Cases reported "Retinal Diseases"

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1/323. Cancer-associated retinopathy in a patient with non-small-cell lung carcinoma.

    Cancer-associated retinopathy (CAR) is a paraneoplastic syndrome most often associated with small-cell lung carcinoma (SCLC), and it has been reported in patients with other malignancies. Antibodies against recoverin, a 23-kDa protein, have been found in patients with CAR suggesting an autoimmune phenomenon. Herein is the first report of a patient with non-small-cell lung cancer (NSCLC) in whom anti-recoverin antibodies were detected in the serum. Steroid therapy, chemotherapy, and radiation therapy did not help the patient's vision. Progressive loss of vision in patients with lung cancer should, potentially, be tested for CAR.
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2/323. Immune-mediated retinopathy in a patient with stiff-man syndrome.

    BACKGROUND: Stiff-man syndrome is a rare neurological disorder characterised by rigidity and violent spasms of the body musculature. In the majority of patients, presence of antibodies against glutamic acid decarboxylase (GAD), the enzyme synthesizing gamma-aminobutyric acid (GABA), suggests an autoimmune attack against GABA-ergic inhibitory neurons. We report a 32-year-old patient with stiff-man syndrome and anti-GAD antibodies who developed subacute progressive loss of vision in the right eye, and in the left eye 18 months thereafter. methods: Ophthalmological work-up included electro-retinogram (ERG), visual evoked potentials (VEP) and fluorescein angiography. Antiretinal antibodies were investigated using an indirect immunofluorescence technique on frozen sections of macaque retina with patients serum and FITC-conjugated goat antihuman immunoglobulin. Staining with monoclonal anti-GAD65 antibodies and with serum from three healthy normals served as controls. RESULTS: visual acuity of both eyes decreased to 0.16 within a span of 6 weeks. Perimetry revealed a central scotoma in the visual field of both eyes. VEP and flash ERG were progressively disturbed on the right eye. On the left eye, initially only pattern ERG and photopic responses were abnormal. Follow-up recordings revealed widespread pathology of photopic single and flicker responses. Immunofluorescence revealed strong reactivity of the inner plexiform layer and to a lesser extent staining of the outer plexiform layer at dilutions of 1:1000 with patients serum. The same retinal staining pattern was obtained with monoclonal anti-GAD65 antibodies. CONCLUSIONS: These findings suggest autoimmune retinopathy, mediated by anti-GAD65 autoantibodies as the underlying cause of visual loss.
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3/323. Cancer-associated retinopathy in a patient with advanced epithelial ovarian carcinoma.

    BACKGROUND: Paraneoplastic phenomena, such as retinopathy, may herald an unsuspected gynecologic malignancy. CASE: A 75-year-old woman presented to a neuro-ophthalmologist with abrupt onset of unilateral visual loss. A diagnosis of branch retinal artery occlusion was made and she was treated with aspirin. An echocardiogram subsequently revealed atrial dilation and she was placed on coumadin therapy. Her vision worsened and a cancer-associated retinopathy was entertained. A serum cancer-associated retinopathy antibody was detected; subsequent computed tomographies of the abdomen and pelvis revealed findings consistent with a primary ovarian carcinoma. CONCLUSION: patients with unexplained ophthalmologic symptoms may harbor an underlying gynecologic cancer.
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4/323. Multiple evanescent white dot syndrome in older patients.

    PURPOSE: To report two patients in their seventh decade who exhibited findings consistent with multiple evanescent white dot syndrome. methods: case reports of two patients referred for evaluation of decreased vision, visual field loss, and retinal white spots. RESULTS: A 60-year-old man and a 67-year-old woman had photopsia, visual field loss, and decreased central visual acuity. Examination disclosed numerous white retinal spots, ranging from 50 to 400 microm, with eventual foveal granularity. Visual field testing showed an enlarged blind spot and peripheral field defects. fluorescein angiography, electroretinography, and electrooculography results were consistent with multiple evanescent white dot syndrome. Eventually, the retinal lesions resolved in both patients and baseline visual acuity was recovered. CONCLUSION: A diagnosis of multiple evanescent white dot syndrome should be considered in patients with retinal findings typical of multiple evanescent white dot syndrome, regardless of age.
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5/323. The 22-kDa antigen in optic nerve and retinal diseases.

