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At least 19 recordsLinked to original sources
PubMed1979

[Central serous retinitis or chorioretinitis (retinopathy or chorioretinopathy) and central hemorrhagic chorioretinitis (juvenile disciform macular detachment; focal hemorrhagic chorioiditis, presumed histoplasmosis) (author's transl)].

There are no clinical or etiological connections between central serous and central hemorrhagic chorioretinitis, Serous chorioretinitis is seen mostly in men; full visual acuity is regained in approx. 80% of all cases. It mainly affects subjects aged between 36 and 45. Hemorrhagic chorioretinitis affects both sexes to about the same extent and causes severe impairment of visual acuity. Both forms should be regarded as genuine inflammations (chorioretinitis centralis serosa, chorioretinitis centralis hemorrhagica), not as "pathies". Whereas the hemorrhagica disease is generally thought to be caused by inflammation, the serous form also often shows signs of inflammation such as varying leakages with inflammatory depigmentation and more frequently inflammatory protein increase (exudate) with precipitation on the posterior surface of the retina/anterior surface of the pigment epithelium.

Adult↗
PubMed2000

Relentless placoid chorioretinitis: A new entity or an unusual variant of serpiginous chorioretinitis?

OBJECTIVE: To characterize an unusual clinical entity resembling acute posterior multifocal placoid pigment epitheliopathy (APMPPE) and serpiginous choroiditis but with an atypical clinical course. PATIENTS: We describe 6 patients, aged 17 through 51 years, exhibiting this unusual entity who were seen at 6 different centers from 1984 to 1997. RESULTS: The acute retinal lesions in this series were similar to those of APMPPE or serpiginous choroiditis, both clinically and on fluorescein and indocyanine green angiography. However, the clinical course, number of lesions, and location of these lesions were atypical. These patients had evidence of numerous posterior and peripheral retinal lesions predating or occurring simultaneously with macular involvement. Older, healing pigmented lesions were often accompanied by the appearance of new active white placoid lesions. Additionally, these cases all demonstrated prolonged periods of activity resulting in the appearance of more than 50 and sometimes hundreds of lesions scattered throughout the fundus. Growth of subacute lesions and the appearance of new lesions continued for 5 to 24 months after initial examination, and relapses were common. CONCLUSIONS: This entity has clinical features similar to APMPPE and serpiginous choroiditis but has a prolonged progressive clinical course and widespread distribution of lesions. It may represent a variant of serpiginous choroiditis or may be a new entity. We call it relentless placoid chorioretinitis. Arch Ophthalmol. 2000;118:931-938

Acute Disease↗
PubMed1998

Clinical course of newly developed or progressive patchy chorioretinal atrophy in pathological myopia.

Regional chorioretinal atrophy in the posterior fundus (patchy chorioretinal atrophy) in pathological myopia impairs vision severely when it covers the macula. The aim of this study was to assess the course of development and progression of patchy chorioretinal atrophy in pathological myopia. The location and progression of patchy chorioretinal atrophy that was either newly developed or had progressed during the follow-up period (mean 5.25 years) were analyzed. A total of 41 lesions of patchy atrophy were newly developed in 30 eyes of 25 patients. These lesions were more likely to occur in marginal regions of a posterior staphyloma but frequency per unit area was highest in the macula. There were 138 lesions of patchy chorioretinal atrophy that progressed in 75 eyes of 53 patients. Sixty percent of the lesions of patchy chorioretinal atrophy in marginal regions of a posterior staphyloma spread toward the center. Seventy percent of the lesions of patchy chorioretinal atrophy in the macula spread in all directions. Fluorescein angiography of newly developed patchy chorioretinal atrophy showed hyperfluorescence in 50% and hypofluorescence in 27%. Fluorescein angiography of progressive lesions of patchy chorioretinal atrophy showed hypofluorescence in 69%. Fluorescein angiography of some progressive areas of patchy chorioretinal atrophy, which showed a change from hyperfluorescence to hypofluorescence within several years, suggested that damage to the retinal pigment epithelium preceded the progression of the patchy chorioretinal atrophy. In conclusion, the patchy chorioretinal atrophy is most likely to occur in the macula and to enlarge in all directions. And it is suggested that the patchy chorioretinal atrophy which shows hyperfluorescence by fluorescein angiography should be kept under observation because our data suggest that this finding indicates progression in the future.

