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PubMed2000

[Micro-perimetric documentation of retinal function in photodynamic therapy of choroid neovascularizations].

PURPOSE: Photodynamic therapy provides occlusion of choroidal neovascularization by intravascular endothelial damage. The photodynamic approach offers the potential to occlude choroidal neovascularization selectively without altering adjacent sensory retina and therefore to preserve visual acuity. To determine the selectivity of photodynamic therapy photoreceptor function was measured by microperimetry allowing topic mapping of retinal function. METHODS: A Rodenstock scanning laser ophthalmoscope was used to document preservation of central visual fields before and after photodynamic therapy. Single photodynamic therapy without known efficient parameters was performed in 13 patients and repeated photodynamic therapy using optimised light doses was performed in 10 patients with subfoveal choroidal neovascularization using benzoporphyrin derivate (verteporfin). Intensity and dimension of central scotomas were measured, using a grading system of stimuli ranging from 0-32 dB. Areas of absolute and relative defect were defined and fixation localisation was monitored. Perimetric testing was done pre photodynamic therapy, one week, one month and three months post photodynamic therapy. RESULTS: Postoperative scotomas after single photodynamic therapy were smaller in 8%, identical in 61% and larger in 31% compared with preoperative findings. After repeated photodynamic therapy postoperative scotomas were smaller in 70%, identical in 30% and larger in no case. The observed increase was less than 25% of the original size. Postoperative defects were always significantly smaller than the entire size of the irradiated area. No new scotomas were found after photodynamic therapy. Angiographically visible occlusion post photodynamic therapy was in general larger than scotoma size. CONCLUSION: Documentation of the retinal function by microperimetry after photodynamic therapy of subfoveal choroidal neovascularization shows no new scotoma in the treated area. This can also be documented in the hypofluorescent area around the lesion one week after the treatment. After repeated treatment a reduced scotoma size due to choroidal neovascularization could be seen in 2/3 of the patients after 3 months. No initial vision loss as seen in conventional photocoagulation could be documented after photodynamic therapy.

Aged↗

PubMed2005

Developmental abnormalities in the Nuc1 rat retina: a spontaneous mutation that affects neuronal and vascular remodeling and retinal function.

The retina serves as an excellent model in which to study vertebrate CNS development. We have discovered a spontaneous mutation in the Sprague-Dawley rat that results in a novel and unusual ocular phenotype, including retinal abnormalities, that we have named Nuc1. We have previously shown that the Nuc1 mutation appears to suppress programmed cell death in the developing retina. Here we report that maturation of both the retinal neurons and the retinal vessels is abnormal in Nuc1 homozygous rats. The developmental changes in the retinal neurons and vasculature are correlated with regard to degree of abnormality. As Nuc1 homozygotes mature, focal retinal detachment begins at approximately 3 months after birth, and near total traction retinal detachment, associated with pre-retinal fibrosis and neovascularization, is evident by 18 months. Electroretinographic studies at 2.5 months of age indicate that functional retinal degeneration precedes retinal detachment. The functional abnormality is most evident in rods and the inner retina, and is present in homozygous but not heterozygous mutants. Immunocytochemical studies of rod and cone photoreceptors indicate abnormalities in rod, but not cone, photoreceptors in Nuc1 homozygotes, consistent with the electroretinographic findings. In Nuc1 animals, the Muller cells are activated. Although such activation may result from inflammation, Muller cells in Nuc1 may be reacting to a neuronal influence. It appears that the Nuc1 mutation plays a regulatory role in both developing and maturing ocular tissues. The Nuc1 mutation may also serve as an important genetic tool to explore the relationships that may exist among gliosis, normal neuronal development, and normal vascular development and how abnormalities in these associations lead to common retinal diseases.

Amacrine Cells↗

PubMed1993

Age-related macular degeneration: the current understanding of the status of clinicopathology, diagnosis and management.

