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PubMed1998

[Choroidal venous dilatation in serous retinal detachment].

We studied the correlation between choroidal venous dilatation, intrachoroidal leakage of dye, and subretinal leakage from the choroid in patients with serous retinal detachment unaccompanied by choroidal neovascularization. We reviewed 13 eyes with anamnesis of serous retinal detachment, 23 eyes without anamnesis, and one eye of unknown status of a total of 37 eyes. Regarding the relationship between subretinal dye leakage from the choroid in fluorescein angiography (FAG) and choroidal venous dilatation in indocyanine green angiography (ICG), the point of subretinal leakage (31 points) was on and/or in the neighborhood of the site of choroidal venous dilatation in 87.1% of the 27 eyes, except for eyes of unknown site of leakage in FAG. The point of subretinal leakage was within and/or in the neighborhood of the intrachoroidal leakage of dye in ICG in 92% of the eyes. In serous retinal detachment without choroidal neovascular membranes, serous retinal detachment may be caused by breakdown of the outer retinal barrier due to choroidal venous congestion and intrachoroidal diffusion.

Choroid↗
PubMed2005

Spontaneous rip of the retinal pigment epithelium with a macular hole in neovascular age-related macular degeneration.

PURPOSE: To report a case of retinal pigment epithelial tear associated with a macular hole in a patient with neovascular age-related macular degeneration (AMD). DESIGN: Observational case report. METHODS: An 87-year-old woman with AMD-related fibrovascular pigment epithelial detachment associated with vision loss was followed with sequential fundus photography, fluorescein angiography, and optical coherence tomography for 8 months. RESULTS: The detachment developed into a retinal pigment epithelium tear with macular hole formation. The temporal evolution of the lesion and optical coherence tomography findings suggested that the retinal pigment epithelium tear led to stretching forces along the posterior surface of the neurosensory retina with secondary foveal dehiscence. CONCLUSION: Macular hole formation is one mechanism by which retinal pigment epithelium tears may cause vision loss in AMD.

Aged↗
PubMedDate not supplied

Neovascular glaucoma associated with cilioretinal artery occlusion combined with perfused central retinal vein occlusion.

BACKGROUND: Cilioretinal artery occlusion rarely results in neovascular glaucoma, especially in cases of extensive cilioretinal infarction and combined retinal vascular occlusion. CASE: A 62-year-old man with diabetes mellitus and essential hypertension showed a visual acuity of counting fingers, retinal whitening temporal to the optic disc with mild dilation and tortuosity of the retinal veins, and retinal hemorrhages in four quadrants of his right eye. Fluorescein angiography demonstrated a delayed filling of the central retinal vein and cilioretinal artery. OBSERVATIONS: Two months later, neovascular glaucoma developed and retinal ablation was performed using an argon laser. Trabeculectomy was also performed due to the intractability of the glaucoma, and central artery occlusion was found. On magnetic resonance angiography, the right distal common carotid artery was irregularly narrowed and the right ophthalmic artery was almost entirely occluded. CONCLUSIONS: In cases of cilioretinal artery occlusion and perfused central retinal vein occlusion with multiple risk factors, close follow-up is advised.

Ciliary Arteries↗
PubMed2001

[Eales].

Eales' disease, first described by Eales Henry in 1880, is an idiopathic obliterative vasculopathy that primarily affects the peripheral retina of adults. From nosologic point of view, we could distinguish the "true Eales disease" affecting males in India and portions of the Middle East and the "Eales' like disease" with no geographical or sex predisposition. Vascular sheathing, peripheral retinal nonperfusion and neovascularization are the principal clinical and angiographic findings. It remains a diagnostic by exclusion and retinal diseases with other causes of inflammation or neovascularization must be excluded. In the absence of a specific treatment, retinal photocoagulation to the nonperfused retina and vitrectomy for recurrent vitreal hemorrhage could be proposed.

Humans↗
PubMed2001

Lack of effect of gender on retinopathy in the mouse.

BACKGROUND: The reported effect of gender on retinopathy of prematurity has been controversial. The goal of this study was to determine the effect of gender on oxygen-induced retinopathy in a mouse model. METHODS: Oxygen-induced retinopathy was produced in C57BL6 mice by exposure to 75% oxygen from postnatal day (P) 7 for 5 days. Animals were returned to room air on P12 and killed on P17-21. Gender was determined by inspection. Retinopathy was evaluated by a retinopathy scoring system and by quantifcation of extraretinal neovascular nuclei on retinal sections. RESULTS: Both males and females developed similar degrees of retinopathy. Males had a median total retinopathy score of 9 (25th, 75th quartile: 8, 11) and females had score of 9 (25th, 75th quartile: 7, 10). Retinal subscores of blood vessel growth, blood vessel tufts, extraretinal neovascularzation, haemorrhage and blood vessel tortuosity were similar in both groups. Males and females had a similar number of neovascular nuclei on retinal sections. CONCLUSIONS: Gender does not alter the development of oxygen-induced retinopathy in the C57BL6 mouse.

