A comparative study on visual field defect in low tension glaucoma

The mode of visual field defect and the change of intraocular pressure (IOP) were analyzed between progressive low tension glaucoma (LTG) and non-progressive LTG. Maximum IOP and phasic fluctuation in IOP during the follow-up period in progressive cases were significantly higher than those in non-progressive cases (p less than 0.01). This greater range in phasic fluctuation may lead to the development of glaucomatous damage. Analysis of the pattern of visual field defect revealed significantly greater frequency of dense defects within 10 degrees of the fixation area in progressive cases. Another analysis on the mode of visual field damage between progressive LTG and POAG demonstrated higher frequency of focal progression of the damage. These results suggest that there are some different etiological factors among progressive LTG, non-progressive LTG and POAG, while focal anatomical weakness at the optic nerve head also influences the development of damage in some case of progressive LTG.     

Morphological changes in glaucomatous eyes and the role of TGFbeta2 for the pathogenesis of the disease

This review summarizes the Ernst H. Bárány Prize Lecture given at the XVI. meeting 2004 of the International Society of Eye Research in Sydney, Australia. The article describes the author's early studies starting with the determination of the site of aqueous humour outflow resistance and its regulation through ciliary muscle contraction, which were performed in collaborations with Bárány. It continues with the qualitative and quantitative evaluation of the trabecular meshwork (TM) changes seen in different kinds of glaucoma diseases. A comparison of correlations between meshwork pathology, IOP, and axon loss in the optic nerve between eyes with pseudoexfoliation glaucoma (PEXG) and primary open angle glaucoma (POAG) indicates that in the secondary glaucoma (PEXG) optic neuropathy is mainly induced by an increase in IOP. In eyes with POAG, the correlations point towards a more complex pathogenesis of the disease. Common factors might be involved in both the TM and the optic nerve changes. In vitro studies performed in cell cultures of human TM cells and optic nerve astrocytes as well as organ culture studies of the anterior eye segment indicate that TGFbeta2 might be one of the factors involved in the development of POAG. The paper is primarily focused on studies performed by the author and complete reference to other previous or contemporary studies is therefore not given as the purpose is not to present a comprehensive review article.     

Cochlin and glaucoma: a mini-review

Primary open angle glaucoma (POAG) is a leading cause of late onset, progressive, irreversible blindness and, although its etiology is poorly understood, elevated intraocular pressure (IOP) often appears to be a contributory factor. Proteomic and Western analyses of trabecular meshwork (TM) from patients with POAG and age-matched controls originally implicated cochlin as possibly contributing to glaucoma pathogenesis. Cochlin deposits were subsequently detected in glaucomatous but not in control TM and older glaucomatous TM was found to contain higher levels of cochlin and significantly lower amounts of collagen type II. More recently, similar results were reported in DBA/2J mice, which at older ages develop elevated IOP, retinal ganglion cell degeneration, and optic nerve damage. Notably, cochlin was absent in TM from C57BL/6J, CD1, and BALBc/ByJ mice, which do not exhibit elevated IOP or glaucoma. Cochlin was found in the TM of very young DBA/2J mice, prior to elevated IOP, suggesting that over time the protein may contribute to the events leading to increased IOP and optic nerve damage. Here we review these findings and describe how future studies in DBA/2J mice can help resolve whether cochlin plays a causal role in mechanisms of POAG and elevated IOP.     

原发性开角型青光眼房水外流通路改变的研究进展

原发性开角型青光眼(POAG)是一种以视神经轴索及相关视网膜神经节细胞丢失为特征的视神经病变.眼压升高是POAG最重要的危险因素.大多数POAG患者眼压升高主要是房水外流阻力异常增高所致.小梁网是产生房水排出阻力的主要部位.目前多数研究者认为POAG患者小梁网功能不良与致炎因子表达、细胞老化、氧化应激损伤及细胞质成分减少等因素有关.小梁网细胞本身及细胞外基质的变化均可以引起房水外流阻力的改变,进而导致眼内压的升高.为了进一步开展对POAG发病机制的研究,有必要就目前有关POAG患者房水外流通路改变的研究进展予以综述,旨在为POAG的深入研究提供参考依据.     

