青光眼与正常人视神经纤维层厚度测量

目的 客观测量和比较青光眼病人与正常人视网膜神经纤维层厚度。方法 用神经纤维分析仪对１５例开角青光眼病人及２５例正常人视盘区神经纤维层厚度进行测量,然后经计算机自动分析求出上,下,颞,鼻４个区ＲＮＦＬ厚度及平均厚度,所得数据经统计学分析。     

人眼视神经组织形态学研究视神经纤维计数和直径及视盘面积的测定

目的通过测量正常人眼视神经纤维数量、直径及视盘面积,为青光眼视神经损害研究奠定基础,并对其相互关系进行分析。方法应用一种计算机图像分析系统对15只正常人眼视神经断面和视盘进行检测。结果平均视神经纤维数为（10.08±1.61）×10⁵,神经纤维平均直径为（0.99±0.04）μm,平均视盘面积为（2.28±0.61）mm²。视神经纤维数随神经断面面积的增加而增加,而与视盘面积无关。结论本研究为临床推测视神经损害的预后及进一步研究青光眼的神经损害奠定了一定的基础。(中华眼底病杂志,1999,15:16-19)     

青光眼视神经损害的研究进展

本全面综述了有关青光眼视神经损害的病因研究。尤其重点阐述了近年来国内外的研究动态，概述了视浮头和解剖和发病机理的两种学说，介绍了关于青光眼视乳头血液改变以及神经胶质，轴索、细胞外基质等的改变对视神经损害的影响，较说细地描述了巩膜筛板在青光眼视神经损害中所起的作用及轴浆流的病理改变特点。这些研究为进一步认识和治疗青光眼提供了有意义的资料。     

益眼明对青光眼视神经的保护作用

目的探讨益眼明口服液对眼压已控制的青光眼患者视神经的保护作用。方法选择有视野缺损、眼压控制在≤18mmHg的原发性开角型青光眼患者52例101眼,随机分为试验组27例53眼和对照组25例48眼。对照组仅用噻吗心胺滴眼液点眼,试验组同时应用噻吗心胺滴眼液点眼及益眼明口服液每日3次口服,连续用药12周;观察用药前后视力、眼底的变化,分别于用药后4、8、12周检测视野平均敏感度（MS）、平均缺损值（MD）和丢失方差（LV）等指标,并与其术前值进行比较。结果用药前后各时间点试验组和对照组视力及眼底均未见明显改变。试验组用药4周后患者视野MS值明显高于用药前,差异有统计学意义（t=4.009,P=0.000）;MD值明显低于用药前,差异有统计学意义（t=-2.587,P=0.013）。用药后8周,患者视野MS值明显高于用药前值,差异有统计学意义（t=8.848,P=0.000）;MD和LV值明显下降,差异均有统计学意义（t=-3.874,P=0.000;t=-2.868,P=0.006）。试验组用药12周后,MS值的升高、MD与LV的下降与用药前比较差异均有统计学意义（t=5.086,P=0.000;t=-2.580,P=0.013;t=-2.765,P=0.008）。结论益眼明口服液对原发性开角型青光眼患者的视神经有一定程度的保护作用。     

青光眼的视神经保护治疗

视网膜神经节细胞死亡是青光眼视神经损伤的最终共同通路,阻断或延缓神经节细胞原发性和(或)继发性损伤的治疗方法称为青光眼视神经保护治疗。目前这一领域的研究包括基因治疗、谷氨酸拮抗剂、钙通道阻滞剂、自由基清除剂、NO合成酶抑制剂、β受体阻滞剂、α2-肾上腺素能受体激动剂、疫苗接种等。在未来的青光眼治疗中视神经保护治疗很可能成为一种重要的辅助治疗措施,将和包括降眼压药在内的其他手段一起来减少各种原发性和(或)继发性致病因素对视网膜神经节细胞的损伤。     

凋亡调节蛋白Bcl-2 相关死亡因子Bad在正常人眼视神经组织中的表达

目的 探讨促凋亡蛋白Bcl-2相关死亡因子Bad在正常人眼视神经组织中的表达及其意义。方法 采用免疫组织化学SP法观察8例正常人眼视神经组织中Bad蛋白的表达情况。结果 Bad蛋白表达在正常人眼视神经髓鞘部位，在无髓鞘组织即筛板前视神经及束间隔处未见表达。结论 Bad蛋白可能参与维持正常人视神经组织的生理过程。     

The effect of age on normal human optic nerve fiber number and diameter

In one optic nerve from each of 19 persons, the authors determined the number of axons, the distribution of fiber diameter, and the total neural area. The mean fiber count was 693,316, the mean neural area was 5.17 mm2, and the mean axonal fiber diameter was 0.96 microns. No significant decline in fiber number or neural area with increasing age was found. The authors found a large variability of axonal number among their patients. This variability would have obscured any small effect of aging. Linear regression analysis of the effect of age on mean axonal diameter yielded a slight negative slope (P less than 0.01), suggesting a redistribution of fiber diameter. This could occur from axonal shrinkage, from preferential large fiber loss, or from the technical features of tissue acquisition and analysis. The authors suspect that the explanation is a selective loss of large nerve fibers.     

