Cases reported "Macular Degeneration"

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1/9. adult-onset foveomacular pigment epithelial dystrophy: clinicopathologic correlation of three cases.

    PURPOSE: The authors describe the clinicopathologic features of three patients with adult onset foveomacular pigment epithelial dystrophy (AOFPED). methods: The eyes of three patients were studied ophthalmoscopically and by fluorescein angiography, and obtained postmortem and studied by light and electron microscopy. RESULTS: Histopathologic study of the three patient's eyes disclosed central loss of the retinal pigment epithelium and photoreceptor cell layer with a moderate number of pigment-containing macrophages present in the subretinal space and outer retina. To either side, the retinal pigment epithelium was distended with much lipofuscin. Basal laminar and basal linear deposits were present throughout the central area. No discontinuities of bruch membrane were present. CONCLUSION: The findings in the eyes of three patients with AOFPED included marked aging changes that are similar to those seen in age-related macular degeneration. Pigmented cells with lipofuscin in the subretinal space account for the vitelliform appearance.
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2/9. radiotherapy of exudative age-related macular degeneration; a clinical and pathologic study.

    BACKGROUND: radiotherapy has recently been employed to treat patients with exudative macular degeneration in order to prevent severe visual loss. radiotherapy affects the evolution of exudative macular degeneration directly by endothelial toxicity, leading to capillary closure, and/or indirectly through its attenuating effects on the inflammatory response, mediated by macrophages and other inflammatory cells. methods: In this study we describe the histopathologic findings in a patient with exudative age-related macular degeneration (AMD) in both eyes whose right eye was treated with radiotherapy (5 times 2 Gy) 3 years before he died. The eyes were enucleated post mortem and investigated by light microscopy. Additionally, immunohistochemical investigation with antibodies against CD34 and CD68 was performed to identify patent endothelial cells and macrophages. RESULTS: Both eyes showed neovascular AMD consisting of mixed fibrocellular and fibrovascular membranes. capillaries in both the choriocapillaris and the neovascular membrane were patent in both eyes. macrophages were present in the choroidal neovascularization of both eyes. Neither preexistent choroidal, intraretinal, nor neovascular vessels showed increased wall thickness as sign of radiation damage. CONCLUSION: No radiation-related histopathologic effect could be demonstrated 3 years after radiation therapy in this patient with AMD.
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3/9. Clinicopathologic studies of age-related macular degeneration with classic subfoveal choroidal neovascularization treated with photodynamic therapy.

    BACKGROUND: Photodynamic therapy (PDT) is a relatively new modality that is currently under clinical and experimental evaluation for treatment of subfoveal choroidal neovascularization (CNV). The authors report the case of an 82-year-old woman who underwent verteporfin-mediated PDT for classic subfoveal CNV. fluorescein angiography performed 2 weeks after treatment disclosed reduction of the initial area of neovascularization and leakage by approximately 60%. Three weeks after PDT, however, the area of leakage was almost the same size as that before treatment. The patient underwent submacular membranectomy almost 4 weeks after treatment. The authors describe the ultrastructural vascular changes after PDT and a clinicopathologic study of classic CNV. methods: The submacular membrane was studied by light and electron microscopy and immunohistochemical techniques. RESULTS: Ultrastructural examination of the peripheral vessels showed evidence of endothelial cell degeneration with platelet aggregation and thrombus formation. Occasional occluded vessels were surrounded by macrophages, a phenomenon previously reported to describe the process of resorption of such blood vessels. The vessels in the center of the membrane were unremarkable. CONCLUSION: Photodynamic therapy causes endothelial cell damage, thrombus formation, and vascular occlusion of classic CNV in age-related macular degeneration.
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4/9. Transmission electron microscopic study of a subretinal choroidal neovascular membrane due to age-related macular degeneration.

    From a patient with age-related macular degeneration we studied ultrastructurally a disciform scar that was removed from an eye with a vitreous hemorrhage. In cross section, the scar was divided by a retinal pigment epithelial (RPE) cell layer. The choroidal side consisted of fibrovascular tissue with active neovascular buds and inflammatory cells, including macrophages attached to the RPE basement membrane. Apart from the RPE, no components of Bruch's membrane could be identified. The retinal side contained organizing hemorrhage and a collagenous matrix with fibroblastlike cells probably of RPE and choroidal origin. The anatomy and the clinical findings at surgery suggest that such scars lie on (rather than within) the inner collagenous layer of Bruch's membrane and contain two components divided by the original RPE layer. The choroidal side is fibrovascular, including active neovascularization, and the retinal side is fibrous and formed by metaplastic RPE cells and choroidal fibrovascular ingrowth.
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5/9. Macular hole and retinal detachment in Best's disease.

