Contributions of the Musculus Uvulae to Velopharyngeal Closure Quantified With a 3-Dimensional Multimuscle Computational Model. (February 2016)

• Record Type: Journal Article
• Authors: Inouye, Joshua M.; Lin, Kant Y.; Perry, Jamie L.; Blemker, Silvia S.
• Is Part Of: Annals of plastic surgery. Volume 77(2016:Jul.)Supplement 1
• Publication Date: 2016-02
• Subjects: musculus uvulae -- velopharyngeal function -- cleft palate surgery -- computational modeling; Surgery, Plastic -- Periodicals; 617.95205
• DOI: 10.1097/SAP.0000000000000777
• Languages: English
• ISSNs: 0148-7043

Abstract

Abstract : Abstract: The convexity of the dorsal surface of the velum is critical for normal velopharyngeal (VP) function and is largely attributed to the levator veli palatini (LVP) and musculus uvulae (MU). Studies have correlated a concave or flat nasal velar surface to symptoms of VP dysfunction including hypernasality and nasal air emission. In the context of surgical repair of cleft palates, the MU has been given relatively little attention in the literature compared with the larger LVP. A greater understanding of the mechanics of the MU will provide insight into understanding the influence of a dysmorphic MU, as seen in cleft palate, as it relates to VP function. The purpose of this study was to quantify the contributions of the MU to VP closure in a computational model. We created a novel 3-dimensional (3D) finite element model of the VP mechanism from magnetic resonance imaging data collected from an individual with healthy noncleft VP anatomy. The model components included the velum, posterior pharyngeal wall (PPW), LVP, and MU. Simulations were based on the muscle and soft tissue mechanical properties from the literature. We found that, similar to previous hypotheses, the MU acts as (i) a space-occupying structure and (ii) a velar extensor. As a space-occupying structure, the MU helps to nearly triple the midline VP contact length. As a velar extensor, the MU acting alone without the LVP decreases the VP distance 62%. Furthermore, activation of the MU decreases the LVP activation required for closure almost 3-fold, from 20% (without MU) to 8% (with MU). Our study suggests that any possible salvaging and anatomical reconstruction of viable MU tissue in a cleft patient may improve VP closure due to its mechanical function. In the absence or dysfunction of MU tissue, implantation of autologous or engineered tissues at the velar midline, as a possible substitute for the MU, may produce a geometric convexity more favorable to VP closure. In the future, more complex models will provide further insight into optimal surgical reconstruction of the VP musculature in normal and cleft palate populations.