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Results for “Retinal Neovascularization”

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PubMed1987

[Results of a survey on the occurrence of neovascular glaucoma after central retinal vein occlusion].

A prospective study, ten years long, has been conducted in 147 cases of retinal central vein occlusion without any photocoagulation treatment, in order to evaluate the frequency and the delay of occurrence of neovascular glaucoma. Neovascular glaucoma occurred in 28 cases (19%) occurrence rate of neovascular glaucoma increases in the first four years and then remains stable during the 10 years of observation. Connections between occurrence of neovascular glaucoma and initial association to ware hypertony of chronic glaucoma or to hypertony are discussed.

Glaucoma↗
PubMed1990

Spontaneous involution of subfoveal neovascularization.

We studied five patients who maintained or spontaneously regained significant central vision despite the presence of a subfoveal neovascular membrane. Sequential photographs and fluorescein angiograms showed a pattern of development common to these patients and not observed in patients who lose all central vision. The pattern involves formation of a pigmented ring around the subfoveal neovascular membrane followed by alteration of the membrane from one that leaks fluorescein to one that stains but does not leak. This pattern is associated with gradual resorption of subretinal fluid and apparent limitation of subretinal hemorrhage and fibrosis. This course suggests the occurrence of spontaneous involution of some subfoveal neovascular membranes and implicates the retinal pigment epithelium in this process.

Adult↗
PubMed1982

Efficacy of panretinal photocoagulation in preventing neovascular glaucoma following ischemic central retinal vein obstruction.

Ninety-three percent of eyes that develop neovascular glaucoma (NVG) following central retinal vein obstruction (CRVO) have an ischemic index greater than 50%. An ischemic index (percentage of retinal capillary nonperfusion) of 50% represents approximately 10 disc areas of retinal ischemia as determined by computer analysis of standard 30 degrees fluorescein angiograms. The difficulties of following patients clinically and angiographically at frequent intervals over extended periods of time, and the tendency for iris neovascularization (NVI) to develop and to progress rapidly to NVG with painful loss of vision emphasizes the importance of early recognition and treatment of high-risk eyes. In this prospective study (1976--81), 100 consecutive eyes with an ischemic CRVO pattern (average ischemic index 82%) received early argon laser panretinal photocoagulation (PRP) and none developed NVG unless another ischemic event occurred following treatment. Prophylactic PRP in high-risk ischemic CRVO eyes appears to eliminate virtually the devastating complications of NVG.

Adult↗
PubMed2004

[Vitreoretinal traction syndrome in multiple sclerosis].

METHODS: From January to December 2001, 89 patients with multiple sclerosis (MS) were treated in our hospital; 24 of them were diagnosed for the first time. All patients underwent a complete ophthalmologic examination including a three-mirror contact lens examination when photopsias were found or the disease was diagnosed primarily. RESULTS: Two patients showed vitreoretinal tractions with signs of periphlebitis before clinical-neurological manifestation of multiple sclerosis. The third patient, in whom the disease had been known for years, showed distinct neovascularizations, vasculitis, and recurrent vitreous hemorrhages. High-dose steroid therapy resulted in stabilization of the retinal situation in one patient, but the tractions remained unchanged. Additional laser coagulation in the second patient achieved stabilization and reduction of the tractions. A pars plana vitrectomy led to stabilization of the retinal proliferation in the third patient. CONCLUSIONS: The vitreoretinal traction syndrome is associated with MS and can precede its clinical-neurological manifestation. The good results after argon laser coagulation and vitreoretinal surgery suggest a vascular pathogenesis of these tractions.

Adult↗
PubMed1977

Preliminary report on effect of retinal panphotocoagulation on rubeosis iridis and neovascular glaucoma.

Eight eyes with central retinal vein occlusion one eye with old central retinal artery occlusion complicated by rubeosis iridis or increased intraocular pressure, or both; and one eye with diabetic retinopathy and rubeosis iridis were treated by retinal panphotocoagulation. Vision did not improve but intraocular pressure was lower and iris neovascularisation regressed in most cases, supporting the hypothesis that retinal hypoxia is a cause of iris neovascularisation and suggesting that retinal panphotocoagulation has a potential prophylactic and therapeutic role in rubeosis iridis and early neovascular glaucoma.

Glaucoma↗
PubMedDate not supplied

Chorioretinal neovascularization after radial optic neurotomy for central retinal vein occlusion.

