原发性开角型青光眼血流动力学研究

目的：探讨原发性开角型青光眼（primary open angle glaucoma,POAG)眼血流动力学的变化, 分析眼血流与视野、视力、眼压、杯盘比的关系。方法：利用彩色多普勒成像（color Doppler imaging,CDI)技术检测POAG患者与正常人各30例59眼的球后血流状态,其中10例,10眼行眼底荧光血管造影（fundus fluorescein angiography,FFA)检测。结果：POAG眼血流速度明显降低（P＜0．01）,血流速度与视功能具有相关性。POAG组表现FFA异常：早期视盘弱荧光,相对性、绝对性视盘局部充盈缺损, 后期视盘强荧光。结论：POAG患者视盘及视网膜血液供应不良,与视神经损害和视野缺损密切相关,首次提出CDI技术检测标准化,实现检测结果的可比性。     

低眼压性青光眼

von Graefe 1957年首次描述低眼压性青光眼(LTG),目前,关于它是否为一独立的病种以及它与原发性开角型青光眼(POAG)的关系尚有争议,同时,还没有一个能够概括临床和发病学两个方面的简明的定义。目前流行的定义仅限于描述性定义,其标准是:1)单眼或双限的后天获得性POAG样视野改变;2)单眼或双眼的后天获得性POAG样视盘改变;3)双眼未经处理时的自然眼压在统计学正常范围内;4)双眼开房角。一般选择21—24mmHg为正常眼压上限。上限眼压值增高使LTG的范围加大,也可能包括更多的交叉重迭的POAG病例。作者以24mmHg作为正常眼压上限,并以有无进行性视野缺损进行再分类。     

正常眼压性青光眼

正常眼压性青光眼患者的眼压在统计学眼压的正常范围之内,却有典型的青光眼性视野缺损及与之相关的视盘改变。故发病隐匿,常造成不可逆的视神经损害。现代研究认为其发病机制是机械因素、血管因素、自身免疫因素等多种因素的共同作用。降眼压是必要的措施,眼压降低30%以上对其病变有利。与此同时,改善视神经血流供应和保护视神经的药物正被关注。     

冷激发对原发性开角型青光眼患者视网膜 光敏感度的影响

目的研究原发性开角型青光眼(primary open angle glauc oma,POAG)患者在寒冷刺激时的视盘血流、视网膜光敏感度变化及二者的相互关系。方法33例眼压已控制的POAG患者的33只患眼和13个正常人 的13只眼纳入研究。用海德堡视网膜血流仪和Topcon计算机自动视野计测量POAG患者及正常人在基础状态和冷激发后的视盘血流及视网膜光敏感度的变化。结果POAG患者在冷激发后视盘平均血流量下降31.5,血管容积下降1.1,视网膜光敏感度下降0.78dB,均较其自身基础状态显著下降(P<0.05),而正常对照组无此趋势。POAG患者冷激发前后的血流变化值与其视网膜光敏感度的变化密切相关(r=0.615,P＜0.001)。在冷激发时,有偏头痛病史的 POAG患者视盘血流下降幅度更大(P<0.001)。结论冷激发可使部分POAG患者的视盘血管痉挛,血流减少,视网膜光敏 感度下降。视网膜光敏感度下降程度与视盘血流减少量密切相关。(中华眼底病杂志, 2001,17:37-40)     

