视神经乳头的微血管构筑

本文采用多种方法对100例200只人眼视乳头微血管构筑进行观察,结果表明:1.Zinn 氏血管环对视乳头的血液供应具有重要作用。该血管环分支供应视乳头的筛板前区,筛板区及筛板后区的软膜血管网。2.筛板前区的血液供应直接来自睫状后短动脉或 Zinn 氏血管环的分支,脉络膜的血管仅发出少数分支供应此区。以上两观察结果与 S、S、Hayreh 的观点不同。3.视网膜中央动脉与睫状后短动脉两系统间可以在筛板后区软膜血管网和视神经内建立吻合,但在视神经眼内段尚未见到明显吻合现象。4.视乳头的微血管构筑与其组织结构相适应。表层最浅层呈放射状;筛板前区及筛板区呈层状;筛板后区呈纵横交错状。筛板前区及筛板区毛细血管口径最细,提示此两区容易发生缺血性改变。     

缺血性视神经病变

缺血性视神经病变是老年人最常见的视神经病变,此病变分为前段缺血性视神经病变与后段缺血性视神经病变。前段缺血病变发生在视神经筛板及其前后,缺血导致视盘水肿并常伴视盘周围出血。后段缺血病变发生在视盘后的眶内段视神经,病变早期视盘外观正常,后期出现视神经萎缩。前后段缺血性视神经病变又再分为动脉炎性与非动脉炎性。     

视神经鞘减压术有关动脉的应用解剖

目的为视神经鞘减压术提供有关动脉解剖学资料。方法采用显微解剖和血管铸型技术对30个甲醛固定成人尸头和4个新鲜尸头视神经的鞘动脉等进行观察。结果鞘动脉可分为视神经管内支和眶内支。眶内支主要来自眼动脉第2段，占63．33％，也可发自眼肌动脉干等，其入鞘点多在眶内部鞘的后1／3段的上面或内侧面。管内支多从眼动脉的内侧壁发起，行于视神经腹侧面，以1支者多见，占61.67％，2支者占11.67％，3支者占5.00％。结论管内视神经鞘切开部位在鞘的外上壁或内上壁较安全，眶内鞘切开部位选在鞘的外侧面较好。     

视神经病眼动脉血流速度的临床研究

视神经疾病为危害视功能的严重疾病,其发病机理尚在研究中。文献报道视神经血液供应不良常导致视神经萎缩。睫状后动脉(眼动脉的主要分枝之一)是筛板区和筛板前区视神经血液供应的唯一源泉,也是筛板后区视神经主要供血来源,而视盘、视盘周围的血液循环与眼内压和睫状后动脉灌注压密切相关。当眼压与血压的平衡失调,睫     

视神经管周围结构解剖的实验研究

目的 了解视神经管周围结构的解剖并为临床视神经管减压术及鼻窦手术提供解剖学依据.方法 实验研究.(1)成人干性颅骨标本50个,观察和测量筛窦和蝶窦的形态和大小;(2)甲醛溶液固定的成年湿性头颅标本15个,观察和测量蝶窦中部外侧壁与颈内动脉的距离、眼动脉起始处与颈内动脉的夹角,测量视神经颅内段的长度、视神经于视交叉前方之间的夹角、视神经颅内段颅口处两侧视神经内侧缘之间的距离,测量眼动脉在视神经管内的长度和直径;(3)选取6例经甲醛溶液防腐固定的完整成年无明显病变的成年湿性头颅标本,应用CT对筛、蝶窦进行轴位和冠状位扫描,观察视神经管与筛、蝶窦的关系;然后将CT扫描后的湿性头颅标本利用工业用钢锯行筛、蝶窦的断面(6例)、水平断面(3例)、冠状断面(3例)解剖,层厚均为6 mm.将筛窦、蝶窦、视神经管的CT扫描图像和相对应的解剖断面标本进行对比、观察.采用SPSS 13.0统计学软件进行数据处理.男性与女性湿性颅骨标本的测量值比较,采用两组独立样本的t检验.结果 全筛窦前后径(39.02±4.89)mm,前部横径(12.26±2.12)mm,前筛窦上下径(11.89±2.56)mm;蝶窦前后径(24.08±4.87)mm,蝶窦中部外侧壁与颈内动脉的距离(1.23±0.56)mm;眼动脉起始处与颈内动脉的夹角54.33°±7.89°;视神经颅内段的长度(9.91±2.89)mm,两侧视神经于视交叉前方之间的夹角59.89°±4.79°,视神经颅口处两侧视神经内侧缘之间的距离(14.26±3.23)mm;眼动脉在管内段的长度(5.38±1.87)mm,眼动脉外径(2.18±0.37)mm.男性与女性间的视神经颅内段长度(t=0.25)、两侧视神经于视交叉前方之间的夹角(t=0.71)、视神经颅口处两侧视神经内侧缘之间的距离(t=0.57)、蝶窦中部外侧壁与颈内动脉的距离(t=0.29)、眼动脉起始处与颈内动脉的夹角(t=0.99)、眼动脉在视神经管内段的长度(t=0.50)、眼动脉外径(t=0.52)测量值比较,差异均无统计学意义(P>0.05).结论 (1)切开视神经管内侧壁时,在蝶窦内切开的深度不宜超过13 mm,否则有可能损伤颈内动脉并引起大出血;(2)在进行视神经管减压术时,穿破前部筛窦的左右深度不宜超过15 mm,上下不宜超过12 mm,否则易穿破到对侧筛窦或向上穿破颅底进入颅内;(3)应特别注意保护眼动脉,防止眼部缺血和失明.     

