Idiopathic central serous chorioretinopathy.
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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)
The pathogenesis of choroidal neovascularization in patients with age-related macular degeneration.
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Laser photocoagulation and several experimental treatments for choroidal neovascularization (CNV) in patients with age-related macular degeneration attempt to ablate the neovascularization, but do not address underlying angiogenic stimuli. As a result, recurrences are a major problem. Drug treatment to counter the growth of CNV would be a major advance, but its development is impeded by lack of knowledge concerning the stimuli and other molecular signals involved in the pathogenesis of CNV. Herein we explore clues that can be gleaned from clinical, epidemiological, pathological, and experimental data. These suggest that abnormalities of the extracellular matrix of retinal pigmented epithelial (RPE) cells may promote a pro-angiogenic RPE phenotype that contributes to the development of CNV. This provides a general hypothesis that can be tested, but it is also necessary to test hypotheses regarding the specific alterations in gene expression that contribute to CNV. Identification of alterations in gene expression will provide targets for rational design of drug treatment. (+info)
Autosomal dominant macular atrophy at 6q14 excludes CORD7 and MCDR1/PBCRA loci.
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PURPOSE: Localization of the gene responsible for autosomal dominant atrophic macular degeneration (adMD) in a large pedigree UM:H785. METHODS: Standard ophthalmologic examinations were performed. Microsatellite markers were used to map the disease gene by linkage and haplotype analyses. RESULTS: The macular degeneration in this family is characterized by progressive retinal pigment epithelial atrophy in the macula without apparent peripheral involvement by ophthalmoscopy or functional studies. Acuity loss progressed with age and generally was worse in the older affected individuals. The rod and cone function remained normal or nearly normal in all tested affected members up to 61 years of age. The phenotype in our family has characteristics similar to Stargardt-like macular degeneration with some differences. Haplotype analysis localized the disease gene in our adMD family to an 8-cM region at 6q14, which is within the 18-cM interval of STGD3 but excludes cone-rod dystrophy 7 (CORD7; centromeric) and North Carolina macular degeneration and progressive bifocal chorioretinal atrophy (MCDR1/PBCRA; telomeric). The mapping interval overlaps with that of recessive retinitis pigmentosa (RP25). CONCLUSIONS: These results implicate at least three genetically distinct loci for forms of macular degeneration that lie within a 30-cM interval on chromosome 6p11-6q16: CORD7, adMD, and MCDR1/PBCRA. Because the critical interval for the adMD family studied overlaps with STGD3 and RP25, these loci could be allelic. (+info)
Fluorescein angiographic features of choroidal insufficiency in anterior ischemic optic neuropathy.
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Anterior ischemic optic neuropathy(AION) is known to be caused by circulatory disturbance in the anterior optic nerve(AON). Because the AON shares blood supply from the paraoptic short posterior ciliary artery with peripapillary choroid, the authors investigated the angiographic evidences of combined choroidal insufficiency in patients with acute AION. Fundus fluorescein angiograms from 30 eyes from 28 patients with acute AION were enrolled in this study. The diagnosis of acute AION was based primarily on angiographic evidences of filling delay of optic nerve head and the various clinical features, such as decreased visual acuity, visual field defects, afferent pupillary defect, and optic disc swelling. Angiographic evidences of combined choroidal filling delay were as follows: 1) circular or localized filling delay of peripapillary choroid in 15 eyes (50%), 2) generalized filling delay of posterior pole in 11 eyes (36.7%), 3) filling delay of unilateral choroid divided by watershed zone in 5 eyes (16.7%), and 4) choriocapillary filling delay in 10 eyes (33.3%). In this study, various types of choroidal insufficiency in patients with AION were observed, which helped us to differentiate AION from the other various diseases of the anterior optic nerve. (+info)
Bullous variant of idiopathic central serous chorioretinopathy.