原发性开角型和闭角型青光眼眼压降低前后视盘改变和筛板顺应性的对比研究

目的比较降跟压前后原发性慢性闭角型青光眼（PACG）与原发性开角型青光眼（POAG）的视盘结构改变,了解两者间筛板顺应性是否存在差异。设计前瞻性对比研究。研究对象PACG36例49眼和POAG35例49眼。方法眼压降低前全部患者进行海德堡视网膜断层扫描（HRT—II）及Humphrey静态视野检查。根据病情选择手术、激光或药物治疗,使眼压降至正常范围。眼压降低后1个月重复HRT检查和视野检查。比较POAG和PACG眼压降低前后HRT视盘参数的变化,采用多元线性逐步回归法校正治疗前眼压、眼压降低幅度、年龄、杯盘比等因素影响。主要指标眼压降低前后HRT视杯面积、盘沿面积、视杯容积、平均视杯深度的差值。结果PACG及POAG组的视杯面积、视杯容积、平均视杯深度等指标在眼压降低后均明显降低（P〈0．05）,盘沿面积在眼压降低后均明显增加（P〈0．05）。视杯面积、盘沿面积、视杯容积、平均视杯深度在跟压降低前后的差值两组间无显著性差异（P〉0．05）。眼压降低前后这4个参数的差值与眼压降低幅度及杯盘比有关（P〈0．05）;与年龄及治疗前眼压无关（P〉0．05）。结论眼压降低后青光眼视盘形态结构有一定回复;但在PACG和POAG间,视盘形态结构回复的程度无明显差异,PACG和POAG的筛板顺应性可能无差异。（眼科,2009,18：264—269）     

低眼压性青光眼

本文介绍了作者对两组病人的临床观察。一组5例为眼压从未超过正常,即<20mmHg,而有进行性视盘凹陷、视神经萎缩及视野缺损;一组4例为开角型青光眼,眼压曾有明显升高伴有青光眼视盘杯状凹陷、萎缩和视野缺损,虽经药物和手术治疗眼压降至正常范围,病情依然继续恶化。作者将此两组病人都归类于“进行性低眼压性青光眼”,而第二组又可称为“继发性进行性低眼压性青光眼”。低眼压性青光眼不是罕见的,其视盘改变绝非单纯由眼压增高的机械性结果,当然最初是由于眼压高,尔后是由于视盘的血管改变和营养障碍所致。视神经一旦出现改变就显得格外易受损     

早期原发性开角型青光眼视盘血流密度的分析研究

目的:探讨早期原发性开角型青光眼(POAG)、高眼压症患者和健康者的视盘血流密度的差异。方法:横断面研究。收集2019-01/2021-04于福州东南眼科医院青光眼科门诊就诊患者,早期POAG组45例70眼,其中男32例49眼,女13例21眼,年龄48.50(26.75,64.50)岁,高眼压症组37例65眼,其中男17例29眼,女20例36眼,年龄37.00(27.00,47.00)岁,健康组51例94眼,其中男23例39眼,女28例55眼,年龄46.00(34.50,56.50)岁。分别对三组进行常规的眼科检查包括最佳矫正视力(BCVA)、眼压、视野、视网膜神经纤维层厚度(RNFL)、中央角膜厚度(CCT)等,通过光相干断层扫描血管成像检查(OCTA)采集并测量三组的视盘中心区、内层区、外层区和完整区的视盘血流密度。结果:三组眼压比较有差异(H=146.876,P<0.001),早期POAG组和高眼压症组与健康组的眼压值有差异(均P<0.01),早期POAG组和高眼压症组患者的眼压无差异(P=0.132)。早期POAG组和高眼压症组的BCVA、RNFL、MD值比较有差异(P=0.005、0.01、<0.01),早期POAG组和健康组两者的BCVA、RNFL、MD值比较有差异(P=0.013、<0.01、<0.01),高眼压症组和健康组两者的BCVA、RNFL、MD值比较无差异(P=1.000、0.660、1.000)。早期POAG组和健康组之间CCT无差异(P=0.074),早期POAG组和高眼压症组之间CCT比较有差异(P=0.006),高眼压症组和健康组之间CCT比较有差异(P<0.01)在中心区、内层区、完整区,早期POAG组和高眼压症组的血流密度比较有差异(均P<0.01),早期POAG组和健康组的血流密度比较有差异(均P<0.01),高眼压症组和健康组比较无差异(均P=1.000)。在外层区,早期POAG组和健康组的血流密度比较有差异(P=0.001),高眼压症组和早期POAG组及健康组比较有差异(P=0.067、0.877)。结论:早期POAG的视盘血流密度相比高眼压症和健康者是减少的,与视野MD、RNFL参数的变化是相一致的,早期POAG视盘不同区域血流密度均减少。     

