青光眼的定义及其研究发展方向

回顾分析了视神经损害性理论的形成与青光眼定义的被改变过程，揭示了目前青光眼的定义及其研究发展方向是不正确的。指出青光眼的定义不是视神经损害性疾病，而是眼压增高病，用两路房水循环的观点，重新认识青光眼、研究青光眼是青光眼研究发展的正确方向。     

青光眼与视神经损害性疾病关系的探讨

在青光眼领域中存在许多问题,其中最主要的问题是青光眼的定义问题,因为它关系到疾病的性质和研究的发展方向。青光眼(Glaucoma)这个病名从何而来?它不是当初就没有自己的定义,而是原青光眼的定义(眼压增高病)被“视神经损害性疾病”的定义取代了。“视神经损害理论”是怎样取代原青光眼的定义?青光眼等于视神经损害性疾病吗?这正是我们要讨论要回答的问题。     

关于青光眼定义之商榷

试图提出一个与目前研究及认识水平相适应的青光眼定义，即“青光眼是由于病理性高眼压以及其他相关因素，引起进行性视神经损害，导致视乳头进行性凹陷性萎缩和视功能、特别是视野损害的一类眼病”。定义强调4点：①视神经对眼压的耐受性有较大的个体差异；②眼压升高的机械压迫和血供障碍共同参与了青光眼的视神经损害，病理性高眼压是主要因素；③青光眼性视神经损害，导致眼底改变的特点是视乳头进行性凹陷性萎缩；④在青光眼性视功能损害方面，视野改变是主要的且具有特征性。本文从眼压、眼底、视野、青光眼视神经损害机制以及视神经保护五个方面对青光眼定义进行了阐述。用比较简明的语言揭示了青光眼的内涵，提出较为全面、科学的青光眼定义。     

我国青光眼研究的现状和发展趋势(上)

目前,青光眼被定义为:病理性眼压升高导致特征性视神经损害和视野缺损的一组疾病.这一定义主要强调了两点:[1]青光眼的发生、发展与个体病理性高眼压关系密切;[2]特征性视神经损害以及相关的视野缺损(视功能损害)是青光眼的主要病理改变.这两点相互联系,提示了青光眼发病机理中眼压的重要作用.围绕青光眼与眼压关系的研究构成了长期以来青光眼的临床和基础研究的基本问题和主要线索,在此基础上其他临床和基础研究得以深入和展开.本文试就我国青光眼的研究现状和发展趋势作一概述,以馈读者.     

青光眼视神经损伤与修复期待精准的个体化治疗

青光眼是临床上常见的以视神经损害为主要特征的致盲眼病,降低眼压仍是目前治疗青光眼的主要方法,但一些患者眼压虽然得到合理控制,视神经损害却难以恢复,甚至持续发展,因此其病理机制的研究和视神经损害的防治研究一直是近年来青光眼治疗研究的热点.最近随着生物医学研究的快速发展,尽管青光眼视神经损伤和修复的基础研究已经取得了显著进展,青光眼视神经损伤的机制已得到阐明,但是鲜见证据充分的、有确定疗效的临床研究报道.目前基因组学研究、干细胞研究、分子生物学研究、电子技术在医学中的应用研究等取得了长足进步,尤其是大数据时代的到来更为临床上青光眼的神经保护研究奠定了良好的基础.眼科医生应关注大数据信息时代为疾病精准化治疗带来的机遇和挑战,聚焦于青光眼视神经保护的精准个体化治疗,降低青光眼的致盲率.     

青光眼与颈动脉相关性研究进展

青光眼是一种进行性特征性视神经损害为共同特征的眼部疾病.在以往的研究中高眼压被认为是导致视神经损害的主要危险因素.其中颈动脉狭窄所致眼部血流调节异常及视神经血流灌注不足导致的缺血缺氧也是青光眼视神经损伤的重要发病机制之一.研究发现颈动脉异常在青光眼的发生、发展中起着十分重要作用.本文就青光眼与颈动脉的相关性研究进行综述.     