    OBJECTIVE: patients with unexplained visual loss were evaluated for the possibility of immunologic involvement. Antibody reactions were sought that might identify a common indication of retinal hypersensitivity. methods: The enzyme-linked immunosorbent assay (ELISA) and Western blot analysis were used to identify autoantibody reactions with retina and optic nerve components. Comparisons were made with the autoantibody reaction of normal subjects and patients with recognized forms of retinal decay: macular degeneration, retinitis pigmentosa, diabetic retinopathy, and paraneoplastic retinopathy. RESULTS: Eight patients, one man and seven women, were found to produce an autoantibody reaction with retina and optic nerve, including a novel 22-kDa neuronal antigen present within the retina and optic nerve. One of the eight had retinopathy associated with melanoma (MAR syndrome). Seven of the eight patients had electroretinogram abnormalities, varying from mild to severe. Six displayed features of optic atrophy. One patient with progressive visual loss had visual function stabilized after immunosuppressive therapy. CONCLUSIONS: In the eight cases described, unexplained visual loss was associated with autoantibody reactions with retina and optic nerve, including a common antibody reaction with a 22-kDa neuronal antigen found in the retina and optic nerve. All the patients had either an abnormal electroretinogram or optic atrophy. Six patients had both. The 22-kDa immunologic marker may not be directly involved in the patient's vision loss, but rather may be related to a nonspecific destruction of retina and optic nerve. However, the marker may be useful in identifying a specific subgroup of patients for further analysis.
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6/323. Nonsurgical management of binocular diplopia induced by macular pathology.

    OBJECTIVE: To treat binocular diplopia secondary to macular pathology. methods: Seven patients underwent evaluation and treatment. All had constant vertical diplopia caused by various maculopathies, including subretinal neovascularization, epiretinal membrane, and central serous retinopathy. visual acuity ranged from 20/20 to 20/30 in the affected eye. All except 1 patient had a small-angle, comitant hyperdeviation with no muscle paresis. Sensory evaluation demonstrated peripheral fusion and reduced stereoacuity. Neither prism correction nor manipulation of the refractive errors corrected the diplopia. A partially occlusive foil (Bangerter) of density ranging from 0.4 to 1.0 was placed in front of the affected eye to restore stable, single vision. RESULTS: The Bangerter foil eliminated the diplopia in all patients. Two patients elected not to wear the foil; 1 patient was afraid of becoming dependent, and the other was bothered by the visual blur. visual acuity in the affected eye was reduced on average by 3 lines. All patients maintained the same level of sensory fusion, with only 2 having reduced stereoacuity. Symptoms returned when the foil was removed or its density was reduced. CONCLUSION: Low-density Bangerter foils provide an effective, inexpensive, and aesthetically acceptable management for refractory binocular diplopia induced by macular pathology, allowing peripheral fusion to be maintained.
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7/323. Progressive changes in the fluorescein and indocyanine green angiogram in acute idiopathic maculopathy.

    AIMS/BACKGROUND: To report progressive changes in the fluorescein and indocyanine green angiograms of a patient with acute idiopathic maculopathy (AIM). methods: Over a two-year period, the patient underwent repeated ophthalmoscopic examinations and fluorescein (FA) and indocyanine green (ICG) angiography. RESULTS: The patient presented with subretinal neovascularization in his right eye. He developed recurrences after laser photocoagulation and surgical removal of the neovascular complex. One year later, he experienced a sudden loss of vision in his left eye with a maculopathy consistent with AIM. The maculopathy resolved after two weeks with poor vision. During the acute stage, FA showed lobular hyperfluorescence in the early phase and pooling in the late phase of the angiogram. In the resolved stage of the disease, FA showed irregular window defects and blockage. ICG revealed late hyperfluorescence of the macula in the acute stage. In the resolved stage of the disease, early hypofluorescence was noted in the ICG, which persisted throughout the late phase. CONCLUSION: This patient had poor vision in his right eye as a result of subretinal retinal neovascularization and poor vision in his left eye from a severe form of AIM. FA and ICG differed markedly during the acute and resolved stages of AIM. All cases of idiopathic subretinal neovascularization should be carefully evaluated to exclude AIM as the primary disease.
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8/323. central serous chorioretinopathy and hiv.

