中西医结合治疗视神经炎

中西医结合治疗视神经炎河南省眼科研究所郭茜如，李舒茵，种平，赵名媛视神经炎是常见眼底病之一．中医根据视力下降的急缓将其归于暴盲，视瞻昏渺范畴．若不进行积极有效的治疗后期可因视神经萎缩而导致祝功能严重损害．由于病因复杂目前对本病尚无规范的治疗方法，我们...     

高压氧治疗管内段视神经间接损伤三例报告

早在19世纪,Battle就将因视神经管骨折或管内段视神经受挫伤所致的视神经损伤称为间接损伤,以区别于因异物穿通伤所致的视神经直接损伤。本病视力受损非常严重,早期诊断及时治疗可挽救部分视力。我们用高压氧对3例管内段视神经间接损伤进行治疗,似有一定疗效,现报告如下。     

中西医结合治疗视神经炎

中西医结合治疗视神经炎山东中医学院附院伊成运视神经炎是一种严重危害病人视力的眼病，亦是目前致盲的主要眼底病之一。根据炎症发病部位、眼底体征表现，分为视神经乳头炎和球后视神经炎。本病发病急，病程短。近几年我们采用以中药为主，部分病例适当配合少量激素的治...     

颅脑外伤合并视神经损伤

目的 探讨颅脑外伤合并视神经损伤的诊断、治疗方法,评价其治疗后的视力恢复情况.方法 对25例(25眼)颅脑外伤合并视神经损伤患者中20眼行非手术保守治疗,5眼进行视神经管减压手术.结果 视神经损伤保守治疗20眼中,13眼视力不同程度提高;5眼进行视神经管减压手术3眼视力提高.结论 对颅脑外伤合并视神经损伤的诊断、治疗要足够重视;在救治颅脑外伤的同时,应注意观察、抢救视神经损伤,挽救残余视力.有手术指征者要争取时间尽早进行视神经管减压术.     

非动脉炎性缺血性视神经病变的相关研究进展

非动脉炎性前部缺血性视神经病变是50岁以上人群较常见的一类缺血性视神经病变,表现为突发无痛性视力下降、典型视野缺损、有特征性进展模式的视乳头水肿等.视乳头血循环短暂的无灌注或低灌注是其主要病因,但可能不是血栓栓塞性疾病.本病高发于高血压病、动脉粥样硬化、糖尿病、缺血性心脏病、高脂血症、代谢综合征等患者.视乳头小视杯是其发病的主要局部因素.夜间动脉低压是重要的发病促成因素.除眼底荧光素血管造影及视野检查外,光学相干断层扫描检查可随访、监测视乳头水肿变化.本病的视力预后与患眼缺血的严重程度和持续时间有关,早期大剂量糖皮质激素治疗有利于改善视力和视野.但目前对其病因、发病机制、临床特点及治疗等仍存在许多争论.     

外伤性玻璃体积血中药疗效分析

目的分析外伤性玻璃体积血患者应用中医辨证治疗效果。方法对56例外伤性玻璃体积血根据其出血早晚分别采用中药凉血止血活血化瘀治疗。结果42例显效(占75.00%),获得满意视力。14例无效,其中7例经玻璃体切除术亦获得满意视力;5例因严重视神经损伤,视功能丧失;其余2例因视神经挫伤合并视网膜脱离。视功能丧失未坚持治疗。结论中医辨证治疗外伤性玻璃体积血是一种有效措施。     

管内段视神经间接损伤

管内段视神经间接损伤,系指视神经管骨折所致或管内段视神经受挫伤所致视神经损伤。本病视力损失严重,甚至无光感。只有早期诊断及时治疗,部份患者尚可不同程度恢复视力。我院近1年半遇15例,现报告如下:     

颅脑外伤合并视神经损伤临床分析

目的分析颅脑外伤合并视神经损伤的临床表现,评价其疗效。方法回顾性颅脑外伤合并视神经损伤26例(28只眼)患者的诊断、手术治疗及药物治疗后的视力恢复情况。结果视神经损伤后光感或光感以上者20只眼中,18只眼视力不同程度提高;无光感8只眼中,3只眼视力提高;3例(3只眼)行视神经管减压术者视力提高。结论在第一时间救治颅脑外伤的同时,应抢救视神经损伤后尚存活的神经元,挽救残余视力。确诊后以CT检查有视神经受压迫的阳性征象者,不论有无光感均应及早手术;无阳性征象者及早药物治疗,多途径给药,疗效较好。伤后立即失明者效果差。     

