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At least 1,729 records · Page 96Linked to original sources
PubMed2003

Retinal detachment rate after vitrectomy for retained lens material after phacoemulsification.

PURPOSE: To report the rate of retinal detachment after vitrectomy for retained intravitreal lens material after phacoemulsification using specific vitrectomy techniques designed to minimize retinal detachment. DESIGN: Consecutive, interventional case series. METHODS: Retrospective chart review of 100 consecutive eyes (one surgeon) of 100 patients undergoing vitrectomy for retained lens material after phacoemulsification and followed up for 3 months or longer unless an outcome event had occurred. Vitrectomy techniques employed to minimize the frequency of retinal detachment included inducing posterior vitreous detachment with maximal vitreous removal before phacofragmentation to avoid vitreous trauma, lens fragment debulking before fragmentation, use of low energy with high aspiration during removal of retained lens material, and intraoperative indirect ophthalmoscopic evaluation of the retinal periphery with scleral indentation to diagnose and treat intraoperative retinal breaks. The main outcome measures included prevalence of coexisting retinal detachment in eyes with retained lens material, incidence of retinal detachment or retinal breaks after vitrectomy for removal of retained lens material, and final visual acuity. RESULTS: The prevalence of previtrectomy retinal detachment was 4%; the incidence of postvitrectomy retinal detachment was 4%; the final visual acuity was 20/40 or better in 53%. One patient had a retinal break recognized during vitrectomy and was treated with retinocryopexy, but postoperative retinal detachment developed from a separate break. Three others were treated during vitrectomy for retinal breaks (including two with known preexisting breaks) and did not have any retinal detachment. Poor previtrectomy visual acuity (hand motions) was a risk factor for postvitrectomy retinal detachment. CONCLUSIONS: The rate of retinal detachment reported after vitrectomy for retained lens material after phacoemulsification can be minimized to approximately the rate expected with cataract extraction complicated by vitreous loss by employing standard surgical techniques. Higher risk eyes may benefit from more frequent postvitrectomy examinations.

Aged↗
PubMed1995

Progressive outer retinal necrosis (PORN) in AIDS patients: a different appearance of varicella-zoster retinitis.

Retinal infections caused by the varicella-zoster virus (VZV) have been reported in immunocompetent and immunocompromised individuals. Two cases of a VZV-related retinitis are described with the characteristic features of the recently described progressive outer retinal necrosis (PORN) syndrome. Both patients suffered from the acquired immunodeficiency syndrome (AIDS) with greatly reduced peripheral blood CD4+ T lymphocyte counts, and presented with macular retinitis without vitritis. The disease was bilateral in one case and unilateral in the other. The clinical course was rapidly progressive with widespread retinal involvement and the development of rhegmatogenous retinal detachment with complete loss of vision in the affected eyes despite intensive intravenous antiviral therapy. VZV DNA was identified in vitreous biopsies, by molecular techniques based on the polymerase chain reaction (PCR), in both patients. At present, the use of very high-dose intravenous acyclovir may be the best therapeutic option in these patients for whom the visual prognosis is poor. Intravitreal antiviral drugs could also contribute to the management of these cases.

AIDS-Related Opportunistic Infections↗
PubMed1990

Effect of the calcium antagonist, nifedipine, on ischemic retinal dysfunction.

