前部缺血性视神经病变

回顾性总结５１例前部缺血性视神经病变。５１例中单眼发病４４例；双眼７例（１３．７％），其中５例对侧眼已有视神经萎缩。平均发病年龄５４．９岁。作为病因的系统疾病，动脉粥样硬化占５４．９％，高血压动脉硬化３３．３％，糖尿病１１．８％。视力中度损害（０．２—０．５）者占１／３。下部视野缺损占３０．２％，大多与生理盲点相连；４只眼各有两处视野缺损。荧光血管造影揭示，脉络膜（含视盘）视网膜充盈倒置占２１．１％；视盘充盈延迟苍白水肿及火焰状出血表明前部视神经（筛板附近）的睫状后短动脉及表浅的中央血管微血管发生缺血损害。经药物治疗视力进步者占７５．８％。     

前部缺血性视神经病变眼底荧光血管造影分析

本文通过眼底荧光血管造影（ＦＦＡ）对前部缺血性视神经病变６６例（７４眼）的造影图像进行分析。结果表明：造影早期视盘缺血区均呈弱荧光，显示缺血累及的部位和范围，伴随相应的视野缺损。造影晚期视盘荧光形态各异，其中主要表现为强荧光者６７眼（９０．５４％），多见于病程早期；视盘仍呈弱荧光者７眼（９．４６％），见于病程较长者。认为ＦＦＡ是本病诊断的重要依据，但应参照临床症状、眼底和视野等资料综合分析才能有利于准确确诊。     

前部缺血性视神经病变的眼底荧光血管造影及视野的改变

目的分析眼底荧光血管造影和视野检查对前部缺血性视神经病变的诊断作用。方法对25例(39眼)前部缺血性视神经病变的造影及视野图像进行分析。结果眼底荧光血管造影早期视盘部分或大部分呈现荧光充盈迟缓,晚期视盘缺血区呈强荧光,并伴有不同的视野缺损。结论眼底荧光血管造影和自动视野分析对前部缺血性视神经病变的诊断有重要意义。     

前部缺血性视神经病变眼底荧光血管造影分析

前部缺血性视神经病变(anterior ischemic optic neuropa-thy,AION)为供应视盘筛板前区及筛板区的睫状后血管的小分支发生缺血,致使视盘发生局部的梗塞。眼底荧光血管造影(fundus fluorescence angiography,FFA)是本病诊断的重要依据。对我院102例(120只眼)AION患者进行FFA检查,现将结果报告如下。一、资料和方法1.一般资料:回顾性分析我院1998年3月～2006年3月间有完整病历记录的AION患者102例(120只眼)的临床资料。其中男性50例,女性52例;单眼93例,占91%,双眼9例,占8%;年龄35～72岁,平均年龄52.5岁。23例伴有糖尿病视网膜病变,30…     

前部缺血性视神经病变38例临床分析

目的：探讨前部缺血性视神经病变的诊断和治疗。方法：本组38例（41只眼）,视力损害严重,视野缺损多与生理盲点相连。眼底视盘边界模糊,水肿、渗出及出血,部分呈现视盘缺血苍白,眼底荧光造影检查;视盘及脉络膜充盈延迟,视盘低荧光。结果;经多种方法治疗视力提高24只眼（58．6％）,21只眼视野扩大,38只眼不同程度视神经萎缩。结论：常规治疗方法效果欠佳,应寻找早期预防、诊断的方法及确切有效的治疗手段。     

前部缺血性视神经病变的不典型荧光素眼底血管造影表现

目的探讨前部缺血性视神经病变(AION)患者的非典型荧光素眼底血管造影(FFA)表现。方法回顾性分析45例(52只眼)经临床确诊为AION患者的临床检查过程,比较分析其不典型的FFA表现等。结果45例(52只眼)呈典型AION表现者23例(25只眼),不典型表现者22例(27只眼)。不典型AION患者FFA表现为造影早中晚期均呈视乳头持续弱荧光等不典型表现。结论前部缺血性视神经病变有多种FFA表现。     

前部缺血性视神经病变的临床分析

观察分析前部缺血性视神经病变（anterior ischemic optic neuropathy,AION）的发病危险因素、临床特征及治疗效果。 方法：回顾性分析46例51眼AION患者全身及眼部危险因素、临床症状、眼底、FFA、视野改变。治疗和控制全身性疾病,全身或局部应用糖皮质激素、血管扩张剂、神经营养剂,评价治疗效果。 结果：患者平均年龄53±10岁,全身性疾病包括高血压、糖尿病、高脂血症、低血压、心脑血管疾病等。47.06%患者诉视力突然下降,64.71%患者眼底检查示视盘呈灰白色水肿,33.33%患者视野表现偏盲性缺损,56.86%患者FFA早期视盘弱荧光,晚期荧光增强。经治疗80.39%患者视力提高,视野缺损改善。 结论：AION是多病因眼病,高血压、糖尿病、高脂血症、心脑血管疾病等是其发生的危险因素。突然视力下降、视盘灰白水肿、偏盲性视野缺损、FFA视盘早期弱荧光、晚期强荧光是其典型表现。综合治疗后患者可恢复一定视力视野。     