Adult↗
PubMed2000

Lymphocytic choriomeningitis virus: an underdiagnosed cause of congenital chorioretinitis.

PURPOSE: To elucidate the role and clinical spectrum of congenital lymphocytic choriomeningitis virus infection as a cause of chorioretinopathy, congenital hydrocephalus, and macrocephaly or microcephaly in the United States. METHODS: We performed complete ophthalmologic surveys of all residents at Misericordia, a home for the severely mentally retarded in Chicago, and prospectively evaluated all patients with chorioretinitis or chorioretinal scars during a 36-month period at Children's Memorial Hospital, also located in Chicago. Sera for patients demonstrating chorioretinal scars (a sign of intrauterine infection) were tested for Toxoplasma gondii, rubella virus, cytomegalovirus, and herpes simplex virus and lymphocytic choriomeningitis virus antibodies. RESULTS: Four of 95 patients examined at the home had chorioretinal scars, and two of these patients had normal T. gondii, rubella virus, cytomegalovirus, and herpes simplex virus titers and dramatically elevated titers for lymphocytic choriomeningitis virus. Three of 14 cases of chorioretinitis at the hospital had normal T. gondii, rubella virus, cytomegalovirus, and herpes sim-plex virus titers and elevated lymphocytic choriomeningitis virus antibody titers. (A fourth case, diagnosed in 1996, was reported 2 years ago.) CONCLUSIONS: Lymphocytic choriomeningitis virus was responsible for visual loss in two of four children secondary to chorioretinitis in a population of severely retarded children. The six new cases of lymphocytic choriomeningitis virus chorioretinitis identified in these two populations over the last 3 years, compared with the total number ever reported in the United States (10 cases), suggests that lymphocytic choriomeningitis virus may be a more common cause of congenital chorioretinitis than previously believed. Because its consequences for visual and psychomotor development are devastating, we conclude that the workup for congenital chorioretinitis should include lymphocytic choriomeningitis virus serology, especially if T. gondii, rubella virus, cytomegalovirus, and herpes simplex virus titers are negative.

Antibodies, Viral↗
PubMed1996

Choroidal neovascularization secondary to Candida albicans chorioretinitis.

PURPOSE: To study the clinical histories and courses of six patients with choroidal neovascularization secondary to endogenous Candida albicans chorioretinitis. METHODS: The medical records, fundus photographs, and fluorescein angiograms of six patients who developed C. albicans chorioretinitis secondary to candidemia and who subsequently developed choroidal neovascularization in one or both eyes were reviewed. RESULTS: The six patients ranged in age from 18 to 79 years. Four were women and two men; all but one showed evidence of bilateral chorioretinal scarring secondary to C. albicans chorioretinitis. All patients had been treated successfully with systemic antifungal therapy (amphotericin B). Two weeks to two years after the chorioretinitis, choroidal neovascularization developed in one eye (four cases) or both eyes (two cases). The neovascularization on initial examination was subfoveal in four eyes, extrafoveal in three eyes, and juxtafoveal in one eye. Laser photocoagulation was used in four of the eight involved eyes. In these cases, the active choroidal neovascularization was brought under control. In one eye, the patient had submacular surgery for excision of the choroidal neovascular membrane. Final visual acuities ranged from 20/20 to 20/200 in treated eyes and from 20/50 to 20/400 in untreated eyes. CONCLUSION: Choroidal neovascularization is a potential cause of late visual loss in patients who have had C. albicans sepsis and endogenous C. albicans chorioretinitis. Eyes that have chorioretinal scarring from C. albicans chorioretinitis should be watched for the development of choroidal neovascularization. Laser photocoagulation or perhaps surgical excision of the neovascular complex may be of benefit in selected cases.

Adolescent↗
PubMed1989

Herpes simplex virus type-1 strain influence on chorioretinal disease patterns following intracameral inoculation in Igh-1 disparate mice.

