Changes of GABA metabolic enzymes in acute retinal ischemia.

It is reported that GABA accumulates in Müller cells in ischemic and diabetic rat retina. To investigate the mechanism of GABA accumulation in Müller cells, we localized GABA and glutamate in ischemic rat retina and measured the activity of GAD and GABA-T, enzymes involved in GABA metabolism. Using general anesthesia, we incised the bulbar conjunctiva of the rat around the limbus and clamped the left optic nerve. A sham operation was performed on the right eyes. Ocular ischemia was sustained for 30, 60 and 90 minutes. Rat eyes were enucleated immediately after ischemia and prepared for immunohistochemistry and enzyme activity measurement. Glutamate-like immunoreactivity (Glu-IR) in the sham-operated rat retina was observed in all retinal layers, showing intense staining in the nerve fiber layer (NFL), ganglion cell layer (GCL), and inner plexiform layer (IPL). Glu-IR increased in the outer plexiform layer (OPL) and outer nuclear layer (ONL) in an ischemic time-dependent manner. GABA-like immunoreactivity (GABA-IR) in sham-operated rat retina was observed in NFL, GCL, IPL and inner nuclear layer (INL). When the ischemic time was extended, GABA-IR intensely stained Müller cells. GAD activity was not changed in ischemic rat retina as compared to normal rat retina, but GABA-T activity was significantly decreased in ischemic rat retina. These results suggested that glutamate was induced by ischemia and was converted to GABA by GAD activity. Increased GABA was not metabolized because GABA-T activity was decreased. GABA accumulation in Müller cells progressed during the change in activity of these metabolic enzymes.     

运用高分辨SD-OCT探测视神经脊髓炎谱系疾病视网膜厚度变化

目的：分析视神经脊髓炎谱系疾病（NMOSD）在超高分辨谱域光学相干断层成像（UHR-OCT）中视网膜神经纤维和轴突损伤、视网膜厚度的亚临床变化,以更好地监测疾病进展和治疗该疾病。方法：病例对照研究。利用UHR-OCT分析21 例NMOSD患者和20 例健康志愿者（健康对照组）的9 个区域视网膜结构厚度,并根据NMOSD患者是否伴有视神经炎又分为非视神经炎（NO-ON）组（13 眼）和视神经炎（ON）组（13 眼）。运用单因素方差分析比较各组之间视网膜厚度的差异。结果：ON组在总厚度上较健康对照组、NO-ON组薄,除中央区外,其余区域差异均有统计学意义（均P < 0.001）。NO-ON组视网膜总厚度较健康对照组视网膜薄,主要在鼻侧内环（P=0.011）、颞侧内环（P=0.003）以及上侧外环（P=0.019）、下侧外环（P=0.002）,差异均有统计学意义。ON组视网膜神经纤维层（RNFL）及神经节细胞层+内丛状层（GCL+IPL）厚度在各象限与健康对照组相比较薄（P < 0.001）,NO-ON组的RNFL厚度较健康对照组鼻侧内环（P=0.049）和颞侧（P < 0.001）薄。NO-ON组的GCL+IPL较健康对照组上侧外环（P < 0.001）和下侧外环（P=0.002）薄。ON组内核层厚度较对照组上侧内环（P=0.001）、下侧内环（P=0.003）、颞侧外环（P=0.043）厚,而NO-ON组较对照组在上侧外环（P=0.015）、下侧外环（P=0.012）薄。NO-ON组的Henle纤维层+外核层厚度较对照组比较在上侧内环（P=0.009）、上侧外环（P=0.018）、下侧内环（P=0.001）、下侧外环（P=0.001）有下降,ON组与对照组比较差异无统计学意义。结论：本研究发现NMOSD患者不同层次的视网膜结构存在改变,在视神经未受累眼视网膜RNFL和GCIPL存在厚度下降,提示NMOSD患者未受累眼存在潜在的视网膜神经结构损伤。     