原发性青光眼视神经损害的发生机制

关于原发性青光眼的发病机制,目前有许多学说,但每种学说都不能完全说明青光眼视神经损害的具体机制。综合分析发现,每个正常人或青光眼患者身上都具有致视神经损害因素和抗视神经损害因素,青光眼发生与否是这两种因素相斗争的结果。眼压虽然不是青光眼视神经损害的唯一因素,但仍然是青光眼最主要和最稳定的危险因素。另外,血循环因素和免疫因素也是导致青光眼视神经损害的重要原因。本文综合分析了近年来有关原发性青光眼视神经损害机制的研究,并以独特的视角分析了眼压对青光眼视神经损害的具体机制。     

低颅压与正常眼压性青光眼的关系

青光眼作为导致人类不可逆性盲的头号杀手,是一组慢性进行性视神经病变疾病。虽然病理性眼压增高是青光眼发展的主要危险因素,但是其视神经病变机制始终不明。而且有部分患者眼压处于正常值范围内,却依然发生了青光眼性视神经损害,被称为“正常眼压性青光眼”。因此,我们不得不考虑,除眼压外还有其他因素参与青光眼视神经的损害。近年来有研究表明:颅内压与眼压的失衡有可能是正常眼压性青光眼的原因之一,本文就颅内压与正常眼压性青光眼的关系做一综述。     

TLR4在青光眼视神经损伤机制中的作用

青光眼是一种以视乳头萎缩凹陷、视野缺损及视力下降为共同特征的不可逆的致盲性疾病,其视神经损伤的本质为视神经节细胞的凋亡。尽管通过药物干预和手术控制眼压可以对青光眼起到一定的治疗作用,但如何从根本上阻止青光眼的进一步发展仍处于探索阶段。因此,研究青光眼视神经损伤机制,通过阻断视神经损伤而治疗青光眼至关重要。近几年,免疫机制对青光眼视神经损伤的影响成为研究热点,本文中主要对Toll样受体4(TLR4)通过不同免疫通路并与神经胶质细胞相互作用引起青光眼患者视神经损伤进行综述。     

原发性房角关闭--闭角型青光眼的新定义?

最近在国际上提出了对原发性闭角型青光眼（PACG）的新定义和分类系统,强调在青光眼视神经病变方面应与原发性开角型青光眼取得相同意义的定义,其中对尚未发生青光眼性视神经损害,但有急性发作或者慢性房角-虹膜前粘连的患者,改称为原发性房角关闭,虽然这个新的分类系统后来为美国眼科学会和东南亚青光眼学会采用,但是对于是否在国内采用这个定义和分类系统,一直存在很大的争议,笔者旨在说明提出这个分类系统的背景,讨论新定义的益处和存在问题,以便与广大眼科同道交流。     

New findings in the evaluation of the optic disc in glaucoma diagnosis

PURPOSE OF REVIEW: Ophthalmoscopical evaluation of the optic disc is a feasible and largely accessible method to diagnose glaucoma. Many qualitative parameters have been described in glaucomatous optic neuropathy. Considering individual variations in the details of topography or tissue components damaged by the glaucomatous process, however, adequate identification of glaucomatous optic disc signs requires training and experience. Without adequate guidelines of optic disc examination, the physician may miss important aspects that could lead to adequate diagnosis or identification of progression in a patient with established glaucoma. This paper presents a systematic approach for the examination of the optic disc and retinal nerve fiber layer to aid the detection of glaucoma. RECENT FINDINGS: Optic disc qualitative parameters are better than quantitative parameters in separating glaucomatous from normal eyes. The sequential evaluation of optic disc size, neuroretinal rim size and shape, retinal nerve fiber layer, presence of peripapillary atrophy, and presence of retinal or optic disc hemorrhages enhances the ability to detect glaucomatous damage and its progression. SUMMARY: Ophthalmologists should be familiar with glaucomatous optic disc signs that can be identified during clinical examination. A simple systematic approach may allow improved diagnosis and management of glaucoma.     

The optic nerve head in normal-tension glaucoma

There is controversy over the definition, appearance, and characteristics of the optic nerve head in normal-tension glaucoma (NTG). Optic disk size is greater in eyes with NTG than in those with primary open-angle glaucoma. However, in an intraindividual bilateral comparison, the eye with the larger optic disk showed neither more marked nor less pronounced glaucomatous optic nerve damage. Optic disk hemorrhage and peripapillary atrophy have been reported to be more frequent in patients with NTG. Nonuse of calcium channel blockers, peripapillary atrophy, and disk hemorrhage were statistically significantly associated with visual field loss progression in NTG. However, there is a possibility that a high IOP may stop disk hemorrhage relatively early. Histopathologic optic nerve head changes correlated with the clinical appearance of the optic nerve head, which is comparable in NTG and primary open-angle glaucoma. However, as novel findings, serum antibodies to retinal proteins and retinal immunoglobulin deposition in the ganglion cells were observed, and the level of serum autoantibodies to optic nerve head glycosaminoglycans was higher in patients with NTG than in patients with primary open-angle glaucoma.     