BACKGROUND: This paper represents an up-to-date review of the current thoughts regarding the etiopathogenesis and management of the various varieties of age-related macular degeneration (ARMD). METHODS: Included is a look at the epidemiology as well as the clinicopathologic basis for the development of the degenerative process. CONCLUSIONS: The clinicopathologic basis for development of ARMD is divided into drusen, lipofuscin development, solar radiation effects, photochemical damage and mediation by antioxidants, choroidal neovascularization, scarification, and retinal pigment epithelial detachment. The clinical presentation of both non-exudative and exudative ARMD is discussed with synopses of the mimickers of both outlined in the text. RESULTS: Current accepted methods of therapy are discussed including; laser intervention, surgical removal of membranes, and investigational modes of treatment including antioxidants. Specific management protocol is discussed based on the current knowledge base.

Aged↗

PubMed1999

Change in retinal sensitivity due to excision of choroidal neovascularization and its influence on visual acuity outcome.

PURPOSE: Excision of choroidal neovascular membranes (CNV) has been attempted as an alternative to photocoagulation for the management of subfoveal CNV. To evaluate functional results of CNV excision, we studied retinal sensitivity in the area corresponding to the CNV (CNV area). METHODS: Static microperimetry using a scanning laser ophthalmoscope was performed on 17 eyes before and after CNV excision. We studied whether CNV excision changed retinal sensitivity in the CNV area. To evaluate the relationship between retinal sensitivity and visual acuity, further testing was performed on nine patients who had subfoveal CNV from age-related macular degeneration (ARMD). RESULTS: Preoperatively, 5 of 17 eyes (29.4%) had retinal sensitivity in the CNV area. Postoperatively, 4 of 17 (23.5%) eyes had retinal sensitivity. Surgery did not significantly change retinal sensitivity in the CNV area (P>0.999). There was a significant correlation between the presence of retinal sensitivity and visual acuity. Postoperative visual acuity of eyes with retinal sensitivity in the CNV area was better than that of the eyes without sensitivity in the patients with subfoveal CNV from ARMD (P = 0.0017). CONCLUSIONS: In most cases, excision of CNV does not improve central retinal sensitivity, and patients have poor visual outcome. In some cases, however, postoperative sensitivity in the bed of CNV is preserved and visual outcome is relatively good. Better or worse preoperative retinal sensitivity does not predict better or worse visual acuity outcome, respectively.

Adult↗

PubMedDate not supplied

Serous retinal pigment epithelial detachment with a notch. A sign of occult choroidal neovascularization.

One or more signs of occult neovascularization usually accompany large serous detachments of the retinal pigment epithelium occurring in patients older than 50 years of age. Evidence is presented that a flattened or notched border of these detachments is a frequently encountered and an important biomicroscopic and fluorescein angiographic sign of hidden choroidal neovascular complex, most of which lies outside the area of the serous detachment of the pigment epithelium. A clinical trial is required to determine the reliability of the various signs of occult neovascularization and the effectiveness of laser photocoagulation in these patients.

Aged↗

PubMed2000

[Siblings with age-related macular degeneration in a pedigree].

BACKGROUND: The pathogenesis of age-related macular degeneration remains unknown. Environmental and genetic factors have been shown to be associated with in this disease. We report siblings with age-related macular degeneration. CASES: The proband (the third of 6 siblings) was found to have retinal pigment epithelial abnormalities and drusen of the right macula, and serous retinal detachment, drusen, and choroidal neovascularization of the left macula. Examination of the eldest siblings showed choroidal neovascularization, subretinal hemorrhage, and serous retinal detachment of the right macula. The left eye of the proband and the right eye of the eldest siblings were treated with laser photocoagulation. The fourth sibling was examined, and findings included retinal pigment epithelial abnormalities of both maculas and drusen of the right eye. The sixth sibling had drusen of the left macula. CONCLUSION: We report a family in which two siblings had age-related macular degeneration and two other siblings had abnormalities of the maculas.

Aged↗

PubMed2006

Hematopoietic stem cells provide repair functions after laser-induced Bruch's membrane rupture model of choroidal neovascularization.