We have previously shown that the Igh-1 locus on chromosome 12 of the mouse influences contralateral disease patterns in the modified von-Szily model. Following intracameral injection with 1.5 X 10(4) PFU of HSV strain KOS (HSV-KOS), 75% of BALB/cByJ (Igh-1a), 30% of C.AL-20 (Igh-1d) and 5% of C.B-17 (Igh-1b) mice develop contralateral chorioretinal necrosis. In contrast, Igh-1 congenic mice do not develop contralateral chorioretinal necrosis following anterior chamber inoculation of the same dose of an HSV-KOS mutant lacking surface glycoprotein-C (HSV-GC-KOS). Similarly, injection of wild type HSV strain mP (HSV-mP) into the anterior chamber of susceptible BALB/cByJ mice induces destructive contralateral chorioretinitis whereas injection of the same dose of the mutant HSV strain MP (HSV-MP) lacking surface glycoprotein-C does not induce a destructive contralateral chorioretinitis. In addition, higher doses of HSV-mP inoculum abrogate the Igh-1-associated contralateral chorioretinal protection seen in C.B-17 mice; protection is restored in C.B-17 mice at lower HSV-mP doses that still cause contralateral chorioretinitis in BALB/cByJ mice. These data demonstrate the influence of the viral isolate on the modified von-Szily model and specifically the requirement for the presence of glycoprotein-C on the surface of HSV for the development of contralateral destructive chorioretinitis.

Animals↗
PubMed1992

[Idiopathic and secondary chorioretinal folds].

Chorioretinal folds may be observed in many choroidal or retinal diseases. In age-related macular degeneration, they are usually associated with retraction of a neovascular membrane and a typically radial pattern of the folds can be seen. In this disease, pigment epithelium folds were recently described. Their clinical and angiographical characteristics are different from chorioretinal folds and the two diseases should not be confused. A 74-old patient presented, in the left eye, with sub foveal new vessels situated at the center of a pigment epithelial detachment (PED). Radial chorioretinal folds surrounded the PED, as frequently observed during follow-up in subretinal neovascular membranes. Nevertheless, right eye fundus examination revealed roughly horizontal, regular and parallel chorioretinal folds. Ultrasonography demonstrated characteristics of idiopathic chorioretinal folds: flattening and thickening of the posterior sclera and choroid. No sign of posterior scleritis was found. These ultrasonographic elements were observed in the left eye away from the central neovascular membrane. The chorioretinal folds therefore seemed to be idiopathic, in a hyperopic patient. The shape of the folds was modified in one eye by a subfoveal neovascular membrane. Chorioretinal folds may occur in different retinal diseases. The associations with many different aetiologies with modification of the shape of the folds, as described in this clinical case, should be emphasized.

Aged↗
PubMed2001

Effect of Fas and Fas ligand deficiency in resistance of C57BL/6 mice to HSV-1 keratitis and chorioretinitis.

PURPOSE: To investigate the effect of Fas and Fas ligand (FasL) deficiency on the development of herpes stromal keratitis and on the von Szily model of herpes retinitis in C57BL/6 mice, which are ordinarily resistant to development of both of these herpetic diseases. METHODS: Anterior chamber inoculation of the right eye of each mouse with various titers of HSV-1 (KOS strain) was performed. Both eyes of each mouse were enucleated on postinoculation day 15 and processed for histopathologic examination. HSV-1 was inoculated into one cornea of other mice, and the severity of stromal keratitis was scored. RESULTS: Contralateral destructive chorioretinitis developed in susceptible Balb/cByj mice (19/23); ipsilateral chorioretinitis did not occur (0/23). Stromal keratitis developed in susceptible C.AL-20 mice (15/16). None of the C57BL/6 (0/10 for keratitis or 0/20 for retinitis) developed inflammation. Neither did B6.SMN.C3H.gld (FasL deficient; 0/12 or 0/28) or B6.MRL.lpr (Fas deficient; 0/11 or 0/34) mice (keratitis or contralateral chorioretinitis). Minimal scattering of inflammatory cells in the contralateral retina but not destructive chorioretinitis was observed in two C57BL/6, three B6.SMN.C3H.gld, and five B6.MRL.lpr mice. Few inflammatory cells were also found in the ipsilateral vitreous and vitreoretinal interface (but not destructive chorioretinitis) of all C57BL/6, two gld, and three lpr mice. CONCLUSIONS: Immune dysregulation secondary to deficiency in Fas or FasL system does not influence the resistance of the C57BL/6 mice to develop herpes simplex keratitis or destructive herpes simplex chorioretinitis.