应用计算机辅助三维重建技术重建和测量视神经管和管内结构

目的　重建人视神经管和管内结构,为视神经减压术提供解剖参考数据,为进一步探索视神经间接损伤的病理机制提供形态学依据。方法　应用计算机辅助三维重建技术重建６ 例成人视神经管及管内结构,并用计算机图像分析系统测量视神经管的厚度,视神经管、管内段视神经、硬膜鞘、蛛网膜下腔的横截面积和蛛网膜下腔的容积。在重建的三维模型上,对管内各结构间的空间关系进行系统观察。结果　视神经管内壁中部厚度为（０－４５ ±０－３５）ｍｍ ,是视神经管壁最薄的部位。管中部横截面积为（１８－２１ ±２－５０）ｍｍ２ ,是视神经管最狭窄的部位。蛛网膜下腔在颅口、中部及眶口处的横截面积分别为（４－４５±１－１２）ｍｍ２、（２－６８±１－３２）ｍｍ２ 、（１－２３±０－８３）ｍｍ２ ,依次呈逐渐减小趋势,其容积为（２１－１６±４－３１）ｍｍ３,可能为损伤后视神经水肿、硬膜出血的代偿空间。结论　视神经管内代偿扩张的空间有限,所以视神经轻度水肿和视神经鞘内少量出血就可能使视神经受压。当视神经间接损伤后,视神经管最狭窄的中部对视神经的束缚作用可能最强,而从视神经管的颅口到眶口段,代偿扩张空间逐渐减小。因此,切实开放视神经管和硬膜鞘的中段和前段是视神经减压术成功     

视神经鞘膜内海绵状血管瘤一例

47岁女性,左眼视力逐渐下降伴色觉减退4年。视力光感,左侧相对性传入性瞳孔功能障碍(RAPD)阳性,鼻侧视盘色偏淡,视野缺损。眼眶MRI:左侧眶尖区眶内段视神经旁占位性病变,T1WI低信号,T2WI明显高信号,增强明显强化。经手术病理证实诊断为视神经鞘膜内海绵状血管瘤。(眼科,2022,31:204-206)     

管内段视神经间接损伤

前言远在西波格拉底时代，人们即知道前额部受到撞击可发生同侧的视力障碍。Berlin于1879年首先对此病描述，并将此种视力障碍称之为视神经管骨折。此后逐渐引起眼科及耳鼻喉科医生的重视和注意。直至今日，人们大多认为外伤性视神经损伤的主要原因是外伤引起的视神经管骨折，但是对于其发生机制及治疗，一直存在争议。视神经按解剖位分，可分为球内段（长0．7mm）眶内段（长30mm），管内段（长6－10mm）颅内段（长10mm）。球内段是指视神经与眼球的连接部，由于外伤，可引起此部的离断，即视神经撕脱。此种情况偶可见到，但非常稀少。眶内…     