Fluorescein fundus angiography of optic nerve head in primary open angle glaucoma and low tension glaucoma]

Fluorescein fundus angiography was performed at angle of 20 degrees in the 58 low tension glaucoma (LTG) eyes (30 cases) and 77 primary open angle glaucoma (POAG) eyes (41 cases) and the relation of the optic nerve head fluorescein changes to visual field disturbances (stage classification of Kosaki) was compared between POAG and LTG groups. The filling defect of fluorescein in the deep area and the decrease in number of superficial capillaries were observed in the optic nerve head. The filling defect area of fluorescein in the optic nerve head corresponding to Bjerrum scotoma was recognized even in the mild visual field disturbance cases of both LTG and POAG. The following findings were noted in both LTG and POAG cases; expansion of the filling defect area and the decrease in number of superficial capillaries in the same area with progression of visual field disturbances. Filling defect area of fluorescein of the optic nerve head accorded with visual field disturbance area in 19 LTG eyes (32.8%) and 61 POAG eyes (79.2%). On the contrary, the filling defect area of the optic nerve head was wider than the visual disturbance area in 37 LTG eyes (63.8%) and 16 POAG eyes (20.8%). These findings suggest that blood circulatory disorders of the optic nerve head occurred earlier in LTG than in POAG and that the development of LTG might be closely associated with the blood circulatory disorders.     

Exfoliation syndrome and exfoliation glaucoma

Exfoliation syndrome abnormal deposition in the anterior segment of the eye of an unknown substance thought to be related to elastic fibres and basement membrane components is associated with accelerated cataract progression. increased frequency of intraoperative and postoperative complications and increased risk for glaucoma and. therefore, is a clinically important finding. A clear association has been shown with age. The syndrome occurs worldwide but its prevalence seems to vary from country to country. The best-known sign of exfoliation syndrome is deposits of greyish-white material on the anterior lens surface. Sometimes exfoliation material can also be seen at the pupillary border, on the anterior iris surface, corneal endothelium, and on the anterior vitreous face. When clinically detected, exfoliation syndrome is somewhat more often unilateral than bilateral. According to recent investigations clinically unilateral exfoliation syndrome is probably never truly unilateral but rather asymmetric, because exfoliation material has been detected ultrastructurally and immunohistochemically around iris blood vessels of the nonexfoliative fellow eyes. Indeed, electron microscopy identifies in various organs of patients with exfoliation syndrome fibrils similar to those seen in intraocular exfoliation deposits. Other clinical signs associated with exfoliation syndrome are pigment dispersion, transillumination defects of the iris and reduced response to mydriatics. In unilateral exfoliation syndrome, intraocular pressure (IOP) of the exfoliative eye is approximately 2 mmHg higher than IOP of the nonexfoliative fellow eye. Whether elevated IOP, vascular changes or exfoliation syndrome itself is the main factor causing optic nerve head damage and conversion of an exfoliative eye to glaucomatous, is not known. Glaucoma in the exfoliation syndrome has been shown to have a more serious clinical course than in primary open-angle glaucoma (POAG). At the time of diagnosis, IOP and its diurnal variation are generally higher and visual field defects tend to be greater in exfoliation glaucoma than in POAG. Because the decrease in lOP variation and lowering of the mean IOP level has been shown to improve visual field prognosis more in exfoliation glaucoma than in POAG, the glaucomatous process is considered to be more pressure-related in exfoliation glaucoma. Furthermore, progression of optic disc damage has been shown to be similar in exfoliation glaucoma and POAG when lOPs are lowered to a comparable level by the treatment. However, vascular disturbances in the posterior segment of the eye might after all be of equal importance in these two types of glaucoma; optic disc haemorrhages and venous occlusions have been reported to be as frequent in exfoliation glaucoma as in POAG. Perhaps in exfoliation glaucoma circullatory disturbances combined with high IOP lead to a particularly relentlessly progressing form of the disease.     

