The myoelastic-aerodynamic theory of phonation has been quantified and tested with mathematical models. The models suggest that vocal fold oscillation is produced as a result of asymmetric forcing functions over closing and opening portions of the glottal cycle. For nearly uniform tissue displacements, as in falsetto voice, the asymmetry in the driving forces can result from the inertia of the air moving through the glottis. This inertia can in turn be enhanced or suppressed by supraglottal or subglottal vocal tract coupling. More obvious and pronounced asymmetries in the driving forces are associated with non-uniform vocal fold tissue displacements. These are combinations of normal tissue modes, and can result in vertical and horizontal phase differences along the surfaces, as observed in chest voice. The ranges of oscillation increase among various models as more freedom in the simulated tissue movement is incorporated. Of particular significance in initiating and maintaining oscillation are the vertical motions that facilitate coupling of aerodynamic energy into the tissues and allow tissue deformations under conditions of incompressibility. Vertical displacements also can have a significant effect on vocal tract excitation. Control of fundamental frequency of oscillation (FO) is basically myoelastic, partially as a result of deliberate or reflex adjustments of laryngeal muscles, and partially as a result of nonlinear tissue strain over the vibrational cycle. This places limits on the control of FO by subglottal pressure, and forces such control to be inseparably connected with vibrational amplitude, or less directly, with vocal intensity.
Birmingham Intervention Tent Technique (BITT): A Technical Note