OCT3检测视盘参数与视野的相关性研究

目的:研究第三代光学相干断层扫描仪(stratus optical co-herence tomography3000,OCT3)检测原发性开角型青光眼(primary open angle glaucoma,POAG)视盘参数与视野平均缺损(mean defect,MD)的相关性,评估OCT3检测视盘参数在POAG早期诊断中的价值。方法:正常人43例(43眼)、48例原发性可疑型青光眼(SOAG)、55例(55眼)原发性开角型青光眼(POAG)。采用OCULUS Easyflied视野计和OCT3分别进行视野和视盘形态检测。比较OCT3检测三组间视盘参数的差异,分析青光眼组视野检测的视野平均缺损(MD)与OCT3视盘参数的关系。结果:OCT3检测三组间的视盘参数均存在显著性差异(P<0.01)。在原发性开角型青光眼组,RA与MD相关性最好(P<0.05)。结论:OCT3能够检测到青光眼的早期视盘结构的改变,且与MD有基本一致的较好相关性。OCT3检测视盘参数可用于POAG的早期诊断。     

前部视神经微循环环异常与青光眼

18 5 7年 Von Graefe[1 ]描述青光眼为一视盘凹陷的黑朦 ,同时可伴有眼压的明显增高、轻度增高或甚至并不增高。然而 ,他仍然认为青光眼是一种眼压增高的疾病。至 1892年Schnabel首次提出视盘萎缩凹陷 ,而无眼压增高 ,也可以认为是青光眼病。自 190 5年 Schiotz[2 ]发明压陷式眼压计之后 ,大多数诊断检查集中于测量眼压 ,长期以来眼压被认为是青光眼的危险因素。最近被人们热衷研究的正常眼压青光眼(NTG )或低眼压青光眼 (L TG ) ,与原发性开角型青光眼(POAG)相似 ,都是属于开角型青光眼 ,具有相似的青光眼性视神经病变和视野缺损。虽…     

应用海德堡视网膜断层扫描仪检测开角型青光眼的视盘改变

目的探讨海德堡视网膜断层扫描仪(Heidelberg retinal tomography,HRT)检测青光眼性视盘改变是否与视野损害的部位相一致,了解正常眼压性青光眼(normal tension glaucoma,NTG)与原发性开角型青光眼(primary open angle glaucoma,POAG)早或中期视盘形态是否异同.方法对64例(64只眼)仅有半侧视野异常的开角型青光眼(POAG27只眼、NTG37只眼)患者进行HRT检测,将Humphery视野与HRT的检测结果以0°～180°为界,分成上下两部分进行对应分析.结果与正常半侧视野对应的1/2视盘比较,显示异常半侧视野对应的1/2视盘HRT参数中,杯盘面积比、视杯形态测量值显著增大,而盘沿面积、视网膜神经纤维层厚度及视网膜神经纤维层横断面积值显著减少 (t=-2.625～3.025,P=0.003～0.05);NTG眼和POAG眼对应与异常半侧视野的HRT视盘参数差异无显著性(t=-0.98～1.511,P=0.14～0.97).结论 HRT参数能较准确反映与视野损害相一致的视盘变化,其中尤以杯盘面积比、盘沿面积、视杯形态测量、平均视网膜神经纤维厚度及视网膜神经纤维层横断面积测量值较为准确.NTG和POAG眼的视盘形态相似,可能具备某些相似的视神经损害发生机制.     

