后部缺血性视神经病变

后部缺血性视神经病变是缺血性视神经病变的一种类型。临床表现以突发视力障碍,视野缺损,单纯性视神经萎缩为特征。血液动力学紊乱和易感性增高所致的眶内视神经梗塞是后部缺血性视神经病变的病理基础。尚无有效治疗方法。本文对其的病因和发病机制、临床表现、诊断及治疗加以综述。     

后部缺血性视神经病变的研究进展

后部缺血性视神经病变(posterior ischemic neuropathy, PION)是缺血性视神经病变的一种,其发病较前部缺血性视神经病变少见,临床特征不明显,阳性体征较少,诊断困难,治疗方法仍有争议.本文从后部视神经的辅助检查、诊断、鉴别诊断及治疗4个方面的研究进展进行综述.     

后部缺血性视神经病变临床观察

目的:通过回顾性研究,探讨后部缺血性视神经病变(pos-teriorischemicopticneuropathy,PION)的临床表现、发病机制、诊断及治疗预后。方法:对9例(12眼)PION患者常规行眼部检查及全身检查,并排除压迫性、炎性、青光眼性或其它视神经疾病。行中医综合治疗。观察视力、视野、眼前节及眼底体征。结果:9例12眼均有不同程度视力下降及视野缺损;眼底视盘及视网膜正常6眼,视盘变淡或苍白6眼。经治疗的8例10眼,有效率70%。结论:PION是一种独立的临床眼病,诊断强调排除其它视神经疾病或眼病,中医综合治疗有助于视力改善。     

白内障手术源性后部缺血性视神经病变一例

1病例患者,女,90岁,因左眼逐渐视物模糊5～6年加重半年,经检查诊断为老年性白内障而入院。患者于3年前右眼曾因白内障行“白内障摘出后房型人工晶状体植入术”,术后视力0．2。既往有“高血压”史30年。     

后部缺血性视神经病变

后部缺血性视神经病变发病率低,国内眼科界对该病的认识尚未统一,本文主要对后部缺血性视神经病变的分类、临床特点、诊断与鉴别诊断、组织病理学表现和病理机制作一综述。     

后部间接外伤性视神经病变41例

目的 观察大剂量皮质类固醇对后部间接外伤性视神经病变的治疗效果。方法 对1995年1月～2002年12月住院的41例后部间接外伤性视神经病变,依据就诊时间及治疗方法的不同分为治疗组和对照组,治疗组每天一次静脉滴注地塞米松1 mg/kg·d,连续5天,对照组静脉滴注地塞米松20 mg,连续7天;然后口服强的松40 mg,每3天减10 mg。结果 治疗组26例经治疗视力恢复至0.05以上者22例(84.62％),对照组15例中7例(46.67％)视力达0.05以上,两组间差异具有显著意义(P<0.05),伤后24 h以内就诊治疗者视力恢复情况明显好于24 h以后就诊治疗者(P<0.05)。结论 早期应用大剂量皮质类固醇治疗后部间接外伤性视神经病变效果明显。     

手术相关性后部缺血性视神经病变

手术相关性后部缺血性视神经病变为后部缺血性视神经病变(posterior ischemic optic neuropathy,PION)的一种类型,其发生率虽低,但视功能损害严重。本综述通过对手术相关性PION的临床病例总结,探讨其诊断、临床特征、组织病理、发病规律、危险因素、致病机制、以及治疗和预防。     

应用彩色多普勒血流成像技术对后部缺血性视神经病变的研究

目的:探讨后部缺血性视神经病变(posterior ischenic optic neuropathy,PION)患者颈动脉及眼血流动力学的改变。方法:应用彩色多普勒血流成像技术(color Doppler flow imaging,CDFI)观察14例19眼PION患者,检测颈总动脉和颈内动脉影像学特征、睫状后动脉(posterior ciliary arteries,PCAs)和视网膜中央动脉(central retinal artery,CRA)血流动力学变化,与患者未受累一侧眼进行比较。结果:14例PION患者中12例(86%)表现为双侧颈总动脉和颈内动脉内膜粗糙、增厚,9例(64%)探查到血管壁斑块回声,硬斑5例,混合斑5例,软斑3例;PCAs的收缩期峰值速度(peaksy stolic velocity,PSV)为27.60±16.7cm/s,阻力指数(resistance index,RI)为0.84±0.038,与对照眼比较PSV无显著降低,RI明显增高(t=2.116,P<0.05);CRA的PSV为11.51±3.47cm/s,RI为0.75±0.036,与对照眼比较PSV无差异,RI增高非常明显(t=2.862,P<0.01)。结论:PION的发生主要与颈动脉粥样硬化导致的颈动脉系统血流变化有关,CDFI对明确PION诊断有重要的应用价值。     