NO在缺血性视网膜病变机制的研究

目的 :研究一氧化氮在短暂高眼压诱导的视网膜缺血性损伤的作用机制。方法 :48只雄性S -D大鼠随机分为两组 ,每组 2 4只。 1组左眼为正常对照组、右眼为视网膜缺血对照组 ;2组左眼为视网膜缺血溶剂对照组 ,右眼为视网膜缺血L -NAME治疗组。视网膜缺血再灌注后 7、 14、 2 8天分别将各组 2 4只眼随机分入 3个时间点 ,每个时间点 8只眼。制备视网膜病理切片 ,定量测量内网状层 (IPL)、内核层 (INL)、外核层 (ONL)的厚度。结果 :在缺血的早期阶段 (第 1周 ) ,内网状层 (IPL)的厚度即下降 ,在缺血的晚期阶段 (第 2周～第 4周 ) ,内核层 (INL)和外核层 (ONL)的厚度才发生显著下降。与对照组相比差异均有显著性 ( χ2 检验 ,P <0 0 5 )。L -NAME ,一氧化氮合酶抑制剂可明显减轻缺血性损伤。减轻视网膜各层的下降幅度。与缺血对照组相比经统计学处理差异均有显著性 ( χ2 检验 ,P <0 0 5 )。结论 :视网膜缺血性损伤的诱导机制除了兴奋性毒性诱导的损伤以外 ,还有其他的机制存在。NO可介导视网膜缺血性损伤 ,并在短暂视网膜缺血后晚期内核层 (INL)与外核层 (ONL)神经元的延迟死亡起到一个主要的作用。     

Analysis of spectral domain optical coherence tomography measurements in optic neuritis: differences in neuromyelitis optica,multiple sclerosis,isolated optic neuritis and normal healthy controls

Purpose: To compare the retinal layer thickness of eyes with optic neuritis (ON) and that of control eyes and ON eyes with and without neuromyelitis optica (NMO) or multiple sclerosis (MS). Methods: Horizontal and vertical SD‐OCT scans of the fovea were undertaken for 56 patients with ON with and without NMO or MS and for 24 healthy controls. Patients with ON were divided into three groups: NMO, MS and isolated ON without NMO or MS. The thickness of each retinal layer was compared between ON and healthy control eyes, and between ON eyes with and without NMO or MS. Results: Compared with healthy control eyes, ON eyes showed significant thinning of the ganglion cell layer plus the inner plexiform layer (GCL + IPL) at all eight inner and outer macular locations. Significant differences in thickness were observed for the retinal layers of NMO, MS and isolated ON without NMO or MS at several retinal locations. Conclusions: Our SD‐OCT data revealed a notable difference in the GCL + IPL thickness between ON and healthy control eyes. It also showed differences in the thickness of several retinal layers for ON subgroups including NMO, MS and isolated ON. This may be helpful for distinguishing the aetiology of ON.     

Optic Disc and Macular Imaging in Blind Eyes from Non-glaucomatous Optic Neuropathy: A Study with Spectral-domain Optical Coherence Tomography

The purpose of this study was to determine and compare the optic disc and macular thickness measurements using two spectral-domain optical coherence tomography (SD-OCT) instruments in long-standing blind eyes diagnosed with non-glaucomatous optic neuropathies (NGON). A prospective observational case-series design was used. Twelve eyes from 12 NGON patients with no light perception for at least 6 months underwent optic disc and macular imaging with Cirrus HD-OCT and Spectralis OCT. The correlation between the peripapillary retinal nerve fibre layer (PRNFL) and macular ganglion cell layer and inner plexiform layer (GCL+IPL) thicknesses, and between the duration of no light perception (NLP) and PRNFL/GCL+IPL thicknesses were determined using Spearman’s correlation analysis. The mean average PRNFL thickness was 55.9 ± 4.8 µm for Cirrus HD-OCT, which was significantly thicker than that measured by Spectralis OCT (31.9 ± 7.4 µm; p < 0.001). The mean central macular thickness on Cirrus HD-OCT was normal, but there was global thinning at the other macular areas. The mean average GCL+IPL thickness on Cirrus HD-OCT was 51.8 ± 5.8 µm. There was a good correlation between average PRNFL thickness and GCL+IPL thickness (r = 0.830, p = 0.002); however, there was no significant correlation between the duration of NLP to the average PRNFL thickness (on either instruments) or GCL+IPL thickness on Cirrus HD-OCT (p > 0.7). These results show that there was residual PRNFL thickness in NGON eyes with NLP, which varied significantly between SD-OCT instruments. The values of the residual PRNFL and GCL+IPL thicknesses in blind eyes (the “floor” effect) may be useful for prognostic purposes for patients with partial optic atrophy.     