以急性视神经炎首发的多发性硬化视神经功能障碍分析

目的 探讨以急性视神经炎(acute optic neuritis,AON)为首发的多发性硬化(multiple sclerosis,MS)视神经功能的改变特点,及时治疗并尽大可能恢复视神经功能.方法 对每例以视神经炎为首发的MS患者行视力、眼底、视野及视诱发电位检查,部分患者行CT或者MRI,脑脊液测定和寡克隆区带检查.采用χ2检验与t检验对患者视神经功能改变的特点进行分析.结果 (1)视神经功能检查:所有患者均有视力下降;不同程度的视神经萎缩、视神经乳头水肿表现;客观检查显示视野损害、视诱发电位、色觉异常;与无伴AON的MS患者进行比较,在视力下降及视神经乳头水肿方面差异均有统计学意义;视诱发电位检查均存在异常,表现在P100潜伏期延长,AON组异常率为63.6%～72.7%,无伴AON的MS组为21.4%～28.5%,两组相比差异有显著性意义(P＜0.05).(2)脑脊液免疫球蛋白检查:视神经炎鞘内IgG合成率低于无伴AON组(P＜0.01).(3)所有患者经大剂量肾上腺素糖皮质激素及时治疗后,视力恢复到0.5以上者约31.2%～36.3%.结论 AON是MS的最常见症状之一,视神经炎与MS视神经脊髓炎型的视神经损害发生频率高且程度重,迫切需要对AON患者进行早期诊断,并及时给予大剂量肾上腺素糖皮质激素治疗.     

中医辩证治疗间接性视神经损伤

头颅、面部损伤 ,特别是眼眶周围损伤 ,常造成视神经损伤 ,致视力锐减。而检眼镜检查无眼球及视神经改变 ,称之为间接性视神经损伤[1] 。它严重影响患者视力 ,给工作、生活造成极大不便及精神痛苦 ,临床治疗比较困难。根据外伤性视神经的发生机制 ,特别是眶部受冲击时的视神经管内视神经的病理学特性[2 ] 等 ,外伤后应早期积极应用药物治疗 ,减少视神经内实质水肿、炎症反应、加强营养并修复受损伤的视神经。对治疗视神经损伤及间接性伤都是有很重要的意义。有关外伤性视神经损伤的治疗有很多方法 ,特别是中药疗法取得了可喜的效果。探讨一…     

原发性开角型青光眼的中医分型与RNFL厚度改变及视野损害关系

目的:探讨原发性开角型青光眼(青风内障)中医辨证分型与视网膜神经纤维层厚度的改变及视野损害之间关系的临床研究。方法:对72例144眼原发性开角型青光眼患者,采用光学相干断层成像术对144眼作围绕视盘3.4mm的环形扫描,记录各个象限视网膜神经纤维层厚度,并采用进口Humphry视野分析仪作中30°全定量视野检测检查,同时根据中医理论对患者作中医辨证分型,观察二者之间的关系。结果:中医的证型与视网膜神经纤维层厚度改变类型有统计学意义,中医证型与视野损害的类型有统计学意义(P<0.05)。结论:视神经损害较严重多见于青风内障的虚证,视神经损害早期多见于实证,因此视神经损害的程度在一定的程度上给予中医辨证治疗一定的指导作用。     