    The authors report a family with Best's vitelliform macular dystrophy in which one member developed a macular hole and retinal detachment. The retinal detachment was repaired by resultant extensive rhegmatogenous pars plana vitrectomy, fluid-air exchange, and photocoagulation. Examination of the vitreous specimen disclosed numerous large macrophages with abundant cytoplasm distended by lipofuscin.
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6/9. Foveomacular vitelliform dystrophy, adult type. A clinicopathologic study including electron microscopic observations.

    Foveomacular vitelliform dystrophy, adult type (FVDAT), is a dystrophy of the retinal pigment epithelium (RPE) characterized in part by autosomal dominant inheritance, midlife onset, mild visual loss, and various patterns of foveal yellow deposits located at the level of the pigment epithelium. Detailed pathologic studies of two postmortem eyes from a 61-year-old woman with documented FVDAT disclosed striking abnormalities involving mainly the foveal RPE and overlying photoreceptors. By light microscopy, marked focal atrophy of the pigment epithelial cells in the foveolar area was bordered by hypertrophic RPE. Interposed between the atrophic RPE and Bruch's membrane were scattered eosinophilic, fusiform collagenous plaques. The sensory retina overlying the deranged RPE displayed marked atrophy of the outer nuclear layer with loss of photoreceptor inner and outer segments. Pigment-laden macrophages containing periodic acid-Schiff-positive material had migrated into the atrophic, outer sensory retina. Ultraviolet fluorescent microscopy demonstrated massive accumulation of lipofuscin pigment within the macular RPE as well as within macrophages in the atrophic outer retina. By scanning electron microscopy, a confluent area of flattened, atrophic retinal pigment epithelial cells was rimmed by taller, hypertrophic RPE cells. By transmission electron microscopy, the pigment epithelial cells contained myriad lipofuscin granules. Bruch's membrane and the intercapillary pillars were slightly thickened and the choriocapillaris was patent. The possible interrelationships between FVDAT and the other pattern dystrophies of the RPE are discussed.
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7/9. Histopathology of Best's macular dystrophy.

    The pathogenesis of Best's macular dystrophy (BMD) is poorly understood. Previous histopathologic descriptions of BMD have been published in the literature; however, all were from elderly persons who clinically exhibited late manifestations of the disease. In this article, light and electron microscopic observations of an earlier stage of BMD are reported. Both globes were from a 28-year-old patient who had a "scrambled egg" lesions in the macula with some features of a pseudohypopyon. Our studies indicate that BMD is a generalized retinal pigment epithelial (RPE) abnormality that results in an abnormal accumulation of lipofuscin granules. Lipopigment accumulates within the RPE, within macrophages in the subretinal space, and within the choroid. These observations help to explain the clinical appearance as well as the fluorescein angiographic and electrophysiologic findings of this conditions.
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8/9. Ultrastructural features of surgically excised idiopathic subfoveal neovascular membranes.

    The ultrastructural features of three surgically excised idiopathic subfoveal neovascular membranes were examined. Ultrastructural features of the cellular components in the membranes included retinal pigment epithelium, endothelial-lined vascular channels, photoreceptor cells, macrophages, myofibroblasts, glial cells, erythrocytes, and ghost erythrocytes. Extracellular constituents included 200-nm to 250-nm collagen fibrils, 100-nm collagen fibrils and fibrin. The findings in this study are consistent with previously reported findings of subfoveal neovascular membranes in age-related macular degeneration and the ocular histoplasmosis syndrome, with the exception of the presence of basal laminar deposit in membranes from age-related macular degeneration.
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9/9. Morphology of early choroidal neovascularisation in age-related macular degeneration: correlation with activity.

    The purpose of this study was to describe the morphology of early choroidal neovascularisation (CNV) and compare the findings in two patients, in the first of whom the vessels appeared inactive and in the second progressive. Changes common to both included a diffuse deposition of membrane coils external to the basement membrane (BsM) of the retinal pigment epithelium (RPE), and macrophages and foreign body giant cells beneath thinned segments of Bruch's membrane (BrM). In the first patient small activated vessels surrounded by enlarged pericytes were found in the choroid beneath these areas and pursued a convoluted course, bulging into or through BrM, but without spreading in the sub-RPE space. This choroidal phase of CNV may be common and unrecognised. In the second patient there was spread of CNV in the sub-RPE space with extravasation of red cells and fibrin. The tips leaking fibrin were covered by a thick BsM-like material and naked endothelial cells were not seen. pericytes were absent here but were observed at the non-leaking edge. The difference in activity of CNV in the two patients appeared to correlate with the quantity of membranous debris present.
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