Histologic analysis of photochemical lesions produced in rhesus retina by short-wave-length light.
(1/1813)
The photopathology of retinal lesions produced by extended exposure (1000 sec) to low corneal power levels (62 microW) of blue light (441 nm) was investigated by light microscopy in 20 rhesus eyes over an interval ranging from 1 hr to 90 days after exposure. Results indicate a nonthermal type of photochemical lesion originating in the retinal pigment epithelium and leading to a histological response with hypopigmentation which requires 48 hr to appear. This type of lesion helps to explain solar retinitis and eclipse blindness and has significance for aging and degenerative changes in the retina. (+info)
Pigment epithelial windows and drusen: an animal model.
(2/1813)
Aging rhesus monkeys, both controls and those undergoing long-term administration of investigational oral contraceptive steroids, developed widespread hyperfluorescent dots at the posterior pole. The dots were considered to represent drusen. Histologic (including electron microscopic) study showed the "drusen" in some of the animals to be almost exclusively pigment epithelial windows produced by a lipoidal degeneration of the pigment epithelial cells. The experiment provided a fortuitous model for direct correlation of clinical and histologic observations of myriad uniform, tiny, depigmented, hyperfluorescent, nonleaking spots at the level of the retinal pigment epithelium. (+info)
Necrosis and apoptosis after retinal ischemia: involvement of NMDA-mediated excitotoxicity and p53.
(3/1813)
PURPOSE: Accumulated evidence has shown that apoptosis and necrosis contribute to neuronal death after ischemia. The present study was performed to study the temporal and spatial patterns of neuronal necrosis and apoptosis after ischemia in retina and to outline mechanisms underlying necrosis and apoptosis. METHODS: Retinal ischemia was induced by increasing intraocular pressure to a range of 160 mm Hg to 180 mm Hg for 90 minutes in adult rats. The patterns of neuronal cell death were determined using light and electron microscopy and were visualized by TdT-dUTP nick-end labeling (TUNEL). The mRNA expression profile of p53 was examined using reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization histochemistry. Immunohistochemistry was performed using anti-p53, anti-microtubule associated protein-2, and anti-glial fibrillary acidic protein antibodies. RESULTS: Within 4 hours after ischemia, neurons in the inner nuclear cell layer (INL) and ganglion cell layer (GCL) underwent marked necrosis, made apparent by swelling of the cell body and mitochondria, early fenestration of the plasma membrane, and irregularly scattered condensation of nuclear chromatin. After 3 days, the INL and GCL neurons showed further degeneration through apoptosis marked by cell body shrinkage, aggregation, and condensation of nuclear chromatin. Apoptotic neurons were also observed sparsely in the outer nuclear cell layer. Intravitreal injections of MK-801 prevented early neuronal degeneration after ischemia. Of note, mRNA and protein levels of p53, the tumor suppressor gene known to induce apoptosis, were increased in the retinal areas undergoing apoptosis 1 to 3 days after ischemic injury. CONCLUSIONS: Ischemia produces the N-methyl-D-aspartate-mediated necrosis and slowly evolving apoptosis of neurons in the retina. The latter may depend on the expression of the p53 proapoptosis gene. (+info)
Idiopathic central serous chorioretinopathy.
(4/1813)
Idiopathic central serous chorioretinopathy (ICSC) is usually seen in young males with Type A personality. Clinical evaluation of the macula with fundoscopy and biomicroscopy, coupled with fluorescein angiography establishes the diagnosis. Indocyanine green angiographic studies have reinformed that the basic pathology lies in choriocapillaries and retinal pigment epithelium. Most of the ICSC resolve completely in four months, and some of them could resolve early with direct photocoagulation of the leaking site. Oral steroids have no role, and could even cause an adverse reaction. (+info)
Rapid pneumatic and Mackey-Marg applanation tonometry to evaluate the postural effect on intraocular pressure.
(5/1813)
A postural study was conducted in three separate groups of subjects. The first group comprised 20 women volunteers with an average age of 20-75 years. In this group, the study was conducted by the pneumatonograph only. Mean pressure recorded was 15-65 +/- 0-25 mmHg and there was an average rise of 1-4 mmHg in supine posture. Groups 2 and 3 comprised 151 non-glaucomatous and 108 glaucomatous eyes respectively in the age range of 30 to 85 years. In these two groups, the study was conducted using the PTG and the Mackay-Marg tonometer. Clinical evaluation of the Mackay-Marg with the PTG gave significant correlation, with mean Mackay-Marg readings being 1-13 mmHg higher. The intraocular pressure when changing from seated to the supine position increased on average by 2-71 and 4-04 mmHg, respectively in Groups 2 and 3 and by 2-51 and 3-72 mmHg by Vackay-Marg, suggesting a higher change in glaucomatous subjects. Pressure on resumption of sitting was found to be lower than the initial pressure. Postural change also showed some direct relationship with age in non-glaucomatous subjects. (+info)
Chronic retinal vein occlusion in glaucoma.