Radial optic neurotomy was recently introduced for the treatment of central retinal vein occlusion. Two patients developed chorioretinal neovascularization through the radial cut of the optic disc after pars plana vitrectomy, radial optic neurotomy, and endophotocoagulation. Patients undergoing radial optic neurotomy should be closely observed to minimize the risk of this complication.

Adult↗
PubMed1996

Basic fibroblast growth factor and vascular endothelial growth factor are present in epiretinal and choroidal neovascular membranes.

PURPOSE: To determine whether vascular endothelial growth factor and basic fibroblast growth factor, which may be critical mitogens for neovascularization, are present together in human retinal and choroidal neovascular membranes. METHODS: Light microscopic immunocytochemistry using antibodies against vascular endothelial growth factor, basic fibroblast growth factor, and several cellular "marker" proteins on frozen sections from three choroidal neovascular membranes from patients with age-related macular degeneration, seven surgically excised epiretinal membranes from patients with proliferative diabetic retinopathy, and six epiretinal membranes from patients with nonischemic proliferative retinopathies. RESULTS: All three choroidal neovascular membranes and all seven epiretinal membranes stained positive for vascular endothelial growth factor. Two choroidal neovascular membranes and six of the epiretinal membranes were positive for basic fibroblast growth factor. The same cells were often positive for both antigens. None of the epiretinal membranes from patients with nonischemic proliferative retinopathies were positive for either growth factor. Many of the cells that demonstrated growth factors were glial cells, vascular endothelial cells, and retinal pigment epithelial cells. CONCLUSIONS: Colocalization of two growth factors in the same cells of ocular neovascular membranes suggests that more than one growth factor may contribute to pathologic angiogenesis. Growth factors in neovascular tissues are not localized exclusively in the vascular endothelium. Because expression of some growth factors is stimulated by hypoxia, their localization within choroidal neovascular membranes suggests that hypoxia may be an etiologic factor for choroidal as well as for retinal neovascularization.

Adult↗
PubMed2005

Riluzole inhibits VEGF-induced endothelial cell proliferation in vitro and hyperoxia-induced abnormal vessel formation in vivo.

PURPOSE: The present study examined the effects of riluzole, a Food and Drug Administration-approved drug for amyotrophic lateral sclerosis, on VEGF-stimulated endothelial cell proliferation in culture, and on neovascularization in a rat model of retinopathy of prematurity (ROP). METHODS: Human umbilical vein endothelial cell and bovine retinal endothelial cell cultures were treated with VEGF to induce endothelial cell proliferation in the presence or absence of riluzole. Activation of PKC betaII was examined by quantifying its phosphorylated form on immunoblots. ROP was induced in 5-day-old rat pups by raising them in hyperoxic conditions for 7 days and in normoxic conditions for the next 5 days. Dextran fluorescence retinal angiography was used to quantitatively assess ROP. RESULTS: Riluzole inhibited VEGF-stimulated PKC betaII activation and cell proliferation in bovine retinal endothelial cell and human umbilical vein endothelial cell cultures. In addition, systemic administration of riluzole substantially ameliorated abnormal new vessel formation in the rat ROP model. CONCLUSIONS: The present results suggest that riluzole is a potent inhibitor of VEGF-induced endothelial cell proliferation both in vivo and in vitro. Since long-term use of riluzole has already been proven safe in humans, the present data indicate that clinical trials of riluzole for proliferative retinopathies should be implemented expeditiously.

Adolescent↗
PubMed2005

Long-term results of submacular surgery combined with macular translocation of the retinal pigment epithelium in neovascular age-related macular degeneration.

PURPOSE: To provide long-term (> or =5 years) follow-up data on patients who had previously undergone macular retinal pigment epithelium (RPE) translocation surgery for choroidal new vessels (CNVs) associated with age-related macular degeneration. DESIGN: Retrospective interventional case series. PARTICIPANTS: Four of 9 patients who originally underwent surgery and whose results were reported after 2 years of follow-up were reviewed again 5 to 6 years after surgery. METHODS: All surviving patients from the original trial were contacted, and those who consented to full ocular examination were called in for review. Examination included best-corrected visual acuity (VA), optical coherence tomography (OCT), fundus autofluorescence, fluorescein angiography (FA), and indocyanine green angiography. MAIN OUTCOME MEASURES: Long-term success of RPE translocation was assessed by VA, imaging, angiography, and maintenance of overlying foveal fixation. Comparisons were made to the original 2-year follow-up data previously published. RESULTS: Over the long term, VA had declined further in 3 patients and improved slightly in 1 patient. Significantly, all 4 patients had lost foveal fixation and autofluorescence of translocated RPE, which had been present at the original 2-year follow-up assessment. The RPE graft, however, seemed viable when assessed by OCT, FA, and indocyanine green angiography, and no patient had suffered a recurrence of CNVs. CONCLUSIONS: In these 4 patients, RPE choroidal grafts had survived in the subfoveal space for at least 5 to 6 years, but rescue of visual function had been transient. The long-term loss of foveal fixation and graft autofluorescence might be explained by chronic photoreceptor apoptosis, initiated by either surgery or the disease process itself. Caution should be applied when drawing firm conclusions from similar studies that provide data after only 2 years' follow-up.