The normal human optic nerve. Axon count and axon diameter distribution

Computerized image analysis was used to determine the normal axonal count and axon diameter distribution in 12 normal human eyes. Mean axon count per nerve was 969,279 +/- 239,740 and mean axon diameter was 0.72 +/- 0.07 micron. Multiple linear regression disclosed 4909 axons lost yearly (P = 0.08). Statistical analysis did not show a relationship between axon diameter and age or time to fixation. The inferotemporal sector of the nerve had the highest fiber density (P = 0.02). The superonasal nerve had higher mean diameters (P = 0.02). This study may provide a baseline for future pathologic studies.     

Expression of myocilin/TIGR in normal and glaucomatous primate optic nerves

Myocilin/TIGR was the first molecule discovered to be linked with primary open angle glaucoma (POAG), a blinding disease characterized by progressive loss of retinal ganglion cells. Mutations in myocilin/TIGR have been associated with age of disease onset and severity. The function of myocilin/TIGR and its role in glaucoma is unknown. Myocilin/TIGR has been studied in the trabecular meshwork to determine a role in regulation of intraocular pressure. The site of damage to the axons of the retinal ganglion cells is the optic nerve head (ONH). The myocilin/TIGR expression was examined in fetal through adult human optic nerve as well as in POAG. Myocilin/TIGR was expressed in the myelinated optic nerve of children and normal adults but not in the fetal optic nerve before myelination. Also examined was the expression in monkeys with experimental glaucoma. The results demonstrate that optic nerve head astrocytes constitutively express myocilin/TIGR in vivo in primates. Nevertheless, myocilin/TIGR is apparently reduced in glaucomatous ONH. The colocalization of myocilin/TIGR to the myelin suggests a role of myocilin/TIGR in the myelinated optic nerve.     

正常成人视乳头筛板细胞外基质的免疫组化研究

目的 用免疫组化法研究正常成人视乳头筛板细胞外基质的结构组成和分布。方法 用免疫过氧化酶法（ＡＢＣ法）观察７例（１４只眼）正常成人眼筛板中,Ⅳ型胶原蛋白、纤维连接蛋白（ＦＮ）和层连接蛋白（ＬＮ）的分布。结果 正常成人筛板中存在大量Ⅳ型胶原蛋白和层连接蛋白,纤维连接蛋白仅在血管处呈阳性染色,筛板中无阳性染色。结论 筛板是中枢神经系统的一种特殊组织,由类似基底膜样物质组成,赋予筛板弹性和基底膜的机械稳     

MRI lesions of the optic nerves in optic neuritis

Magnetic resonance imaging (MRI) was performed in 14 patients with optic neuritis. Three patients suffered from multiple sclerosis but the etiologies of the remaining 11 cases could not be identified. They were bilateral in 6, and unilateral in 8. The MR images were compared with the symptomatic lesions of optic neuritis and pattern reversal VECP. The STIR mode (short time inversion recovery), was employed for the MRI in the orbit and T2-weighted mode in the brain. In 11 eyes with hyperemia of the optic disc, 7 eyes showed a high signal in the optic nerve with the MRI, and 9 eyes showed an abnormal pattern VECP. Seven eyes with normal disc and two eyes with a pale disc showed a high signal in the optic nerve with MRI, those 9 eyes had abnormal pattern VECP. The high signal in the optic nerve was not related to visual acuity or visual field abnormalities of patients. However, the degree of the high signal of the optic nerve lesion in MRI was associated with the clinical course and prognosis of the optic neuritis. The degree of the high signal of the optic nerve lesion decreased with the recovery of visual acuity in optic neuritis.     

外伤性眼球萎缩眼视神经组织中bcl-2相关死亡基因bad的表达及其意义

目的 探讨外伤性眼球萎缩眼视神经组织中bcl-2相关死亡基因bad表达情况及其意义。 方法 用免疫组织化学的方法观察8只正常对照尸体眼、31只外伤性眼球萎缩眼视神经组织中bad的表达情况。 结果 眼球萎缩眼视神经退行性变表现为视神经髓鞘进行性脱失，神经胶质细胞增生补充。bad表达于正常视神经髓鞘组织及眼球萎缩眼视神经残存髓鞘组织，束间隔及神经胶质细胞中无bad表达。眼球萎缩眼残存的视神经组织较正常视神经组织bad表达量有增高趋势(P＜0.05)；但与眼球萎缩病程长短及导致眼球萎缩的病因之间无直接线性关系(P＞0.05)。 结论 bad可能具有促进外伤性眼球萎缩眼视神经退行性变的作用。 (中华眼底病杂志, 2002, 18: 276-278)     

Aplasia of the optic nerves

At birth, a full term baby showed marked cyanosis and respiratory distress, resulting from transposition of the great vessels. In spite of intensive care, and of balloon septostomies, the child died at the age of five days. The right eye was small and had an almost fully opaque cornea, together with other abnormalities of the anterior segment; the left eye was slightly larger, with a clear cornea. Both eyes showed varying degress of retinal dysplasia, and foci of microcystoid change. Macroscopically, and on histological examination of serial sections, the central retinal vessels were completely absent (a focus of neovascularisation in the vitreous of the right eye was apparently of choroidal origin). Furthermore, no optic discs, retinal ganglion cells and nerve fibres could be demonstrated. The optic nerves were missing. The findings are discussed.