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At least 973 records · Page 54Linked to original sources
PubMed1976

Autosomal recessive retinitis pigmentosa and Coats disease: a presumed familial incidence.

Three of four siblings of normal parents had a combination of Coats disease and retinitis pigmentosa bilaterally. Our report of their respective cases is, to our knowledge, the first report of a familial incidence of the combination of the two diseases in an individual and supports the implication that Coats disease may be a genetic abnormality. The pathological process was essentially the same in all three patients, although it occurred differently in one of the three siblings and gave rise to an altered functional and clinical picture. The similarities may indicate that the convenient categories of "tapeto-retinal degenerations" are clinical variations of the same genetic abnormality.

Adolescent↗
PubMed1976

Clinicopathologic correlations in diabetic retinopathy. I. Histology and fluorescein angiography of microaneurysms.

A patient with adult-onset diabetes mellitus was referred with a diagnosis of malignant melanoma of the choroid of the left eye. A nonproliferative type of diabetic retinopathy was present, which was studied and documented by stereoscopic fundus photographs and fluorescein angiograms. Following enucleation, the microangiopathies were correlated histologically, using the retinal trypsin digest technique. Four types of microaneurysms were seen histologically that were believed to represent stages in the development of this lesion. Most thin-walled aneurysms tightly packed with erythrocytes did not fluoresce. Aneurysms that were hypercellular and those with thick walls showed early and late fluorescence. Intraretinal microvascular abnormalities were hypercellular dilated channels. Those that take origin from terminal arterioles are believed to represent attempts at neovascularization.

Aneurysm↗
PubMed1977

Herpes simplex retinitis and encephalitis in an adult.

A 17-year-old girl developed a viral encephalitis that was followed by massive exudative retinal detachments in both eyes. A diagnosis of herpes simplex encephalitis and retinitis was made as a result of finding rising herpes simplex viral titers. An examination of the patient's cell-mediated immune system showed it to be grossly intact.

Adolescent↗
PubMed1982

Idiopathic juxtafoveolar retinal telangiectasis.

Twenty-seven healthy adult patients had visual loss in one or both eyes because of exudation from juxtafoveolar retinal capillary telangiectasis of uncertain cause. These patients were subdivided as follows: group 1, men with uniocular involvement, intraretinal lipid exudation, and telangiectasis largely confined to the temporal half of the juxtafoveolar area; group 2, mostly men with symmetric areas of telangiectasis affecting the temporal half of the juxtafoveolar areas and minimal intraretinal exudation; group 3, both sexes with symmetric involvement of all of the parafoveolar capillary bed an minimal exudation; and group 4, one case of telangiectasis with occlusive perifoveolar capillary changes and familial optic disc pallor. The visual acuity prognosis in groups 1 through 3 is relatively good. Photocoagulation may be of some value in the treatment of patients in group 1.

Adult↗
PubMed1983

Retinal abnormalities associated with anemia.

The incidence of clinically apparent retinal changes in 35 anemic patients and 35 age- and sex-matched control subjects was studied. Retinal photographs of all subjects were obtained. From these, all vascular and extravascular retinal lesions were noted. No retinal abnormalities were observed in the control subjects. Seven (20%) of the anemic patients exhibited extravascular lesions. There was no relationship detected between the occurrence of these changes and the severity or the cause of the anemia. Employing the assumption that true venous length for a given net distance traveled correlates with the degree of venous tortuosity, venous length over a standard radial distance from the optic disc was assessed with a curvometer. A significant negative correlation was determined between venous length and the level of hematocrit, thereby implying that retinal venous tortuosity is directly related to severity of anemia.

Adolescent↗
PubMed1984

Manifestations of Whipple's disease in the posterior segment of the eye.