Animals↗
PubMed1989

Chorioretinal disease patterns in congenic mice following intraocular inoculation with HSV-1.

Disease patterns and immunologic parameters were studied employing inbred and Igh-1 disparate congenic mice to determine the role of host genetics and Igh-1-linked gene products in the von Szily model of viral chorioretinitis. Following intracameral inoculation of 1.5 x 10(4) PFU HSV-1 (KOS), 100% of BALB/c (Igh-1a), 62% of A/J (Igh-1e) and none of the C57BL/6J (Igh-1b) inbred mice developed contralateral necrotizing chorioretinitis. Multigenic differences between inbred mice prohibit conclusions about the specific role of Igh-1-linked immune regulation in this model. In order to more exactly define Igh-1-specific restriction of HSV-1-mediated chorioretinitis, Igh-1-disparate, congenic BALB/c mice were studied following both anterior chamber and intravitreal inoculation protocols. Anterior chamber inoculation resulted in contralateral retinal necrosis in 75% of BALB/c (Igh-1a) mice, 30% of C.AL-20 (Igh-1d) and 5% of the C.B-17 (Igh-1b) congenic mice; all strains showed ipsilateral retinal sparing. Following intravitreal inoculation of HSV-1 a similar restricted disease pattern was found in contralateral eyes. Contralateral chorioretinitis developed in 30% of BALB/c, 15% of C.AL-20 and 6% of C.B-17 mice. Ipsilateral disease, however, was found in all murine strains. These disease patterns developed despite equivalent suppression of systemic DTH and equivalent RPE permissivity to viral replication. These data demonstrate that host genetics strongly regulates contralateral HSV-1-mediated chorioretinal disease patterns by a mechanism unrelated to the development of systemic suppression of DTH and specifically support a dominant role for gene products linked to the Igh-1 locus in the immunomodulation of ocular disease.

Animals↗
PubMed1996

Choroidal neovascular membrane after laser-induced chorioretinal anastomosis.

PURPOSE: To treat a patient who had a choroidal neovascular membrane after laser-induced chorioretinal anastomosis for nonischemic central retinal vein occlusion. METHODS: A 70-year-old man underwent successful formation of a chorioretinal anastomosis for nonischemic central retinal vein occlusion. He subsequently developed a choroidal neovascular membrane at the site of the chorioretinal anastomosis. RESULTS: The choroidal neovascular membrane at the site of the chorioretinal anastomosis was treated successfully with argon laser photocoagulation. The anastomosis remained functional. CONCLUSION: We recommend that patients who have undergone laser-induced chorioretinal anastomosis for nonischemic central retinal vein occlusion be followed up closely for choroidal neovascular membrane formation.

Aged↗
PubMed1990

Electroretinograms in microcephaly with chorioretinal degeneration.

We recorded full-field electroretinograms from a family with two daughters with microcephaly and chorioretinal degeneration and a third daughter and mother with microcephaly without chorioretinal degeneration. The two siblings with inferior chorioretinal degeneration showed electroretinographic responses to 0.5-Hz white light that were reduced 60% to 70% below normal, suggesting that the loss of photoreceptor function exceeded the areas of visible atrophy. The mother and third daughter had normal electroretinograms. The two siblings, ages 12 and 21 years, had virtually the same electroretinographic amplitudes. In a second family, a man with microcephaly and inferior chorioretinal degeneration, examined at ages 9 and 23 years, also showed 60% to 70% reduction in electroretinographic responses to 0.5-Hz white light and showed no change in amplitudes over the 14-year interval. These findings suggest that the chorioretinal degeneration sometimes associated with microcephaly is stable in young adult life, although the long-term prognosis remains to be defined.

Adolescent↗
PubMed1993

The role of chorioretinal biopsy in the management of posterior uveitis.

