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At least 541 records · Page 30Linked to original sources
PubMed1978

Bilateral retinal detachment following cytomegalovirus retinitis.

Bilateral retinal detachments developed in a renal allograft patient several months after the onset of cytomegalovirus retinitis. Laser photocoagulation was used to limit the posterior extent of one detachment until the detachment was surgically repaired. The thinned, atrophic retina that results from the necrotizing retinitis makes localization of retinal holes difficult and, in this case, contributed to the initial impression that these detachments were nonrhegmatogenous in origin.

Cytomegalovirus Infections↗
PubMed1986

Measurement of blood-retinal barrier function in central retinal vein occlusion.

Vitreous fluorophotometry was used to measure blood-retinal barrier permeability to fluorescein in eight patients (mean age, 42.9 years; range, 30 to 55 years) with central retinal vein occlusion (CRVO). Permeability coefficient was derived by fitting a mathematical model to the posterior vitreous fluorescence scan and plasma-free fluorescein concentration curve at 60 minutes after intravenous fluorescein sodium (14 mg X kg-1). A permeability index (PI) was estimated by dividing the area under the vitreous fluorescence scan by the area under the plasma-free fluorescein curve. The permeability coefficient and PI were comparable and highly correlated. Initial mean permeability coefficient was 28.78 X 10(-7) cm X s-1 (range, 14.42 X 10(-7) to 41.10 X 10(-7) and 1.89 X 10(-7) cm X s-2 (range, 0.96 X 10(-7) to 2.76 X 10(-7) in eight affected and seven unaffected eyes, respectively. The permeability coefficient and PI in unaffected eyes did not differ significantly from 18 eyes of ten normal subjects. After three to 12 months, permeability coefficient and PI in affected eyes approached the values in the contralateral eyes of four patients with mild and one patient with moderate CRVO but remained elevated in the remaining patients. The permeability coefficient and PI correlated well with changes in severity of retinal appearances on color photographs and fluorescein angiograms. Vitreous fluorophotometry quantitated changes in blood-retinal barrier permeability in CRVO.

Adult↗
PubMed2002

Loss of retinal ganglion cells following retinal ischemia: the role of inducible nitric oxide synthase.

Following experimental, transient, retinal ischemia in the rat, there is loss of retinal neurons, which occurs over several weeks. Retinal ganglion cells (RGCs) are particularly susceptible and there is early, massive degeneration of these neurons after ischemia. We have determined the early mechanisms by which RGCs are killed following ischemia. Retinal ischemia/reperfusion was produced in rats by transient unilateral elevation of intraocular pressure above systolic blood pressure. Retinas were studied by immunohistochemistry for the presence of inducible nitric oxide synthase (NOS-2) at several time points post-ischemia and specific cell types were identified. Rats were also treated orally with L -N(6) -(1-iminoethyl)lysine 5-tetrazole amide (SC-51), a prodrug of an inhibitor of NOS-2 or with aminoguanidine (AG) for a period of 14 days. Retrograde labelling with Fluoro-Gold quantitated the loss of RGCs. NOS-2 was not present in the normal retina and was not present in the eyes that were contralateral to the ischemic eyes. Within 24hr after ischemia, polymorphonuclear leukocytes containing NOS-2 had entered the ganglion cell layer and surrounded RGCs. Within 5 days after ischemia, NOS-2 was present in many inner retina cells and in invading monocytes in the vitreous. Between 7 and 14 days post-ischemia, there were few hematogenous cells in the retina but NOS-2 was sparsely detectable in microglia and other cells of the inner retina. Two weeks after ischemia, rat eyes lost approximately 50% of the RGCs. Treatment with AG for 14 days following ischemia was partially neuroprotective; approximately 28% of the RGCs were lost. Treatment with SC-51 for 14 days following ischemia almost completely prevented the loss of RGCs. Thus, within 24hr following ischemia, polymorphonuclear leukocytes containing NOS-2 attack and kill neurons in the ganglion cell layer. For 2 weeks after ischemia, NOS-2 appears transiently in the retina in several different cell types at different times. Continuous pharmacological treatment with inhibitors of NOS-2 activity during the 2 weeks post-ischemia period provides significant neuroprotection against the loss of RGCs.

Animals↗
PubMedDate not supplied

Retinal vessel responses to systemic autonomic stimulation in fellow eyes of patients with retinal vein occlusion.