前部缺血性视神经病变的眼底荧光血管造影及视野分析

目的　探讨眼底荧光血管造影和自动视野检查对诊断前部缺血性视神经病变的作用。方法　对 6 0例 (6 5眼 )前部缺血性视神经病变的造影及视野图象进行分析。结果　造影早期缺血区呈弱荧光 ,造影晚期比弱荧光区有明显的荧光渗漏而呈强荧光 ,伴随相应的视野缺损。结论　眼底荧光血管造影和自动视野是诊断前部缺血性视神经病变的重要依据 ,对于治疗及预后具有重要的临床意义。     

前部缺血性视神经病变并发视网膜分支动脉阻塞1例

目的:报告1例前部缺血性视神经病变(anterior ischemicoptic neuropathy,AION)并发视网膜分支动脉阻塞(branchretinal artery obstruction,BRAO)。方法:患者,女,42岁,因视力障碍进行如下眼科检查:眼底照相、荧光血管造影(fluorescent angiography,FAG)和视野测试。结果:第一次就诊时,患者视盘肿胀,动脉循环完整,发病1wk后,视网膜下支动脉开始萎缩并火焰状出血加剧。16mo后,视盘呈萎缩性改变,此外,发现视网膜下分支动脉血管影一条。结论:AION并发BRAO可造成动脉循环的机械性压迫。     

非动脉炎性AION中缺血部位及水肿程度对中心视力的影响

目的 :探讨非动脉炎性前部缺血性视神经病变 (nonarteriticanteriorischemicopticneuropathy ,NAION)中视盘水肿程度、缺血部位对中心视力的影响 ,以利于疗效评定及预后判断。方法 :2 40例NAION患者 (160例接受住院治疗 )的临床资料 ,结合视野和荧光眼底血管造影 (fundusfluoresceinangiography ,FFA)检查进行治疗前中心视力与水肿程度、缺血部位两方面统计分析 ,并分析治疗效果。结果 :2 40例NAION患者发病时中心视力的损害程度 ,依视盘缺血部位、水肿程度之不同而均有显著的差异 (P <0 0 0 5 )。 160例住院患者 ,视盘水肿消退时间最长为 3 5天 ,最短 11天 ,平均时间 2 1 5天 ,FFA复查四项指标改善率 88 1% ,中心视力两行行上者 10 4例 ,占 65 %。结论 :视盘的缺血部位及水肿程度是影响NAION中心视力的重要因素之一 ,积极针对性的治疗对防止NAION致盲有重要意义。     

Uveal effusion syndrome complicated by anterior ischemic optic neuropathy

We report on a case of idiopathic uveal effusion syndrome complicated by AION. To our knowledge such an association hasn't been previously described. We suggest that scleral thickening caused obstruction of vortex veins followed by uveal effusion and compression of posterior ciliary arteries within their intrascleral tract, leading to AION. Nevertheless it can't be excluded that AION was the result of mechanical compression on ciliary vessels of optic disc by choroidal detachment.     

Familial non-arteritic anterior ischemic optic neuropathy

PURPOSE: Primary objective was to investigate clinical characteristics of nonarteritic anterior ischemic optic neuropathy (NA-AION) in three families; secondarily, to test these families for a previously detected mitochondrial mutation in a pedigree with familial NA-AION. METHODS: Study comprised three families where more than one member developed NA-AION. All patients with NA-AION had a detailed ophthalmic, medical and family history, and comprehensive ophthalmic evaluation at initial visit and on follow-up. One patient from family 1, one from family 2, 41 non-familial NA-AION patients, 97 control subjects and 1,488 patients with suspected Leber hereditary optic neuropathy (LHON) were tested for the presence of mitochondrial mutation (G4132A) in a previously reported genetic study of family 3. RESULTS: Familial NA-AION was found in seven individuals of family 1, four of family 2 and six of family 3. Symptoms, signs and clinical findings of familial NA-AION were similar to classical NA-AION, with two exceptions: familial NA-AION had an earlier onset (47.3 + 8.6 years versus 60.1 + 13.6 years) and a higher frequency of bilateral disease. The G4132A mitochondrial variant was not detected outside family 3. None of the three major mutations associated with LHON (G3460A, G11778A, T14484C) was found among Familial NA-AION patients. CONCLUSIONS: The only difference in clinical features between familial NA-AION and classical NA-AION is that the former has an earlier onset and a higher frequency of bilateral disease. The G4132A mutation is not commonly associated with familial NA-AION, and was not detected in patients with non-familial NA-AION. The role of hereditary factors in familial NA-AION remains largely unknown.     