Vascular repair by adult hematopoietic stem cells (HSCs) is well-appreciated because these cells are known for their plasticity. We have shown that adult HSCs differentiate into endothelial cells and participate in both retinal and choroidal neovascularization. We asked whether HSCs participated in the wounding response by forming astrocytes, retinal pigment epithelia (RPE), macrophages, and pericytes. Lethally irradiated C57BL6/J mice were reconstituted with HSCs from mice homozygous for green fluorescent protein (GFP) and then subjected to laser-induced rupture of Bruch's membrane. After immunohistochemical examination of ocular tissue, GFP(+) astrocytes were observed concentrated along the edge of the laser wound, where they and mural cells closely ensheathed the neovasculature. GFP(+) vascular endothelial cells and macrophages/microglia were also evident. Large irregularly shaped GFP(+) RPE cells constituted approximately 93% of RPE cells adjacent to the edge of the denuded RPE area. In regions farther away from the wound, GFP(+) RPE cells were integrated among the GFP(-) host RPE. Thus, postnatal HSCs can differentiate into cells expressing markers specific to astrocytes, macrophages/microglia, mural cells, or RPE. These studies suggest that HSCs could serve as a therapeutic source for long-term regeneration of injured retina and choroid in diseases such as age-related macular degeneration and retinitis pigmentosa.

Animals↗

PubMed2003

Focal inner retinal hemorrhages in patients with drusen: an early sign of occult choroidal neovascularization and chorioretinal anastomosis.

PURPOSE: To present evidence that superficial retinal hemorrhage in the macula of patients with age-related macular degeneration (ARMD) may be an early sign of occult chorioretinal anastomosis (OCRA) and type 1 occult choroidal neovascularization (OCNV). METHODS: Retrospective follow-up study of 16 patients presenting with a small focal area of superficial retinal hemorrhages and drusen in the juxtafoveolar area in 24 eyes. RESULTS: OCRA and OCNV occurred in an older subset of patients with ARMD (mean age, 75 years). Of 22 eyes with the early stages of chorioretinal anastomosis (CRA), 18 had evidence of a piggyback neovascular complex, with the smaller subsensory retinal type 2 complex lying anterior to the larger subretinal pigment epithelial type 1 complex. At initial presentation, three patients had OCRA and OCNV bilaterally, and three patients had large disciform cicatricial lesions with overt CRA in the fellow eye. Nine patients had one or more laser photocoagulation treatments for early stages of CRA. Only one patient maintained visual acuity of better than 20/200 for >1 year. At the last follow-up, 24 of 26 eyes with CRA had visual acuity of 20/200 or less. CONCLUSION: Superficial retinal hemorrhage in the paracentral area of patients with drusen is the earliest sign of OCRA and OCNV. Fluorescein angiography and indocyanine green angiography are important in detecting the dual nature of the subretinal neovascular network. Photocoagulation and photodynamic treatment is usually unsuccessful in preserving central vision.

Aged↗

PubMed2003

RPE cells modulate subretinal neovascularization, but do not cause regression in mice with sustained expression of VEGF.