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。     

Ischemic optic neuropathy

Ischemic optic neuropathy (ION), based on vascular anatomy of the optic nerve, pathogenesis and clinical picture, consists of two distinct entities: anterior (AION) and posterior (PION) ischemic optic neuropathies. AION is due to interference with posterior ciliary artery supply to the optic nerve head and retrolaminar part of the optic nerve; it initially presents with visual loss and optic disc edema which progresses to optic atrophy in a month or two. PION is due to occlusion of nutrient arteries to the posterior part of the optic nerve; in this condition during the initial stages the optic disc is normal in spite of marked visual loss, but the atrophy develops later on. Their pathogeneses, causes, clinical pictures, diagnosis and management are discussed briefly.Some of the figures have been reproduced by courtesy of the British Journal of Ophthalmology (Figs. 2, 5, 7), American Academy of Ophthalmology and Otolarngology (Fig. 1) and Springer-Verslag (Fig. 8). This investigation was supported by Public Health Service Grant EY-01151.     

白内障超声乳化吸出术后并发前部缺血性视神经病变(AION)危险因素分析

目的 筛选出白内障超声乳化吸出术后并发前部缺血性视神经病变(anterior ischemic optic neuropathy,AION)的危险因素,初步探讨术后并发AION的发病机制.方法 收集2010年9月1日至2016年9月1日在郑州大学第一附属医院眼科行白内障超声乳化吸出术的手术病例,符合条件的病例为11 206例(13 320眼),其中白内障术后并发AION 30例30眼(AION组),以1∶3比例在纳入的其余病例中随机选取90例90眼作为对照组.记录AION组和对照组小视盘、既往手术史、心脏病、糖尿病、高血压、高脂血症、吸烟、颈动脉疾病、眼压等情况,采用x2检验、Logistic回归分析、t检验,筛选出白内障术后并发AION的相关因素及危险因素.结果 小视盘、糖尿病、高血压、高脂血症、颈动脉疾病为白内障术后并发AION的相关因素.高脂血症、颈动脉疾病为白内障术后并发AION的危险因素.术前两组患者眼压差异无统计学意义(P＞0.05);术后1d和7dAION组眼压均高于对照组,差异均有统计学意义(均为P＜0.05).结论 高脂血症、颈动脉疾病均为白内障术后发生AION的危险因素,术后眼压高可能是发生AION的诱因.     

前部缺血性视神经病变颈动脉超声改变的观察研究

目的：：探讨前部缺血性视神经病变( anterior ischemic optic neuropathy, AION)患者与颈动脉血管超声改变的关系。方法：对54例AION患者及同期进行健康体检者54例作为对照组,应用彩色超声诊断仪检测颈动脉超声影像学特征变化。结果：AION患者54例中38例出现颈动脉粥样硬化病变,占接受该项检查总数的70％,其中硬斑18例(33％),软斑13例(24％),混合斑7例(13％);对照组中检出粥样硬化20例,占接受该项检查总数的37％,其中硬斑12例(22％),软斑5例(9％),混合斑3例(6％);均未见颈动脉狭窄及明显流速改变。 AION患者组与对照组粥样硬化斑块的例数比较,差异有统计学意义(χ2=12.836,P=0.005)结论：AION的发生与颈动脉粥样硬化有相关性,颈动脉超声检查对查找AION的病因及诊断有重要的价值。     

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...     

Systemic corticosteroids in nonarteritic ischemic optic neuropathy

Nonarteritic ischemic optic neuropathy (NAION) is one of the most prevalent optic nerve disorders seen in ophthalmic practice. The role of corticosteroid therapy in NAION remains a highly controversial area of debate in ophthalmology. This brief review will provide an overview of the current clinical evidence on this topic as well as some comment on the medical debate.     

