Magnetic Resonance Imaging of Glaucoma

青光眼是世界上不可逆失明的主要原因，其特征在于： 视网膜神经节细胞（RGC）、视网膜神经纤维层的进行性变性，以及 视神经青光眼通常与眼内压（IOP）升高有关， 因为增加的IOP对眼睛中的血管施加压缩力， 长期以来一直假设RGC损伤是由轻度但慢性的基础胰岛素水平降低引起的。 血流和/或血流失调。对于许多患者来说，当检测到青光眼时， 在检查中或患者注意到视力丧失时，超过一半的RGC已经 堕落了最终的结果往往是失明。因此，非侵入性成像 能够检测深度分辨血流、氧合和刺激诱发的 血流动力学变化，以评估视网膜和视网膜中的血流减少和失调。 视神经乳头可以实现客观的早期检测，纵向疾病分期， 监测治疗干预措施。 尽管基于光学的成像技术提供高空间分辨率，但是它们 深度有限，妨碍视网膜、脉络膜和视神经血的定量分辨率 流我们的实验室率先应用多模态MRI成像高分辨率 无深度视网膜的特定层解剖、血流、氧合和功能 限制.在这里，我们建议：i）开发一种多模式MRI方法，以显着改善 通过使用3D，对比度和空间分辨率（35x35x300 <$m）无MRI敏感性伪影 平衡稳态自由进动（bSSFP）数据采集方案，以及ii）应用该方案 在已建立的遗传性（DBA/2J）小鼠青光眼模型中， 可以在早期检测到昏迷的变化，并检查可能的机制， 青光眼发病机制 我们假设：1）MRI可以提供高分辨率，深度分辨，层流- 特定的解剖、血流和功能图像，无磁敏感伪影;以及2） 青光眼的发病机制是由青光眼中血流减少和/或血流失调介导的。 早期阶段，导致缺血性缺氧导致RGCs的最终损失，如果这是原因， 高氧治疗应该停止昏迷损害。

Glaucoma, a leading cause of irreversible blindness in the world, is characterized by progressive degeneration of the retinal ganglion cells (RGCs), the retinal nerve fiber layer, and the optic nerve. Glaucoma is often associated with elevated intraocular pressure (IOP), and because the increased IOP exerts a compressing force on the blood vessels in the eye, it has long been hypothesized that the RGC damage is caused by mild, but chronic, reduction of basal blood flow and/or blood-flow dysregulation. For many patients, by the time glaucoma is detected in examinations or patients notice vision loss, more than half of the RGCs have already degenerated. The eventual outcome is often blindness. Thus, non-invasive imaging technologies capable of detecting depth-resolved blood flow, oxygenation, and stimulus-evoked hemodynamic changes to evaluate blood flow reduction and dysregulation in the retina and the optic nerve head could enable objective early detection, longitudinal disease staging, and monitoring of therapeutic interventions. Although optically based imaging techniques provide high spatial resolution, they are depth limited which precludes quantitative resolution of retinal, choroidal, and optic nerve blood flow. Our laboratory pioneered the application of multimodal MRI to image high-resolution lamina-specific anatomy, blood flow, oxygenation, and function of the retina without depth limitation. Here we propose: i) to develop a multimodal MRI approach to markedly improve contrast and spatial resolution (35x35x300 ¿m) without MRI susceptibility artifact by using a 3D balanced Steady State Free Precession (bSSFP) data acquisition scheme, and ii) to apply this approach in an established genetic (DBA/2J) mouse glaucoma model to determine whether MRI can detect glaucomatous changes in early stage and examine a plausible mechanism of glaucoma pathogenesis. We hypothesize that: 1) MRI can provide high resolution, depth-resolved, laminar- specific anatomical, blood flow, and functional images free of susceptibility artifacts; and 2) the pathogenesis of glaucoma is mediated by reduced blood flow and/or blood-flow dysregulation in the early stage, resulting in eventual loss of RGCs by ischemic hypoxia, and, if this is the cause, hyperoxia treatment should halt glaucomatous damage.