Relationship between optic nerve head microcirculation and visual field loss in glaucoma

PURPOSE: To study the relationship between optic nerve head blood flow velocity and visual field loss in patients with primary open-angle glaucoma (POAG) and normal tension glaucoma (NTG). METHODS: This study included 44 eyes of 44 patients with POAG and 44 eyes of 44 patients with NTG. To evaluate optic nerve head blood flow velocity, the square blur rate (SBR) was measured by means of laser speckle flowgraphy. The correlation between SBR and Humphrey visual field indices was evaluated with linear regression analysis. RESULTS: In the NTG group, the average SBR at the superior and inferior temporal neuroretinal rim was positively correlated with mean deviation (MD) (r = 0.349, p = 0.020). The SBR at the superior or inferior temporal neuroretinal rim was positively correlated with the sum of the total deviations in the corresponding hemifields (r = 0.299, p = 0.049; r = 0.354, p = 0.019, respectively). The correlations between SBR and MD did not differ statistically between the NTG and POAG groups; however, no significant correlation between SBR and visual field indices was observed in the POAG group. CONCLUSION: These results suggested that the change in the circulation of the optic nerve head may be related to visual field damage in the NTG group but may be less involved in visual field damage in the POAG group.     

Glaucoma in a rural population of southern India: the Aravind comprehensive eye survey

PURPOSE: To determine the prevalence of glaucoma and risk factors for primary open-angle glaucoma in a rural population of southern India. DESIGN: A population-based cross-sectional study. PARTICIPANTS: A total of 5150 subjects aged 40 years and older from 50 clusters representative of three southern districts of Tamil Nadu in southern India. METHODS: All participants had a comprehensive eye examination at the base hospital, including visual acuity using logarithm of the minimum angle of resolution illiterate E charts and refraction, slit-lamp biomicroscopy, gonioscopy, applanation tonometry, dilated fundus examinations, and automated central 24-2 full-threshold perimetry. MAIN OUTCOME MEASURES: Definite primary open-angle glaucoma (POAG) was defined as angles open on gonioscopy and glaucomatous optic disc changes with matching visual field defects, whereas ocular hypertension was defined as intraocular pressure (IOP) greater than 21 mmHg without glaucomatous optic disc damage and visual field defects in the presence of an open angle. Manifest primary angle-closure glaucoma (PACG) was defined as glaucomatous optic disc damage or glaucomatous visual field defects with the anterior chamber angle partly or totally closed, appositional angle closure or synechiae in the angle, and absence of signs of secondary angle closure. Secondary glaucoma was defined as glaucomatous optic nerve damage and/or visual field abnormalities suggestive of glaucoma with ocular disorders that contribute to a secondary elevation in IOP. RESULTS: The prevalence (95% confidence interval) of any glaucoma was 2.6% (2.2, 3.0), of POAG it was 1.7% (1.3, 2.1), and if PACG it was 0.5% (0.3, 0.7), and secondary glaucoma excluding pseudoexfoliation was 0.3% (0.2,0.5). On multivariate analysis, increasing age, male gender, myopia greater than 1 diopter, and pseudoexfoliation were significantly associated with POAG. After best correction, 18 persons (20.9%) with POAG were blind in either eye because of glaucoma, including 6 who were bilaterally blind and an additional 12 persons with unilateral blindness because of glaucomatous optic neuropathy in that eye. Of those identified with POAG, 93.0% had not been previously diagnosed with POAG. CONCLUSIONS: The prevalence of glaucoma in this population is not lower than that reported for white populations elsewhere. A large proportion of those with POAG had not been previously diagnosed. One fifth of those with POAG had blindness in one or both eyes from glaucoma. Early detection of glaucoma in this population will reduce the burden of blindness in India.     

Primary open angle glaucoma and low tension glaucoma--pathogenesis and mechanism of optic nerve damage]