Aged↗
PubMed1997

Experimental preretinal neovascularization by laser-induced venous thrombosis in rats.

PURPOSE: Retinal ischemia and neovascularization (NV) are important components of many retinal disorders. To facilitate further investigation of retinal ischemia and neovascularization, we sought to develop a reproducible in vivo experimental model of venous occlusion by photodynamic thrombosis in rats. METHODS: After anesthesia, 27 eyes of pigmented rats received an intraperitoneal injection of 0.2 ml of, 10% sodium fluorescein 15 minutes prior to laser treatment. With a blue-green argon laser, selected venous sites next to the optic nerve head were photocoagulated indirectly with a 78 diopter lens. Venous occlusion was accomplished using laser parameters of 1.0 second, 50 microns, and 50-100 mW. For a control group, 10 eyes were coagulated on the retina between major vessels using the same parameters after fluorescein injection. For a second control group, 1% sodium hyaluronate was injected into the subretinal space to make a long-standing retinal detachment in 5 eyes. RESULTS: With 1-8 laser impulses, each venous occlusion was obtained and was associated with extreme venous constriction and tortuousity. Retinal edema became evident 10-30 minutes after treatment in the sectors associated with the occluded veins. This edema became a bullous retinal detachment (RD) within 12 hours and intra-retinal hemorrhage was observed. The retinal edema continued for 3-10 days and the retinas reattached spontaneously. Prior to or after retinal reattachment 70% (19/27) of eyes developed retinal NV and tractional RD. Of these, 11 developed NV of the optic disc (NVD), 6 developed NV elsewhere (NVE), and 2 developed NVD and NVE. In 30% (8/27) of the eyes, retinal edema resolved without evidence of NV. In control groups no eyes showed either circulatory disorders or evidence of NV. CONCLUSIONS: This is a new model of retinal ischemia and associated neovascularization established by venous thrombosis that is easily reproducible. Many aspects of rat retinal physiology are known and this model has promise as an avenue for further investigation.

Animals↗
PubMed1989

Subretinal choroidal neovascularization as a response to penetrating retinal injury in the pigmented rabbit.

Subretinal choroidal neovascularization has been identified in the pigmented rabbit in association with penetrating retinal injury. In this study, the subretinal new vessels were not contained within the fibrous scar, but were located posterior to it and impinged on the visual streak. Histology revealed subretinal neovascularization in the region of transition from normal to atrophic retina. These new vessels originated from the choroidal vessels and extended through a spontaneous break in Bruch's membrane into the retinal pigment epithelium. There was degeneration of the photoreceptors and hyperplasia of the retinal pigment epithelium in the region of neovascularization. The subretinal new vessels identified in the pigmented rabbit have many of the morphological features seen in the human clinical condition, and therefore this animal model may be useful in studying human choroidal neovascularization.

Animals↗
PubMed1998

Branch retinal vein obstruction secondary to retinal arteriovenous communication.

PURPOSE: To document a branch retinal vein obstruction secondary to a congenital arteriovenous communication. METHOD: Case report of a young patient with retinal arteriovenous communication. RESULTS: A 12-year-old girl had a grade 2 retinal arteriovenous communication in her right eye. She was asymptomatic and was subsequently followed up. Magnetic resonance imaging of the brain was normal and disclosed no signs of Wyburn-Mason syndrome. Nine years later, she developed a branch retinal vein obstruction in the area of the arteriovenous communication. Six months later, the patient was free of secondary complications of branch retinal vein obstruction; however, she is being followed up to detect any retinal or iris neovascularization. CONCLUSION: Awareness of retinal vascular obstruction associated with arteriovenous communication may help its timely recognition, as well as prompt treatment of potential complications, such as retinal and iris neovascularization.