PURPOSE: Previous studies using models of choroidal neovascularization (CNV) in which the angiogenic stimulus is not sustained, have concluded that the retinal pigmented epithelium (RPE) causes regression of neovascularization (NV). However, the withdrawal of angiogenic stimuli may actually be the major modulator of NV, and RPE cells may simply be responding to withdrawal of the angiogenic stimuli or something released by NV because of the withdrawal. In this study, the long-term course of NV and the behavior of the RPE in rhodopsin/VEGF transgenic mice, in which there is a sustained angiogenic stimulus, was investigated. METHODS: Hemizygous mice from the V-6 line were killed at 0.75, 1, 3, 6, and 12 months after birth, and at each time point mRNA for VEGF, VEGF-R1, and VEGF-R2 was measured by RT-PCR. Some mice were perfused with fluorescein-labeled dextran and retinal flatmounts were examined by fluorescence microscopy. Light and electron microscopy was performed on Epon-embedded eyes. RESULTS: The mRNA levels for VEGF, VEGF-R1, and VEGF-R2 remained constant from the earliest to the latest time point. Retinal flatmounts showed numerous small areas of subretinal NV at 3 weeks and at 1 month, and there were a similar number of larger lesions. By 6 months, many of the individual NV lesions had grown together to form large networks of new vessels. At 12 months, NV networks were similar to those at 6 months, but some of the vessels were not perfused. Light microscopy showed serous retinal detachments overlying NV lesions in mice up to 3 months of age, but at 6 and 12 months, the RPE completely surrounded new vessels and formed tight junctions to reestablish the outer blood-retinal barrier, and there were no serous detachments. Electron microscopy showed that compared with more acute NV lesions, chronic lesions contained thinner endothelial cells, similar to those of the choriocapillaris in that they had scant cytoplasm and numerous fenestrations, or pinocytotic vesicles with thick basement membrane surrounded by extracellular matrix (ECM). Bruch's membrane remained intact. CONCLUSIONS: Despite persistent high expression of VEGF and its receptors, NV stopped growing and reached a plateau in older V-6 mice. RPE cells modulated the NV by surrounding it and reestablishing the blood-retinal barrier, but did not cause regression, although some vessels in chronic lesions were not perfused. These data do not support the conclusion of several previously reported studies, that RPE cells cause regression of CNV.

Animals↗

PubMed2004

Increased expression of VEGF in retinal pigmented epithelial cells is not sufficient to cause choroidal neovascularization.

Increased expression of vascular endothelial cell growth factor (VEGF) in the retina is sufficient to stimulate sprouting of neovascularization from the deep capillary bed of the retina, but not the superficial retinal capillaries or the choriocapillaris. Coexpression of VEGF and angiopoietin 2 (Ang2) results in sprouting of neovascularization from superficial and deep retinal capillaries, but not the choriocapillaris. However, retina-derived VEGF and Ang2 may not reach the choriocapillaris, because of tight junctions between retinal pigmented epithelial (RPE) cells. To eliminate this possible confounding factor, we used the human vitelliform macular dystrophy 2 (VMD2) promoter, an RPE-specific promoter, combined with the tetracycline-inducible promoter system, to generate double transgenic mice with inducible expression of VEGF in RPE cells. Adult mice with increased expression of VEGF in RPE cells had normal retinas and choroids with no choroidal neovascularization (CNV), but when increased expression of VEGF in RPE cells was combined with subretinal injection of a gutless adenoviral vector containing an expression construct for Ang2 (AGVAng2), CNV consistently occurred. In contrast, triple transgenic mice with induced expression of Ang2 and VEGF in RPE cells, did not develop CNV. These data suggest that increased expression of VEGF and/or Ang2 in RPE cells is not sufficient to cause CNV unless it is combined with a subretinal injection of a gutless adenoviral vector, which is likely to perturb RPE cells. These data also suggest that the effects of angiogenic proteins may vary among vascular beds, even those that are closely related, and, therefore, generalizations should be avoided.

Angiopoietin-2↗

PubMed2006

Role of the angiotensin II type 1 receptor in the pathogenesis of diabetic retinopathy: effects of blood pressure control and beyond.

Diabetic retinopathy is characterized by both functional and morphological changes in the retinal microvessels that can lead to macular edema, neovascularization, and vision loss. Hypertension has been identified as a major risk factor for diabetic retinopathy and randomized clinical trials have shown that reduction of blood pressure using angiotensin converting enzyme (ACE) inhibitors reduces the progression of diabetic retinopathy. The major components of the renin-angiotensin system have been identified in ocular tissues. Activation of angiotensin II type 1 (AT1) receptors expressed on retinal endothelial cells and pericytes has been implicated in contributing to the microvascular abnormalities in diabetic retinopathy. We have examined the experimental and clinical evidence for the role of the renin-angiotensin system in the pathogenesis of diabetic retinopathy, including the effects of ACE inhibition and AT1-receptor antagonism on diabetes-induced abnormalities in retinal hemodynamics, vascular permeability, and leukostasis; retinal neovascularization in rodent models of oxygen-induced retinopathy; and results from randomized clinical trials that have investigated the effects of ACE inhibitors on the progression of diabetic retinopathy in diabetic patients in the absence or presence of hypertension. The effects of AT1-receptor antagonism on the retina have been attributed to decreases in systemic blood pressure and the concomitant reduction in mechanical vascular stretch, in addition to the intraocular effects blocking AT1-receptor stimulation of retinal endothelial cells and pericytes. Results from the current DIabetic REtinopathy Candesartan Trials program will evaluate the potential of the AT1-receptor as a therapeutic target for diabetic retinopathy.

