海德堡视网膜断层扫描仪在青光眼诊断中的应用

世界上有近50％的青光眼患者没有被诊断。临床对于青光眼的评价通常包括眼压测量、视野检查和对视乳头的分析。眼压升高是青光眼神经病变发展最重要的危险因素。研究显示，不同个体对眼压及其波动有不同的耐受性。在多数情况下，不管是对青光眼的诊断还是随访监测，仅测量眼压是不够的。视野检查是评价视神经功能很好的检查方法。     

青光眼视神经病变的视乳头改变

原发性开角型青光眼是青光眼最常见的类型，其特征为视神经轴突的不可逆性的丧失，以前对人和猴青光眼的研究提示，轴突的损害部位在视乳头内的筛板水平，在青光眼性视乳头，视盘上视杯的进行性扩大来自筛板结缔组织（细胞外间质）的压缩，牵张和重构。星形细胞是视神经中的主要细胞类型，并且可能主动参与了细胞外间质的重构，神经神经轴突支持组的构成，结构或者反应过程可能存在着个体差异，这或许解释了在眼压反应和神经病变进展     

HRT在青光眼诊断和视神经监测中的应用

HRT是一种自动化的电子计算机控制的共焦激光眼底断层扫描仪。利用它可以获取视盘的三维地形图,通过对图像的分析处理,得到视盘和视网膜神经纤维层厚度的定量描述,并且可用于地形图变化的定量分析。本文就HRT的工作原理和技术参数及其在青光眼诊断和视神经损害监测中的应用作一综述。     

青光眼性与非青光眼性视神经病变的鉴别诊断

青光眼性与非青光眼性视神经病变的鉴别是临床上的重点和难点之一。鉴别要点包括病史、症状、体征、眼底检查、视野检查、眼科或神经影像学检查和其他特殊检查等方面。视盘形态学是两者鉴别的关键,也仍然是目前早期诊断的核心。非青光眼视物显大症(大视杯)的患者有20%被误诊为青光眼视神经损害。加强神经眼科基本知识的学习,重视交叉学科的协同合作,是解决临床实际问题和困惑的有效途径。     

青光眼的视神经乳头

所有类型的青光眼都会有青光眼视神经病变。检查和处理青光眼的关键在于清楚如何检查视乳头（ONH）     

海德堡第三代视网膜断层扫描仪(HRT-3)在青光眼诊断中的应用

青光眼是最主要的致盲眼病之一。在人群中青光眼的患病率为1%-2%，并且世界上有50%的青光眼患者没有破诊断。临床对于青光眼的评价通常包括眼压测量，视野检查和对视神经乳头的分析。     

如何鉴别青光眼与非青光眼性视神经病变

视乳头视杯扩大并非只见于青光眼,还可见于多种神经眼科疾病,其鉴别诊断是临床工作的重点与难点.据国外统计,非青光眼大视杯的患者有20％被误诊为青光眼视神经损害.因此,总结并准确地理解青光眼与非青光眼大视杯的鉴别要点显得非常重要.盘沿色泽以及视功能异常和视盘改变的相关性是视盘形态学上的重要鉴别点.另外,盘沿局限性丢失对于两者的鉴别具有重要的意义.现有的证据显示,其鉴别需详细地询问病史、仔细地观察视盘视杯形态和血管形态,综合视野、神经影像学检查等信息综合判断.     

TRPV4在青光眼性视神经病变中的研究进展

青光眼性视神经病变(GON)是青光眼治疗难点所在。近年来,关于GON的发病机制提出了多种学说,但其中任何一种均无法解释所有类型青光眼造成的视神经病变原理,使得该病在临床治疗中顾此失彼,且不利于早期干预。最新研究发现,存在于视网膜中的瞬时受体电位通道香草酸亚家族4(TRPV4)在GON多种发病机制中均占有重要地位。本文将对TRPV4及其在GON发生发展过程中所发挥的作用作一综述,以期为GON的多种机制学说寻找一共同“连接点”,这将有助于对该病的进一步认识和临床治疗。     

糖尿病性视神经病变的临床分析

目的 观察糖尿病性视神经病变的临床表现、眼底血管造影和视野特征.方法 对173例321眼0～Ⅴ期糖尿病视网膜病变患者的临床表现、视力、视野、荧光造影等临床资料进行分析.结果 321眼中有视神经病变者共155眼,占48.3%.临床表现多样,轻者无任何症状,重者视力下降明显.眼底检查可有视盘水肿、色淡、充血等多种改变.荧光造影中主要表现为视盘新生血管40眼,占25.8%、视盘充盈缺损21眼,占13.5%、视盘水肿45眼,占29.0%及视盘晚期染色49眼,占31.6%.0期DR患者中,25.9%视神经有异常改变.Ⅰ～Ⅴ期DR患者视神经异常率分别为25.0%,37.5%,43.0%,65.1%,85.1%.结论 糖尿病性视神经病变发生率高,临床表现多种多样.糖尿病视网膜病变越严重,发生糖尿病视神经病变的可能性越大,但两者不平行.荧光造影检查对糖尿病视神经病变的早期诊断有重要意义.糖尿病性视神经病变是影响视力和预后的重要因素,应引起眼科医生的高度重视.     

