PURPOSE: The purpose of this study was to evaluate the etiology and physiology of vocal hyperfunction (VH) using the acoustical measure of voice onset time (VOT).
METHOD: Twenty-eight women enrolled as participants in the study, including speakers with a diagnosis of VH (n=14), and age- and sex-matched control participants (n=14). Participants produced three repetitions of distinct VCV combinations of the vowels /α/ and /u/, and stopped voiced and voiceless cognates (e.g., /p/, /b/). Mean VOT was calculated for the three repetitions, and a coefficient of variation (CoV) was calculated for each set to determine variance of VOT. Two separate ANOVAs were completed for mean VOT and CoV of VOT with main effects of group, voiced vs. voiceless plosive, vowel, and place of articulation, and interactions between each variable and group.
RESULTS: The first ANOVA model revealed no differences in mean VOT between groups. The second ANOVA revealed statistically significant main effects between groups (p <.001) for the CoV data with a small effect size. No interaction effects were significant for either model.
Conclusion: We determined that CoV, a measure of variation in VOTs, was significantly different between healthy speakers and speakers with VH. These results provide further evidence of a speech-motor control deficit in individuals diagnosed with VH, in that they may have more variable targets during voice production.2020-07-06T00:00:00