The retinal vessel calibre responses to systemic autonomic stimulation were studied in fellow eyes of 11 patients with central retinal vein occlusion (CRVO) and 10 patients with branch retinal vein occlusion (BRVO), using sustained isometric muscle contraction as the stimulus. These vessel responses were compared to those of a control group of 11 subjects of similar ages. The changes in retinal vessel calibre were measured using the Quantimet Image Analyser. There was no significant difference in mean arteriolar constriction during isometric muscle contraction (mean +/- SEM) between the CRVO group (6.0 +/- 1.34%) and the BRVO group (5.4 +/- 0.31%), (p greater than 0.05), and between either of these groups compared with the control group (7.4 +/- 1.20%), (p greater than 0.50). Similarly there was no significant difference in mean venule responses between the groups (CRVO 4.9 +/- 0.48%; BRVO 4.6 +/- 0.63%; control subjects 3.8 +/- 0.90%; p greater than 0.05). The diastolic blood pressure responses were similarly not significantly different between the 3 groups (CRVO 22.3 +/- 1.27, range + 17 to 29 mmHg; BRVO 25.8 +/- 2.9 mmHg, range 18 to 45 mmHg; control subjects 21.3 +/- 1.7 mmHg, range 16 to 35 mmHg), (p greater than 0.10). The implications of the results are discussed.

Adult↗
PubMed1975

[Peripheral retinal circulation times in connection with retinal detachment (author's transl)].

Concerning the pathogenesis of retinal detachment 4 groups of each 10 eyes have been examined by fluorescein angiography: the periphery of normal eyes (Table 2), ophthalmoscopically inconspicuous sectors of patients with detachment (Table 3), the area of lattice degeneration, radial perivascular degeneration and round holes without detachment (Table 4) and the area of tears and holes, when detachment has taken place (Table 5). The time passing between the injection of dye into the cubital vein and the first arterial filling in the retinal periphery is practically equal in all groups. The prolongation of retinal circulation time II from the first arterial to the complete venous filling in areas of lattice degeneration etc. without detachment seems to be in connection with small vessel closures. The striking short retinal circulation time I from the first arterial to the first venous filling in the cases of detachment is apparently caused by capillary dilatations central of the tears and holes; the dilated capillaries seem to have the function of a arteriovenous anastomosis. Own measurements of circulation times in the area of optic disc (Table 1), performed for comparisments, are accordant to literature.

Adolescent↗
PubMed1990

Retinal break type and proliferative vitreoretinopathy in nontraumatic retinal detachment.

In a retrospective study of 1180 consecutive eyes operated for retinal detachment, vitreous traction on the rent was the determining factor for the development of proliferative vitreoretinopathy (PVR). Round, multiple, small holes in equatorial degeneration (retinogenic) and macular holes in which no vitreous traction on the rent was found did not complicate with PVR. Retinal detachment caused by horseshoe or crescent-shaped tears with evidence of vitreous traction (vitreogenic) developed PVR to a variable degree: in 171 (25.8%) senile myopic, 19 (44.2%) senile-myopic aphakic, 23 (20.2%) typical aphakic, and 32 (78.1%) patients with giant tears. We also found that retinogenic retinal detachments affected younger age groups more than did vitreogenic retinal detachments.

Adolescent↗
PubMed1977

Dissociation of the vitreo-retinal junction following experimental embolization of retinal circulation.

Spheric plastic beads (7-25 mu in diameter) were injected into the central retinal artery of the owl monkey (Aotus trivirgatus) using a micro-surgical technique. The occlusion of retinal arteriolar branches resulted in posterior vitreous detachment and microcystoid degeneration in inner retinal layers. The dissociation of the vitreoretinal junction showed three different entities: detachment of the vitreous from the basal lamina (inner limiting lamina of the retina), separation of the basal lamina from the retina, and detachment of shreds of glial cells and other degenerated retinal tissue (intraretinal schisis).

Animals↗
PubMed1998

[Acute retinal necrosis syndrome. Argon laser coagulation for prevention of rhegmatogenic retinal detachment].

BACKGROUND: ARN syndrome follows severeintraocular infection by herpes viruses and primarily affects the peripheral retina. Following scar formation, despite antiviral treatment, rhegmatogenous retinal detachment occurs very often. Prophylactic argon laser photocoagulation has therefore been proposed. We report our experience. PATIENTS: We treated five patients presenting clinically with advanced unilateral ARN with acyclovir. All eyes received a prophylactic confluent double row of argon laser treatment (500 microns, 0.2 s, gray-white lesions) central to the affected area as soon as was possible, depending on the vitreous clouding. Four patients were treated with Aspirin. RESULTS: One of the five patients had a peripheral rhegmatogenous retinal detachment that was limited by the argon laser row. Another patient had a tractional detachment needing vitreoretinal surgery. Two eyes developed vitreal hemorrhage of unknown origin. CONCLUSION: A lower rate of rhegmatogenous retinal detachments than expected occurred post-laser treatment. Vitreal hemorrhage was more frequent than previously reported. The bleeding probably originated from anterior retinal neovascularization and may have been enhanced by Aspirin treatment. We recommend early prophylactic argon laser photocoagulation in all ARN patients in agreement with the results of previous studies.