急性后部缺血性视神经病变

急性缺血性视神经病变系视神经的营养血管发生急性循环障碍而出现的一种营养不良性疾患。若以视网膜中央动脉进入视神经处为界(约在眼球后10mm),可将视神经分为前、后两部分。那末,由于这两部分的血液供应不同,发生缺血时的临床表现也迥然不同。在缺血的早期,前者呈特征性的视乳头水肿,而后者却表现为正常的视乳头外观。关于急性前部缺血性视神经病变的临床特征、诊断及治疗,本刊已有综述。而对于后部缺血性视神经病变(简称PION),由于人们对视神经后部(包括眶内段、管内段及颅内段)     

视神经胶质细胞的培养及其特征观察

目的 体外培养、分离、纯化P2期小鼠视神经胶质细胞，并观察其生物学特性。方法 经颅开眶获取P2期小鼠管内段视神经2mm，组织块法培养，振荡法分离纯化，免疫组织化学方法鉴定，流式细胞仪检测纯度。结果 视神经星形胶质细胞体外迅速分裂增殖，少突胶质细胞生长缓慢，传代困难，振荡法分离纯化的细胞纯度高，星形胶质细胞GFAP染色阳性，阳性率96．2％，少突胶质细胞MBP染色阳性，阳性率96％。结论 组织块法培养、振荡法分离纯化P2期小鼠视神经星形和少突胶质细胞纯度高，是进一步研究视神经胶质细胞的结构和功能的可靠材料。     

Lack of blood-brain barrier properties in microvessels of the prelaminar optic nerve head

PURPOSE: To define the blood-brain barrier (BBB) characteristics of microvessels in the optic nerve head (ONH). METHODS: Immunohistochemical staining of different regions of the ONH, retro-laminar optic nerve, and retina of human and monkey eyes was carried out, using antibodies against BBB markers (glucose transporter 1, transferrin receptor, and P-glycoprotein), the non-BBB marker PAL-E, and against plasma proteins fibrinogen and IgG, which serve as endogenous markers of nonspecific microvascular permeability. In the ONH of monkey eyes, the number of transport-related endothelial pinocytotic vesicles and their cellular distribution within the microvessels were determined by electron microscopy. RESULTS: In both human and monkey eyes, only microvessels in the prelaminar region of the ONH were positive for the PAL-E antigen. The prelaminar region microvessels showed either no or weak expression of the transferrin receptor and P-glycoprotein but stained positive for glucose transporter 1. In human ONH, fibrinogen and IgG were present around microvessels in the prelaminar region but not in other parts of the optic nerve or retina. By electron microscopy, endothelial cells of prelaminar region microvessels contained a higher number of pinocytotic vesicles, located at the luminal and abluminal side of the endothelial cell membrane, in contrast to a mainly abluminal localization in microvessels of the retina and other parts of the optic nerve. CONCLUSIONS: Microvessels in the prelaminar region of the ONH lack classical BBB characteristics and display nonspecific permeability, possibly mediated by vesicular transport.     

Cyclooxygenase-1 and Cyclooxygenase-2 in the Human Optic Nerve Head

To investigate the hypothesis that eicosanoids act as cellular mediators in the optic nerve head of normals and of patients with glaucoma, we have determined the presence of the two cyclooxygenase (COX) isoforms in human tissue. Histological sections of optic nerve heads were studied by immunohistochemistry. Age matched normal donors were compared with eyes from glaucoma patients with moderate to severe nerve damage. Polyclonal antibodies to human COX-1 and COX-2 were localized with immunoperoxidase staining. Specific antibodies for vascular endothelia and microglia were also co-localized. In normal and glaucomatous eyes, COX-1 was localized exclusively to the prelaminar and lamina cribrosa regions of the optic nerve head. No staining for COX-1 was observed in the nerve fiber layer or the myelinated optic nerve. COX-1 was associated with the astrocytes of the glial columns and the cribriform plates, but not with the endothelia lining the capillaries. In glaucoma, more astrocytes appeared to be stained with antibody to COX-1 than in normals and staining was intensely perinuclear. There was no staining for COX-2 in normal tissue. A few COX-2 positive cells were found in the prelaminar, lamina cribrosa and postlaminar regions of the glaucomatous optic nerves. Positive staining for COX-2 was not associated with microglia. COX-1 is constitutively present in astrocytes that are localized exclusively to the prelaminar and lamina cribrosa regions of the human optic nerve head. Eicosanoids, synthesized by COX-1 in this tissue, may have a homeostatic and a neuroprotective role related to the axons of the retinal ganglion cells. The sparse presence of COX-2 in glaucomatous tissue probably reflects the lack of inflammation associated with glaucomatous optic neuropathy.     

