Sound wave propagation was modeled using a wave reflection analog method. An effective single-degree-of-freedom model was designed to model vocal-fold vibrations. The effects of orifice geometry changes on the flow were considered by enforcing a time-varying discharge coefficient within a Bernoulli flow model. The resulting single-degree-of-freedom model allowed for energy transfer from flow to structural vibrations, an essential feature usually incorporated through the use of higher order models. The relative importance of acoustic loading and the time-varying flow resistance for fluid-structure energy transfer was established for various configurations. The results showed that acoustic loading contributed more significantly to the net energy transfer than the time-varying flow resistance, especially for less inertive supraglottal loads. The contribution of supraglottal loading was found to be more significant than that of subglottal loading. Subglottal loading was found to reduce the net energy transfer to the vocal-fold oscillation during phonation, balancing the effects of the supraglottal load.