早产儿视网膜内外层厚度与视力的关系研究

目的　探讨早产儿视网膜内外各层厚度与视力的关系。方法　选取本院2007年1月至2009年1月出生的早产儿60例（120眼）作为早产组,另选取同期在本院出生的足月儿60例（120眼）作为足月组,早产组根据出生时是否有早产儿视网膜病变（retinopathy of prematurity,ROP）、是否接受治疗分为无ROP亚组（32例）、未治疗ROP亚组（20例）和治疗ROP亚组（8例）。测量各组最佳矫正视力（best corrected visualacuity,BCVA）和屈光度,频域光学相干断层扫描(spectral domain optical coherence tomography,SD-OCT)检测视网膜内外各层厚度。比较足月组和早产各亚组间 BCVA及视网膜内外各层厚度,分析早产儿视网膜内外各层厚度与BCVA的关系。结果　足月组BCVA明显优于早产组（P＜0.05）,早产组中治疗ROP亚组BCVA明显弱于未治疗ROP亚组和无ROP亚组（均为P＜0.05）。足月组与早产组年龄、屈光度比较,差异均无统计学意义（均为P>0.05）。早产组各亚组视网膜内层总厚度、视网膜神经纤维层（retinal nerve fiber layer,RNFL）、神经节细胞层（ganglion cell layer,GCL）、内网层（inner plexiform layer,IPL）及内核层（inner nuclear layer,INL）厚度均显著厚于足月组（均为P＜0.05）;未治疗ROP亚组和无ROP亚组视网膜内层总厚度、GCL厚度均显著薄于治疗ROP亚组（均为P＜0.05）。早产组各亚组视网膜外层总厚度、外网层（outer plexiform layer,OPL）和外核层（outer nuclear layer,ONL）、视网膜色素上皮（retinal pigment epithelium,RPE）层厚度均显著厚于足月组（均为P＜0.05）;未治疗ROP亚组和无ROP亚组视网膜外层总厚度、OPL、ONL厚度均显著薄于治疗ROP亚组（均为P＜0.05）。早产组儿童视网膜内层总厚度及GCL厚度与BCVA均呈正相关（均为P＜0.05）,视网膜外层厚度与BCVA无明显相关性（均为P＞0.05）;GCL是影响BCVA的独立危险因素（P＜0.05）。结论　与足月儿相比,早产儿视网膜内外层厚度增加,视力降低,且接受ROP治疗的早产儿视网膜各层厚度和视力所受影响更大,GCL厚度增厚是引起BCVA恶化的独立危险因素。     

增强深度成像OCT对急性期视神经炎患者早期视网膜和脉络膜变化的定量评估

背景 视神经炎是常见的神经眼科疾病之一.频域OCT(SD-OCT)是客观评价视网膜厚度变化的有用工具,而增强深度成像(EDI)OCT则可进一步对视网膜和脉络膜的形态进行定量评估.目前关于视神经炎的早期视网膜和脉络膜形态变化尚未阐明. 目的 采用SD-OCT和EDI OCT对视神经炎早期的视网膜和脉络膜形态进行定量检测,了解视神经炎早期的视网膜和脉络膜变化特征. 方法 采用前瞻性队列研究方法,于2015年7月至2016年5月纳入天津市眼科医院确诊的急性发作期视神经炎患者20例20眼,同期纳入性别和年龄匹配的健康体检者22人22眼.采用SD-OCT及EDI OCT测量受检者视盘周围3.4mm区域上、下、鼻、颞侧4个象限的视网膜神经纤维层(RNFL)平均厚度及上、下、鼻、颞侧4个象限的脉络膜厚度以及黄斑区RNFL、神经节细胞层(GCL)、内丛状层(IPL)、内核层(INL)、外丛状层(OPL)、外核层(ONL)、光感受器层的平均厚度.所有受检者均行图形视觉诱发电位(P-VEP)及视野检查,评价视野平均缺损(MD)与视盘周围RNFL平均厚度、脉络膜厚度、黄斑区RNFL、GCL、IPL、INL、OPL、ONL、光感受器层厚度的相关性. 结果 视神经炎患者视盘周围3.4 mim区域上方、下方及鼻侧3个象限的RNFL厚度分别为(424.00±160.30)、(428.40±169.83)和(108.15±50.66) μm,较正常对照组的(265.68±26.25)、(283.27±52.81)和(72.68±12.01) μm均明显增加,差异均有统计学意义(t=4.571、3.814、3.190,均P＜0.01),2个组间颞侧象限的RNFL厚度差异无统计学意义(t=0.849,P=0.401);2个组间上方、下方、鼻侧、颞侧4个象限的脉络膜厚度的差异均无统计学意义(均P＞0.05).视神经炎组患者黄斑1 mm区域RNFL、GCL、IPL平均厚度较正常对照组受检者明显变薄,视神经炎组患者黄斑3 mm区域GCL、IPL、INL平均厚度较正常对照组受检者明显变薄,差异均有统计学意义(均P＜0.05).视神经炎组患者P-VEP P100波潜伏期为(133.15±11.11)s,较正常对照组的(94.59±4.38)s明显延长,差异有统计学意义(t=15.058,P＜0.05).MD与视盘周围上方、下方、鼻侧3个象限的RNFL平均厚度呈中等线性正相关(r=O.649、0.649、0.635,均P＜0.05),而各象限脉络膜厚度与MD均无明显线性相关(r=-0.120、-0.102、-0.415、0.120,均P＞0.05);黄斑区RNFL、GCL、IPL、INL、OPL、ONL、光感受器层厚度与MD均无明显线性相关. 结论 EDI OCT检测发现视神经炎早期患者视盘周围RNFL发生水肿,厚度增加,黄斑区各层视网膜厚度均不同程度地变薄,但患者的脉络膜厚度无明显改变.EDI OCT是客观和定量评价视神经炎早期视网膜和脉络膜形态学的有用工具.     