Animals↗
PubMed2003

Choroidal osteoma: observations from a community setting.

PURPOSE: To determine the characteristics of choroidal osteoma arising from a previously unreported patient population and to document new observations in this condition. DESIGN: Retrospective, observational case series. PARTICIPANTS: Eleven consecutive patients seen from 1986 through 2002 with choroidal osteoma from one community-based retina practice. INTERVENTION: Laser ablation of subretinal neovascularization in two cases and focal laser treatment of retinal pigment epithelial leaks in one case. METHODS: Photographs, fluorescein and indocyanine green angiograms, and clinical records were analyzed. MAIN OUTCOME MEASURES: Demographic variables, visual acuity, complications of laser treatment, growth of lesions, and associated funduscopic changes. RESULTS: Choroidal osteoma from a community setting is more frequently asymptomatic (5/11 cases; 45%) than in previously reported university series, is usually initially misdiagnosed, and is not rare. Light-intensity focal laser photocoagulation for serous retinal detachment unaccompanied by subretinal neovascularization can resolve fluid (1/11 cases; 9%). Laser ablation of secondary subretinal neovascularization stimulates rapid choroidal osteoma vascular remodeling (2/11 cases; 18%) and can cause retina-osteoma venous and arterial anastomoses (1/11 cases; 9%). Spontaneous choroidal hemorrhage unaccompanied by subretinal neovascularization can occur with confinement to the osteoma borders (1/11 cases; 9%). Association of choroidal osteoma with retinitis pigmentosa is reported. CONCLUSIONS: These data on choroidal osteoma natural history and treatment help clinicians managing these lesions. In the community, a higher index of suspicion for choroidal osteoma is warranted.

Adolescent↗
PubMed2005

Retinal vascular development and pathologic retinal angiogenesis are not impaired in matrix metalloproteinase-2 deficient mice.

PURPOSE: Earlier studies have suggested a role for metalloproteinase-2 (MMP-2) in retinal angiogenesis. To investigate this further, we have studied retinal vascular development and pathologic ischemia-induced retinal angiogenesis in MMP-2-deficient and wild-type mice. METHODS: Vascular development of the retina was studied in retinal flatmounts, whereas pathologic retinal angiogenesis was analyzed in retinal flatmounts and on histologic sections using a model of ischemia-induced retinopathy. The time course of MMP-2 mRNA expression was determined by in situ hybridization and real-time polymerase chain reaction (PCR). RESULTS: Formation of the retinal vascular plexus was not significantly different in MMP-2-deficient mice as compared to wild-type mice. In ischemia-induced retinopathy, there was an increased formation of extraretinal neovascular tufts in the MMP-2-deficient mice (p < 0.05). MMP-2 mRNA expression did not correlate to either retinal vascular development or to ischemia-induced formation of extraretinal vascular tufts. CONCLUSIONS: The current data suggest that MMP-2 is not essential for either retinal vascular development or pathologic retinal neovascularization in the mouse.

Animals↗
PubMed2001

Presenilin-2 (PS2) expression up-regulation in a model of retinopathy of prematurity and pathoangiogenesis.

Presenilin-2 (PS2; AD4), a regulator of intercellular signaling during CNS development and cell fate determination, appears to be involved in pathogenic processing of beta-amyloid precursor protein (betaAPP) into potentially neurotoxic beta-amyloid (Abeta) peptides. The PS2 gene promoter contains multiple DNA binding sites for the relatively rare hypoxia-inducible transcription factor HIF-1, suggesting that PS2 expression may be a sensitive indicator of decreased oxygen availability. We have used a cycled hypoxia/hyperoxia (10-50% O2) protocol followed by normoxia (20% O2) as a retinal model of retinopathy of prematurity to induce neovascularization (NV) in rat pups. Retinal cell nuclear extracts from pups undergoing hypoxia exhibited a dramatic increase in HIF-1-DNA binding, followed by a delayed (2-7 day) elevation of PS2 RNA message and protein. PS2 gene activation during hypoxia may direct cellular fate towards pathoangiogenesis and intercellular PS2-mediated signaling dysfunction.

Animals↗
PubMed1999

[Ocular manifestations of Behçet's disease].