超声乳化白内障手术对剥脱综合征性青光眼的降眼压作用

目的 观察和分析剥脱综合征性青光眼患者行超声乳化白内障摘除人工晶体植入术后的眼压变化。方法 对7例伴有高眼压、明显影响视力的白内障但尚无严重的视神经、视野损害的剥脱综合征患者施行超声乳化白内障摘除人工晶体植入术，比较手术前后的眼压变化。结果 术前平均眼压31．57mmHg，术后1周时平均眼压18．19mmHg，降幅为13．38mmHg，术前术后眼压差异极显著。结论 伴有明显影响视力白内障的剥脱综合征性青光眼病人在行超声乳化白内障摘除人工晶体植入术后眼压会显著下降，对那些尚未发生明显视神经视野损害的剥脱综合征性青光眼患者，行超声乳化白内障摘除人工晶体植入术可有效降低眼压。     

选择性激光小梁成形术治疗原发性开角型青光眼

目的:选择性激光小梁成形术(selective laser trabeculoplasty,SLT)治疗原发性开角型青光眼(primary open angle glaucoma,POAG)观察。方法:原发性开角型青光眼80例160眼,蓝黄视野检查未见明显损害或轻度损害,眼压>30mmHg者20例40眼,眼压<30mmHg者60例120眼。使用倍频Q开关,波长532nm,Nd∶YAG激光,照射180°~360°小梁网,光斑400nm,脉宽3μs,能量设置0.3~1.0mJ。光斑点数50~80点,术后1d;1wk;1,3,6mo测眼压。结果:对于眼压在>30mmHg的POAG患者眼压控制不理想。眼压<30mmHg的POAG患者效果明显。结论:SLT的降眼压效果,虽然针对性较强,适宜患者人群窄,但给POAG的治疗提供了新思路和新希望。     

高眼压性和正常眼压性原发性开角型青光眼视神经损害特征的比较

目的探讨高眼压性原发性开角型青光眼(POAG)和正常眼压性青光眼(NTG)患者视神经损害的不同特点。方法应用德国Heidelberg公司生产的视网膜断层扫描仪对高眼压性POAG39例(47只眼)和NTG32例(38只眼)进行定量视盘参数和神经纤维层检查,并行眼底立体照相观察视网膜神经纤维层(RNFL)缺损类型,检测静态定量视野,并对检查结果进行比较。结果(1)NTG组视盘总体参数和分区(除颞侧外)盘沿面积、沿/盘面积小于高眼压性POAG组,而C/D大于高眼压性POAG组;平均RNFL厚度和RNFL面积在颞下和颞上小于高眼压性POAG组;总体盘沿容积小于高眼压性POAG组,总体平均视杯深度和颞下视杯面积大于高眼压性POAG组,两组差异均有统计学意义(P<005)。两组颞侧视盘各参数比较,差异无统计学意义(P>005)。(2)RNFL缺损类型高眼压性POAG组RNFL弥漫性缺损占5319%,局限性缺损占426%;NTG组弥漫性缺损占2105%,局限性缺损占5526%。两组RNFL缺损类型构成比比较,差异有统计学意义(P<001)。结论NTG较高眼压性POAG具有较大的C/D值、C/D面积比和窄盘沿面积,RNFL丢失严重。高眼压性POAG患者的RNFL以弥漫性缺损为主,NTG患者的RNFL以局限性缺损为主。两者视神经损害具有不同特点,其损害机制可能不同。(中华眼科杂志,2005,41136140)     

Expression of myocilin/TIGR in normal and glaucomatous primate optic nerves

Myocilin/TIGR was the first molecule discovered to be linked with primary open angle glaucoma (POAG), a blinding disease characterized by progressive loss of retinal ganglion cells. Mutations in myocilin/TIGR have been associated with age of disease onset and severity. The function of myocilin/TIGR and its role in glaucoma is unknown. Myocilin/TIGR has been studied in the trabecular meshwork to determine a role in regulation of intraocular pressure. The site of damage to the axons of the retinal ganglion cells is the optic nerve head (ONH). The myocilin/TIGR expression was examined in fetal through adult human optic nerve as well as in POAG. Myocilin/TIGR was expressed in the myelinated optic nerve of children and normal adults but not in the fetal optic nerve before myelination. Also examined was the expression in monkeys with experimental glaucoma. The results demonstrate that optic nerve head astrocytes constitutively express myocilin/TIGR in vivo in primates. Nevertheless, myocilin/TIGR is apparently reduced in glaucomatous ONH. The colocalization of myocilin/TIGR to the myelin suggests a role of myocilin/TIGR in the myelinated optic nerve.     