缺血后适应对视网膜缺血-再灌注损伤的保护作用

背景研究证明,缺血后适应（IPC）对多种组织器官的缺血缺氧损伤均有一定的抵抗作用,但其对视网膜缺血缺氧的作用仍受到关注。目的探讨IPC对大鼠视网膜缺血-再灌注损伤（RIRI）后视网膜结构和功能的保护作用。方法将36只健康雄性Wistar大鼠以随机数字表法分为正常对照组、伪手术组、缺血-再灌注组、IPC组。利用前房灌注生理盐水升高眼压至100mmHg（1mmHg=0．133kPa）维持60min的方法制备RIRI大鼠模型,实施IPC处理鼠亚分为再灌注后即刻、1min、10min组（即IPCⅠ组、IPCⅡ组、IPCⅢ组）,分别于实验后1d、7d行大鼠视网膜电图（ERG）检测,然后用过量麻醉法处死大鼠并制备视网膜切片,行苏木精-伊红染色,对各组大鼠视网膜厚度的变化和视网膜形态进行观察。采用SPSS13．0统计学软件的单因素方差分析对各组大鼠ERG各波振幅恢复率和视网膜厚度值的差异进行比较。结果实验后1d,与正常对照组大鼠比较,伪手术组大鼠视网膜结构接近正常,而缺血-再灌注组及IPCⅠ组、IPCⅡ组、IPCⅢ组大鼠视网膜均出现水肿,可见空泡变性,主要在内丛状层（IPL）及内核层（INL）。缺血-再灌注组及IPCⅠ组、IPCⅡ组、IPCⅢ组大鼠视网膜全层、INL、IPL及视网膜外层厚度值均明显高于正常对照组,差异均有统计学意义（均P〈0．05）。再灌注后7d,缺血-再灌注组大鼠视网膜全层厚度值明显低于正常对照组,差异均有统计学意义（均P〈0．05）,尤以INL、IPL显著。IPCⅠ组、IPCⅡ组、IPCⅢ组大鼠视网膜全层、INL、IPL及视网膜外层厚度值均明显高于缺血-再灌注组,差异均有统计学意义（均P〈0．05）。再灌注后7d,缺血-再灌注组、IPC各组大鼠ERG a波、b波和OPs振幅恢复率明显低于伪手术组和正常对照组大鼠,差异均有统计学意义（均P〈0．05）;而IPCⅠ组、IPCⅡ组、IPCⅢ组大鼠ERG a波、b波和OPs振幅恢复率明显高于缺血-再灌注组,差异均有统计学意义（均P〈0,05）。结论IPC对RIRI具有保护作用,在大鼠模型中,这种保护作用在再灌注后即刻至1min时最强。     

Chronic bilateral common carotid artery occlusion: a model for ocular ischemic syndrome in the rat