疏肝通窍法对青光眼视神经损害大鼠视网膜神经节细胞凋亡及视网膜、视神经超微结构的影响

目的：通过观察视网膜神经节细胞（RGCs）计数和视网膜、视神经超微结构及形态学变化,研究疏肝通窍法保护高眼压损害的视神经的作用机制,为开发保护青光眼视神经的有效中药方剂提供参考。方法：实验研究。以SD大鼠为实验动物,右眼前房注射复方卡波姆溶液建立慢性高眼压模型（90只）。将不同时间窗（1周、2周、3周）的慢性高眼压大鼠模型分别分为模型组（5只）、阴性对照组（5只）、阳性对照组（5只）、低剂量通窍明目4号治疗组（低剂量治疗组） （10 gkg-1d-1,5只）、中剂量治疗组（20 gkg-1d-1,5 只）和高剂量治疗组（40 gkg-1d-1,5 只）,以具有疏肝通窍作用的通窍明目4 号灌胃为干预手段,运用CMIAS系列数码医学图像分析系统观察RGCs计数,电镜观察视网膜、视神经超微结构,采用one-way ANOVA法和LSD法进行数据分析。结果：①RGCs计数：随着高眼压持续的时间延长,RGCs计数逐渐减少（F=87.67、29.69、33.38、38.03、33.67、23.36,P<0.001）,经药物治疗后,高眼压持续1周、2周和3周各组的高中剂量治疗组RGCs的存活量明显增加,与阴性对照组和阳性对照组比较差异均有统计学意义（P<0.001）。②模型组和阴性对照组视网膜结构排列紊乱,厚度变薄,空泡变性,细胞萎缩坏死,各治疗组视网膜的结构紊乱减轻,各层厚度略增加,空泡变性减少,细胞萎缩程度减轻。③模型组和阴性对照组视神经轴突排列紊乱,密度降低,微丝溶解,空泡样变,细胞器肿胀破坏,髓鞘变性,各治疗组视神经髓鞘的水肿程度减轻,髓索的变性有所修复,线粒体的水肿程度也减轻。结论：通窍明目4 号可以改善高眼压大鼠模型RGCs生存的微环境,保护未受损的细胞,修复轻度受损的RGCs,延缓或阻止部分受损细胞的下行性改变,减少高眼压大鼠模型RGCs的凋亡。疏肝通窍法对青光眼视神经损害具有保护作用。     

非动脉炎性前部缺血性视神经病变的治疗进展

非动脉炎性前部缺血性视神经病变(NAION)作为一组常见的严重危害视功能的视神经疾病,是由于睫状后短动脉灌注不足,使视神经发生急性缺血、结构以及功能紊乱,最终导致视力下降、甚至视力丧失。该病的病因和发病机制复杂,目前认为是局部解剖因素、全身血管危险因素等多因素共同参与,导致治疗上没有明确、统一、公认的治疗方案,早期发现、诊断和治疗对NAION的预后影响极大。目前治疗主要包括:对因治疗、药物治疗、中医治疗、联合用药、视神经鞘减压术、辅助治疗及外泌体治疗。随着近年各类抗NAION药物的不断发展和运用,提出了多种治疗方法,尤其以外泌体为研究热点,被广泛关注。为了更好地治疗NAION、提高治愈率、指导临床工作,本文主要对NAION的近年来的治疗进展做出以下综述。     

Hereditäre Optikusneuropathien

Hereditary optic neuropathies are caused by mutations either in the nuclear or mitochondrial genome and lead to retinal ganglion cell death mediated by reduced oxidative phosphorylation, fragmentation of the mitochondrial network, and increased sensitivity to apoptosis. Nuclear mutations result in autosomal dominant optic atrophy, autosomal recessive optic atrophy, or X-linked recessive optic atrophy, whereas mitochondrial mutations result in Leber’s hereditary optic neuropathy, which is maternally inherited. A tentative diagnosis of a hereditary optic neuropathy can usually be made on the grounds of a thorough patient and family history, visual field and color vision tests, and a detailed assessment of the optic nerve head. The rarity of hereditary optic neuropathies makes it difficult to include these disorders in the differential diagnosis. Molecular genetic testing of a blood DNA sample should be performed on every patient, with implications for future genetic counseling and prediction of the disease course.     

Dominant infantile optic nerve atrophy

The authors present an account of a family with an autosomal dominant infantile atrophy of the optic nerve. In three generations two men and three women were affected. With the clinical picture of simple atrophy of the optic nerve with a different degree of expressivity corresponded functional and fluoroangiographic changes. Disorders of colour vision were within the range of deuteroanomaly, deuteroanopia. The proband suffered also from tritanopia. The disease did not call for amaurotic training.     

Acquired optociliary shunt vessels in papilloedema.

Seven cases are presented in which prolonged papilloedema led to the development of acquired optociliary shunt vessels. These vessels may also be found with optic nerve tumours, particularly spheno-orbital meningiomas, optic nerve drusen, glaucoma, and after central retinal vein occlusion. Two patients had intracranial tumours, 4 benign intracranial hypertension, and one Crouzon's disease. Three had marked atrophic changes of the disc. The pathophysiology of the disc changes is discussed. The triad of long-standing poor vision, acquired optociliary shunts, and optic atrophy with blurred disc margins should not be regarded as specific for spheno-orbital meningioma.     

