青光眼中血管因素作用的相关研究

视乳头出血和视乳头旁萎缩是青光眼患者的两个重要体征，系统血管疾病如低血压、夜间低血压、高血压，与血管痉挛有关的异常会导致视乳头周围和球后区域血流量下降，血液流变学异常如血黏度升高、红细胞变形能力下降，微血管疾病如糖尿病等，这些都提示血管因素与青光眼的发病有关。血管因素作用的可能机制是血管自身调节异常。总之，青光眼中存在血管、血流等诸多改变，这可能是原发的，也可能是继发的，单纯缺血是否能导致青光眼，还需进一步的研究。     

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。     

光相干断层扫描血管成像对青光眼视网膜微循环的评估

视网膜的微循环改变与青光眼密切相关。光相干断层扫描血管成像(OCTA)是一种无创检查,可同时提供视网膜以及其血管信息,对视网膜各层微循环的检测效果良好,近年被运用到青光眼的研究和监测中。放射状盘周毛细血管(RPC)密度与视网膜神经纤维层厚度呈正相关,因而在青光眼评估中尤为重要。OCTA对视网膜微循环改变的评估主要在视盘...     

视神经乳头微循环及其在青光眼性损害中的作用

长期以来,机械学说在青光眼的发病机制中占有统治地位,然而越来越多的证据表明,眼压升高并不是导致青光眼视功能损害的唯一因素。视神经乳头微循环在青光眼性损害中扮演着重要角色。该文就视神经乳头微循环的解剖生理、实验研究、临床研究等几个方面进行了综述。     

视神经乳头微循环及其在青光眼性损害中的作用

长期以来,机械学说在青光眼的发病机制中占有统治地位,然而越来赵多的证据表明,眼压升高并不是导致青光眼视功能损害的因素,视神经乳头微循环在青光眼性损害中扮演着重要角色。该文就视神经乳头微循环的解剖生理,实验研究,临床研究等几个方面进行了综述。     

降眼压后青光眼视杯回复性缩小的形态特征

根据Ｑｕｉｇｌｅｙ的学说视神经筛板上、下极区域的结缔组织少、筛孔大最容易导致视神经的青光眼特征性损害。为了获得此学说的临床证据，本研究对降低眼压后回复性缩小的视杯（此变化主要是由于原受压向后膨隆变形的筛板向前回弹致视杯变小）进行监测观察。视杯监测采用立体视下图象闪烁比较法，即交替显示两幅叠加好的立体象对，变化的部分呈跳动感。通过立体镜下的观察，可发现视杯三维的变化，还能鉴别有否照象角度不一致、血管搏动等所致的假阳性。观察对象为高眼压的青光眼，共３ｌ只眼。经服Ｄｉａｒｎｏｘ或行小梁切除术降低眼压，降眼压前后分别拍立体眼底象。结果减压后视杯回弹性缩小不匀称，尤以上、下极回复为主。经多元逐步回归法分析，其改变量仅与初始眼压相关。我们认为：由于视神经筛板结缔组织及筛孔分布上的特点，其耐压力因人而异，因部位而异。正是筛板薄弱区的扭曲、变形所致的剪切力造成青光眼性形态、功能上的损害。     

青光眼视神经损害的研究进展

本文全面综述了有关青光眼视神经损害的病因研究，尤其重点阐述了近年来国内外的研究动态。概述了视乳头和解剖和发病机理的两种学说。介绍了关于青光眼视乳头血流改变以及神经胶质、轴索、细胞外基质等的改变对视神经损害的影响。较详细地描述了巩膜筛板在青光眼视神经损害中所起的作用及轴浆流的病理改变特点。这些研究为进一步认识和治疗青光眼提供了有意义的资料。     