    BACKGROUND: patients with central serous chorioretinopathy (CSC) have sudden-onset, painless, uniocular blur that is typically diagnosed via fundus and fluorescein angiographic appearance. The etiology and pathophysiology are not fully understood; however, there may be an association with an infectious etiology. This article presents two cases of hiv-positive patients in whom central serous chorioretinopathy developed and discusses the possible relationship between the two cases. The differential diagnosis, clinical features, angiographic appearance, management options, and proposed etiologies of CSC will be presented. case reports: A 34-year-old black man hiv reported to the eye clinic with decreased vision in his right eye. A diagnosis of central serous chorioretinopathy (CSC) was made on the basis of the clinical and fluorescein appearance. He is currently being monitored for resolution. A 44-year-old black man with profoundly compromised immunity also came to the eye clinic with CSC and hiv retinopathy. He later progressed to CMV retinitis and subsequently died. CONCLUSION: Although considered in many cases to be idiopathic, central serous chorioretinopathy has been associated with infectious etiologies, one of which could be hiv.
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9/323. Ocular toxocariasis: a rare presentation of a posterior pole granuloma with an associated choroidal neovascular membrane.

    BACKGROUND: Ocular toxocariasis is a rare infection caused by the nematode larvae of toxocara canis, which is commonly found in dogs. Human transmission is usually via geophagia, the ingestion of food contaminated with the toxocara eggs, or contact with infected puppies, often resulting in devastating ocular and/or systemic effects. Distribution is worldwide; however, a higher incidence is demonstrated in the united states. methods: A 17-year-old black woman sought treatment at a neighborhood health center with a report of gradual decrease in vision from her left eye over a 3-month period. Her ocular and systemic histories were unremarkable. Anterior segment evaluation revealed no signs of anterior uveitis. The posterior pole showed a 1.5 DD, round, raised, white, subretinal lesion adjacent to the fovea with an overlying serous retinal detachment and retinal hemorrhage. RESULTS: She was referred to a retinologist who performed both fluorescein and indocyanine green (ICG) angiographies. A serum toxocara ELISA test was also ordered. fluorescein angiography revealed hyperfluorescence consistent with the granuloma. The ICG demonstrated an occult choroidal neovascular membrane (CNV) underlying the area of hemorrhage inferotemporal to the granuloma. CONCLUSION: This paper illustrates the case presentation and includes an extensive review of the ocular and systemic manifestations of toxocariases. A description of ICG videoangiography, therapeutic approaches, and management will also be discussed.
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10/323. Postprandial transient visual loss.

    BACKGROUND: Temporary loss of vision after ingestion of a large meal is a phenomenon that has been reported in only a small number of cases in the ophthalmic literature. CASE REPORT: A 60-year-old man reported episodes of blurred vision associated with visual aberrations in his left eye for 5 minutes after eating large meals. His medical history was significant for carotid artery disease, hypertension, "diet-controlled" diabetes, and hypercholesterolemia. The patient's symptoms abated when he ate in smaller quantities and was placed on a regimen of IOP-lowering eye drops. CONCLUSIONS: Postprandial transient visual loss can occur when blood gets shunted to the mesenteric system after eating, leaving the eye hypoperfused. It most commonly takes place in individuals whose ocular perfusion is already compromised by carotid disease, in combination with other vascular conditions that result in the inability to compensate for decreased perfusion to the eye. The signs and symptoms of postprandial visual loss--as well as the mechanisms thought to contribute to it--are discussed.
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