Acyclovir↗
PubMed2002

Intentional complete interruption of a retinal vein after vitrectomy might improve the rate of successful chorioretinal venous anastomosis formation in central retinal vein occlusion.

BACKGROUND: Laser or surgical chorioretinal venous anastomosis has not become widespread as suitable treatment for central retinal vein occlusion (CRVO). We report here the effectiveness of cutting off a retinal vein with vitrectomy in making a chorioretinal venous anastomosis in CRVO. METHODS: We performed a vitrectomy accompanied by a chorioretinal venous anastomosis procedure for seven consecutive patients with CRVO. These patients had shown no improvement in their visual acuity in the month following their first visit to our hospital and had a visual acuity of less than 20/200. Their preoperative visual acuity ranged from counting fingers to 20/300. The procedure included the complete cutting of the affected retinal vein, and the making of a small incision at both sides of the vein interruption through the full thickness of the retina, the retinal pigment epithelium and Bruch's membrane. RESULTS: In five of the seven patients, successful chorioretinal venous anastomosis was observed. All five patients showed an improvement of two or more lines in visual acuity 6 months postoperatively. In three of the five, visual acuity was 20/100 or better. A postoperative complication of recurrent vitreous hemorrhage and fibrous proliferation was observed in one patient, and a second operation was necessary. CONCLUSIONS: Surgical interruption of an affected vein was a feasible procedure and could raise the rate of successful chorioretinal venous anastomosis in CRVO.

Aged↗
PubMed1978

Retinal depression sign indicating a small retinal infarct.

Retinal depression, a newly observed sign, has been observed as an abnormality in the reflection from the internal limiting lamina produced by depression of the inner surface of the retina after a small retinal infarct. These depressions were first observed in 16 patients with sickling hemoglobinopathies. Additionally, I examined a patient with systemic hypertension, a patient with retinal arteriolitis, and a patient with juvenile onset diabetes mellitus who also had retinal depression.

Adolescent↗
PubMed1979

Rhegmatogenous retinal detachment complicating cytomegalovirus retinitis.

Six eyes in four patients with cytomegalovirus retinitis developed retinal holes and retinal detachment. Holes appeared in areas of necrosis and were typically large and round with shaggy edges. Differentiation from exudative detachment was sometimes difficult because of obscuration of the fundus by vitreous haze. Cryotherapy was successful in closing open breaks without detachment; cryotherapy and exoplant surgery were used effectively to treat the initial detachments. The occurrence of massive periretinal proliferation and late development of new areas of hole formation or retinitis complicated therapy for these detachments.

Adult↗
PubMed1979

Rhegmatogenous retinal detachment with retinal telangiectasia.

A 34-year-old man with unilateral retinal telangiectasia developed a bullous retinal detachment. A horseshoe retinal tear was found at 12 o'clock. The detachment resolved with placement of an encircling scleral buckle. The prompt and permanent resolution of subretinal fluid supported our belief that this was a rhegmatogenous retinal detachment.

Adult↗
PubMed1984

Surgical treatment of giant retinal tears with inverted posterior retinal flaps.

We treated 23 consecutive cases of giant retinal tears with inverted retinal flaps. We used pars plana vitrectomy together with an intravitreal bubble to unfold the posterior retinal flap, combined with cryotherapy to cause a chorioretinal adhesion and a broad scleral buckle. The vitrectomy was done after applying cryotherapy so viable retinal pigment epithelial cells in the vitreous cavity could also be removed. Thirteen eyes had giant tears measuring 90 to 180 degrees (Group 1), eight eyes had giant tears measuring 180 to 270 degrees (Group 2), and two eyes had giant tears larger than 270 degrees (Group 3). The retina was successfully reattached in 11 of the 13 eyes in Group 1, each of the eight eyes in Group 2, and one of the two eyes in Group 3. We believe that vitrectomy and lavage of the vitreous cavity after applying cryotherapy was important in reducing the incidence of proliferative vitreoretinopathy and improving our success rate.

Adolescent↗
PubMed2006

Retinal ischemia with neovascularization in cisplatin related retinal toxicity.

PURPOSE: To report a case of macular ischemia and retinal neovascularization in a patient who received cisplatin related chemotherapy. DESIGN: Interventional case report. METHODS: A patient with germ cell testicular tumor received polychemotherapy (bleomycin, etoposide, and cisplatin or BEP) for a recurrence of his tumor. Ten weeks after completion of treatment, he presented with loss of vision in his left eye. RESULTS: Fluorescein angiography revealed bilateral retinal ischemia and left retinal neovascularization. Panretinal laser photocoagulation was performed. Unfortunately, his vision did not improve. CONCLUSIONS: Like interferon, cisplatin related chemotherapy could cause considerable ocular morbidity. It can cause marked irreversible visual loss at therapeutic dose, and it is not well recognized. Retinal neovascularization related to cisplatin therapy has not been previously reported. Physicians should be aware and warn patients of the potential ophthalmic side effects of cisplatin related chemotherapy.

