## 4 Discussion
### Clinical Implications  
One of the most common causes of voice disorders is phonation-related trauma to vocal fold tissue which can cause the loss (e.g., scarring) of normal superficial lamina propria and/or the formation of benign lesions on the vocal folds (e.g., vocal fold nodules). Such damage to the phonatory mucosa is believed to be associated with excessive perilaryngeal muscle activity, termed vocal hyperfunction; however, the actual underlying mechanisms that produce varied vocal fold traumatic injury are poorly understood. The direct measurement of vocal fold collision pressures during phonation, in addition to frictional shearing  
Figure 7: Comparison of the intraglottal pressure signal during phonation of the current study with exemplary intraglottal pressure signals observed in the literature according to numerical models [18; 19], physical (synthetic material) models [12; 14], excised larynx studies [13; 22; 25], and an in vivo animal study [29]. Figures reused with permission.  
stresses on vocal fold tissue and dissipated energy dose [50; 51], has important implications in understanding the role of vocal fold collision in the etiology and pathophysiology of phonotraumatic vocal hyperfunction [3]. It is believed that a primary contributing factor to phonotrauma is an increase in level and/or duration above safe thresholds of the collision forces that are generated by the vibrating vocal folds during voice production. However, valid measures of vocal fold collision forces are lacking/incomplete, particularly with respect to what constitutes safe versus damaging levels of such forces.  
Of particular interest is the development of measures that can be applied to ambulatory voice monitoring technologies, with the ultimate goal to better differentiate what constitutes healthy versus damaging vocal function. Real-world voice monitoring devices often use sensors placed on the surface of the neck below the larynx as a way to track features of voice production in a way that is confidential, non-obtrusive, and robust to environmental noise artifacts [40; 41; 52; 53]. The vibration accelerometer used in the current study was similarly placed on the neck surface above the sternal notch and below the thyroid prominence to mimic the sensor positioning of an accelerometer used for ambulatory voice monitoring. Several recent studies have started to elucidate vocal features and behaviors during daily life that may be associated with the presence of hyperfunctional voice disorders [39; 54; 55; 56; 57; 58]. Traditional in-field accelerometer features include estimates of sound pressure level [59] and fundamental frequency that have been combined with voice activity detection to yield vocal dose measures that are designed to indirectly quantify the accumulated effects of phonotrauma [60]. Later formulations of vocal dose measures have attempted to incorporate the effects of vocal fold collision [50], which is important since phonotrauma is hypothesized to be caused by repetitive stress on the mid-membranous portion of the vocal folds [5; 6; 7]. Since the data in this study point toward a potential 1:1 correspondence between vocal fold collision pressure and subglottal pressure in certain scenarios, we can take advantage of work aimed at estimating subglottal pressure from neck-surface vibration and apply this analysis to ambulatory voice signals [61; 62; 63; 64].