BACKGROUND: The ideal management of intraocular inflammation may require a tissue diagnosis. Diagnostic vitrectomy is a well-established method for acquiring such tissue. However, in some patients, the diagnostic pathology is limited to the choroid and retina and vitrectomy may yield no useful information. In such cases, a more aggressive surgical approach to obtain tissue may be useful. METHODS: The authors performed chorioretinal biopsies on seven patients with progressive chorioretinal lesions of unknown etiology. Indications for biopsy included: (1) macular-threatening lesions unresponsive to therapy, (2) suspicion of malignancy, or (3) suspicion of an infectious etiology. In all cases, it was expected that the results would alter therapy or other aspects of clinical care. Preoperative visual acuity was 20/200 or worse in each eye biopsied with one or more peripheral chorioretinal lesions present. Biopsy specimens were divided into three parts and submitted for light and electron microscopy, immunohistochemistry, and tissue culture. RESULTS: On the basis of the biopsy findings, a diagnosis of multifocal choroiditis and subretinal fibrosis was rendered in three eyes, sarcoidosis in two eyes, and viral retinitis in two eyes. Therapy was changed in five patients. Final visual acuity was unchanged or improved in five eyes. Complications included the progression of lens opacity in all eyes and the development of phthisis in one eye that was extensively diseased preoperatively. CONCLUSION: Chorioretinal biopsy may provide useful information for determining the diagnosis and guiding the subsequent management of patients with progressive chorioretinal lesions of unknown etiology.

Adult↗
PubMed1998

Hereditary pigmented paravenous chorioretinal atrophy.

Pigmented paravenous chorioretinal atrophy (PPCRA) is a rare disorder which is diagnosed primarily because of the typical fundoscopic appearance of retinal pigment epithelial (RPE) atrophy and clumping in a paravenous distribution. A mildly affected and asymptomatic 54-year-old mother and her mildly affected daughter and severely affected son presented with pigmented paravenous chorioretinal atrophy. The severely affected (proband) 28-year-old man manifested the characteristic paravenous chorioretinal atrophy with pigment clusters in both eyes with macular involvement. Besides the characteristic fundus picture, he also had chronic angle closure glaucoma. His 23-year-old sister presented with unilateral involvement. Her right eye showed focal perivenular retinal pigment epithelial hyperplasia at the 2 o'clock position and dilated, tortuous retinal veins, while her left eye had only dilated and tortuous retinal veins. Both patients were hyperopic. Their mother had an area of chorioretinal atrophy in one eye near a retinal vein. The scotopic ERG responses were markedly abnormal in the male patient, while his sister had a mild decrease in amplitude of both a and b waves in both eyes. One of the children of an unaffected family member was found to have dilated and tortuous retinal veins and hyperopia (III-12). To our knowledge, this is the fourth report of familial occurrence of pigmented paravenous chorioretinal atrophy. The present pedigree is compatible with X-linked recessive or dominant inheritance.

Adult↗
PubMed1990

Chorioretinal folds and a macular hole secondary to craniofacial surgery.

Chorioretinal folds have been reported as a result of many intraocular and extraocular inflammatory processes or tumors. Visual loss is usually secondary to a combination of the underlying process and chorioretinal folds involving the macula. We report a patient who developed decreased vision, metamorphopsia, chorioretinal folds, and a lamellar macular hole secondary to global compression by a bone fragment. The chorioretinal folds regressed and his vision stabilized following surgical decompression. Chorioretinal folds and lamellar macular hold formation are previously unrecognized complications of reconstructive craniofacial surgery.

Adult↗
PubMed1995

Digital indocyanine green angiography in chorioretinal diseases.

BACKGROUND: Fluorescein angiography (FA) is important in the diagnosis of chorioretinal diseases; however, it has some limitations. We conducted this study to evaluate whether digital indocyanine green (ICG) angiography can offer enhanced image in chorioretinal diseases. METHODS: Digital indocyanine green angiography with scanning laser ophthalmoscope (SLO) was performed in 314 patients with various chorioretinal diseases. This coupled digital imaging system can offer instant images, process and store data by computer, and give convenient hardcopy generation. RESULTS: The digital ICG angiography provided enhanced image resolution of the choroid compared with FA. The disease categories included choroidal neovascularization (CNV), choroidal tumor, inflammatory choroidal disease, ischemic choroidal disorder, idiopathic central serous chorioretinopathy and retinal macroaneurysm. CONCLUSIONS: ICG angiography is a useful adjunctive diagnostic technique to fluorescein angiography for various chorioretinal diseases. It is especially useful in the diagnosis of occult and recurrent CNV, as well as choroidal tumor and choroiditis. With greater clinical experience, ICG angiography is promising in giving additional clinical information for many other chorioretinal diseases.

