慢性原发性闭角型青光眼患者视觉信息处理网络改变机制的磁共振成像研究

Glaucoma is not pure eye disorders. The intraocular pressure (IOP) of glaucoma was simple reduced only delay disease progression. It was considered that the degeneration of the optic nerve to the optic radiation is an important feature of glaucoma, but the neuroimaging study is relatively ignored in chronic primary angle closure glaucoma (PACG). In recently study, we have found that the alteration and re-plasticity in visual cortex, and it was not consistent in spatial distribution and plasticity ability of the ventral and dorsal areas, suggesting a differently pathological mechanism in the ventral and dorsal pathways of visual information processing network. Moreover, it is still not clear in chronic PACG patients: the altered visual information processing how to impact the visual cognition. In this study, we hypothesis that the chronic ocular hypertension could selectively influenced visual information processing network in chronic PACG patients. Therefore, the purpose of this project is: (1) to detect the influenced characteristics of content and spatial information processing of the visual information processing network of chronic PACG by task and resting-state fMRI, and the basis structural foundation of functional alteration by high-resolution volumetric MRI and DTI, then discuss the visual information processing network change mechanism of patients by combining with the clinical function evaluation; (2) to explore the characteristics and possible mechanism of visual information processing network selective damage to patients' visual cognition by visual cognitive task of chronic PACG patients with visual impairment. Our study could contribute to comprehensively understand the characteristics and mechanisms of visual information processing in patients with chronic PACG, but also provide a theoretical basis and technical support for the discovery of new strategies for the rehabilitation or therapy in chronic PACG patients.

青光眼并非单纯眼病，简单降低眼内压仅能延缓疾病进展。中枢神经退行性变已成为青光眼备受关注的病理机制，然国内发病率较高的原发性闭角型青光眼(PACG)的脑影像研究并不多。本组前期MR研究发现，PACG患者初级视皮层存在独特结构和功能改变模式，同时注意到作为视认知重要加工厂的腹、背侧视觉信息处理通路受影响可不同。基于此，本研究假设：慢性眼高压相关的神经退变可选择性影响PACG患者“视觉信息处理网络”的结构和功能，进而影响视认知。为此，本项目拟通过任务和静息态fMRI检测慢性眼高压对慢性PACG患者的内容和空间信息处理影响特点，以高分辨容积MRI和DTI研究上述改变的结构基础，结合临床功能评估，探讨(1)“视觉信息处理网络”选择性损害特点和重构的可能机制，(2)其对患者视觉认知的影响及可能机制。本研究有助于全面理解慢性PACG患者视觉信息处理中枢的损害和重构机制，并为患者提供潜在的治疗靶点。

研究采用静息态基于种子点的功能连接、脑功能连接密度、特定波段低频振幅、脑网络分析、体素-镜像同伦连接等手段对原发性闭角型青光眼患者脑功能进行研究，发现：（1）原发性闭角型青光眼患者在两个频段（slow-5、slow-4）视觉皮层、感觉运动皮层、额叶、额顶网络和默认模式网络出现异常自发神经活动，可能表明原发性闭角型青光眼患者个体的视觉、认知和情绪功能受损。Slow-5频段的区域同质性信号与病情严重程度密切相关。（2）对比单眼发病的原发性闭角型青光眼患者，双眼发病患者的情绪认知、视觉及人脑默认网络表现出更为明显的自发神经活动异常。（3）原发性闭角型青光眼患者存在半球间功能协调异常及与半球间镜像功能连接下降脑区相关的全脑功能连接减弱。（4）原发性闭角型青光眼患者脑白质结构网络具有小世界属性，其视觉及情感认知相关脑区局部属性存在异常。（5）原发性闭角型青光眼患者具有广泛的脑功能连接密度异常，短程功能连接密度减低脑区与视觉皮层紧密相关并可能与视网膜神经纤维层退变有相同机制，长程功能连接密度增加的脑区主要位于非视觉相关脑区，而短程功能连接密度增加的脑区既涉及到视觉相关脑区也涉及非视觉相关脑区，进一步证明异常长程和短程功能连接密度在原发性闭角型青光眼患者大脑中具有不同的意义。以上结果表明原发性闭角型青光眼患者存在广泛性的脑功能及结构异常，包括视觉相关脑区及视觉外脑区，为进一步理解及研究原发性闭角型青光眼患者的中枢神经病理损害机制提供了思路。