MRI-Based Modeling to Understand Anatomical Basis of Velopharyngeal Dysfuntion

 描述(申请人提供)：预计有25%-35%的修复腭裂的儿童将会有VPD，这是由上鼻音证明的。如果儿童的腭帆提肌(提上提肌)有一次修复(即在说话过程中，一次修复腭帆上提的肌肉) 这不符合正常的解剖学，孩子很可能会发展成高鼻音，并需要二次腭部手术。VPD的主要原因是我们所说的“不利的生物力学”。具体地说，术后腭咽闭合机制的解剖学和力学机制不足以保证其正常的功能。我们的研究团队已经证明，手术前的肌肉排列和功能被用来确定手术后的结构，手术计划对成功的演讲结果至关重要。这项提案的目标将是根据磁共振成像数据开发特定对象的模型，以确定某些儿童在手术后如何以及为什么会发生VPD。我们的愿景是通过提供 一种手术前肌肉排列和功能被用来指导手术计划以优化手术后结构的框架。我们在这个项目中的目标是：(I)确定哪些解剖特征导致VPD儿童的生物力学不利，以及(Ii)揭示如何改变解剖结构以恢复正常的VP功能。我们打算通过以下具体目标来实现这些目标：(目标1)建立患有和不患有VPD的儿童进行腭裂修复的计算模型；以及(目标2)使用特定于对象的模型来确定每个儿童VPD的原因。在成功完成这个R21项目后，我们将证明特定于对象的模型可以预测儿童腭裂修复后的功能。这些结果将使我们能够在修复前对患者进行建模，并确定患者特定的模型是否可以用作做出患者特定手术决定的指南。这项研究和后续研究将解决手术后语音结果的长期问题，以及VP结构的生长和成熟对VP功能的影响。

 DESCRIPTION (provided by applicant): It is expected that 25-35% of children with repaired cleft palate will have VPD as evidenced by hypernasal speech. If a child has a primary repair of the levator veli palatini (levator) muscle (i.e., primary muscle for velar elevation during speech) that does not conform to that of normal anatomy, it is likely that the child will develop hypernasa speech and will require secondary palate surgery. The primary cause of VPD is due to what we term "disadvantageous biomechanics." Specifically, the anatomy and mechanics of the velopharyngeal (VP) mechanism post-surgically are not adequate for proper VP function. Our research team has demonstrated that surgical planning in which pre-surgical muscle arrangement and function are used to determine post-surgical structure is critical to a successful speech outcome. The goal of this proposal will be to develop subject-specific models based on magnetic resonance imaging data to determine how and why certain children have VPD following surgery. Our vision is to ultimately improve outcomes of cleft palate repair by providing a framework in which pre-surgical muscle arrangement and function are used to inform surgical plans to optimize post-surgical structure. Our goals are in this project are to: (i) determine whic anatomical features lead to disadvantageous biomechanics in children who have VPD, and (ii) reveal the ways in which the anatomy could be changed to restore normal VP function. We intend to achieve these goals through the following specific aims: (Aim 1) Create computational models of children with and without VPD who have had cleft palate repair; and (Aim 2) Use the subject-specific models to determine the cause of VPD in each child. After successful completion of this R21 project, we will have demonstrated that the subject-specific models are predictive of function in children post-cleft palate repair. These results will empower us to move towards modeling patients pre-repair and determining if patient-specific models can be used as a guide for making patient-specific surgical decisions. This and follow-on studies will address long-standing questions of speech outcomes following surgery and the effect of growth and maturation of the VP structures on VP function.