Choroid Diseases↗
PubMed1998

Peripheral multifocal chorioretinitis with panuveitis: clinical and immunogenetic characterization in older patients.

BACKGROUND: The etiology of peripheral multifocal chorioretinitis with panuveitis (MCP) is unclear. Characteristic signs of MCP are punched-out, white chorioretinal lesions of the lower fundus periphery, chronic smoldering chorioretinal inflammation, vitritis, and mild inflammation of the anterior chamber. In this retrospective study we investigated clinical and immunogenetic abnormalities in MCP in older patients. PATIENTS AND METHODS: 20 patients (18 women, 2 men), median age 70.5 years, were investigated clinically by ophthalmologists and were typed for HLA class I antigens using the standard microlymphocytotoxicity test. Typing for HLA-DR antigens was performed by polymerase chain reaction with sequence-specific primers (PCR-SSP). The HLA controls consisted of healthy people (108 for HLA class I, 114 for HLA class II). RESULTS: MCP was bilateral in 18 patients. Disease-related symptoms were present for 8 months (median) before diagnosis. The main presenting symptoms or findings were glaucoma (in 11 patients), visual loss (7), iritis (5), and vitritis (2). Anterior segment changes were frequently seen: keratitic precipitates (32 eyes), anterior chamber cells (25 eyes), aqueous flare (26 eyes), posterior synechiae (22 eyes), secondary glaucoma (15 eyes), and iris neovascularization (8 eyes). All patients had vitritis and typical chorioretinal fundus lesions. Fourteen patients developed cystoid macular edema (bilateral in seven cases). Subretinal neovascularization occurred in three patients. Although systemic medication was given to 17 patients and surgical treatment was performed in 25 eyes, improvement in vision was found in only 6 eyes, but 18 eyes deteriorated markedly (median 5 lines) during follow-up (median 24.5 months). Immunogenetically significant reduced frequencies of HLA-B7 and HLA-DR1 were found; also HLD-DR15(2) was reduced. However, several alleles were increased in MCP, although not significantly: HLA-A31; HLA-B57, HLA-B62; HLA-Cw3, HLA-Cw6; HLA-DR4, HLA-DR7, and HLA-DR8. CONCLUSIONS: MCP is clinically and immunogenetically open to speculation. The present diagnosis and treatment of MCP are insufficient. Further DNA typing methods should clarify, whether HLA-DQ antigens are associated with the disease.

Aged↗
PubMed1975

Cytomegalovirus in tears from patients with normal eyes and with acute cytomegalovirus chorioretinitis.

Cytomegalovirus (CMV) was recovered from the tears in eight of 41 (19.5%) children excreting CMV in their urine or saliva. Tear excretors were all immunosuppressed children with acute lymphocytic leukemia. Three had active CMV chorioretinitis and five did not develop retinal disease in nine to 15 months of observation. To our knowledge this was the first report of the recovery of CMV from tears and of acquired CMV chorioretinitis in children. One patient with active chorioretinitis presented with a disciform elevation of the macula. Therapy with adenine arabinoside (ara-A) or idoxuridine was ineffective in two patients while a third patient treated with ara-Apossibly had a more rapid recovery. However, the significance is uncertain due to the unusual disease presentation and lack of data regarding the nature of cytomegalic inclusion disease chorioretinitis. Areas of retinal calcification were present at autopsy in one patient.

Adult↗
PubMed1983

Herpes simplex chorioretinitis in a healthy adult.

A previously healthy 20-year-old man developed bilateral chorioretinitis that included mild anterior uveitis, vitreous cells, multifocal chorioretinitis, and optic nerve swelling that progressed to severe optic neuropathy in one eye. Chorioretinal biopsy specimens cultured herpes simplex type 1 from separate chorioretinal and vitreous samples. Although the visual acuity of one eye remained at light perception, sight in the second eye was saved when treatment with systemic acyclovir and corticosteroids led to resolution of the inflammation. A recurrence was successfully treated with acyclovir alone and the patient shows no evidence of active disease.

Acyclovir↗