The therapeutic effectiveness of calcium channel antagonists (CCA) in hypertension and angina are well established. More recently, CCAs have also been demonstrated to ameliorate neurologic dysfunction that often accompanies ischemia associated with subarachnoid hemorrhage and stroke. We have hypothesized that retinal degeneration associated with ischemia may also result from the accumulation of calcium intracellularly, so-called "Ca++ overload". To test this hypothesis, a rat model of acute retinal ischemia, produced by direct occlusion of posterior ciliary and central retinal arteries, was developed. The extent of retinal dysfunction induced by ischemia was evaluated by electroretinograms (ERGs). Occlusion of the retinal arteries resulted in the disappearance of both a- and b-waves during the occlusion period (30 minutes) in vehicle-treated rats. Total retinal ischemia did not produce any significant change in magnitude of ERG a-wave amplitude during three-hours of reperfusion. However, ERG b-waves amplitudes were significantly reduced by more than 60%. In rats, pretreatment with nifedipine (0.33 to 3.3 mg/kg, i.p.) 30 minutes prior to the occlusion of the retinal vessels produced a significant dose-dependent increase in the recovery of b-wave amplitude when compared to vehicle-treated rats. These data support the idea that "Ca++ overload", resulting from the deregulation of intracellular Ca++ homeostasis, is a primary factor involved in ischemic retinal degeneration and that CCAs can protect the retina from ischemic damage.

Animals↗
PubMed2004

Neuro-optic cell apoptosis and microangiopathy in KKAY mouse retina.

Diabetic retinopathy is one of the common complications of diabetes and is the leading cause for patients' visual dysfunction and sight loss. However, the mechanism of diabetic retinopathy is not clearly defined. The present study was undertaken to investigate neuroretinal apoptosis in different stages in a mouse model for type 2 diabetes mellitus and the mechanism of diabetic retinopathy. KKAY mouse with genetic diabetes, an animal model for type 2 diabetes, was used in this study. Mice were divided into a control group and a diabetic group. The mice in both groups were sacrificed at one month and three months, and the mouse eyeballs were used for making retinal histologic sections. We showed in this study that the apoptotic cell numbers for retinal neural cells in the ganglion cell layer were significantly greater in the diabetic group than in the control group (p<0.01), as determined by the TUNEL assay. In addition, many more apoptotic retinal neuronal cells were found in the retinal ganglion cell layer and medial part of the inner nuclear layer in the diabetic group when the mice were sacrificed at three months as compared to those sacrificed at one month (p<0.01). We also studied the ultrastructure of the retinal nerve cells and microvesseles by electron microscopy and demonstrated that the ultrastructure changes for retinal neural cells and retinal microangiopathy were observed in, as early as, the early stage of diabetes. These findings indicate that: i). retinal neuropathy and microangiopathy occur in the early stage of diabetes, ii). apoptosis may be an important mechanism through which retinal neurodegeneration is developed, and iii). both retinal neurodegeneration and retinal microangiopathy should be considered as the diabetic retinopathy.

Animals↗
PubMedDate not supplied

Minimally invasive method for repair of rhegmatogenous retinal detachment following treatment for retinoblastoma.

A minimally invasive method for repair of rhegmatogenous retinal detachment following treatment of retinoblastoma is described. Two children with retinoblastoma developed rhegmatogenous retinal detachments following treatment with a combination of chemotherapy and cryotherapy. Each eye underwent a non-drainage scleral buckling procedure without retinopexy of the retinal break. Postoperatively, the retinas reattached and retinopexy with indirect laser photocoagulation was performed during subsequent examinations under anesthesia. The retinas have remained attached with 2 to 5 years of follow-up. The tumor recurred in case 2, was treated with additional chemotherapy, and has undergone type 1 regression. Non-drainage scleral buckling without retinopexy is a useful technique for repairing rhegmatogenous retinal detachment in eyes with retinoblastoma. The retinal break can be treated postoperatively with indirect laser photocoagulation to minimize the chance of viable tumor cell dissemination.

Antineoplastic Agents↗
PubMed1984

Occlusive retinal vascular disease in systemic lupus erythematosus.

Ocular involvement in patients with systemic lupus erythematosus (SLE) is most commonly noted in the form of retinal hemorrhage, exudates and cotton wool spots resulting from occlusion of small retinal blood vessels. Less frequently, SLE is associated with extensive obliteration of larger retinal vessels, as demonstrated in the 2 cases reported here. In both cases large parts of the retina lost their function due to extensive occlusions of retinal arteries and veins. Marked retinal neovascularizations developed in one of the 2 cases. Awareness and early detection of retinal vascular occlusive disease and its complications are important in averting serious visual loss in SLE.