Background Ocular ischemic syndrome is a devastating eye disease caused by severe carotid artery stenosis. The reduction of blood flow produced by bilateral common carotid artery occlusion (BCCAO) of rats for 7 days induces events related to gliosis with no evident histological damage. However, retinal degeneration and cellular death occur after 90 days of BCCAO. Our purpose has been to investigate the effects of BCCAO for 30 days in the retina of adult rats. Methods Adult Wistar rats were submitted to BCCAO or sham surgery. Both direct and consensual pupillary light reflexes were investigated before and after surgery, everyday for the first week and weekly for 30 days. After 1 month, eyes were enucleated and embedded in paraffin. The retinal ganglion cell (RGC) density and thickness of the internal plexiform (IPL), internal nuclear, outer plexiform, and outer nuclear layers were estimated. Results Four rats of the BCCAO group (50%) lost the direct pupillary reflex in both eyes, three rats (37%) lost this reflex in one eye, and only one (13%) maintained it in both eyes. RGC density (cells/mm) was diminished in the BCCAO group, and a significant decrease was found in the total retina and IPL thickness; however, no changes were evident in the other layers. BCCAO pupillary-reflex-negative rats presented with a significant decrease in total retinal thickness and retinal ganglion cell density compared with the sham group. Both BCCAO pupillary-reflex-positive) and -negative rats showed a decrease in IPL compared with the sham group. Conclusion This study demonstrates that BCCAO for 30 days induces functional and morphological damage to the retina with loss of the pupillary reflex and a decrease in IPL thickness and RGC number. We suggest that this protocol might be used as a model for ocular ischemic syndrome in the rat.     

POAG患者视网膜各层厚度的OCT分析

目的利用RTVue OCT对POAG患者黄斑区视网膜各层厚度进行分析,尤其是视神经节细胞层,探讨其在原发性开角型青光眼诊断中的价值。方法前瞻性对照研究。临床诊断为POAG的病例76例（91眼）纳入本研究,分为早期30例（30眼）,中期25例（29眼）,晚期21例（32眼）;选择32例（32眼）年龄、性别构成相匹配的健康体检者作为正常对照组。采用RTVue OCT对受检眼黄斑区视网膜进行扫描,用自编程序图像处理软件将视网膜结构分为9层,早、中、晚期POAG与正常对照组黄斑区视网膜各层厚度比较采用LSD-t检验。结果早期POAG组视网膜神经纤维层（RNFL）、节细胞层（GCL）平均厚度分别为（31.6±9.2）μm、（33.9±5.0）μm,较对照组薄（P＜0.05）,中期POAG组RNFL、GCL平均厚度分别为（31.2±3.4）μm、（34.1±3.9）μm,较正常组薄（P＜0.05）;晚期POAG组RNFL、GCL、内丛状层（IPL）、锥杆细胞内节（IS）、全视网膜（TR）平均厚度分别为（18.8±7.6）μm、（24.2±7.9）μm、（38.0±6.4）μm、（22.8±4.4）μm、（299.5±15.1）μm,均较正常组薄（均P＜0.05）;INL平均厚度（39.1±6.6）μm,较正常组厚（P＜0.05）。结论POAG患者黄斑区视网膜厚度明显变薄,早期POAG对GCL的影响尤为突出,结合临床有助于POAG的早期诊断。     

Aprotinin reduces ischemia-reperfusion injury in the retina of guinea pigs

PURPOSE: The aim of this study was investigate the role of aprotinin on retinal lipid peroxidation and histopathological changes during ischemia/reperfusion (I/R) of guinea pigs. METHODS: Three groups of seven pigmented guinea pigs each were formed: a control (group 1), ischemia/saline (group 2) and ischemia/aprotinin (group 3). One eye of each animal was selected for histopathological evaluation and the other for biochemical assay. Bilateral pressure-induced retinal ischemia was instigated for 90 min and was followed by 24 hours of reperfusion. Animals in the ischemia/aprotinin and ischemia/saline groups received either 20,000 KIU/kg of aprotinin or saline, repeated four times at 6-hour intervals, with the first dose administered 5 min prior to the ischemic insult. The animals were killed at 24 hours of reperfusion. Retinal malondialdehyde (MDA) levels and the thickness of the inner plexiform layers were measured. RESULTS: The level of MDA in group 1 was significantly (p<0.001) lower than the other groups. The mean MDA level in group 2 was significantly (p<0.01) higher than in group 3. The inner plexiform layer in group 1 was significantly (p<0.001) thinner than in the other groups. The mean thickness of the inner plexiform layer in group 2 was significantly (p<0.01) higher than in group 3. CONCLUSIONS: These data indicate that intraperitoneally administrated aprotinin has a protective effect against I/R injury in the retina of guinea pig as evidenced by reduced retinal MDA level and retinal thickness.     