青光眼视神经损害的研究进展

本全面综述了有关青光眼视神经损害的病因研究。尤其重点阐述了近年来国内外的研究动态，概述了视浮头和解剖和发病机理的两种学说，介绍了关于青光眼视乳头血液改变以及神经胶质，轴索、细胞外基质等的改变对视神经损害的影响，较说细地描述了巩膜筛板在青光眼视神经损害中所起的作用及轴浆流的病理改变特点。这些研究为进一步认识和治疗青光眼提供了有意义的资料。     

血管因素在青光眼发病机制中的作用

临床和实验资料证明青光眼损害的发病机制涉及眼压升高和微循环障碍二方面 ,在众多因素中 ,血压降低和血管痉挛是最重要的。这些因素 ,至少在部分上是对治疗有影响的。其基本的改变可能是血管的功能障碍导致局部的血管痉挛和低血压。     

血液粘稠度与开角型青光眼的关系

青光眼性视神经萎缩的血管源性学说指出,眼压升高使视乳头血液循环受阻是导致视乳头凹陷的原因之一。尽管最近的实验证明并非如此,但这种论点仍被许多眼科学者所接受。血液粘稠度对血流率有决定作用,前者的增高有时可致局部缺血。业已报道,心绞痛、外周血管性疾病和缺血性糖尿病性视网膜病变等都与血液粘稠度的增高有关。原发性开角型     

视盘倾斜及其相关性研究现状

视盘在垂直和水平轴位上出现的一侧表面抬高被称之为视盘倾斜.倾斜视盘在人群中并不少见,而倾斜的形态对于视盘结构自身以及盘周如神经纤维层厚度、脉络膜厚度等结构的临床测量及视野等结果分析造成困难.视盘倾斜的方向和程度及视盘周围眼部结构与眼病如近视、青光眼等可能具有相关性.对视盘倾斜程度进行量化研究,可确切评估视盘形态和校正其对周围视网膜结构的测量误差.通过准确的视盘倾斜程度的测量,并前瞻性观察视盘倾斜的程度变化,有助于揭示近视、青光眼相关的发病机制,并为分析相关疾病进展提供科研基础以及临床生物学指标.     

Relationship between structure of optic nerve/nerve fiber layer and functional measurements in glaucoma

PURPOSE OF REVIEW: Glaucoma is a progressive optic neuropathy characterized by structural changes of the optic nerve and retina that are associated with the development of visual functional defects. The temporal relation between structural signs of the disease with psychophysical measures such as visual field tests is important to clarify to determine the best methods to detect glaucoma and progressive glaucomatous damage in the clinical setting. This paper reviews recent advancement in the perception of this structure-function relation. RECENT FINDINGS: Quantitative measurement of optic disc and nerve fiber layer integrity have shown initial promise in early longitudinal studies in detecting progressive glaucoma before the development of progression using standard perimetry. Additionally, selective measures of visual function may be able to detect glaucoma before conventional methods as well; however, the relation between these newer specialized functional tests and optic disc analyzers in detecting progression awaits further study. SUMMARY: Defining the clinical relation between structure and function cannot be done outside of the context of the instrumentation used to assess these parameters. Unfortunately, longitudinal studies that compare newer clinical instruments that measure the structural and functional characteristics of the optic nerve to current conventional testing are lacking, but are required to validate these emerging technologies.     

Is the nasal optic disc sector important for morphometric glaucoma diagnosis?

BACKGROUND/AIM: Since the central retinal vessel trunk usually located in the nasal optic disc sector can render difficult the delineation of the neuroretinal rim and optic disc, the aim of this study was to evaluate whether the nasal region of the optic nerve head is important, or can be left out, for the morphometric glaucoma diagnosis. METHODS: The clinical observational study included 1337 patients with primary or secondary open angle glaucoma and 649 normal subjects. The glaucoma group was divided into 1187 patients with glaucomatous visual field defects ("perimetric glaucoma"), and into 150 patients with optic nerve head changes and normal visual fields ("preperimetric glaucoma"). Colour stereo optic disc photographs were morphometrically evaluated. RESULTS: Highest diagnostic power for the separation between the normal group and the perimetric glaucoma group, and for the differentiation between the normal group and the preperimetric glaucoma group, had the sum of inferotemporal rim area plus superotemporal rim area, the sum of inferotemporal rim area plus superotemporal rim area plus temporal rim area, and the inferotemporal rim area as single parameter. The lowest diagnostic precision had the nasal rim area as single parameter or in combination with rim measurements in other disc sectors. CONCLUSION: Excluding the nasal optic disc sector does not markedly decrease the diagnostic power of morphometric optic disc analysis in glaucoma diagnosis. It may have importance for an automated computerised morphometric detection of glaucomatous optic nerve damage.     