Adolescent↗
PubMedDate not supplied

Retinal breaks in diabetic retinopathy: vitreoretinal relationships.

We retrospectively reviewed the eyes of 143 patients with tractional retinal detachment caused by diabetes that had been studied biomicroscopically, and, after some exclusions, divided them into two groups: those with retinal breaks (group 1) (16 patients, 16 eyes), and those without retinal breaks (group 2) (127 patients, 161 eyes). The group 1 eyes were further divided into three subgroups: those with retinal tears from limited anteroposterior vitreous traction (subgroup A), those with macular holes in an area without posterior vitreous detachment (subgroup B), and those with oval retinal holes anterior to the anteroposterior vitreous traction (subgroup C). Subgroup C comprised most of the eyes in group 1 (10 eyes) and was the only subgroup that we compared with group 2. Significant differences between subgroup C and group 2 were found in terms of the extent of tractional retinal detachment (P = .002) and the degree of preretinal fibrosis (P = .009). These data suggest that large tractional retinal detachments and extensive preretinal fibrosis are significant risk factors for the development of retinal breaks in proliferative diabetic retinopathy.

Diabetic Retinopathy↗
PubMed1994

Purification and characterization of neurotrophic factor for retinal cholinergic neurons derived from cultured hippocampal neurons.

A neurotrophic factor that supports the development of cholinergic retinal neurons was purified from media conditioned by a primary culture of embryonic hippocampal neurons. Retinal choline acetyltransferase (ChAT), which is located exclusively in amacrine cells, served as a marker for the development of retinal cholinergic neurons. In a serum-free control culture, retinal neurons from 17-day-old rat fetus displayed little increase in the enzyme activity and a low proportion of neurite-bearing cells (15-20%) within 7 days. The conditioned media, when added to the retinal neuron culture, dose-dependently increased ChAT activity and the number of neurite-bearing cells (40-60%), the maximum ChAT activity being approximately sixfold higher than that in the control. The fraction with these stimulatory activities was purified by Sephadex G-15 column chromatography and two times reverse-phase HPLC. The final fraction showed approximately 3,000-fold higher purification as compared with that in the Sephadex G-15 fraction. Gas-phase protein sequencing analysis of the final fraction yielded a peptide sequence: Tyr-Leu-Leu-Pro-Ala-Gln-Val-Asn-Ile-Asp. A synthetic peptide with this sequence dose-dependently stimulated ChAT activity in the retinal cell culture and dissociated cell culture of the septal nucleus. These findings suggest that the developing hippocampal neurons produce a neurotrophic peptide that stimulates the development of cholinergic neurons.

Amino Acid Sequence↗
PubMed1996

[Central retinal vein occlusion after embolization for spontaneous carotid cavernous sinus fistula].

A patient with spontaneous carotid-cavernous sinus fistula, who developed central retinal vein occlusion (CRVO) after interventional surgery, was reported. A 78-year-old woman was admitted with symptoms of right abducens palsy and conjunctival injection. Digital subtraction angiography (DSA) revealed bilateral carotid cavernous sinus fistulas supplied by dural branches of the carotid arteries. After embolization of the feeding arteries and the right cavernous sinus using PVA and platinum coils respectively, her symptom improved gradually. Six months after the embolization, she was readmitted because of blurred vision and abducens palsy on the left side. Engorgements of the cavernous sinuses and draining veins, and the shunt flow of the fistula were much less on DSA than those seen previously, but ophthalmologic studies showed an impending central retinal vein occlusion (CRVO) in her left eye. Prognosis of CRVO is generally poor. We discussed the mechanism of CRVO occurring after interventional surgery for CCF and the tactics for preventing it, and early detection of its development.