Macular changes of neuromyelitis optica through spectral-domain optical coherence tomography

AIM: To evaluate the thickness of the retinal layers in the macula using spectral-domain optical coherence tomography (SD-OCT) in patients with neuromyelitis optica (NMO). METHODS: Spectralis SD-OCT, utilizing automated macular layer segmentation, was performed in 26 NMO patients and 26 healthy controls. Visual function including visual field tests and pattern visual evoked potential were recorded in study subjects. RESULTS: Forty-one eyes from 26 NMO patients and 52 eyes from 26 age- and sex-matched healthy controls were included. Besides total macular volume, peri-paipillary retinal nerve fiber layer (RNFL) thickness, the thickness of macular RNFL, ganglion cell layer (GCL) and inner plexiform layer (IPL) were also significantly reduced in NMO patients compared to those inhealthy controls (P<0.000). No differences were found in the thickness of macular inner nuclear layer (INL), outer plexiform layer (OPL), and outer nuclear layer (ONL) between the two groups. Reversely, the outer retinal layer (ORL) was shown to be thicker in NMO than controls (P<0.05). Compared with the peri-papillary RNFL thickness, the GCL thickness was demonstrated to correlate with visual function better. CONCLUSION: The study provides in vivo evidence of retinal neural loss in NMO patients and demonstrates a better structure-function correlation between retinal ganglion cell and visual function than peri-papillary RNFL does. In addition, no evidence of primary neural damage is found. Besides, the photoreceptor cells and retinal pigments epithelial (RPE) cells presumably proliferated in compensation in NMO after retinal neural loss.     

Estrogen protects the inner retina from apoptosis and ischemia-induced loss of Vesl-1L/Homer 1c immunoreactive synaptic connections

PURPOSE: Protective effects of estrogen on nerve cells including retinal neurons have been described previously. However, subcellular effects on synaptic connectivity in mild ischemia more closely resembling ischemic conditions found in diabetic or sickle cell retinopathy and stenosis of the carotid artery have not been identified. The present study quantitatively analyzed effects of estrogen administration on synaptic connections of neurons in the ganglion cell layer (GCL) of the retina. METHODS: Staining of Vesl-1L/Homer 1c (V-1L) immunoreactivity and TUNEL cytochemistry were used to quantify neuroprotective effects at the synaptic level in a model of mild retinal ischemia induced by temporary middle cerebral artery occlusion in the adult rat. RESULTS: V-1L immunoreactivity was found in both synaptic layers, postsynaptic to glutamatergic ribbon synapses. Mild retinal ischemia led to a significantly higher percentage reduction in the number of V-1L-positive synapses in the inner plexiform layer (IPL) compared with the percentage of TUNEL-positive apoptotic neurons in the GCL. Estrogen prevented ischemia-induced loss of V-1L-immunoreactive synapses in the IPL and apoptosis of cells in the GCL. CONCLUSIONS: Immunoreactivity for V-1L can be used as a synaptic marker for early changes before more severe neurodegenerative events. The present results suggest that estrogen protects neurons in the GCL including RGCs from both apoptosis and early changes in synaptic connections associated with ischemia and potentially preceding apoptosis.     

Assessment of inner retina layers thickness values in eyes with pituitary tumours before visual field defects occur

BackgroundThe purpose of this study was to evaluate macula, retinal nerve layer (RNFL), ganglion cell layer (GCL), inner plexiform layer (IPL) and macular nerve fibre layer (mNFL) thickness in patients with pituitary tumours who has normal visual field (VF).MethodsThirty-five eyes of 35 patients with pituitary tumours with normal VF and 41 eyes of 41-healthy subjects were underwent a complete ophthalmic examination. The spectral domain- optical coherence tomography (OCT) was used to measure macular and optic disc parameters. Layer-by-layer segmentation was done automatically by using the new software. Data analyses were performed by using SPSS for Windows, version 22.0.ResultsAverage of total macula thickness inner temporal (p: 0.006), outer temporal (p < 0.001), inner nasal (p: 0.03), outer nasal (<0.001) were significantly lower in pituitary tumour group than normal group. Average of RNFL (p:0.009), temporal (p: 0.001), superiotemporal (p:0.004) and inferiotemporal (p: 0.01) were significantly lower in pituitary tumour group than normal group. Average of central GCL (p: 0.01) and central NFL (p: 0.03) were significantly lower in pituitary tumour group than normal group. There was no statistically significant difference between the two groups in IPL averages.ConclusionsPituitary tumour patients with normal VF had reduced nasal and temporal section of the total macula, temporal RNFL, central mGCL and mNFL thicknesses, reflecting the corresponding to the anatomical substrate of the underlying pathology of chiasmal compression. This indicates that the presence of retinal thinning may be a sign of early detection of anterior visual pathway injury before VF loss becomes apparent.Subject terms: Outcomes research, Optic nerve diseases     