Ocular complications of Behçet's disease are considered one of the major criteria upon which the diagnosis is based. The ocular disease is characterized by repeated, explosive ocular inflammatory attacks which can healed spontaneously. During in-between attacks there is little or no evidence of inflammation in the eyes. The anterior segment can be involved alone presenting as a severe anterior uveitis with hypopyon. Posterior pole involvement is often sight threatening presenting as recurrent retinal vaso-occlusive disease. The fundus changes most frequently encountered are hyperhemia of the optic nerve, macular edema, retinal edema, vascular sheathing retinal exudate, and retinal hemorrhages. Complications of the inflammation include retinal and optic disc atrophy, neovascular glaucoma, vitreous hemorrhage, retinal detachment. Treatment is with topical steroids, systemic medications, including corticosteroids, colchicine, and immunosuppressive drugs. These complications are sight threatening and require a close follow up and a collaboration between ophthalmologists and Internal Medicine physicians.

Behcet Syndrome↗
PubMed1992

[Segmental retinal arteritis and retinochorioiditis].

Acute ocular toxoplasmosis is characterized by a focal retinochoroidal infiltrate, often appearing in the immediate vicinity of an old retinochoroidal scar (satellite lesion). There are atypical forms of ocular toxoplasmosis, including retinal granulomas, intraretinal and subretinal neovascularization, preretinal gliosis and retinal detachment. In rare instances, associated immunological phenomena, i.e. concomitant vasculitis and perivasculitis, have been described. We report on a 28-year-old male patient presenting with signs of congenital toxoplasmosis with intracerebral calcifications and internal hydrocephalus (Whytt's disease). Ocular manifestations included an acute retinochoroidal infiltrate adjacent to a retinochoroidal scar and segmental retinal periarteritis. All arterioles were involved, but there was no inflammation of the venules. Fluorescein angiography revealed filling irregularities of the vessel segments involved. Like a tubercular patient with segmental periarteritis reported on as long ago as 1939, our patient had undergone treatment for active tuberculosis of the lung 6 years earlier. Considering the fact that segmental periarteritis without concomitant periphlebitis is very rarely seen, the coincidence of acute toxoplasmosis and previous tuberculosis suggests a complex immunological etiology of retinal vasculitis. This assumption may be supported by the fact that a combined systemic treatment with pyrimethamine, trimethoprim, sulfamethoxazole and prednisolone reduced the retinochoroidal inflammation and periarterial infiltrates.

Adult↗
PubMed1987

Central retinal artery occlusion with an irido-embolus following carotid endarterectomy.

Endarterectomy is often the treatment of choice in carotid artery disease displaying significant stenosis of the internal carotid artery. This procedure is not without its complications, the most visually devastating being central retinal artery occlusion and secondary neovascularization. Such a case is presented here along with the interesting finding of a cholesterol irido-embolus, apparently the first citation in the ophthalmic literature to date.

Aged↗
PubMed1995

Retinal vasculitis in Lyme borreliosis.

We observed retinal vasculitis in seven patients with clinical and serologic evidence of Borrelia burgdorferi infection. Three patients presented with abrupt loss of vision due to acute retinal vasculitis. Funduscopy demonstrated engorged veins, hemorrhages, perivenous infiltrates and retinal white spots. Fluorescein angiography showed leakage from the veins, from the white spots and from the optic disc. Moreover arterial occlusions were observed in two patients. Four patients had signs of chronic uveitis with vitritis, cystoid macular oedema and retinal vasculitis, which was associated with neovascularization and vitreous hemorrhage in one patient, and with optic neuritis in another patient. Six patients received antibiotic treatment and three patients received systemic corticosteroids. Marked improvement in the three acute retinal vasculitis cases occurred within several weeks, the fundus changes disappeared in another few months, and no recurrences were observed. The final visual acuity was excellent in these patients, although optic disc pallor and visual field loss persisted in one case. In the four patients with chronic uveitis visual blurring improved following antibiotic treatment and the retinal vasculitis and vitritis slowly regressed. The proliferative retinopathy of one patient required panretinal laser treatment.

Adult↗
PubMed1999

[Repeat laser coagulation of subretinal neovascularization in age-related macular degeneration].

INTRODUCTION: Retinal laser coagulation (LC) of extrafoveal subretinal neovascularization (SRN) due to age-related macular degeneration (AMD) is the only sure therapy. Diagnostics, therapy and follow-up are presented in a case report. CASE REPORT: A 55-year-old woman had suffered from progressive reduction of visual acuity (with metamorphopsia) in both eyes (LE > RE) for 3 years. In the RE the visual acuity was 0.32 and in the LE 0.05. Funduscopy and fluorescein angiography revealed in both eyes the wet form of AMD. The extrafovealy located SRN of the RE was photocoagulated and had to be retreated three-times in 6 weeks due to persistence. For 8 months the findings in the RE have been stable. VA has been improved to 0.4 and no metamorphopsia has been found. CONCLUSION: Extrafoveal SRN should be treated by LC. Short-term follow-up (including FA) and in most cases several LCs are necessary to close the SRN and save the patients' reading vision.

Female↗
PubMed2006

Central retinal venous occlusion in an otherwise-healthy child.