Optic nerve gray crescent can confound neuroretinal rim interpretation: review of the literature

The optic nerve gray crescent can be of clinical significance if unrecognized during assessment for glaucoma. It has a characteristic appearance of a slate gray area of pigmentation within the disc margins and commonly appears along the inferotemporal or temporal neuroretinal rim areas. This type of disc rim pigmentation can create the impression of neuroretinal rim thinning, and thus lead to the misdiagnosis of glaucoma or “glaucoma suspect” with attendant implications for overtreatment or unnecessary close monitoring of such patients. The gray crescent is more common in African Americans than whites (prevalence rate 27% vs 7%) and is bilateral in at least 58% of cases. It has been reported in association with Kjer optic atrophy type 1. Suggested causes of the gray crescent include an accumulation of melanocytes, or retinal pigment epithelium cells partially located in the optic nerve head region if Bruch’s membrane extends internal to the peripapillary scleral ring. Other causes of pigmentation that may resemble gray crescent are conus pigmentosus and variations of peripapillary atrophy. When a gray crescent is present, clinicians should endeavour to identify the true anatomical disc margins via the scleral lip and, if necessary, evaluate the patient further with imaging and visual field studies.     

Failure of medical therapy despite normal intraocular pressure

The disease glaucoma is now defined by characteristic optic disc and visual field change, without specific reference to the intraocular pressure (IOP). Success of treatment is no longer judged by the mere attainment of IOP less than 21 mmHg. Controversy remains, however, in deciding appropriate management where optic disc and/or visual field damage continues to progress despite a 'normal' IOP having been achieved with medical treatment. A panel of international glaucoma experts has provided management recommendations in four clinical scenarios--open-angle glaucoma, open-angle glaucoma in a myopic contact lens wearer, uveitic glaucoma and open-angle glaucoma in combination with visually significant cataract--where optic nerve and visual field progression has continued despite an IOP less than 21 mmHg on full medical treatment. Surgical intervention with mitomycin trabeculectomy is the most favoured further therapy.     

Is open‐angle glaucoma caused by impaired cerebrospinal fluid circulation: around the optic nerve?

Chronic open-angle glaucoma is the most frequent type of glaucoma and a leading cause for blindness. The role of intraocular pressure (IOP) in the pathogenesis of open-angle glaucoma has been challenged by patients with typical glaucomatous optic disc changes and visual field loss in whom the IOP never exceeded normal values (normal-tension glaucoma), as well as by patients with persistently elevated IOP who do not develop glaucomatous disc or field changes. Recent research has demonstrated that the cerebrospinal fluid (CSF) is not evenly distributed in all CSF spaces and that the subarachnoid space of the optic nerve can turn into a CSF compartment on its own. The biochemical components in this optic nerve compartment can differ markedly from normal CSF and some of its components (such as L-PGDS) may produce a toxic effect on the optic nerve and may therefore play an important role in the pathophysiology of open-angle glaucoma.     