Posterior ischemic optic neuropathy. I. Blood supply of the optic nerve

The blood supply of the posterior optic nerve was investigated in 10 monkeys after an injection of synthetic resin into the carotid arteries. The posterior intraorbital and intracanalicular optic nerves were supplied by a centripetal vascular system, formed by the pial vessels arising from the first branches of the ophthalmic artery. Superior and inferior vascular semicircles were detected in the intracanalicular optic nerve. The intracranial optic nerve was supplied by branches of the internal carotid artery, anterior cerebral artery and/or anterior communicating artery, and ophthalmic artery.     

Axonal transport and cytoskeletal changes in the laminar regions after elevated intraocular pressure

PURPOSE: To investigate the axonal cytoskeleton changes occurring in the prelaminar region, lamina cribrosa, and postlaminar region of the porcine optic nerve after an acute increase in intraocular pressure (IOP) and whether this corresponds with axonal transport abnormalities. METHODS: Six white Landrace pigs were used. The left eye IOP was elevated to 40 to 45 mm Hg for 6 hours, and the right eye IOP was maintained between 10 and 15 mm Hg. Rhodamine-beta-isothiocyanate (RITC) was injected into the vitreous of each eye at the beginning of the experiment, to study axonal transport. After euthanasia, optic nerves were removed and prepared for axonal transport and cytoskeleton studies. Antibodies to phosphorylated neurofilament heavy (NFHp), phosphorylation-independent neurofilament heavy (NFH), neurofilament light (NFL), neurofilament medium (NFM), microtubule, and microtubule-associated protein (MAP) were used to study the axonal cytoskeleton. Montages of confocal microscopy images were quantitatively analyzed to investigate simultaneous changes in optic nerve axonal transport and cytoskeletal proteins in the high-IOP and control eyes. RESULTS: Axonal transport of RITC was reduced in the prelaminar, lamina cribrosa, and proximal 400 mum of the postlaminar optic nerve regions in the high-IOP eye. NFHp, NFM, and NFH were significantly reduced in the prelaminar, lamina cribrosa, and proximal postlaminar regions in the high-IOP eye. No differences in NFL, MAP, and tubulin staining were detected. CONCLUSIONS: Elevated IOP induced both axonal transport and cytoskeleton changes in the optic nerve head. Changes to the cytoskeleton may contribute to the axonal transport abnormalities that occur in elevated IOP.     

Role of axoplasmic transport in the pathophysiology of ischaemic disc swelling.

Pathological changes in the optic disc and anterior part of the optic nerve of monkeys were studied 5 hours and several days after occlusion of the temporal short posterior ciliary arteries. Ischaemic vacuolation of neural tissue was observed in some of the animals studied and was restricted to the lamina cribrosa and the immediately retrolaminar portion of the optic nerve. Axonal swelling and organelle aggregation were demonstrated in the prelaminar region, and autoradiography after intravitreal injection of tritiated leucine revealed an associated obstruction of rapid and slow orthograde axoplasmic transport. The experimental findings correlate with those seen clinically in acute ischaemic optic neuropathy. The pale swelling of the optic disc in this condition represents an accumulation of axoplasmic debris in retinal ganglion-cell axons owing to obstruction of axoplasmic transport at the lamina cribrosa; it is thus equivalent to a 'cotton-wool spot' of the disc.     

筛板前组织的OCT影像检测及其与眼病的关系

筛板前组织是位于视乳头筛板前区的结构性组织,其与筛板组织一样均为青光眼性视神经损害中不可缺少的部分.筛板前组织厚度可通过OCT观察,其在眼压增高及缺血时会变薄,在青光眼术后眼压降低时会增厚.所以探索筛板前组织的变化可能有利于揭示青光眼的发病机制,并为青光眼随诊提供临床生物学指标.此外,也有些研究发现筛板前组织变化与缺血性视神经病变、糖尿病视神经病变、视网膜色素变性相关.     