Angiotensin II Type 1 Receptor Blockers↗

PubMed1989

[Vitreous hemorrhage and neovascular proliferation in multiple sclerosis].

We report the case of a 40 year-old man with multiple sclerosis, who presented a bilateral proliferative retinopathy responsible for a vitreous hemorrhage. Examination of the periphery of the retina showed diffuse retinal periphlebitis; fluorescein angiograms showed a peripheral retinal ischemic syndrome with secondary neovascularization. Several recent studies have show that retinal periphlebitis is a frequent finding in multiple sclerosis; but to our knowledge a retinal ischemic syndrome with neovascularization has seldom been reported.

Adult↗

PubMed2002

Angiopoietin-2 plays an important role in retinal angiogenesis.

Angiopoietin 2 (Ang2) expression in the retina is increased during physiologic and pathologic neovascularization suggesting that it may be involved. In this study, we used Ang2-deficient mice to test that hypothesis. Mice deficient in Ang2 showed delayed and incomplete development of the superficial vascular bed of the retina, which develops primarily by vasculogenesis, and complete absence of the intermediate and deep vascular beds which develop by angiogenesis. In addition to incomplete retinal vascular development, Ang2-deficient mice showed lack of regression of the hyaloid vasculature, resulting in a phenotype that mimics infants with persistent fetal vasculature (PFV), a relatively common congenital abnormality. Exposure to high levels of oxygen resulted in partial regression of the retinal vessels, indicating that oxygen-induced regression of retinal vessels does not require Ang2. When these oxygen-exposed mice with few retinal vessels were moved to room air, there was no ischemia-induced retinal neovascularization. These data support the hypothesis that Ang2 plays a critical role in physiologic and pathologic angiogenesis, and physiologic, but not oxygen-induced vascular regression. The data also suggest that infants with PFV should be examined for genetic modifications that would be expected to cause perturbations in Tie2 signaling.

Angiopoietin-2↗

PubMed1976

Hemorrhagic detachment of the peripheral retinal pigment epithelium.

Six patients had hemorrhagic detachment of the peripheral retinal pigment epithelium. Abnormal neovascular nets in older individuals, under the retinal pigment epithelium and originating from the choriocapillaris, may well be the cause of such hemorrhagic detachments. This lesion must be differentiated from choroidal tumors, choroidal detachment, and uveal effusion.

Adult↗

PubMed2004

Anomalous posterior vitreous detachment: a unifying concept in vitreo-retinal disease.

Posterior vitreous detachment (PVD) is the consequence of changes in the macromolecular structure of gel vitreous that result in liquefaction, concurrent with alterations in the extracellular matrix at the vitro-retinal interface that allow the posterior vitreous cortex to detach from the internal limiting lamina of the retina. Gel liquefaction that exceeds the degree of vitro-retinal dehiscence results in anomalous PVD (APVD). APVD varies in its clinical manifestations depending upon where in the fundus vitreo-retinal adhesion is strongest. At the periphery, APVD results in retinal tears and detachments. In the macula, APVD causes vitreo-macular traction syndrome, results in vitreoeschisis with macular pucker or macular holes, or contributes to some cases of diabetic macular edema. At the optic disc and retina, APVD causes vitreo-papillary traction and promotes retinal and optic disc neovascularization. Unifying the spectrum of vitreo-retinal diseases into the conceptual frame-work of APVD underscores that to more effectively treat, and ultimately prevent, these disorders it is necessary to replicate the two components of an innocuous PVD, i.e., gel liquefaction and vitreo-retinal dehiscence. Pharmacologic vitreolysis is designed to mitigate against APVD by chemically breaking down vitreous macromolecules and weakening vitro-retinal adhesion to safely detach the posterior vitreous cortex. This would not only facilitate surgery, but if performed early in the natural history of disease, it should prevent progressive disease.