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BACKGROUND: Spontaneous bullous serous retinal detachment (RD) with subretinal exudation complicating idiopathic central serous chorioretinopathy (ICSC) is a rare and infrequently described clinical entity. Clinical observations are described on this variant form in 11 patients, the largest series reported to date. METHODS: 13 eyes of 11 Indian patients having this entity were followed up clinically and angiographically for 12-24 months (retrospective, longitudinal). None of the patients had any previous history of other diseases nor were they on any medications. Four eyes received laser treatment (group A); nine eyes were not treated (group B). RESULTS: All 11 patients were male, aged 23-49 years (median 37 years). The clinical and photographic records revealed subretinal exudation and inferior bullous serous RD complicating ICSC with evidence of large, single or multiple, leaking retinal pigment epithelial detachments (PEDs) in all the cases. In group A, resolution of serous RD occurred in 12 weeks (median) with a visual recovery of >/=20/30 in three out of four eyes while in group B resolution of serous retinal detachment was observed in 14 weeks (median) with eight out of nine eyes achieving a visual acuity of >/=20/30. Subretinal fibrosis developed in two eyes in group A and none of the eyes in group B. CONCLUSION: The disease is an exaggerated form of ICSC and can occur spontaneously without any history of corticosteroid therapy. Recognition of this atypical presentation is important to avoid inappropriate treatment. These observations suggest that with respect to the duration of the disease and the final visual outcome laser therapy offers no additional benefit over the natural course of this variant form of ICSC. (+info)
CT-revealed choroidal effusions as a sign of carotid cavernous fistula.
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Choroidal effusions may appear as subtle abnormalities on CT scans. Recognition of choroidal effusions, however, is critical because they may be an early sign of ocular pathologic abnormality. After detection, the various causes of choroidal effusions, such as carotid cavernous fistulas, ocular hypotony, tumors, and inflammatory conditions, should be considered. (+info)
Choroidal thickness changes during altered eye growth and refractive state in a primate.
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PURPOSE: In the chick, compensation for experimentally induced defocus involves changes in the thickness of the choroid. The choroid thickens in response to imposed myopic defocus and thins in response to imposed hyperopic defocus. This study was undertaken to determine whether similar choroidal changes occur in the primate eye with induced refractive errors. METHODS: Thirty-three common marmosets were used. Eyes in 26 monkeys served as untreated control eyes, and eyes in 7 received 3 weeks of monocular lid suture to induce changes in eye growth and refractive state. Refractive errors were measured using refractometry and retinoscopy, and axial ocular dimensions, including choroidal thickness, were measured using high-frequency A-scan ultrasonography. Eyes were measured before the lids were sutured and at frequent intervals after lid opening. RESULTS: In the marmoset, choroidal thickness ranges from 88 to 150 microm and increases significantly during the first year of life. Monocular lid suture initially results in short, hyperopic eyes that then become elongated and myopic. In these animals the choroids of both the experimental and the fellow control eyes also increase in thickness with age but additionally show interocular differences that vary significantly with the relative changes in vitreous chamber depth and refraction. In eyes that are shorter and more hyperopic than control eyes the choroids are thicker, and in eyes that are longer and more myopic than control eyes the choroids are thinner. CONCLUSIONS: In marmosets, the thickness of the choroid increases during postnatal eye growth. Superimposed on this developmental increase in choroidal thickness there are changes in thickness that are correlated with the induced changes in eye size. These changes are small (<50 microm) in comparison with those observed in the chick, contributing to less than a diopter change in refractive error. (+info)
Early treatment with cyclosporin in serpiginous choroidopathy maintains remission and good visual outcome.
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AIMS: To describe management and clinical outcomes of serpiginous choroidopathy treated primarily with cyclosporin at a tertiary uveitis referral centre METHODS: A case series of 14 eyes of seven patients with serpiginous choroidopathy with follow up ranging from 1.3 to 13 years is described. All patients had fundus lesions consistent with serpiginous choroidopathy, were investigated for systemic disease, had fluorescein angiography, and were treated with combined immunosuppressive therapy including cyclosporin. RESULTS: No patients suffered significant loss of acuity after starting systemic immunosuppression with cyclosporin as the primary agent. All but one patient achieved remission and were able to stop medications with no recurrences in the follow up period. Side effects from cyclosporin were well tolerated and there were no serious complications from immunosuppression. CONCLUSIONS: Cyclosporin is a safe and effective option with which to manage serpiginous choroidopathy. Significantly, adequate immunosuppression can result in clinical remission and cessation of therapy in some patients. (+info)