Inhibition of cyclooxygenase-2 expression by zinc-chelator in retinal ischemia

The zinc ion (Zn2+) is abundant in neurons. However, excessive Zn2+ can induce neuronal cell death. This study examined the role of Zn2+ in transient retinal ischemia in adult male rats. The rats were sacrificed 4-24 h after retinal ischemia by high intra-ocular pressure, and the retinas were prepared for microscopic examination of retinal cell degeneration, and fluorescence microscopy using zinquin ethyl ester as the zinc ion-specific probe. Moreover, COX-2 expression was observed by Western blotting. In control retinas, there was a low Zn2+ concentration in the inner plexiform layer (IPL), a high Zn2+ concentration in the outer plexiform layer (OPL), and no detectable Zn2+ in either the ganglion cell layer (GCL) or the inner nuclear layer (INL). In contrast, in the retinas exposed to ischemia without the administration of the zinc ion chelators (Ca2+-EDTA and TPEN), Zn2+ deposits were found in the IPL and INL beginning 4 h after ischemia and degeneration of neurons was found in the GCL and INL. Less Zn2+ accumulation in the IPL and INL and less neuronal degeneration in the GCL and INL were found in the retinas treated with Ca2+-EDTA or TPEN before ischemia. Furthermore, the COX-2 protein levels increased 4-8 h after retinal ischemia, and chelation of zinc ion inhibited this effect. These results suggest that the accumulation of Zn2+ following an ischemic insult can cause retinal degeneration and induce abnormal COX-2 expression.     

Retinal Ganglion Cell Loss in X-linked Adrenoleukodystrophy with an ABCD1 Mutation (Gly266Arg)

The authors here report a single case of a 10-year-old male patient who presented with severe vision loss associated with progressive demyelination. The patient was diagnosed with X-linked childhood cerebral adrenoleukodystrophy (ALD). Genetic analysis demonstrated a missense mutation (Gly266Arg) in exon 1 of the ABCD1 gene. His corrected visual acuity confirmed the absolute lack of light perception in both eyes. Funduscopy revealed severe pallor of the optic disc in both eyes. Spectral-domain optical coherence tomography showed thinning of the retinal ganglion cell and inner plexiform layers (GCL and IPL). Thinning of the GCL and IPL may be due to transneuronal retrograde degeneration of ganglion cells secondary to optic tract demyelination.     

Quantitative Analysis of Changes in Macular Layers Following Optic Neuritis

The effects of optic neuritis in patients with multiple sclerosis (MS) on the thickness of individual macular layers was analysed by means of optical coherence tomography (OCT). Data of 15 patients (mean age 37.2 years, range 16–50) with multiple sclerosis and 15 normal subjects (mean age 37.7 years, range 17–67) were analysed. Twelve patients had suffered from an attack of acute unilateral optic neuritis in one or both eyes. OCT scans of the circumpapillary retinal nerve fibre layer (RNFL) and of the macula were obtained by means of fast scan protocols. The characteristic sequence of five intensity maxima and four intensity minima was attributed to the mean location of the individual macular layers. The eyes affected by optic neuritis showed significant (p < 0.05) reductions of RNFL thickness by 30.5%, of macular volume (MV) by 12.8%, and of inner macular layers. The mean reduction was 16.2% (macular nerve fibre layer), 31.1% (ganglion cell layer [GCL]), and 25.9% (inner plexiform layer [IPL]), respectively. However, significant reductions of RNFL thickness (by 9.0%), MV (by 5.0%), CGL (by 10.3%), and IPL (by 10.8%) were found also in the unaffected eyes of MS patients. Thus, the quantitative analysis of the axial reflectivity profiles from exported OCT images offers an appropriate method for the characterisation of the location of macular changes after optic neuritis. The shrinking of inner macular layers is a more sensitive parameter of postneuritic optic atrophies than the reduction of MV.     