Aged↗
PubMed1981

Bilateral central retinal vein occlusion in a patient with scleroderma.

A 53-year-old man with scleroderma, pulmonary fibrosis, cardiac decompensation and secondary polycythaemia, but no arterial hypertension, developed central retinal vein occlusion (CRVO) in the left eye. 1.5 years later, during the treatment with systemic steroids and anticoagulants, he developed CRVO in the right eye, and a further half year later, secondary glaucoma in the left eye and loss of the visual acuity to counting fingers at 2.5 m in the right eye and at 0.5 m in the left. Retinal vascular changes, pulmonary and cardiac insufficiency and secondary polycythemia, symptoms of scleroderma, most probably contributed to the development of bilateral CRVO.

Glaucoma↗
PubMed1982

Retinal 's' antigen disease in rats.

The form of experimental allergic uveoretinitis induced by sensitization with retinal 's' antigen in rats actually begins as a pars planitis and juxtapapillary choroiditis. Retinal inflammation develops at the middle limiting vascular layer of the retina and extends outward with focal destruction of photoreceptors and inward as a perivasculitis of small retinal vessels. Extensive choroiditis is a late development in severely diseased animals. Significant strain differences in susceptibility to disease were observed.

Animals↗
PubMedDate not supplied

[Ocular function in beta-thalassemia patients].

The eyes were examined in 118 inpatients with various thalassemia forms. The examinations included viso- and perimetry, biomicro- and ophthalmoscopy, fluorescent angiography of the fundus oculi and retinophotography. Patients with thalassemia were found to develop a variety of changes in the eye, whose manifestations depended on the length and severity of the underlying disease and on the treatment administered. Changes in the conjunctival and retinal vessels develop as early as in the initial stages of thalassemia, presenting as twisting, dilatation, and irregular calibre of the veins, dilatation of the arteries and reduction of their light reflex. Later dystrophic and atrophic changes develop: obliteration of the iris pattern and thinning of its peripheral zone, deterioration of blood circulation in the central retinal zone. Multiple blood transfusions and hemosiderosis lead to the development of hyperpigmentation of the limb, sclera, fundus oculi and appearance of retinal angioid strips. These findings should be taken into consideration when assessing the ocular status of thalassemia patients and defining the indications for treatment for angiopathic and dystrophic processes in the eye.

Adolescent↗
PubMed1981

Central retinal vein occlusion and scleroderma: implications for sclerodermatous vascular disease.

A patient with scleroderma (progressive systemic sclerosis) who developed central retinal vein occlusion is described. The aetiology of this condition is discussed and the role of possible sclerodermatous vascular disease is highlighted. It is suggested that studies of fundal vasculature could be useful in the clinical assessment of sclerodermatous vascular disease.

Constriction, Pathologic↗
PubMed2006

Incremental retinal-defocus theory of myopia development--schematic analysis and computer simulation.

Previous theories of myopia development involved subtle and complex processes such as the sensing and analyzing of chromatic aberration, spherical aberration, spatial gradient of blur, or spatial frequency content of the retinal image, but they have not been able to explain satisfactorily the diverse experimental results reported in the literature. On the other hand, our newly proposed incremental retinal-defocus theory (IRDT) has been able to explain all of these results. This theory is based on a relatively simple and direct mechanism for the regulation of ocular growth. It states that a time-averaged decrease in retinal-image defocus area decreases the rate of release of retinal neuromodulators, which decreases the rate of retinal proteoglycan synthesis with an associated decrease in scleral structural integrity. This increases the rate of scleral growth, and in turn the eye's axial length, which leads to myopia. Our schematic analysis has provided a clear explanation for the eye's ability to grow in the appropriate direction under a wide range of experimental conditions. In addition, the theory has been able to explain how repeated cycles of nearwork-induced transient myopia leads to repeated periods of decreased retinal-image defocus, whose cumulative effect over an extended period of time results in an increase in axial growth that leads to permanent myopia. Thus, this unifying theory forms the basis for understanding the underlying retinal and scleral mechanisms of myopia development.