Trombophilic screening for nonarteritic anterior ischemic optic neuropathy

Background Nonarteritic anterior ischemic optic neuropathy (NAION) is an ischemic infarction of the optic nerve head, frequently leading to sudden, mostly irreversible loss of vision. In this study blood thrombophilic factors, as well as cardiovascular risk factors were investigated for their relevance to this pathology. Trombophilic risk factors so far not evaluated were included in the study. Patients and methods 37 NAION patients (4 with sequential second eye involvement) and 81 matched control subjects were examined. From blood, protein C, protein S, antithrombin, von Willebrand antigen levels (vWFAg), and factor V (Leiden) mutation, factor VIIIC level, plasminogen activity, lipoprotein (a) and fibrinogen levels, and presence of anticardiolipin antibodies were investigated. Possibly relevant pathologies [e.g. diabetes mellitus (DM), hypertension, and ischemic heart disease] were also registered. Results Elevated Lp(a) and vWFAg levels, DM, F V (Leiden), hypercholesterolemia, and hyperfibinogenemia proved to be significant risk factors associated with NAION. Forward stepwise logistic regression analysis revealed that high Lp(a), DM, and FV (Leiden) were the main predictive components, with odds ratios 16.88 (p=0.012), 5.78 (p=0.022) and 4.44 (p=0.033), respectively. Conclusions Based on our results it appears that thrombophilia is likely to contribute to the development of NAION besides vascular damage due to the presence of cardiovascular risk factors. Further data are needed, however, to justify the suggested use of secondary prophylaxis using anticoagulant/antiplatelet therapy.     

非动脉炎性前部缺血性视神经病变治疗进展

非动脉炎性前部缺血性视神经病变(nonarteritic anterior ischemic optic neuropathy,NAION)是全身血管危险因素及局部解剖因素等多因素共同参与的、发病机制复杂的视神经缺血性疾病.控制全身危险因素是治疗关键.目前三大治疗尝试包括改善循环(如眼压干预、体外反搏、手术),减轻视盘...     

非动脉炎性前部缺血性视神经病变视盘形态学定量研究

目的 研究非动脉炎性前部缺血性视神经病变(NAION)视盘形态结构特征,探讨 NAION 的发病机制.方法 应用海德堡视网膜断层扫描仪(HRT)对71例NAION患者对侧未发病眼及69名正常人随机选择一眼的视盘进行检测,对NAION患者和正常人的视盘参数进行比较分析.结果 NAION组视盘面积,视杯面积,杯盘面积比,平均视杯深度,最大视杯深度,视杯形态测量均小于正常对照组(P<0.05. NAION患者与正常组盘沿面积无差异(P>0.05. NAION组杯盘面积比小于等于0.2占91.5%,而对照组占40.6%,其中NAION组无视杯为14例,对照组仅为1例,NAION组无视杯的发生率明显高于对照组;两组杯盘面积比分布的差异具有统计学意义(P<0.05).结论 小视盘,小视杯及浅视杯是NAION患者视盘的形态学特点,也是导致NAION的解剖基础.     

前部缺血性视神经病变的回顾分析

目的:掌握前部缺血性视神经病变的临床检查、诊断、治疗方法,挽救视功能。方法:回顾性分析32例缺血性视神经病变患者的临床检查治疗过程,观察治疗前后的视力变化、视野变化、OCT、眼底荧光血管造影结果等。结果:32例前部缺血性视神经病变病例中,通过控制全身疾病,局部激素治疗,扩张血管药物促循环,营养神经治疗,大部分病例视力有所提高,视盘水肿减轻,视野不同程度扩大,患眼OCT示:盘周神经纤维层变薄。结论:前部缺血性视神经病变的正确诊断,及时系统的治疗,可有效提高视力,改善视盘缺血状态,扩大视野、提高视敏度。     

Bilateral arteritic anterior ischemic optic neuropathy

Background

Arteritic anterior ischemic optic neuropathy (AION) is a disease of the optic nerve head seen in patients over the age of 50 and more commonly over the age of 70. With few exceptions, arteritic AION is caused by giant cell arteritis. Early diagnosis and prompt treatment with corticosteroids are essential for preventing potentially devastating visual loss from this disease.

Case Report

A 63-year-old white man presented with the complaints of blurred vision of the right eye and visual field loss of the left eye. Ocular examination found bilateral swollen optic nerve heads. Visual field testing showed altitudinal defects in each eye. Laboratory testing was significant for elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels. The patient was treated with oral prednisone for arteritic AION and referred to a rheumatologist. At follow-up, the patient’s ESR and CRP levels showed significant improvement. The optic nerve head of the left eye showed a reduction in swelling, and the visual field finding was stable.

Conclusion

Arteritic AION is an ocular emergency. Optometrists need to be able to recognize and diagnose this condition quickly to initiate critical corticosteroid treatment.     

Optic disc structure in anterior ischemic optic neuropathy

The etiology of anterior ischemic optic neuropathy (AION), when not associated with giant cell arteritis, is usually unknown. Clinical, pathologic, and experimental studies have not determined a cause. The optic disc appearance in both the involved and normal fellow eye was studied in 51 patients with acute nonarteritic AION. The number of discs (both involved and fellow) without a physiologic cup was significantly greater than would be expected from normal population studies. The etiology of nonarteritic AION may be related to the anatomic configuration of the optic nerve.