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.     

免疫系统调节在青光眼性视神经病变中的作用

青光眼是一种以进行性视网膜神经节细胞及其轴突丧失为特征且伴有视野敏感度降低的慢性视神经变性疾病。随着近年来免疫学研究的深入,免疫系统调节在青光眼性视神经保护中的作用越来越引起了研究者的高度重视。当机体免疫系统出现异常调节时,自身免疫反应和应激介导的免疫反应也将导致视神经的退行性改变。全面、系统地了解免疫系统在青光眼视神经病变中的作用,对于确立有效的视神经保护策略具有重要的指导意义。因此,有必要就免疫系统在青光眼性视神经病变中的作用予以综述。     

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)     

青光眼视神经损害的三要素及其盘沿丢失的识别

诊断青光眼视神经损害的三要素为盘沿丢失、视网膜神经纤维层缺损（RNFLD）及视盘线状出血。三要素中如有两要素改变应诊断为视神经损害。对于盘沿丢失已往的教科书中均无明确描述,笔者认为识别盘沿丢失必须首先认识正常盘沿形态及其影响因素。大多数的正常盘沿形态符合ISNT法则,生理性大视杯也符合该法则。不符合ISNT法则者为盘沿丢失,或者为正常盘沿形态变异。后者如部分小视盘下方盘沿可比上方盘沿窄,判断是否上、下方盘沿丢失时应将其与鼻侧盘沿进行比较;横椭圆视盘鼻侧盘沿较宽,应上、下盘沿比较;视盘主干血管发出位置偏位、视盘倾斜也会影响盘沿形态。如果参照ISNT法则认识正常盘沿变异因素,就不难发现盘沿丢失。然而不是所有的盘沿丢失均为青光眼所致,应鉴别非青光眼性视神经损害。     

非动脉炎型前部缺血性视神经病变的光相干断层扫描特征

目的 观察非动脉炎型前部缺血性视神经病变（NAION）患者视盘及盘周视网膜神经纤维(RNFL)厚度变化特征。方法 利用光相干断层扫描（OCT）对NAION患者96例108只眼的视盘进行环形和十字交叉纵横扫描,分析患者视盘及盘周RNFL厚度变化。其中,水肿期96例96只眼,水肿消退期37例41只眼。同时选取单眼发病患者的84只对侧健康眼作为对照。随访时间2周~24个月,平均随访时间6个月。结果 视盘水肿期患者十字交叉纵横扫描显示,盘周RNFL较对侧健康眼增厚,59只眼非缺血区RNFL增厚更显著,即盘周RNFL厚度非缺血区大于缺血区,占视盘水肿期患者的61%;26只眼缺血区RNFL厚度大于非缺血区,非缺血区RNFL厚度在正常范围,占视盘水肿期患者的27%;11例11只眼盘周缺血区与非缺血区RNFL厚度无差异,隆起厚度均大于对侧健康眼厚度,占视盘水肿期患者的12%。十字交叉纵横扫描显示,除视杯狭窄较浅或无杯的形态外,其他与环形扫描一样均显示以视盘缺血区水肿消退最快,平均时间为2周左右,而非缺血区水肿消退时间为3~6周。水肿消退期患者在水肿消退1个月内视盘缺血区RNFL均变薄,其厚度低于非缺血区和对侧健康眼,占本期患者的95%;在水肿消退≥3个月时,26例患者整个盘周RNFL厚度≤对侧健康眼,视盘缺血区与非缺血区RNFL均表现为持续性萎缩性薄变,且盘周缺血区RNFL厚度薄于非缺血区;占本期患者的70%。结论 NAION水肿期盘周RNFL厚度较对侧健康眼增厚,且多数患者非缺血区高于缺血区;水肿消退期盘RNFL厚度均低于对侧健康眼。     