Animals↗

PubMed1984

Characteristics of the hemispheric retinal vein occlusion.

Hemispheric retinal vein occlusions involve the venous return from approximately one-half of the retina and have characteristics of both central retinal vein occlusions and branch retinal vein occlusions. One hundred six such occlusions were studied in 104 patients whose average age was 66 years. The site of the hemispheric vein occlusion was located in a branch retinal vein in 90% of the eyes, and in 10% of the eyes it was located in one of the dual intraneural trunks of the central retinal vein. Of these eyes, 11% developed neovascularization of the disc, 9% developed neovascularization of the retina elsewhere, 9% developed neovascularization of the iris, and 3% developed neovascular glaucoma. Neovascularization was positively correlated with an increasing percentage of capillary nonperfusion (ischemic index) within the area of occlusion. Prophylactic argon laser treatment was effective in reducing the incidence of neovascularization in eyes with significant capillary nonperfusion.

Adult↗

PubMed1985

Vitreous hemorrhage secondary to presumed ocular histoplasmosis syndrome.

Hemorrhagic retinal pigment epithelium detachment caused by choroidal neovascular membrane progressed to massive vitreous hemorrhage in two patients with presumed ocular histoplasmosis syndrome. When the hemorrhage cleared, a diskiform mass became visible. In one patient, this was located near the midnasal periphery. In endemic areas of histoplasmosis, presumed ocular histoplasmosis syndrome should be considered as a possible cause of spontaneous vitreous hemorrhage.

Eye Diseases↗

PubMed2000

A comparison of digital nonmydriatic fundus imaging with standard 35-millimeter slides for diabetic retinopathy.

PURPOSE: The purpose of this study was to compare nonmydriatic digital images with 35-mm slide images for the detection of diabetic retinal findings. STUDY DESIGN: Comparative, observational case series. PARTICIPANTS: Twenty-two patients with diabetes. METHODS: Diabetic patients underwent digital (nonmydriatic fundus camera attached to a digital back) and standard dilated 35-mm retinal photography of three areas: posterior pole, nasal retina, and temporal retina. The images were reviewed by a single masked grader for the presence or absence of specific retinal findings. PRIMARY OUTCOME MEASURES: Presence or absence of neovascularization of the disc (NVD), neovascularization elsewhere (NVE), venous beading (VB), nerve fiber layer (NFL) hemorrhage, dot-blot hemorrhage, microaneurysm (MA), clinically significant macular edema, cotton wool spot, intraretinal microvascular anomaly (IRMA), hard exudate (HE), and retinal pigment epithelial (RPE) pigmentary changes. RESULTS: Forty eyes of 22 patients underwent both imaging procedures. The agreement between image type was highest for IRMA (97.5%) and VB (95%) and lowest for RPE pigmentary changes (65%) and MA (62.5%). Sensitivity ranged from 25% (NVD) to 100% (VB). Specificity ranged from 90% (RPE pigmentary changes) to 100% (NVD, NVE, VB, NFL hemorrhage, HE). Positive predictive value ranged from 50% (IRMA) to 100% (NVD, NVE, HE, NFL, VB). Negative predictive value ranged from 48% (MA) to 100% (IRMA). CONCLUSIONS: Nonmydriatic digital fundus imaging for detection of diabetic retionopathy has a low sensitivity rate and a high specificity rate and is less clinically useful than standard dilated 35-mm fundus slide images.

Adult↗