Ocular manifestations of Whipple's disease result from CNS involvement, direct intraocular involvement, or both. Ocular signs caused by CNS involvement occurred in 30 of the 34 patients with ocular manifestations described in the literature. In only four of the 34 cases were ocular manifestations due solely to intraocular involvement. Two cases reported herein had unique intraocular involvement, manifested as diffuse chorioretinal inflammation. Fluorescein angiography showed diffuse vasculitis, with hemorrhages, exudates, retinal capillary occlusion in the perifoveal and midperipheral areas, capillary dilation at the optic disc, and choroidal folds. Proper antibiotic treatment resulted in ocular and systemic recovery. Follow-up is mandatory because of possible recurrences, which may start with intraocular signs, followed by systemic manifestations. Some cases progress to fetal CNS involvement. Therefore, when intraocular signs recur in treated patients, antibiotic therapy should be restarted or dose should be increased.

Adult↗
PubMed1984

Actin filaments in contracting preretinal membranes.

In 14 patients, preretinal membranes, causing retinal traction and severe visual impairment, were removed by vitrectomy and evaluated by light and electron microscopy using myosin subfragment-1 to stain actin filaments. Eight membranes were of vascular origin, six of nonvascular origin. All but one contained bundles of oriented actin filaments within a number of their nonvascular stroma cells, suggesting that the contractile protein action may have been involved in their clinically observed contraction.

Actins↗
PubMed1989

Anterior location of the crossing artery in branch retinal vein obstruction.

We evaluated retrospectively the cases of 25 patients (26 eyes) with a recent, temporal, branch retinal vein obstruction to determine the relative anatomic position of the obstructed vein in relation to its crossing artery. In 26 (100%) of 26 eyes, the artery lay anterior to the vein, toward the vitreous cavity. A control group was obtained by evaluating the relative anatomic position between the branch retinal artery and vein at an equivalent crossing site along the opposite vascular arcade within the same eye. In the control crossing sites, the artery lay anterior to the vein 65% (15/23) of the time. We conclude that the likelihood that the artery will lie anterior to the obstructed vein at the site of blockage in a branch retinal vein obstruction is substantially greater than what would be expected by chance alone. This anatomic relationship between artery and vein probably plays a role in the cause of a branch retinal vein obstruction and may have therapeutic significance in light of a recent report concerning surgical treatment of such obstructions.

Adult↗
PubMed1989

Central retinal vein obstruction with lipid exudate.

Four patients with a central retinal vein obstruction associated with excessive deposits of hard exudate are described. When compared with a control group of 15 consecutive patients with a central retinal vein obstruction, those with large amounts of hard exudate were noted to have significantly elevated triglyceride levels, poorer visual acuity, and increased degrees of retinal ischemia on fluorescein angiography.

Adult↗
PubMed1990

Retinal toxicity of recombinant tissue plasminogen activator in the rabbit.

We studied the dose-dependent retinal toxicity of the available commercial preparation of human recombinant tissue plasminogen activator in the normal rabbit eye. Tissue plasminogen activator was injected into the midvitreous cavity of albino rabbits in doses (per 100 microL) of 25, 50, 75, and 100 micrograms. Control eyes received 100 microL of balanced salt solution or tissue plasminogen activator vehicle. No evidence of a retinal toxic reaction was seen in eyes receiving 25 micrograms of tissue plasminogen activator. One of four eyes injected with 50 micrograms showed loss of photoreceptor cells by light microscopy. Severe retinal damage was seen by ophthalmoscopy, electroretinography, and light microscopy in three of four eyes receiving 75 micrograms of tissue plasminogen activator and in all eyes treated with 100 micrograms of tissue plasminogen activator or equivalent vehicle. These results suggest that the commercial recombinant tissue plasminogen activator formulation has a narrow margin of safety in nonvitrectomized eyes and that a component of the vehicle is the toxic factor.

Animals↗
PubMedDate not supplied

Doppler assessment of hemodynamic changes after hemodilution in retinal vein occlusion.