玻璃体切除联合内界膜剥除翻转填塞治疗特发性黄斑裂孔的短期疗效及影响因素

目的 观察玻璃体切除联合内界膜剥除翻转填塞治疗特发性黄斑裂孔的疗效和预后影响因素。设计 回顾性病例系列。研究对象 特发性黄斑裂孔患者36例（37眼）。方法 所有患者行玻璃体切除联合内界膜剥除翻转填塞手术。术后随访时间4个月。观察眼压、最佳矫正视力（best-corrected visual acuity, BCVA）、裂隙灯、间接检眼镜、眼轴长度（axial length, AL）、黄斑裂孔直径;频域相干光断层扫描（spectral domain optical coherence tomography, SD-OCT）测量术前及术后黄斑区视网膜各层厚度,包括视网膜神经纤维层（retinal nerve fiber layer, RNFL）、视网膜神经节细胞层（ganglion cell layer, GCL）、内丛状层（inner plexiform layer, IPL）、内核层（inner nuclear layer, INL）、外丛状层（outer plexiform layer, OPL）、外核层（outer nuclear layer, ONL）、视网膜色素上皮层（retinal pigment epithelium, RPE）;Spearman相关性分析术后BCVA与术前BCVA、AL、年龄、黄斑裂孔大小等的关系。主要指标 裂孔闭合率,BCVA,视网膜厚度。结果 术后黄斑裂孔闭合率100%。术前、术后平均BCVA （LogMRA）分别为1.23±0.64和0.28±0.17（P<0.05）。SD-OCT测量术后黄斑区鼻侧和颞侧的RNFL、GCL、IPL、INL厚度明显变薄(P均<0.05);黄斑区鼻侧和颞侧OPL、ONL、RPE厚度变化无统计学意义（P均>0.05）。术后BCVA与术前BCVA（r=0.641）、黄斑裂孔最小直径（r=0.662）、白内障手术（r=0.438）、黄斑区鼻侧RNFL厚度变化（r=0.349）、黄斑区鼻侧IPL厚度变化（r=0.383）有相关性（P均<0.05）。结论 玻璃体切除联合内界膜剥除翻转填塞治疗黄斑裂孔能改善术后BCVA。术前BCVA、黄斑裂孔最小直径、白内障手术、黄斑区鼻侧RNFL厚度变化、黄斑区鼻侧IPL厚度变化是影响术后BCVA的因素。     

Retinal Ganglion Cell Loss in X-linked Adrenoleukodystrophy with an ABCD1 Mutation (Gly266Arg)

Abstract

The authors here report a single case of a 10-year-old male patient who presented with severe vision loss associated with progressive demyelination. The patient was diagnosed with X-linked childhood cerebral adrenoleukodystrophy (ALD). Genetic analysis demonstrated a missense mutation (Gly266Arg) in exon 1 of the ABCD1 gene. His corrected visual acuity confirmed the absolute lack of light perception in both eyes. Funduscopy revealed severe pallor of the optic disc in both eyes. Spectral-domain optical coherence tomography showed thinning of the retinal ganglion cell and inner plexiform layers (GCL and IPL). Thinning of the GCL and IPL may be due to transneuronal retrograde degeneration of ganglion cells secondary to optic tract demyelination.     

Retinal neuroprotection against ischemic injury mediated by intraocular gene transfer of pigment epithelium-derived factor

PURPOSE. To determine whether intraocular gene transfer of pigment epithelium-derived factor (PEDF) protects the retina from ischemia-reperfusion injury. METHODS. Four days before induction of pressure-induced ischemia, Lewis rats received intravitreous injection of 3 x 10(9) particles of an adenovirus vector expressing PEDF (AdPEDF.11) in one eye and 3 x 10(9) particles of an empty adenovirus vector (AdNull.11) in the contralateral eye. Seven days after reperfusion, eyes were enucleated and processed for morphometric analysis. Apoptotic cells stained by TdT-dUTP terminal nick-end labeling (TUNEL) in the retina were counted 12 hours after initiation of reperfusion. Retina levels of PEDF were measured by enzyme-linked immunosorbent assay. RESULTS. PEDF levels in retinal homogenates from eyes receiving AdPEDF.11 injection were well above the background levels in the untreated baseline and control eyes (P = 0.04). Retinal thickness was preserved in AdPEDF.11-treated eyes. Retinal cell density was significantly greater in the ganglion cell layer (GCL; P = 0.014), inner nuclear layer (INL; P = 0.008), and outer nuclear layer (ONL; P = 0.008) of AdPEDF.11-treated eyes compared with the corresponding layers in AdNull.11-treated eyes. AdNull.11-treated eyes also had significantly more TUNEL-positive cells in these layers than AdPEDF.11-treated eyes (P < 0.05). CONCLUSIONS. Adenoviral vector-mediated intraocular expression of PEDF significantly increases cell survival after ischemia-reperfusion injury of the retina. The protective effect may result from inhibition of ischemia-induced apoptosis. This study provides proof of concept for a gene transfer approach directed at interrupting programmed cell death induced by retinal ischemic insult.