Fluorescein leakage of the optic disc in glaucomatous optic neuropathy

Purpose To identify and quantify the role of capillary leakage of the optic nerve head in digital fluorescein angiography in normal subjects and patients with open-angle glaucoma.Methods We conducted a prospective cross-sectional study in the Department of Ophthalmology of the Technical University of Aachen. Thirty patients with primary open-angle glaucoma (POAG) and 30 healthy age-matched subjects were included. Fluorescein angiograms were performed using the scanning laser ophthalmoscope. The fluorescence of the optic nerve head and the surrounding retina (ratio of leakage) was measured using digital imaging analysis in the late phases of the angiogram (9–10 min).Results The ratio of optic nerve head fluorescence to retinal reference loci was significantly increased (p=0.01) in patients with glaucoma (POAG, 1.38±0.34) compared with normal subjects (1.20±0.19). Intraocular pressure (p=0.0001), visual field indices (mean deviation, p<0.0001; pattern standard deviation, p<0.0001; corrected pattern standard deviation, p<0.0001), and cup to disc ratios (p=0.02) differed significantly between the groups. Age and systolic and diastolic blood pressure showed no significant differences between groups.Conclusion Fluorescein angiography revealed significantly increased vascular leakage of glaucomatous optic nerve heads. An endothelial disruption and fluorescein leakage might be the result of mechanical stress at the level of the lamina cribrosa and/or a sign of ischemic damage. This measurement approach might enable us to judge the severity of optic nerve head leakage, and it is a potential way to evaluate therapeutic regimens.     

Agreement in identification of glaucomatous progression between the optic disc photography and Heidelberg retina tomography in young glaucomatous patients

AIM:To evaluate concordance between the clinical assessment of glaucomatous progression of the optic disc photography and progression identified by Heidelberg Retina Tomograph (HRT) in patients with suspected primary juvenile open angle glaucoma (JOAG).METHODS:Optic disc photographs and corresponding HRT Ⅱ series were reviewed. Optic disc changes between first and final photographs were noted as well as progression identified by HRT topographic change analysis (TCA) and rim area regression line (RARL) Agreement between progression indentified by photography and HRT methods was assessed. Progression, determined from optic disc photographs by consensus assessment was used as the reference standard.RESULTS: A total of 31 patients (59 eyes) with suspected JOAG were studied. Agreement for progression/no progression between TCA and photography was obtained in 4 progressing eyes and 38 stable eyes (71.19%, k=0.11). Agreement for progression/no progression between RARL and photography was detected in 5 progressing eyes and in 34 stable eyes (66.10%, k=0.15). The number of HRT per patient was statistically higher in the progressing group (P=0.034).CONCLUSION:Agreement for detection of longitudinal changes between photography and HRT analysis was poor. One way to improve the chance of discovery of the progression could be increasing the number of HRT examinations.     

放射性视神经病变临床分析

目的 探讨放射性视神经病变(RON)的临床特点、影响因素、诊治方法及其转归.方法 回顾性系列病例研究.对1999年6月至2010年10月中山大学中山眼科中心收治的35例(60只眼)RON住院患者的临床资料进行回顾性分析.结果 共收集35例(61只眼)RON患者的临床资料.所有患者均以进行性、无痛性单眼或双眼视力下降为主要表现.18例(51.4％)在完成放射治疗后3年内出现眼部症状.43只眼(70.5％)的患眼入院时中心最佳矫正视力＜0.05或视野0°.可窥见眼底的52只眼中,41只眼(78.8％)视乳头边界清晰,11只眼(21.2％)视乳头水肿和(或)出血、渗出.视乳头边界清晰的41只眼中,视乳头正常6只眼(14.6％),视乳头色较淡30只眼(73.2％),视乳头苍白5只眼(12.2％).14只眼有视野检查记录,主要表现为神经纤维束损害性视野缺损,其中7只眼(50％)表现为上方和(或)下方弓形暗点,3只眼(21.4％)出现中心和(或)旁中心暗点,2只眼伴生理肓点扩大,1只眼伴旁中心暗点,1只眼见鼻上象限缺损.23只眼有视网膜荧光血管造影检查结果,主要的改变为视乳头低荧光和视网膜毛细血管无灌注区.图形视觉诱发电位检查发现,83.3％出现振幅降低和(或)潜伏期延长.分别用糖皮质激素治疗、高压氧、高压氧联合糖皮质激素、视网膜激光光凝等治疗,只有10只眼(16.4％)视力有不同程度的改善.结论 RON潜伏期变异大,造成的视力和视野损伤重,视功能预后极差,主要眼部损伤为视网膜血管闭塞和不同程度视神经萎缩.目前针对并发症的保守治疗能短期改善视力.     

局灶性筛板缺损对青光眼进展的影响

筛板一直被认为是青光眼视网膜神经节细胞和轴突发生损伤的初始部位,观察筛板的形态学改变有助于认识青光眼的病理机制。以往研究结果显示局灶性筛板缺损与青光眼进展相关,但两者的因果关系和作用机制并不清楚。本文指出相干光层析成像术发展,首次揭示了青光眼局灶性筛板缺损可以平衡跨筛板压力梯度,从而起到延缓或终止青光眼视神经损伤进展的作用,该发现为跨筛板压力梯度学说在青光眼发病机制中的作用提供了直接的临床依据,深化了临床对局灶性筛板缺损与青光眼进展的认识,从另一角度阐述了原发性开角型青光眼的发病机制,为该疾病的治疗和预后判断提供了新的思路。