青光眼视神经保护的研究进展

视网膜神经节细胞死亡是青光眼视神经损伤的最终共同通路,阻断视神经损伤通路和增强视神经存活机制的方法称为视神经保护。目前这一研究领域主要包括抗凋亡途径,促红细胞生成素,谷氨酸拮抗剂,钙离子拮抗剂,一氧化氮合酶抑制剂,神经营养因子,自身保护性免疫,抗青光眼药物等方面。将来视神经保护将成为一种重要的青光眼辅助治疗措施     

Research progress of stem cells on glaucomatous optic nerve injury

Glaucoma, the second leading cause of blindness, is an irreversible optic neuropathy. The mechanism of optic nerve injury caused by glaucoma is undefined at present. There is no effective treatment method for the injury. Stem cells have the capacity of self-renewal and differentiation. These two features have made them become the research focus on improving the injury at present. This paper reviews the application progress on different types of stem cells therapy for optic nerve injury caused by glaucoma.     

青光眼视神经损伤机制的研究进展

青光眼是目前全球范围内致盲性最高的疾病之一,是以进行性视网膜神经节细胞丧失、不可逆的视野损害等病理性改变为特征,最终导致视神经萎缩及视功能丧失的疾病。目前青光眼的发病机制并不完全清楚,其中视神经损伤的机制有多种学说,包括眼压因素及非眼压因素,非眼压因素包括血管因素、免疫作用、远端轴突病变、氧化应激作用、细胞因子的变化及自噬等机制。本文综述了有关青光眼视神经损伤机制的研究进展,为进一步研究青光眼视神经病变提供依据。     

鼠青光眼模型

青光眼是一组以特征性视神经萎缩和视野缺损为共同特征的疾病,是主要的致盲性眼病之一,青光眼动物模型的建立为研究该病的发生发展和预后提供了良好的基础。鼠类较容易利用转基因技术改造和繁殖,并且鼠眼的结构在很多方面与人眼相似,近年来青光眼鼠模型得到了越来越多的应用。从高眼压模型和非高眼压模型两个方面对国内外研究者的建模方法做一综述。     

Autophagy in axonal degeneration in glaucomatous optic neuropathy

The role of autophagy in retinal ganglion cell (RGC) death is still controversial. Several studies focused on RGC body death, although the axonal degeneration pathway in the optic nerve has not been well documented in spite of evidence that the mechanisms of degeneration of neuronal cell bodies and their axons differ. Axonal degeneration of RGCs is a hallmark of glaucoma, and a pattern of localized retinal nerve fiber layer defects in glaucoma patients indicates that axonal degeneration may precede RGC body death in this condition. As models of preceding axonal degeneration, both the tumor necrosis factor (TNF) injection model and hypertensive glaucoma model may be useful in understanding the mechanism of axonal degeneration of RGCs, and the concept of axonal protection can be an attractive approach to the prevention of neurodegenerative optic nerve disease. Since mitochondria play crucial roles in glaucomatous optic neuropathy and can themselves serve as a part of the autophagosome, it seems that mitochondrial function may alter autophagy machinery. Like other neurodegenerative diseases, optic nerve degeneration may exhibit autophagic flux impairment resulting from elevated intraocular pressure, TNF, traumatic injury, ischemia, oxidative stress, and aging. As a model of aging, we used senescence-accelerated mice to provide new insights. In this review, we attempt to describe the relationship between autophagy and recently reported noteworthy factors including Nmnat, ROCK, and SIRT1 in the degeneration of RGCs and their axons and propose possible mechanisms of axonal protection via modulation of autophagy machinery.     

Investigations into a vascular etiology for low-tension glaucoma

Increased intraocular pressure is accepted as a primary etiologic factor for the atrophy of the optic nerve head and visual field defects of high-tension glaucoma. Other factors must be present to explain these findings in low-tension glaucoma. One of the current theories is that low-tension glaucoma is the result of decreased optic nerve perfusion on the basis of vascular disease or other factors such as altered blood viscosity. This study compared the non-invasive vascular profiles, coagulation tests, and rheological profiles of 46 consecutive cases of low-tension glaucoma with 69 similarly unselected cases of high-tension glaucoma and 47 age-matched controls. Despite the multifactorial approach and the use of previously validated objective tests, no significant group differences were detected with any of the above investigations. If vascular disease is important in the etiology of low-tension glaucoma, then it must be localized or vasospastic since this study does not support the concept of a generalized vascular etiology, either of an atheromatous or hyperviscous nature, for the genesis of low-tension glaucoma.