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We used scanning laser ophthalmoscope (SLO) microperimetry to evaluate scotomas in patients with clinically significant diabetic macular edema (CSME) in type 2 diabetes mellitus.We studied 19 patients (mean age = 63 years; range, 45-78 years) (19 eyes). SLO microperimetry was performed in all eyes. We divided patients into three groups as follows: dense scotoma, relative scotoma, and no scotoma. The following variables were documented: age; duration of diabetes, hemoglobin A(1c) levels; logarithm of the minimum angle of resolution (Log(MAR)) visual acuity; refractive power; a history of panretinal photocoagulation; presence or absence of proliferative diabetic retinopathy, vitreomacular separation, and cystoid changes; the type of macular edema; and stability of fixation. All variables were compared in the three groups.We identified 4 eyes (21.1%) with dense scotoma, 10 (52.6%) with relative scotoma, and 5 (26.3%) with no scotoma. There were significant differences in log(MAR) visual acuity among those with dense scotoma (1.4 +/- 0.5), relative scotoma (0.6 +/- 0.2), and no scotoma (0.2 +/- 0.3) (P.05), and in the prevalence of cystoid changes, diffuse edema, and unstable fixation among those with dense scotoma (75%, 75%, and 100%, respectively), relative scotoma (20%, 30% and 50%, respectively) and no scotoma (0%, 0% and 0%, respectively) (P.05).Macular scotoma was observed by SLO microperimetry in 74% of the patients in this study. A scotoma in CSME is related to the formation of cystoid changes and the type of macular edema. In eyes with CSME in type 2 diabetes mellitus, a scotoma in the macula causes visual acuity impairment and unstable fixation.

We developed a tree shrew model of diabetes using streptozotocin (STZ), and studied early ocular changes of diabetes (after one week of diabetes) by fluorophotometry. STZ was injected intraperitoneally at doses of sixty to 400 mg/kg body weight. Animals injected with more than 300 mg/kg of STZ developed diabetes. Corneal autofluorescence was significantly increased one week after STZ injection. These changes may be related to impairment of the ocular homeostatic mechanisms due to the onset of diabetes. Using this model, we might be able to obtain diabetic ocular impairment data closer to human data than in previous models of diabetes, because tree shrews are primates.

Nitric oxide (NO) plays an important role in homeostatic vasodilation and the regulation of blood flow. On the other hand, excess release of NO causes various vascular complications. There are only a few reports on the relationship between plasma NO levels and microvascular complications, especially diabetic retinopathy (DR) in patients with type 2 diabetes. The purpose of this study was to determine the relationship between plasma NO levels and DR.In a prospective study, blood samples were obtained from 36 patients with diabetes and no diabetic retinopathy (NDR), 43 patients with nonproliferative diabetic retinopathy (NPDR), 18 patients with proliferative diabetic retinopathy (PDR), and 40 subjects without diabetes mellitus, who served as controls. The levels of plasma NOx (nitrite and nitrate), the stable metabolites of NO, were measured by high-performance liquid chromatography with the Griess method.The plasma NOx levels were 92.8 +/- 16.0, 70.2 +/- 6.8, 90.3 +/- 9.1, and 53.8 +/- 6.1 micromol/l in patients with NDR, NPDR, or PDR, and in the controls, respectively. The plasma NOx levels in the three diabetic groups were significantly higher than those in the control group (P0.05 in each case).The increased plasma NO levels in patients with type 2 diabetes indicate that NO may be associated with the pathogenesis of DR.

To evaluate quantitatively the effects of bucillamine on the entrapment of leukocytes in the retinal microcirculation of diabetic rats.13 male Brown Norway rats were injected with streptozotocin (STZ). After the animals developed diabetes, they were divided into two groups. Group 1 (n=7) received fresh drinking water without bucillamine, and group 2 (n=6) received fresh drinking water supplemented with bucillamine (200 mg/kg per day). Rats that were not injected with STZ and received water without bucillamine served as controls (n=6). Four weeks after the injection of STZ, the leukocytes in the retina were observed by acridine orange digital fluorography. The number of leukocytes trapped in the retinal vessels was compared among the three groups.In the untreated diabetic rats, the number of trapped leukocytes was significantly higher than in control rats or bucillamine-treated diabetic rats (P0.05).We demonstrated an inhibitory effect of bucillamine on leukocyte entrapment in the retinal vessels of diabetic rats. Bucillamine may have therapeutic efficacy in preventing the development of diabetic retinopathy.

To determine the changes in the pulse amplitude (PA) and the pulsatile ocular blood flow (POBF) after scleral buckling (SB).Retrospectively, we studied 24 patients (average age, 52 years) who had undergone SB to repair a retinal detachment in one eye. The patients were divided into two groups: those in whom SB had been performed less than 6 months earlier (n = 10), and those in whom the procedure had been performed more than 6 months previously (n = 14). In each group, the PA and the POBF were determined with a computerized tonometry system, and the values in the SB eyes were compared with those in the control fellow eyes.Within 6 months postoperatively, the mean PA in the SB eyes (0.66 +/- 0.30 mmHg) was significantly lower than that in the control eyes (1.43 +/- 0.34 mmHg; P0.05). The mean POBF in the SB eyes (349.5 +/- 154.1 microl/min) was also significantly lower than that in the control eyes (631.0 +/- 226.6 microl/min; P0.05). After more than 6 months postoperatively, there were no significant differences in the PA or the POBF between the SB eyes (1.08 +/- 0.49 mmHg and 612.4 +/- 341.2 microl/min, respectively) and the control eyes (1.50 +/- 0.51 mmHg and 589.5 +/- 278.4 microl/min, respectively).These results indicate that the choroidal blood flow decreases after SB but returns to normal levels after 6 months.

Background: To report an Asian patient with branch retinal vein occlusion secondary to neurofibromatosis 1. Case: A 64-year-old woman presented with a loss of vision in her right eye of 9-month duration. A diagnosis of neurofibromatosis 1 was made. A general medical examination showed no abnormalities except the signs of neurofibromatosis 1. Observations: Fundus examination of the right eye revealed irregularities of the venous caliber, partial sheathing of the corresponding vein and macular edema. Multiple dilated and tortuous collateral channels and an arteriovenous communication bridged the perfused and nonperfused retina. Fundus examination of the left eye showed a tortuous vein in the temporal region of the fovea. Fluorescein angiography of the right eye confirmed delayed filling in a superotemporal artery and in the corresponding vein. The temporal region of the fovea had large areas of capillary loss. The collaterals were tortuous and mimicked a neovascularization. Fluorescein angiography of the left eye confirmed that the vein in the temporal part of the fovea was tortuous and not leaking. A diagnosis of branch retinal vein occlusion of the superotemporal vein was made. Conclusions: Neurofibromatosis 1 should be considered in the differential diagnosis of retinal vascular occlusive disease without other risk factors.