(6/1813)
Asymptomatic chronic retinal vein occlusion that occurs in chronic simple glaucoma is described. The condition is characterized by marked elevation of retinal vein pressure with collateral vessels and vein loops at the optic disc in cases of central vein occlusion, or retinal veno-venous anastomoses along a horizontal line temporal and nasal to the disc in hemisphere vein occlusion. No patient had visible arterial changes, capillary closure, fluorescein leakage, or haemorrhages. The vein occlusion was not limited to "end stage" glaucoma. The role of increased intraocular pressure and glaucomatous enlargement of the optic cup with retinal vein distortion in the pathogenesis of the condition was stressed. Follow-up of these patients revealed persistence of the retinal vein occlusion shown by elevated retinal vein pressures. This would reduce effective perfusion of the inner retina and optic disc and may affect the long-term visual prognosis. (+info)
Apoptosis and caspases after ischemia-reperfusion injury in rat retina.
(7/1813)
PURPOSE: Extensive cell loss in the retinal ganglion cell layer (RGCL) and the inner nuclear layer (INL) was noted in a rat model of retinal ischemia-reperfusion injury by transient elevated intraocular pressure (IOP). The possible involvement of apoptosis and caspases was examined in this model of neuronal loss. METHODS: Transient elevated IOP was induced in albino Lewis rats through the insertion of a needle into the anterior chamber connected to a saline column. Elevated IOP at 110 mm Hg was maintained for 60 minutes. Groups of animals were euthanatized at various times after reperfusion, and their retinas were evaluated by morphology, agarose gel electrophoresis of DNA, in situ terminal deoxynucleotidyl transferase-mediated biotin-deoxyuridine triphosphate nick-end labeling (TUNEL), immunohistochemistry of caspases II (ICH1) and III (CPP32), and morphometry. YVAD.CMK, a tetrapeptide inhibitor of caspases, was used to examine the involvement of caspases. RESULTS: A marked ladder pattern in retinal DNA gel analysis, typical of internucleosomal DNA fragmentation and characteristic of apoptosis, was present 12 and 18 hours after reperfusion. Labeling of nuclei in the RGCL and the inner nuclear layer (INL) by TUNEL was noted between 8 and 18 hours after reperfusion. Histologic and ultrastructural features typical of apoptosis were also observed in the inner retina after ischemia. YVAD.CMK administered during the ischemic period inhibited apoptotic fragmentation of retinal DNA and ameliorated the tissue damage. When administered intravitreally 0, 2, or 4 hours after reperfusion, YVAD.CMK was also effective in preserving the inner retina but had no significant effect when administered 6 or 8 hours after reperfusion. The inner retina showed transient elevated immunoreactivity of caspases II and III 4 and 8 hours after reperfusion. CONCLUSIONS: Retinal ischemia-reperfusion after transient elevated IOP induced apoptosis of cells in the retinal ganglion cell layer and the INL. Caspases may have a pivotal role in the early events of the apoptotic pathway(s). Rescue by using anti-apoptotic agents after ischemia-reperfusion is feasible. (+info)
Retinopathy of prematurity-mimicking retinopathy in full-term babies.
(8/1813)
The purpose of this study was to analyze the fundus findings and associated abnormalities in full-term babies with retinopathy of prematurity (ROP)-mimicking retinopathy. In twenty-seven such babies suffering from this condition, retinal findings were retrospectively analyzed. These babies were not premature and had not required supplementary oxygen; there was no family history of the disease, and no known causes. Bilaterality and severity of retinopathy were compared between groups with associated systemic abnormalities and those without. Forty eyes in twenty-seven full-term babies had abnormal retinal findings; dragged retina accounted for 42.5%, and falciform retinal fold for 47.5%, and retrolental membrane for 10%. Nine babies had associated brain abnormalities, and in these, severe bilateral retinopathy was more likely to occur than in those without abnormalities. These results suggest that if full-term babies have associated abnormalities of the brain, the presence of retinopathy should be ascertained postnatally by cautious examination of the retina. (+info)