Rho激酶抑制剂在青光眼治疗中的应用进展

青光眼是以特征性视神经萎缩和视野缺损为共同特征的不可逆性致盲性眼病,高眼压是其最主要的发病机制,而导致高眼压的主要原因是房水传统流出途径中小梁网的病理学改变导致的房水流出阻力增加。Rho激酶抑制剂(ROCKi)是直接作用于小梁网(TM)的降眼压药物,主要通过影响细胞骨架改变TM细胞形态、细胞运动、胞质分裂和平滑肌收缩等,从而增加房水流出、降低眼压,在美国和日本已被批准用于临床; 具有改善视网膜血管灌注、促进视神经再生等作用,可能存在视神经保护作用; 此外,具有减少滤过泡瘢痕化等作用。因此,ROCKi作为新型抗青光眼药物备受关注,本文将针对Rho/Rho激酶信号通路、ROCKi的作用机制及其临床应用展开综述。     

Influence of prostaglandins on aqueous humour dynamics and intraocular pressure

In the glaucoma disease the disturbed trabecular outflow results not only in an increase in the intraocular pressure (IOP) level, but also in an increase in the intraocular pressure fluctuations in the majority of patients. This induces a biomechanical stress that may damage the optic nerve head over time and may result in the typical glaucomatous excavation. Prostaglandin analogues show positive effects on both risk factors. They enhance the uveoscleral outflow of the aqueous humour, improve the trabecular outflow facility and probably the regulatory capacity of the trabecular meshwork itself. This dual mechanism might explain the strong IOP-lowering efficacy of the prostaglandins and their additional property to reduce IOP fluctuations leading to a general improvement of the aqueous humour dynamics. Therefore, it makes sense pharmacologically to combine prostaglandins with those medications that also reduce aqueous humour production.     

谁动了我的视神经？ -正常眼压性青光眼视神经损害探因

正常眼压性青光眼和高眼压原发性开角型青光眼是一个“连续体”。本文基于病理生理学,探讨了正常眼压性青光眼中眼压与视神经损害的关系,认为视盘筛板是上述关系及其“连续体”概念的中间环节,眼压和筛板共同构成青光眼视神经损害的始动因素。（眼科,2020, 29： 87-89）     

Open-angle glaucoma in an urban population in southern India: the Andhra Pradesh eye disease study

OBJECTIVE: To assess the prevalence and features of open-angle glaucoma in an urban population in southern India. DESIGN: A population-based cross-sectional study. PARTICIPANTS: A total of 2522 persons (85.4% of those eligible) of all ages, including 1399 persons 30 years of age or older, from 24 clusters representative of the population of Hyderabad city. TESTING: The participants underwent an interview and detailed eye examination that included logarithm of minimum angle of resolution visual acuity, refraction, slit-lamp biomicroscopy, applanation tonometry, gonioscopy, dilatation, cataract grading, and stereoscopic fundus evaluation. Automated Humphrey threshold 24-2 visual fields (Humphrey Instruments Inc., San Leandro, CA) and optic disc photography were performed when indicated by standardized criteria for disc damage or if intraocular pressure (IOP) was 22 mmHg or more. MAIN OUTCOME MEASURES: Definite primary open-angle glaucoma (POAG) was defined as obvious glaucomatous optic disc damage and visual field loss in the presence of an open-angle, and suspected POAG was defined as suspected glaucomatous optic disc damage without definite visual field loss. Ocular hypertension (OHT) was defined as IOP of 22 mmHg or more without glaucomatous optic disc damage or visual field loss in the presence of an open-angle. Glaucomatous optic disc damage or IOP of 22 mmHg or more secondary to an obvious cause and with an open-angle was defined as secondary open-angle glaucoma. RESULTS: Definite POAG, suspected POAG, and OHT were present in 27, 14, and 7 participants, respectively, with age- and gender-adjusted prevalence (95% confidence interval) of 1.62% (0.77%-2.48%), 0.79% (0.39%-1.41%), and 0.32% (0.10%-0.78%) in those 30 years of age or older, and 2.56% (1.22%-3.91%), 1.11% (0.43%-1.78%), and 0.42% (0.11%-1.12%) in those 40 years of age or older, respectively. The prevalence of POAG increased significantly with age using multivariate analysis (P < 0.001). Only two of 27 participants (7.4%) with definite POAG had been previously diagnosed and treated, and 66.7% of the previously undiagnosed had IOP less than 22 mmHg. Fourteen of 27 participants (51.9%) with definite POAG had severe glaucomatous damage based on optic disc and visual field criteria, of which five participants (18.5%) had at least one blind eye as a result of POAG (all with best-corrected distance visual acuity less than 20/400 or central visual field less than 10 degrees); the other 13 participants (48.1%) had moderate glaucomatous damage. Because visual fields and optic disc photography were not performed on all participants, the prevalence of POAG may have been underestimated. Secondary open-angle glaucoma was present in one participant as a result of angle recession. CONCLUSIONS: The prevalence of open-angle glaucoma in this urban population in southern India is at least as much as that reported recently from white populations in developed countries. However, the vast majority of persons with glaucoma were undiagnosed in this population, and a large proportion of those having definite POAG already had severe glaucomatous damage.     