Adult↗
PubMed2006

Combining surgical ablation of retinal inflow and outflow vessels with photodynamic therapy for retinal angiomatous proliferation.

PURPOSE: To evaluate short-term efficacy of combining surgical ablation of retinal inflow and outflow vessels and photodynamic therapy (PDT) for stage 3 retinal angiomatous proliferation (RAP). DESIGN: Prospective interventional case series. METHODS: Five eyes (five patients) underwent surgical ablation of inflow and outflow vessels and PDT for stage 3 RAP. RESULTS: Inflow and outflow vessels were ablated in four eyes, and only inflow was ablated in one eye. In four eyes starting PDT within six weeks of surgical ablation, choroidal neovascularization (CNV) disappeared or shrank after one PDT session (three months follow-up). However, CNV enlarged again in three of the four (final follow-up) because of reperfusion from newly formed inflow vessels. In one eye starting PDT seven months after ablation, a new retinal inflow vessel feeding the CNV appeared by the time of the first PDT session. The CNV continued to expand, despite two PDT sessions. CONCLUSIONS: Combining surgical ablation and PDT was not useful on account of a high frequency of reperfusion from retinal inflow vessels.

Arterioles↗
PubMed2003

Cdh23 mutations in the mouse are associated with retinal dysfunction but not retinal degeneration.

Mutations in the cadherin 23 gene (CDH23) cause Usher syndrome type 1D in humans, a disease that results in retinitis pigmentosa and deafness. Cdh23 is also mutated in the waltzer mouse. In order to determine if the retina of the waltzer mouse undergoes retinal degeneration and to gain insight into the function of cadherin 23 in the retina, we have characterized the anatomy and physiology of retinas of waltzer mouse mutants. Three mutant alleles of Cdh23 were examined by histology and electroretinography (ERG). ERGs of the three Cdh23 mutant groups revealed two of them to have abnormal retinal function. One allele had a- and b-waves that were only approximately 80% of Cdh23 heterozygotes. Another allele had a significantly faster implicit time for both the a- and b-waves of the ERG. No anatomical abnormality was detected in any of the Cdh23 mutants by light microscopy. Because the mutant Cdh23 phenotype was found to be similar to the previously reported retinal phenotype of Myo7a mutant mice, the orthologue of another Usher syndrome (type 1B) gene, we generated mice that carried mutations in both genes to test for genetic interaction in the retina. No functional interaction between cadherin 23 and myosin VIIa was detected by either microscopy or ERG.

Alleles↗
PubMed2006

Identical mutation in a novel retinal gene causes progressive rod-cone degeneration in dogs and retinitis pigmentosa in humans.

Progressive rod-cone degeneration (prcd) is a late-onset, autosomal recessive photoreceptor degeneration of dogs and a homolog for some forms of human retinitis pigmentosa (RP). Previously, the disease-relevant interval was reduced to a 106-kb region on CFA9, and a common phenotype-specific haplotype was identified in all affected dogs from several different breeds and breed varieties. Screening of a canine retinal EST library identified partial cDNAs for novel candidate genes in the disease-relevant interval. The complete cDNA of one of these, PRCD, was cloned in dog, human, and mouse. The gene codes for a 54-amino-acid (aa) protein in dog and human and a 53-aa protein in the mouse; the first 24 aa, coded for by exon 1, are highly conserved in 14 vertebrate species. A homozygous mutation (TGC --> TAC) in the second codon shows complete concordance with the disorder in 18 different dog breeds/breed varieties tested. The same homozygous mutation was identified in a human patient from Bangladesh with autosomal recessive RP. Expression studies support the predominant expression of this gene in the retina, with equal expression in the retinal pigment epithelium, photoreceptor, and ganglion cell layers. This study provides strong evidence that a mutation in the novel gene PRCD is the cause of autosomal recessive retinal degeneration in both dogs and humans.

Amino Acid Sequence↗
PubMed1987

Assessment of angiographic retinal capillary nonperfusion in central retinal vein occlusion.

We studied the reproducibility and accuracy of eight retinal specialists in assessing the extent of retinal capillary nonperfusion on fluorescein angiograms of 26 central retinal vein occlusions. Each specialist was asked to classify the retinal capillary perfusion status on every angiogram as nonischemic, minimally ischemic, moderately ischemic, markedly ischemic, or uncertain. Criteria for classification of each angiogram were specified in advance for each reviewer. Each examiner individually reviewed every angiogram on two separate occasions separated by at least one month. Intraexaminer and interexaminer reproducibility were both substantially better than the agreement predicted by chance alone (P less than .05); however, the proportion of agreement with the correct classification was less than 60% for all eight specialists.

Capillaries↗