Hypovolemic ischemic optic neuropathy.

BACKGROUND: Ischemic optic neuropathy refers to an acute event of ischemia, or decreased blood flow, to the optic nerve resulting in varying degrees of vision loss and visual field defects. Typically this disease affects the elderly population who experience systemic diseases that compromise the blood flow efficiency of the optic nerve head (e.g., giant-cell arteritis, hypertension, diabetes, etc.). However, cases of blood loss to the optic nerve, secondary to traumatic injuries or surgeries, have also been shown to result in ischemic optic neuropathy, regardless of age. It seems that in these cases, the resulting anemia and hypotension play contributing roles in the development of ischemic optic neuropathy. METHODS: A 41-year-old black man came to us with optic nerve head pallor O.S., count-fingers vision O.S., positive afferent pupillary defect O.S., and a central scotoma O.S. after being hospitalized and treated for a stab wound to his left neck that severed his left carotid artery at the bifurcation. RESULTS: This patient had been seen in the Optometry Clinic two years before the stab-wound incident. At that time, he had 20/20 vision in his left eye and no remarkable neurological deficits. His ocular presentation after the traumatic hypovolemic event was probably a direct result of the hypoperfusion to the left optic nerve head. This patient was diagnosed with a hypovolemic, or blood loss-related, ischemic optic neuropathy (O.S.). CONCLUSIONS: Patients who experience large amounts of blood loss due to trauma, surgery, internal bleeding, etc. and report vision loss should be screened for possible optic nerve ischemia. As eye care providers, when we are presented with patients who have optic nerve head atrophy, we should inquire about events that may have precipitated blood loss, potentially triggering ischemic optic neuropathy.     

甲状腺相关视神经病变的研究进展

甲状腺相关视神经病变是甲状腺相关眼病的继发性病变，临床表现包括视力下降、色觉受损、相对性传入性瞳孔障碍、视盘水肿或萎缩等。眼科辅助检查表现为视野异常和视觉诱发电位异常等，影像学检查显示眶尖拥挤可辅助诊断。目前此病的发病机制未明，既往研究提出其与视神经压迫、牵拉和缺血有关。治疗方法包括大剂量糖皮质激素静脉冲击治疗、眼眶减压手术、眼眶放射治疗和生物制剂等。本文主要回顾流行病学特征、发病机制及临床诊治等方面的进展，以期为临床实践和研究提供参考。     

低视力患者视力与色觉的相关性

为了解低视力患者视力与色觉的相关关系,选取了视网膜色素变性,青光眼及视神经萎缩患者对其进行视力与色觉水平的测定。根据视力与色觉的相关关系可指导低视力患者的视觉康复。     

X-recessive angiopathic opticopathy

A familial optic atrophy with X-recessive heredity, distinct from Leber's optic atrophy (LOA), is described. The symptoms are: slight to moderate pallor of the papillomacular bundle at the disc possibly preceded by some hyperaemia of the disc, telangiectasia on the disc with normal retinal vessels, occurrence in the second decade of life, slow progression with often subclinical visual loss, a small relative central scotoma with an intact peripheral visual field, slight acquired tritanopia and deuteranopia, and vasomotor headaches. The disease may exhibit severe exacerbations with loss of vision to 1/60, provoked by vasoconstrictors and reacting favourably to vasodialators. This acute loss of vision is associated with ischaemia of the disc, a deep central scotoma with marked disturbance of colour vision in the form of an acquired deuteranopia, and sensoparalytic pupils. This is followed by increasing pallor of the disc, slow resolution of the central scotoma with a permanent reduction in the central light sensitivity, markedly disturbed Visual Evoked Potentials (VEP), acquired deuteranopia and normal ERG and EOG.In contrast to all hereditary opticopathies so far described, fluorescein angiography showed a disturbance of perfusion in the peripapillary choroid and the prelaminar part of the optic nerve. A similar disturbance of perfusion is described in anterior ischaemic optic neuropathy (AION) and low-tension glaucoma. To these acquired, non-hereditary vascular opticopathies, which usually occur late in life, will have to be added the X-recessive vascular optic atrophy which we describe here, for which we propose the name: X-recessive angiopathic opticopathy. The differential diagnosis from some other hereditary, especially X-recessive, optic atrophies is discussed.