New directions in the treatment of normal tension glaucoma

Glaucoma is a progressive optic neuropathy that causes characteristic changes of the optic nerve and visual field in relation to intraocular pressure (IOP). It is now known that glaucoma can occur at statistically normal IOPs and prevalence studies have shown that normal tension glaucoma (NTG) is more common than previously thought. While IOP is believed to be the predominant risk factor in primary open angle glaucoma (POAG), IOP-independent risk factors, such as vascular dysregulation, are believed to play an important part in the pathogenesis of NTG. Though certain distinguishing phenotypic features of NTG have been reported, such as an increased frequency of disc hemorrhages, acquired pits of the optic nerve and characteristic patterns of disc cupping and visual field loss, there is much overlap of the clinical findings in NTG with POAG, suggesting that NTG is likely part of a continuum of open angle glaucomas. However, IOP modification is still the mainstay of treatment in NTG. As in traditional POAG, reduction of IOP can be achieved with the use of medications, laser trabeculoplasty or surgery. Studies now show that the choice of medication may also be important in determining the outcomes of these patients. Though it is likely that future treatment of NTG will involve modification of both IOP and IOP-independent risk factors, current efforts to develop IOP-independent neuroprotective treatments have not yet proven to be effective in humans.     

Optic disc size and optic nerve damage in normal pressure glaucoma.

BACKGROUND--Recent reports indicate that eyes with normal pressure glaucoma have larger optic discs than eyes with primary open angle glaucoma or normal eyes. This study was performed to find whether, in normal pressure glaucoma, a large disc is associated with more optic nerve damage than a small disc. METHODS--Colour optic disc photographs of 74 patients with normal pressure glaucoma were assessed morphometrically. RESULTS--Taking the study group as a whole, the optic disc size decreased significantly (p = 0.04) with increasing visual field defect. In an intraindividual bilateral comparison, the side differences in the disc area of the right minus the left eye of the same individual were not significantly correlated with the side differences in the mean visual field defect. CONCLUSIONS--The results indicate that the eye with the larger optic disc, when compared with the contralateral eye with the smaller optic nerve head, showed neither a significantly more marked nor less pronounced glaucomatous optic nerve damage. It suggests that for a given patient the degree of glaucomatous optic nerve atrophy was not markedly associated with the optic disc size. The finding that patients with large visual field defects had smaller discs than patients with moderate perimetric loss may indicate that the results of previous cross sectional studies reporting on an unusually large disc size in normal pressure glaucoma may be due partially to selection.     

The histology of human glaucoma cupping and optic nerve damage: clinicopathologic correlation in 21 eyes

We have examined by light and electron microscopy the retina, optic nervehead, and optic nerves of 21 human eyes from glaucoma patients in whom clinical information was available for comparison. In several cases it was possible to correlate the degree and distribution of optic nerve damage with the clinical appearance of the optic disc and visual field studies. There was no selective loss of astrocytes of the optic nervehead in early glaucoma cupping. Acquired increases in optic disc cup size prior to detectable visual field loss probably represent loss of ganglion cell axonal fibers which is not yet significant enough to produce field defects. It is unlikely that the mechanism of axonal damage in chronic human glaucoma involves early loss of astrocytic glial cells at the optic nervehead. At the level of the retrobulbar optic nerve, the ganglion cell axonal fibers of the superior and inferior quadrants seem to be lost earlier than the fibers of the nasal and temporal nerve periphery. Since the superior and inferior poles of the optic nerve may contain the fibers of arcuate area ganglion cells, these data confirm the presumption from visual field testing that arcuate area ganglion cell fibers are selectively more susceptible to damage in chronic glaucoma.     

视盘倾斜在高度近视中的研究进展

随着近视在亚洲地区的流行,高度近视的患病率也在逐步上升,高度近视无疑已经成为亚洲地区甚至全球范围内的公共卫生问题。视盘倾斜作为一种相对常见的病理改变多出现于高度近视的患者眼中,并且还有可能成为青光眼和黄斑病变等疾病的危险因素,从而增加对视力损害的风险。然而目前对于高度近视中出现视盘倾斜的机制以及视盘倾斜在高度近视并发症加重过程中所发挥的作用还需深入探究。因此,该文章收集整理视盘倾斜的相关文献,从高度近视导致视盘形态改变的机制以及对于各种并发症的影响做出综合性论述,以便为临床针对高度近视及其并发症的诊治提供一定依据。