Optic nerve axoplasm and papilledema

A detailed review of optic nerve axoplasm is presented. A number of hypotheses have been postulated for the pathogenesis of papilledema associated with increased intracranial pressure. These hypotheses, mechanical and nonmechanical, are critically evaluated in relation to five essential features of papilledema. Theories, as well as clinical and experimental studies, of axonal transport are reviewed, and a new hypothesis is proposed: Papilledema is primarily a mechanical, nonvascular phenomenon in which an excess amount of extracellular fluid is present in the prelaminar region ofthe optic disc and the accumulation of that fluid results from the leakage of axoplasm from optic nerve fibers which are compressed posterior to the lamina cribrosa of the optic disc. The authors believe that this is the only existing hypothesis consistent with all the known facts about papilledema. Discussions by Drs. J. Terry Ernest, Thomas R. Hedges, and S. S. Hayreh follow the review.     

Does the blood-brain barrier play a role in Glaucoma?

The optic nerve head, although part of the central nervous system, lacks classical blood-brain barrier properties. The tissue of Elschnig does not totally separate the optic nerve head from fenestrated peripapillary choriocapillaries. The microvessels in the prelaminar region of the optic nerve head have less effective barriers than those in the laminar or retrolaminar regions. In glaucoma, the blood-brain barrier in the optic nerve head may even be weaker. Incomplete blood-brain barrier renders circulating molecules, such as endothelin-1 (ET-1), direct access to smooth vascular muscle cells and pericytes both in the prelaminar part of the optic nerve head and to adjacent retinal tissue. This potentially leads to some vasoconstriction as observed in the peri-papillary retinal vessel in glaucoma patients. In extreme situations, this may provoke retinal vein occlusion. The direct access of these molecules also influences the barrier function. If, simultaneously, ET-1 reduces endothelial tight-junctions and matrix-metalloproteinase (MMP)-9 degrades the basement membrane, not only macromolecules but even red blood cells may cross the blood-brain barrier and lead to what is clinically observed as optic disk hemorrhages.     

应用OCT探究眼压与筛板参数的关系

筛板的变形与血流减少一直被视作青光眼视神经轴突损伤的首发因素.病理性眼压升高与青光眼的发生发展间有紧密关系.通过OCT技术衡量筛板及周边参数随眼压变化来研究青光眼发病机制受到了广泛关注.研究表明筛板深度(LCD)、筛板前表面厚度(PTT)、筛板曲率指数(LCCI)以及视盘血管密度等参数均与眼压具有相关性.眼压升高可对筛...     

The interaction between intracranial pressure,intraocular pressure and lamina cribrosal compression in glaucoma

This review examines some of the biomechanical consequences associated with the opposing intraocular and intracranial forces. These forces compress the lamina cribrosa and are a potential source of glaucomatous pathology. A difference between them creates a displacement force on the lamina cribrosa. Increasing intraocular pressure and/or decreasing intracranial pressure will increase the trans‐lamina cribrosa pressure difference and the risk of its posterior displacement, canal expansion and the formation of pathological cupping. Both intraocular pressure and intracranial pressure can be elevated during a Valsalva manoeuvre with associated increases in both anterior and posterior lamina cribrosa loading as well as its compression. Any resulting thinning of or damage to the lamina cribrosa and/or retinal ganglion cell axons and/or astrocyte and glial cells attached to the matrix of the lamina cribrosa and/or reduction in blood flow to the lamina cribrosa may contribute to glaucomatous neuropathy. Thinning of the lamina cribrosa reduces its stiffness and increases the risk of its posterior displacement. Optic nerve head posterior displacement warrants medical or surgical lowering of intraocular pressure; however, compared to intraocular pressure, the trans‐lamina cribrosa pressure difference may be more important in pressure‐related pathology of the optic nerve head region. Similarly important could be increased compression loading of the lamina cribrosa. Reducing participation in activities which elevate intraocular and intracranial pressure will decrease lamina cribrosa compression exposure and may contribute to glaucoma management and may have prognostic significance for glaucoma suspects.