Objective To measure optic disc parameters in Mongolian and Han healthy subjects with or without family history of glaucoma, to explore the causes of the differences and their significance in the diagnosis of early glaucoma. Methods Fifteen healthy Mongolian individuals (30 eyes), 30 healthy Han individuals (60 eyes) with a family history of open-angle (30 eyes) or angle-closure (30 eyes) glaucoma, and 45 healthy Han individuals (90 eyes) without a family history of glaucoma were enrolled in this study. The 45 healthy Han individuals without a family history of glaucoma included three age-groups: 20 to 29 years old group, 30 to 39 years old group and 40 to 49 years old group, each group have 15 subjects (30 eyes). Thirteen parameters were measured by Heidelberg retina tomography (HRT) for all subjects, including disc area, cup area, rim area, cup volume, rim volume, cup/disc area ratio, linear cup/disc ratio, mean cup depth, maximum cup depth, cup shape, disc height variation contour, mean retinal nerve fiber layer (RNFL) thickness and optic nerve fiber layer crosssectional area. The results were analyzed and compared between the above groups. Results There was no statistically significant (t=0.791,P=0.132) of the height variation contour between Mongolian and Han without a family history of glaucoma (20 to 29 years old) group. The other parameters of Mongolian were smaller than Han without a family history of glaucoma (20 to 29 years old) group, but the difference was not statistically significant (t=-1.039, -0.799, -0.840,-1.108, -0.956, -0.695, -0.931, -1.099, -1.074, -0.580, -0.204, -1.425; P＞0.05). The parameters in Han with a family history of open-angle glaucoma group were bigger than Han without a family history of glaucoma (30 to 39 years old) group. The differences were statistically significant for disc area, cup area, rim area, cup volume, rim volume, cup area ratio, linear cup/disc ratio, mean cup depth, cup shape measure, nerve fiber layer cross-sectional area (t=4.758, 3.187, 2.544, 2.674, 1.798, 3.676, 2.721, 2.715, 2.510, 2.373; P＜0.05), but were not statistically significant for maximum cup depth, disc height variation contour and mean RNFL thickness (t=1.649, 1.565, 0.767; P＞0.05). Most parameters in Han with a family history of angle-closure glaucoma group were the same as that in Han without a family history of glaucoma (40 to 49 years old) group, including cup area, rim area, cup volume, rim volume, cup/disc area ratio, linear cup/disc ratio, mean optic cup depth, maximum cup depth, cup shape, disc height variation contour, mean RNFL thickness, optic nerve fiber layer cross-section (t=1.201, 1.697, 1.000, 0.516, 0.740, -0.172, -0.070, -0.972, 1.530, -0.390, -0.091, 0.659; P＞0.05); but the difference of disc area between these 2 groups was statistically significant (t=2.224,P＜0.05). Conclusions The family history of glaucoma can change the optic disc parameters of healthy individuals, especially those with a family history of open-angle glaucoma. There is no difference of optic disc parameters between healthy Mongolian and Han subjects.
Objective To monitor the release of amino acids of the whole retina during and after experimental glaucoma by increasing the intraocular pressure （IOP）． Methods Experimental glaucoma was induced in one of the two eyes of rabbits by increasing IOP at 120 mm Hg for 45 min under infusion of saline in anterior chamber；then the pressure was released and the needle inserted into the anterior chamber was removed，this state was maintained for another 45 min．Every 15 min during the experiment 5 rabbits were killed and experimental eyes were enucleated．Aliquots（20 μl）of the retinal extracts（see below）were mixed with ophthaldialdehyde reagent and analysed for amino acid content by the HPLC method of Wangwei，using a 150 mm×4.6 mm,5 μm C18 column． Results A large increase in the release of glutamate，but not of the other three amino acids monitored，occurred during initial experimental ocular hypertension．It reached peak value of（111.73±17.46）10-5 mmol/g at 15 min of hypertension．15 min after release of intraocular pressure，again，immediately large and specific increase in the concentration of glutamate was reached to（102.96±51.91）10-5 mmol/g．In eyes subjected to paracentesis of anterior chamber，no difference was found between experimental eyes and controls. Conclusion These results suggest that glutamate is triggered by increasing the IOP，and it releases not only during the period of experimental ocular hypertension，but also afterwards. (Chin J Ocul Fundus Dis, 2002, 18: 146-148)
Through the different image technologies, peripapillary atrophy can be classified into four types: α zone, β zone, γ zone and δ zone. Each type of them has different imaging and histological features. Peripapillary atrophy is a common structure in peoples’ eyes and it is correlated with many factors and diseases such as age, myopia, glaucoma, non-arteritic anterior ischemic optic neuropathy and age-related macular degeneration which bring difficulties to our diagnosis and antidiastole. Classifying and qualifying peripapillary atrophy properly, which can evaluate the changes and degrees, can benefit our studies about their mechanism and offer the clinical biological indictors and research basis.