Animals↗
PubMed1994

Postnatal development of different classes of cat retinal ganglion cells.

Previous investigators have documented the postnatal development of alpha and beta type ganglion cells in cat retinae (Ramoa et al. [1987] Science 237:522-525; Ramoa et al. [1988] J. Neurosci. 8:4239-4261; Dann et al. [1987] Neurosci. Lett. 80:21-26; Dann et al. [1988] J. Neurosci. 8(5):1485-1499). The development of the remaining cells (about 50%), which constitute a heterogeneous group and are referred to here collectively as gamma cells (Boycott and Wässle, '74), has not been studied in detail. The purpose of this study was to compare the postnatal development of alpha, beta, and gamma cells in kitten and adult retinae using horseradish peroxidase histochemistry and the fluorescent dye DiI. In the kitten, alpha, beta, and gamma cells are recognizable. We find, as have others, that kitten alpha and beta cell bodies and dendritic fields are significantly smaller than in the adult. However, kitten gamma cells are nearly adult sized. In fact, at birth the cell bodies of beta cells throughout the retina are significantly smaller than those of gamma cells. During the first 12 weeks of life, alpha and beta cell bodies increase in size from 90% to 680% depending upon eccentricity. Gamma cells hardly increase in size at all. Also, the normal adult center-to-peripheral cell size gradient for alpha and beta cells is not seen in the neonate. Gamma cells show no such gradient in the neonate or adult. Our results suggest that the morphological development of alpha and beta cells occurs later than that of gamma cells and may explain some of the differences in the effects of visual deprivation and surgical manipulation upon the parallel Y-, X-, and W-cell pathways.

Animals↗
PubMed2006

Regulation of the retinal determination gene dachshund in the embryonic head and developing eye of Drosophila.

The retinal determination gene dachshund is distantly related to the family of Ski/Sno proto-oncogenes and influences the development of a wide range of tissues including the embryonic head, optic lobes, brain, central nervous system as well as the post-embryonic leg, wing, genital and eye-antennal discs. We were interested in the regulatory mechanisms that control the dynamic expression pattern of dachshund and in this report we set out to ascertain how the transcription of dachshund is modulated in the embryonic head and developing eye-antennal imaginal disc. We demonstrate that the TGFbeta signaling cascade, the transcription factor zerknullt and several other patterning genes prevent dachshund from being expressed inappropriately within the embryonic head. Additionally, we show that several members of the eye specification cascade influence the transcription of dachshund during normal and ectopic eye development. Our results suggest that dachshund is regulated by a complex combinatorial code of transcription factors and signaling pathways. Unraveling this code may lead to an understanding of how dachshund regulates the development of many diverse tissue types including the eye.

Animals↗
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↗
PubMed1987

Abrupt loss of dependence of retinopetal neurons on their target cells, as shown by intraocular injections of kainate in chick embryos.

We have examined the capacity of neurons in the chick isthmo-optic nucleus (ION) to survive when their target neurons in the contralateral retinal are destroyed by intraocular injections of kainate (KA) at different stages in development. The retinal vulnerability to KA builds up progressively from embryonic day 10 (E10) until a plateau is reached at E15 (see accompanying paper); and the effects on the ION increase in parallel, almost all the ION neurons being rapidly lost after the E15 injections. KA injection before E15 lesioned only part of the retina and caused degeneration only in the topographically corresponding region of the ION. Near the end of the natural cell death period in the ION (E17), this initial dependence on the target cells is rapidly lost. Already at E16 the injections kill less ION neurons, and by E19 they kill none of them. The ION neurons have become completely insensitive to the KA injections and appear normal more than 4 months later, although axotomy (by eye removal) at a similar age would by then have killed them. The ectopic ION neurons, scattered outside the ION but projecting to the retina, are never affected by KA injections at any age.

Animals↗