Abstract

Purpose: The goal of this study was to experimentally evaluate how compensating for the adverse acoustic effects of a posterior glottal opening (PGO) by increasing subglottal pressure and changing supraglottal compression, as have been associated with vocal hyperfunction, influences the risk of vocal fold (VF) trauma. Method: A self-oscillating synthetic silicone model of the VFs with an airflow bypass that modeled a PGO was investigated in a hemilaryngeal flow facility. The influence of compensatory mechanisms on collision pressure and dissipated collision power was investigated for different PGO areas and supraglottal compression. Compensatory behaviors were mimicked by increasing the sub -glottal pressure to achieve a target sound pressure level (SPL). Results: Increasing the subglottal pressure to compensate for decreased SPL due to a PGO produced higher values for both collision pressure and dissipated collision power. Whereas a 10-mm2 PGO area produced a 12% increase in the peak collision pressure, the dissipated collision power increased by 122%, mainly due to an increase in the magnitude of the collision velocity. This suggests that the value of peak collision pressure may not fully capture the mechanisms by which phonotrauma occurs. It was also found that an optimal value of supraglottal compression exists that maximizes the radiated SPL, indicating the potential utility of supraglottal compression as a compensatory mechanism. Conclusions: Larger PGO areas are expected to increase the risk of phono-trauma due to the concomitant increase in dissipated collision power associ-ated with maintaining SPL. Furthermore, the risk of VF damage may not be fully characterized by only the peak collision pressure.