Arteriovenous Fistula↗
PubMed1990

[Intraretinal neovascularization in rats with experimental renovascular hypertension].

Newly formed intraretinal vessels caused by experimental renovascular hypertension were studied histopathologically in rats. In these rats, dystrophy of the outer retinal layer and disappearance of retinal small capillaries were found in correlation with the duration of hypertensive state. In particular, retina obtained from rats with severe hypertension maintained for 6 months or more showed marked tissue damage and intraretinal proliferation of pigment epithelial cell with numerous microvessels. Most of these vessels were characterized by endothelial cell with large nuclei and slit-like narrowed lumina. Similar microvessels were also frequently observed in neighboring pigment epithelial cell layer. Endothelial fenestrations were observed in these vessels, although no findings were observed suggesting vessels penetrating through Bruch's membrane from the choroid. Similar vessels were also found in the inner plexiform layer and rarely in the nerve fiber layer. They were surrounded by processes resembling basal infolding of pigment epithelial cell. However, no fenestration of endothelial cells was found in these vessels.

Animals↗
PubMed1997

Retinal venous beading with recurrent preretinal hemorrhage.

PURPOSE: To report a patient with idiopathic retinal venous beading and recurrent preretinal hemorrhage. METHOD: Case report of a 17-year-old girl with bilateral retinal venous beading, greater in the left eye than in the right eye, and recurrent preretinal hemorrhage in the left eye. RESULTS: Complete blood cell count, platelet count, blood glucose level, and hemoglobin electrophoresis were normal. Fluorescein angiography showed normal retinal arterial and venous filling with no evidence of retinal capillary nonperfusion or neovascularization. CONCLUSION: Idiopathic retinal venous beading may be associated with recurrent preretinal hemorrhage, even in the absence of retinal ischemia or neovascularization.

Adolescent↗
PubMed2001

Clinical variations and complications of Coats disease in 150 cases: the 2000 Sanford Gifford Memorial Lecture.

PURPOSE: The purpose of this report is to review the clinical variations and natural course of Coats disease, using strict diagnostic guidelines. METHODS: In a retrospective, consecutive series, Coats disease was defined as idiopathic retinal telangiectasia with intraretinal or subretinal exudation without appreciable signs of retinal or vitreal traction. We reviewed our experience with the clinical features, complications, and diagnostic approaches to Coats disease. RESULTS: In 150 consecutive patients (158 eyes), Coats disease was diagnosed at a median age of 5 years (range, 1 month to 63 years), occurred in 114 males (76%), and was unilateral in 142 patients (95%). There was no predilection for race or laterality. The most common referral diagnoses were Coats disease in 64 cases (41%) and retinoblastoma in 43 (27%). The first symptom or sign was decreased visual acuity in 68 cases (34%), strabismus in 37 (23%), leukocoria in 31 (20%), and 13 patients (8%) were asymptomatic. Visual acuity at presentation was 20/200 to no light perception in 121 eyes (76%). The anterior segment was normal in 142 eyes (90%). The retinal telangiectasia involved the midperipheral or peripheral fundus in 156 of the 158 eyes (99%) and was restricted to the macular area in two eyes (1%); involved mainly the temporal fundus in 66 eyes (42%), inferior fundus in 41 eyes (26%), and more than one sector in 34 eyes (22%). Retinal exudation was present in all 12 clock hours in 86 eyes (55%) and six or more clock hours in 115 eyes (73%). There was a total retinal detachment in 74 eyes (47%) and neovascular glaucoma in 12 (8%). Retinal macrocysts were present in 18 eyes (11%), a vasoproliferative tumor in nine eyes (6%) and retinal neovascularization in four eyes (3%). Fluorescein angiography in 49 of the 158 eyes (37%) disclosed early hyperfluorescence of the telangiectasias and macular edema in 18 of eyes (37%). Ultrasonography typically showed a retinal detachment but no solid mass. CONCLUSIONS: Coats disease is a distinct clinical entity characterized by idiopathic retinal telangiectasia and retinal exudation. It is usually unilateral, occurs mostly in young males, and can cause severe visual loss resulting from exudative retinal detachment. The clinician should follow strict criteria in making the diagnosis, to avoid confusing Coats disease with other forms of exudative retinopathy.

Adolescent↗