PURPOSE: We assessed the usefulness of color Doppler imaging and spectral analysis in monitoring the effect of isovolemic hemodilution on retinal vein occlusion. METHODS: Color Doppler imaging was used to measure the systolic and diastolic blood flow velocities and the resistance index (RI) in the central retinal artery and the maximum and minimum blood flow velocities in the central retinal vein of affected eyes and contralateral unaffected eyes before and 1 day after isovolemic hemodilution in 70 adults (40 men and 30 women; mean age, 62.4 +/- 13.7 years) who presented with retinal vein occlusion. RESULTS: With hemodilution, the hematocrit value was decreased from 41.8 +/- 3.0 to 33.0 +/- 3.0. In central retinal vein occlusion, the pretreatment arterial and venous flow velocities of affected eyes were significantly lower than those of unaffected eyes. After hemodilution in eyes affected by ischemic occlusion, a significant improvement in the RI in the central retinal artery was observed without changes in venous flow velocity. After hemodilution in eyes affected by non-ischemic occlusion, a significant increase in maximal venous flow velocity only was noted. In branch retinal vein occlusion, no significant difference was observed in the RI between affected and unaffected eyes. After hemodilution, an improvement in RI was noted only for affected eyes. CONCLUSIONS: The present results confirm the potential value of Doppler analysis in monitoring the impact of hemodilution on arterial and venous velocity in patients with central retinal vein occlusion.

Adult↗
PubMed1985

Chronic lymphocytic leukemia with hyperleukocytosis. The hyperviscosity syndrome.

A 47-year-old man with hyperleukocytic chronic lymphocytic leukemia progressively developed retinal hemorrhages, headache, diplopia, dysequilibrium, slurred speech, nystagmus, ataxic gait, and hearing loss as his leukocyte count rose to a maximum of 968,000/mm3. All of these symptoms and signs resolved promptly after leukapheresis. The authors reviewed records of 210 patients with chronic lymphocytic leukemia seen at our institution over a 12-year period, and found 16 patients with sustained hyperleukocytosis above 500,000/mm3, 3 of whom had features of the hyperviscosity syndrome. No laboratory values consistently predicted the occurrence or lack of occurrence of the hyperviscosity syndrome. The key to the management of hyperviscosity syndrome in the setting of hyperleukocytic chronic lymphocytic leukemia is to consider the diagnosis and to rapidly lower the lymphocyte count.

Adult↗
PubMed1988

Reversible ocular toxicity related to tamoxifen therapy.

A 42-year-old woman with metastatic breast cancer developed bilateral optic disc swelling, retinal hemorrhages, and visual impairment three weeks after starting treatment with low doses of tamoxifen. Neurologic evaluation failed to provide an explanation for the ocular findings which resolved completely after cessation of tamoxifen therapy. This case suggests that tamoxifen has the potential for causing serious ophthalmologic toxicity which may be reversible if recognized early.

Adult↗
PubMed2003

Type I glutaric aciduria, part 1: natural history of 77 patients.

Type I glutaric aciduria (GA1) results from mitochondrial matrix flavoprotein glutaryl-CoA dehydrogenase deficiency and is a cause of acute striatal necrosis in infancy. We present detailed clinical, neuroradiologic, molecular, biochemical, and functional data on 77 patients with GA1 representative of a 14-year clinical experience. Microencephalic macrocephaly at birth is the earliest sign of GA1 and is associated with stretched bridging veins that can be a cause of subdural hematoma and acute retinal hemorrhage. Acute striatal necrosis during infancy is the principal cause of morbidity and mortality and leads to chronic oromotor, gastroesophageal, skeletal, and respiratory complications of dystonia. Injury to the putamen is heralded by abrupt-onset behavioral arrest. Tissue degeneration is stroke-like in pace, radiologic appearance, and irreversibility. It is uniformly symmetric, regionally selective, confined to children under 18 months of age, and occurs almost always during an infectious illness. Our knowledge of disease mechanisms, though incomplete, is sufficient to allow a rational approach to management of encephalopathic crises. Screening of asymptomatic newborns with GA1 followed by thoughtful prospective care reduces the incidence of radiologically and clinically evident basal ganglia injury from approximately 90% to 35%. Uninjured children have good developmental outcomes and thrive within Amish and non-Amish communities.

Brain Diseases, Metabolic, Inborn↗