MECHANISMS OF POSTERIOR VAGINAL PROLAPSE

阴道后壁脱垂（PVP），包括肠膨出和直肠膨出，是一种神秘的疾病， 病理生理学知之甚少。ORWH、NICHD和NIDDK各自确定女性骨盆 诸如PVP之类的底部疾病迫切需要病理生理学研究。相互竞争的假设有 已经提出与盆内筋膜或提肛肌衰竭的因果关系有关。但数据 解决这些冲突是不可用的，需要建立筋膜的相对贡献， 和肌肉异常的症状这项研究将测试的机制假设，发生 PVP不是由单一机制解释的，而是涉及筋膜和肌肉之间的相互作用 异常为了验证这些假设，我们将招募75例PVP患者和75例年龄相似的对照组 和种族。目标1.“筋膜”，我们将使用最大Valsalva期间制作的正中矢状位MR图像来记录 后壁的位置和形态在4个区域受到筋膜支持的影响：1）后壁的位置 阴道后尖，2）阴道后壁的长度，3）远端倾斜度的变化 阴道壁; 4）会阴体的位置。通过比较病例和对照组之间的测量结果， 我们将确定每个区域的异常对PVP发生和大小的贡献。目的 2.“肌肉”，我们将使用多平面质子密度MR扫描来比较1） 肛提肌，2）肌肉的横截面积，以及测量和3）骨盆肌 在最大收缩期间的收缩力。利用这些数据，我们将确定 肌肉异常然后，我们将使用统计建模来确定 筋膜和肌肉异常目标3：“直肠膨出与肠膨出”，我们将测试的力量， 4种筋膜和3种肌肉异常与两种类型PVP之间的相关性使用一般线性 建模目的四，生物力学建模，我们将使用筋膜和肌肉的生物力学分析 以计算机为基础的模型中的相互作用，以研究肌肉和结缔组织支持部位的模式 导致PVP的失败。需要这些见解来推进我们对疾病机制的理解 这样我们就可以降低30%的脱垂术后复发率， 每年减少20万妇女手术需求的战略。

Posterior vaginal wall prolapse (PVP), including enterocele and rectocele, is an enigmatic condition whose pathophysiology is poorly understood. ORWH, NICHD and NIDDK have each identified that female pelvic floor disorders such as PVP are in critical need of pathophysiology research. Competing hypotheses have been proposed relating to the causal roles of endopelvic fascia or levator ani muscle failure. However, data to resolve these conflicts are not available and are needed to establish the relative contributions of fascial and muscular abnormalities to PVP. This study will test the mechanistic hypothesis that the occurrence of PVP is not explained by a single mechanism but involves the interaction between fascial and muscle abnormalities. To test these hypotheses, we will recruit 75 cases with PVP and 75 controls of similar age and race. Aim 1. "Fascia", we will use mid-sagittal MR images made during maximal Valsalva to document the posterior wall location and morphology in 4 regions influenced by fascial support: 1) location of the posterior vaginal apex, 2) length of the posterior vaginal wall, 3) changes in the inclination of the distal vaginal wall, and 4) location of the perineal body. By comparing measurements between cases and controls, we will determine the contributions of abnormalities in each region to the occurrence and size of PVP. Aim 2. "Muscle", we will use multiplanar proton density MR scans to compare 1) presence of visible defects in the levator ani muscles, 2) cross sectional areas of the muscle, as well as measuring and 3) pelvic muscle contraction force during a maximal contraction. Using these data we will determine the contribution of muscular abnormalities. We will then use statistical modeling to determine the relative contributions of fascial versus muscular abnormalities. Aim 3. "Rectocele vs. Enterocele", we will test the strength of association between the 4 fascial and 3 muscle abnormalities and the two types of PVP using general linear modeling. Aim 4, "Biomechanical Modeling", we will use biomechanical analyses of fascia and muscle interactions in computer-based models to investigate patterns of muscle and connective tissue support site failures that lead to PVP. These insights are needed to advance our understanding of disease mechanisms so that we can reduce the 30% recurrence rate of prolapse after surgery, and develop preventative strategies to reduce the need for surgery in 200,000 women each year.