MRI-Based Modeling to Understand Anatomical Basis of Velopharyngeal Dysfuntion

 描述（由申请人提供）：预计25-35%的腭裂修复儿童将有VPD，表现为鼻音过强。如果孩子有一个初步修复腭帆提肌（提肌）肌肉（即，在讲话期间用于软腭提升的主要肌肉） 不符合正常解剖结构的，很可能孩子会发展hypernasa语言，需要进行二次腭部手术。VPD的主要原因是由于我们所说的“不利的生物力学”。“具体来说，手术后咽（VP）机制的解剖和力学不足以实现适当的VP功能。我们的研究小组已经证明，手术计划，其中术前肌肉的安排和功能，用于确定手术后的结构是一个成功的语音结果的关键。该提案的目标是根据磁共振成像数据开发特定对象模型，以确定某些儿童手术后如何以及为什么会发生VPD。我们的愿景是通过提供 一个框架，其中术前肌肉排列和功能用于通知手术计划，以优化术后结构。我们的目标是在这个项目中：（i）确定哪些解剖特征导致VPD儿童的不利生物力学，以及（ii）揭示解剖结构可以改变以恢复正常VP功能的方式。我们打算通过以下具体目标来实现这些目标：（目标1）创建计算模型的儿童和没有VPD谁有腭裂修复;和（目标2）使用特定主题的模型，以确定VPD的原因，在每个孩子。在成功完成R21项目后，我们将证明受试者特异性模型可预测腭裂修复后儿童的功能。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制定患者特定手术决策的指南。这项研究和后续研究将解决长期存在的问题，手术后的语音结果和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.