Two presentations of nonarteritic ischemic optic neuropathy

Background

Nonarteritic ischemic optic neuropathy (NAION) is the most common acute optic neuropathy in adults over the age of 50. Patients affected notice sudden and painless loss of vision in 1 eye, often upon awaking. Studies have found that the opposite eye may be affected in approximately 15% to 20% of cases within a 5-year period. NAION vision loss results from an ischemic event often affecting the short posterior ciliary arteries. This results in optic nerve pallor, nerve fiber layer defects, and corresponding visual field defects.

Case Reports

Two cases of NAION are discussed here. The first patient, a 57-year-old woman, had a 10-year history of visual symptoms, and the second, a 66-year-old man, presented in less than a week after first noticing symptoms. Both had predisposing systemic risk factors and resultant visual field loss and decreased visual acuity.

Conclusions

Predisposing factors for NAION include small cup-to-disc ratios of the optic nerve, obstructive sleep apnea, nocturnal hypotension, diabetes, and other vascular diseases. The vision loss is irreversible, and there is no known effective treatment to prevent subsequent disc atrophy or recurring episodes.     

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.     

前部缺血性视神经病变疗效欠佳临床分析

目的:分析非动脉炎性前部缺血性视神经病变(nonarteritic anterior ischemic optic neuropathy,NAION)治疗效果不满意原因,结合近年研究探讨治疗选择用药的依据。方法:NAION患者78例84眼,均提供有当地医院或首诊医院的荧光素眼底血管造影、眼底彩色相、视野、视力等资料,并符合NAION的诊断标准。治疗药物常选择糖皮质激素、血管扩张剂、高渗性脱水剂、营养神经药物等,同时应用或部分交叉应用,治疗时间1mo以上,从视力、视野、眼底、FFA,OCT检查结果分析药物治疗不满意的因素。结果:84眼经治疗后效果不满意患者,再次就诊时视盘水肿均消退,颜色明显变淡色泽不一致者65眼;视盘全部色淡不易分辨者19眼。复查造影,视盘部分轻度着色9例,其余视盘表现为无渗漏无着色。OCT检查31眼中盘周颞侧神经纤维厚度较正常人均值减少2/3者9眼,减少1/2者11眼,减少1/3者11眼,纵横十字扫描无视杯27眼,浅窄视杯4眼。所有病例在就诊时中心视力均较首诊医院治疗前下降4行以上,最多由1.5下降到0.04。11眼复查视野,结果缺损范围扩大>10°,或原相对缺损区变成绝对缺损区。糖皮质激素、血管扩张剂、高渗性脱水剂、营养神经药物等同时或部分交叉长期非个性化应用是导致疗效不满意的主要原因。结论:除疾病自身特点外,在发病后采取药物积极治疗及选择药物得当与否与疗效和预后密切相关,应尽可能缩短糖皮质激素应用时间,在NAION水肿期根据血黏度、血压、血糖、血脂、视杯形态采取针对性药物的个性化治疗,以提高疗效。     

Studies on the pathogenesis of anterior ischemic optic neuropathy

The pathogenesis of nonarteritic anterior ischemic optic neuropathy (AION) was investigated, on the basis of clinical findings from a patient with nonarteritic AION and experimental study of the vascular architecture of the human optic nerve head. The patient's visual field examination revealed a wide Bjerrum scotoma. This visual field defect suggests that the mechanism of the onset of nonarteritic AION might be similar to that of glaucoma. Fluorescein fundus angiography (FFA) findings suggest that the peripapillary choroidal circulation might recover more easily from perfusion disturbance than the rest. Further, experimental study of the human optic nerve heads revealed that the circle of Zinn forms a complete vascular circle and that small branches from this circle extend to the peripapillary choroid or the optic nerve head, and that the intraneural vascular meshwork is less dense than that in the retrolaminar portion. Based upon the above clinical findings and experimental results, the pathogenesis of nonarteritic AION is postulated as follows: (1) The blood flow in the circle of Zinn is decreased by stenosis of the posterior ciliary artery (PCA). (2) Hypoperfusion is produced in the whole optic nerve head. (3) As in glaucoma, arcuate nerve fibers are first affected, resulting in the onset of nonarteritic AION with arcuate visual field defect or altitudinal defect.