Objective To investigate the risk factors associated with neovascular glaucoma (NVG) after pars plana vitrectomy (PPV) in eyes with proliferative diabetic retinopathy (PDR). Methods Retrospective study. One hundred and thirty-seven patients (137 eyes) with PDR who underwent PPV were recruited. There were 85 males and 52 females. The average age was (60.1±8.8) years old. The duration of diabetes was (10.2±3.6) years. There were 49 patients with ipsilateral carotid artery stenosis. Fifty-three eyes underwent intravitreal ranibizumab or conbercept injection before PPV. All eyes were treated with 23G standard three-port PPV. The average follow-up time after PPV was 11.5 months. Fundus fluorescein angiography (FFA) was conducted in postoperative 4-6 weeks to observe non-perfused retinal areas. Risk factors, such as ipsilateral carotid artery stenosis, the presence of non-perfusion in retina after PPV and the application of anti-vascular endothelial growth factor (VEGF) drugs before PPV, were identified by logistic regression. Results Twenty of 137 patients (14.6%) developed postoperative NVG after PPV. Ipsilateral carotid artery stenosis [odds ratio (OR) =5.048, 95% confidence interval (CI) 2.057-12.389,P=0.000] and the presence of non-perfusion in retina after PPV (OR=4.274, 95%CI 1.426-12.809,P=0.009) were significant risk factors for postoperative NVG, while the application of anti-VEGF drugs was not (OR=1.426, 95%CI 0.463-4.395,P=0.536). But the time from PPV to the onset of NVG varies significantly between the two groups of injection of anti-VEGF drugs or not (t=−4.370,P=0.000). Conclusions Risk factors associated with NVG after PPV in eyes with PDR included ipsilateral carotid artery stenosis and the presence of non-perfusion in retina after PPV. The application of anti-VEGF drugs before PPV can delay the onset of NVG in PDR eyes after vitrectomy.
ObjectiveTo observe the difference of retinal vessel oxygen saturation in glaucoma and normal eyes. MethodsA cross sectional study design was performed. Fifty eyes of 30 glaucoma patients (glaucoma group) and 41 eyes of 27 age-and sex-matched healthy subjects (control group) were included. Retinal vessel oxygen saturation was measured with a spectrophotometric retinal oximeter in darkness and visual fields were obtained by Humphrey filed analyzer. The glaucoma eyes were divided into two groups: mean defect (MD)<6 dB (28 eyes) and MD≥6 dB (22 eyes) according to mean defect of visual field. ResultsRetinal arteriolar oxygen saturation values in glaucoma group and control group were (94.52±6.51)% and (93.47±6.30)% respectively. No statistical difference was found in retinal oxygen saturation in arterioles (H=-0.949, P=0.343). Retinal venous oxygen saturation values in glaucoma group and control group were (57.57±7.96)% and (52.60±7.70)% respectively. The retinal venous oxygen saturation values in glaucoma group was higher than that in control group (H=-3.318,P=0.001). The retinal arteriovenous difference in glaucoma group and control group were (36.59±4.69)% and (42.41±6.73)% respectively. The retinal arteriovenous difference in glaucoma group was lower than that in control group (H=-4.148,P<0.01). The retinal arteriolar oxygen saturation values in glaucoma eyes with MD<6 dB and MD≥6 dB were (93.38±6.33)% and (95.71±6.54)% respectively, with no statistical difference (H=-1.857,P=0.063). Retinal venous oxygen saturation values in glaucoma eyes with MD<6 dB and MD≥6 dB were (54.83±6.10)% and (61.07±8.79)% respectively. The retinal venous oxygen saturation values in MD≥6 dB glaucoma eyes was higher than that in MD<6 dB glaucoma eyes (H=-2.599, P=0.009). The retinal arteriovenous difference in glaucoma eyes with MD<6 dB and MD≥6 dB were (38.12±4.34)% and (34.64±4.49)% respectively. The retinal arteriovenous difference in MD≥6 dB glaucoma eyes was lower than that in MD<6 dB glaucoma eyes (H=-2.463,P<0.05). ConclusionsCompared with healthy eyes, there is no change in the retinal arteriolar oxygen saturation, but the retinal venous oxygen saturation is higher and the retinal arteriovenous difference is lower. This feature is more obvious in MD≥6 dB glaucoma eyes.
Objective To observe the affection of optic nerve under acute ocular hypertension and the effect of protection of bFGF on optic nerve. Methods BSS was perfused into anterior chamber of rabbits to increase the intraocular pressure to cause retinal ischemia. A computer image analysis system was used to count the optic nerve axons.Eyes were intravitreally injected with bFGF and then the number of optic nerve axons of the normal rabbits,and hypertension with and without bFGE treatment groups were counted respectively. Results The number of optic nerve axons in ocular hypertension eyes was less than the normal eyes(P=0.00003).The bFGF treated eyes had more optic nerve axons than the controls(P=0.0078). Conclusions The acute ocular hypertension may cause the loss of the nerve axons,and bFGF may be effective in protecting optic nerve in acute ocular hypertension. (Chin J Ocul Fundus Dis,2000,16:94-96)