Isolated retinal venous occlusion rarely occurs in otherwise-healthy children.(1-3) We report a unilateral case of central retinal vein occlusion with secondary proliferative retinopathy and neovascular glaucoma in a 6-year-old girl. Despite an extensive workup, no etiology was identified.

Antihypertensive Agents↗
PubMed2001

Reduced severity of oxygen-induced retinopathy in eNOS-deficient mice.

PURPOSE: Exposure of premature human infants to hyperoxia results in the obliteration of developing retina capillaries, leading to a vision-threatening retinopathy termed retinopathy of prematurity (ROP). The authors hypothesized that this process may be mediated in part by endothelial nitric oxide (NO)-derived oxidants such as peroxynitrite and tested this hypothesis in a mouse model of ROP. METHODS: Normal mice, mice treated with the nitric oxide synthase (NOS) inhibitor N:(G)-nitro-L-arginine (L-NNA), and knockout mice carrying a homozygous targeted disruption of the gene for endothelial NOS (eNOS) were studied in an experimental model of ROP. Retinas were compared for extent of capillary obliteration in hyperoxia, vascular endothelial growth factor (VEGF) expression, nitrotyrosine formation, and vitreous neovascularization. RESULTS: Oxygen-induced retinal vaso-obliteration was significantly reduced by L-NNA treatment (43% decrease from controls). The eNOS-deficient mice showed a similar reduction in vaso-obliteration (46% decrease from controls), and vitreous neovascularization was also substantially reduced (threefold decrease). Retinal nitrotyrosine formation, a measure of in situ peroxynitrite modification of proteins, was significantly elevated in normal mice during hyperoxia, in a spatial and temporal pattern consistent with a role in oxygen-induced vaso-obliteration. This was not seen in eNOS-deficient mice. VEGF expression was similar in both groups of mice, although suppression in hyperoxia was slightly blunted in eNOS-deficient mice. CONCLUSIONS: These data suggest a role for NO and peroxynitrite in the pathogenesis of ROP. Therapies aimed at modulation of eNOS activity may have therapeutic potential for preventing ROP.

Animals↗
PubMed1997

Growth factors and diabetic retinopathy.

Preretinal neovascularization and chronic retinal oedema are the two major sight-threatening complications that can occur during diabetic retinopathy. Ocular neovascularization is strongly associated with retinal ischaemia, and growth factors have been implicated in its pathogenesis. The ischaemic retina is assumed to secrete growth factors that stimulate residual vessels to proliferate. Interest has focused on basic fibroblast growth factor (bFGF), insulin-like growth factor-1 (IGF-1), platelet-derived growth factor (PDGF), transforming growth factor beta (TGF beta) and more recently vascular endothelial cell growth factor (VEGF). Histologic studies have demonstrated the presence of growth factor proteins and receptors and/or their mRNA, mainly VEGF, PDGF, and bFGF, in preretinal membranes of patients with proliferative diabetic retinopathy. Elevated intravitreal levels of IGF-1 and VEGF correlating with neovascular activity have been found in some patients. However, a direct causal relationship between ischaemia, growth factors and neovascularization has not been clearly demonstrated despite considerable research work. To date, the growth factor correlating most closely with neovascularization is VEGF. As many growth factors seem to be produced during the neovascular process, their specific inhibition probably will have limited effects. Laser photocoagulation of the retina has proved beneficial for regression of new vessels, probably through destruction of the ischaemic retina producing neovascular growth factors, and is currently the only treatment for proliferative diabetic retinopathy. Inhibition of IGF-1 by somatostatin analogs has produced unsatisfactory results. Other vascular inhibitors are currently being studied.

Animals↗
PubMed1994

[Ophthalmological aspects of systemic vasculitis].

Ocular findings of systemic vasculitis, such as polyarteritis nodosa, giant cell angitis, and aortitis syndrome were reviewed. Systemic lupus erythematosus is not categorized as systemic vasculitis, however its ocular findings are microangiopathic. Therefore review of its ocular findings was included in this paper. The most common fundus finding in these diseases is ischemic optic neuropathy or retinal vascular occlusions. Therefore several points in diagnosis or pathogenesis of optic neuropathy and retinal and choroidal vaso occlusion were discussed. Choroidal ischemia has come to be able to diagnosed clinically, since fluorescein angiography was applied in these lesions. When choroidal arteries are occluded, overlying retinal pigment epithelium is damaged. This causes disruption of barrier function of the epithelium and allows fluid from choroidal vasculatures to pass into subsensory retinal spaces. This is a pathogenesis of serous detachment of the retina. The retinal arterial occlusion formed non-perfused retina. Such hypoxic retina released angiogenetic factors which stimulate retinal and iris neovascularizations and iris neovascularization may cause neovascular glaucoma.

Blood-Retinal Barrier↗