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The Eales disease is a retinal idiopathic vasculitis which has raised big problems in diagnosis and especially in therapeutic approach. The complications secondary to neovascularization as well as fibrovascular proliferation has surpassed for many times the therapeutical possibilities from nowadays.
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A case of highly asymmetric retinitis pigmentosa is reported. Signs of pigmentary retinopathy appeared in the first eye following optic disc vasculitis or neuroretinitis of unknown etiology. Within 2 years the visual field became markedly restricted and the dark adaptation thresholds elevated. Twelve years later this eye was almost blind and the ERG was non-recordable. In the fellow eye, the first pigmentary changes were observed 5 years after the initial presentation, and the progression was slow. Nineteen years after the initial examination the visual field of the less affected eye was constricted to 30 degrees nasally and 60 degrees temporally, the dark adaptation threshold was only slightly elevated, and the full-field ERG was within normal range. It is possible that neuroretinitis or vasculitis of the optic disc caused the earlier onset and the more progressive course of pigmentary retinopathy in the initially affected eye.
Four cases of acute retinal necrosis accompanied by acute uveitis, retinal obliterative vasculitis and confluent yellow-white lesions in the peripheral fundus followed by retinal detachment are reported. The clinical course was rapidly progressive and the prognosis was poor despite various treatments. No systemic abnormality was found and etiology could not be identified. In reviewing the 40 cases so far reported, including our 4 cases, we came to the conclusion that acute retinal necrosis and Kirisawa's uveitis fall into the same clinical study.
Linear scleroderma 'en coup de sabre' (LSCS) has been reported in association with intracranial abnormalities. We report the case of an 11-year-old boy with LSCS who presented with recurrent headaches. Cranial magnetic resonance imaging (MRI) and angiography were consistent with the diagnosis of a cerebral vasculitis. In addition, retinal examination showed an exudative inflammatory lesion consistent with vasculitis.
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A 45-year-old woman with a 4-year history of systemic lupus erythematosus (SLE) developed fever, decreased visual acuity and skin ulceration. A biopsy of a cutaneous ulcer demonstrated small vessel vasculitis with characteristic cytomegalovirus (CMV) inclusions in the vascular endothelium. The presence of CMV was confirmed by DNA hybridization immuno-histochemistry. Retinal artery vasculitis, previously associated with flares of her SLE, was also noted on ophthalmologic examination. Our case demonstrates that CMV infection can mimic the cutaneous manifestations of collagen vascular disease and that early identification can be made by biopsy of suspicious skin lesions.
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PURPOSE: To investigate by ERG the effects of Toxoplasma gondii infection on the visual function of interferon gamma knockout (GKO) mice, as a model of immunocompromised hosts. METHODS: Susceptible wild-type (WT) C57BL/6 and GKO C57BL/6 mice were infected with five cysts of the avirulent T. gondii perorally. ERGs were recorded before and after the infection. The eyes of WT and GKO mice were enucleated and prepared for histologic studies 4 weeks and 12 days after infection, respectively. RESULTS: The a- and b-waves of ERGs did not change significantly up to 1 month after infection in WT mice, but those of GKO mice were significantly reduced 11 days after infection. Histopathology revealed focal retinitis and vasculitis in WT mice 4 weeks after infection. Mild inflammation and sludging of blood in the retina and choroid were found in GKO mice 12 days after infection, just before death. Cysts were found in the inner nuclear layer, with little disturbance of the surrounding retinal architecture in both WT and GKO mice. CONCLUSIONS: ERG clearly showed deterioration of visual function in GKO but not in WT mice after T. gondii infection. ERG is a sensitive and reliable method for observing activity in mice severely affected with experimental toxoplasmic retinochoroiditis.
The histopathologic ocular findings in a case of presumed Rocky Mountain Spotted Fever (RMSF) include retinal hemorrhages, vasculitis, and vascular occlusion. A review of earlier literature concerning the clinical ocular findings in the disease is presented.
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The ocular lesions of bovine malignant catarrhal fever were characterized in 15 naturally occurring and eight experimentally induced cases of the disease. Consistent findings included: lymphocytic vasculitis of retinal, scleral, posterior ciliary, and uveal vessels; uveitis, especially involving ciliary processes, ciliary body, and iris; and keratitis with corneal edema, neovascularization, and epithelial and endothelial degeneration. Lymphocytic ciliary neuritis and optic meningitis were found less frequently. Ultrastructural examination of the ciliary body and iris from one experimental calf confirmed that most infiltrating mononuclear cells were lymphocytes. The uveitis, vasculitis, and keratitis of malignant catarrhal fever were probably immune-mediated.