小梁网泵调控理论及其对青光眼诊疗的启示

小梁网房水引流功能异常导致眼压升高,是原发性开角型青光眼发生发展的最主要危险因素。房水具有搏动外流的特征,说明小梁网是弹性组织,其弹性状态与Schlemm管腔开放程度、管类瓣膜结构联动和深层巩膜静脉丛的开放与闭合密切相关,表明小梁网对房水的引流具有泵调控机制。本文对小梁网泵调控机制的理论基础、相关检查的临床应用及对青光眼微创手术的启示进行了系统介绍。希望小梁网泵调控理论为了解原发性开角型青光眼发病机制、选择治疗策略、优化和创新手术设计提供新的视角。(眼科,2022,31:405-412)     

小梁网的干细胞移植治疗原发性开角型青光眼的研究进展

原发性开角型青光眼(primary open angle glaucoma,POAG)是以持续性眼压增高导致视神经损伤为主要临床表现的一种疾病,其发病机制复杂,尚未明确,现阶段临床治疗相对困难。影响眼内压(intraocular pressure,IOP)高低的重要因素是房水引流是否通畅,而房水引流途径中小梁网(trabecular meshwork,TM)起重要调控作用。TM细胞的形态、数量、结构和功能改变均可使房水外流阻力增大,从而导致IOP升高。研究证实诱导多功能干细胞(induced pluripotent stem cells,iPSCs)、骨髓间充质干细胞(bone mesenchymal stem cells,BMSCs)和脂肪干细胞(adipose-derived stem cells,ADSCs)已被用于TM细胞的分化和再生,为POAG小梁网的干细胞替代治疗提供可靠的细胞来源。近年研究发现,小梁网干细胞(trabecular meshwork stem cells,TMSCs)在分化为TM细胞方面具有绝对优势,为细胞移植治疗青光眼提供新的靶向,这标志着干细胞治疗POAG进入一个新纪元,为青光眼治疗带来新的曙光。本文将对不同种类干细胞的小梁网移植进行综述,为细胞移植治疗POAG提供新思路。     

颅内压与青光眼及其无创测量技术的研究进展

青光眼是世界上第二位致盲性眼病,第一位不可复性致盲性眼病。尽管眼压增高被认为是青光眼性视神经损害的主要危险因素,但是50%的原发性开角型青光眼患者的日常眼压正常,还有一些患者尽管眼压控制良好,但青光眼性视神经损害仍继续发展。这些现象无法用高眼压理论来解释,青光眼患者视神经损害的发病机制仍待探讨。目前国内外的一些研究表明：（1）视神经周围的生物力学的解剖结构包括眼内压,筛板和球后的脑脊液压力在原发性开角型青光眼的发病机制中发挥重要的作用;（2）正常眼压性青光眼患者的脑脊液压力比正常人低,而跨筛板压力差比正常人高;（3）高眼压症患者的脑脊液压力比正常人群高,而跨筛板压力差和正常人之间没有统计学意义。基于以上研究,本文就颅内压与青光眼性视神经损害之间关系的相关研究进展及临床上可行的无创颅内压测量方法作一综述。