The etiology, pathogenesis and mechanism of optic nerve damage in primary open angle glaucoma (POAG) and low tension glaucoma (LTG) were investigated by experimental glaucoma in monkey and by follow-up studies of many patients over 15 years, by pathohistological and immunohistochemical analysis. 1) LTG was proved to be a real glaucoma, showing pressure-dependent optic nerve damage. The pathological entity was a primary weakness of the lamina cribrosa (LC), and therefore even normal pressure could deform the LC. Due to backward distortion of LC the channels were disarranged and twisted, inducing mechanical optic nerve damage. There was no active vascular damage or vascular constriction at the site of the optic nerve damage. The filling defects of the advanced glaucomatous optic disc were not the cause of optic nerve damage, but the result of regressive vascular change after axon bundle loss. Splinter hemorrhage of the optic disc might be the result of the same process. 2) The weakness of LC might be induced by the abnormal metabolism of the extracellular matrix of the LC. 3) To arrest the progressive optic nerve damage in LTG, the intraocular pressure (IOP) should be maintained under 12, or ideally, 10 mmHg. 4) The optic nerve damage in POAG was not only pressure-dependent, but also dependent on the weakness of the LC, as in the case of LTG. In the early stage the IOP should be under 19 mmHg, in the advanced stage under 14 mmHg in order to arrest progression for over 15 years. 5) In advanced experimental glaucoma of monkeys, the LC showed reduction of elastin, fragmentation of collagen, and change of proteoglycans. 6) As in the LC, the trabecular meshwork also showed abnormal metabolism and abnormal deposits on the extracellular matrix in POAG, and LTG as well. 7) POAG and LTG might belong to the same family in which common abnormal metabolism of LC and trabecular meshwork induce various clinical features.     

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.     

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.     

Absolute filling defects of the optic disc in fluorescein angiograms in glaucoma--a retrospective clinical study

BACKGROUND: Analysis of clinical importance of the size of filling defects in fluorescein angiograms in primary open-angle glaucoma (POAG), normal-tension glaucoma (NTG), ocular hypertension and subjects with physiological excavations in comparison to visual field loss, optic nerve head morphology and hemodynamics. PATIENTS AND METHODS: 75 patients (POAG, NTG, ocular hypertension) and 10 healthy subjects with physiological excavations were included in this study. In digitized video fluorescein angiograms (Scanning Laser Ophthalmoscope) the size of absolute filling defects of the optic disc was quantified in the early venous phase and expressed by percentage of the optic disc. Visual fields were obtained by conventional static perimetry (Humphrey 24-2) and graded in stages of glaucoma visual field defects (Aulhorn I-V). Optic disc excavations were evaluated as cup-to-disc-area-ratios. RESULTS: The filling defects correlated with the visual-field loss stages of Aulhorn and the visual field indices MD (mean deviation), PSD (pattern standard deviation) and CPSD (corrected pattern standard deviation). There was no correlation with the index SF (short-term fluctuation) and with systemic hemodynamics (blood pressure, perfusion pressure) or the IOP. Absolute filling defects correlated with the cup-to-disc-area-ratio in NTG. The absolute filling defects were larger in patients with glaucoma (POAG, NTG) in comparison to patients without glaucomatous visual field loss (ocular hypertension, glaucoma-like discs). No difference of filling defects was found in the glaucoma group (POAG, NTG). Patients with NTG had larger excavations and lower systolic blood pressures than patients with POAG. CONCLUSION: The size of fluorescein filling defects may be useful as a parameter for the evaluation of an ischemic lesion of the optic nerve head. Absolute filling defects may differentiate POAG from ocular hypertension and NTG from glaucoma-like discs without field defects. The results support the hypothesis that in POAG and NTG disturbances of the circulation result in similar filling defects of the optic disc and visual field loss.     

原发性开角型青光眼与24h眼压及眼灌注压的研究进展

原发性开角型青光眼是一类早期无明显临床症状,但随病情进展将导致不可逆的视神经损害及视野缺损的致盲性眼病。眼压是原发性开角型青光眼诊断及评定治疗效果的简单而又重要的指标。临床上,一些治疗中的原发性开角型青光眼患者白天就诊时间所测眼压已达靶眼压,但视神经损害却仍在进展,研究表明可能与夜间眼压的升高、24 h较大的眼压波动及夜间眼灌注压的降低有关。因此,我们对原发性开角型青光眼与眼压及眼灌注压波动的相关文献予以综述,以更好的理解三者之间的关系。     

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。     

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.