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At least 451 records · Page 25Linked to original sources
PubMed2002

Capillary density and retinal diameter measurements and their impact on altered retinal circulation in glaucoma: a digital fluorescein angiographic study.

AIM: Normal pressure glaucoma (NPG) patients exhibit prolonged retinal arteriovenous passage times in fluorescein angiography and colour Doppler imaging suggests increased resistance downstream from the central retinal and posterior ciliary arteries. The aim of the study was to elucidate the morphological source of decreased perfusion and increased resistance of the ocular circulation in NPG. METHODS: Retinal arteriovenous passage time (AVP) and peripapillary arterial and venous diameters were measured in digital scanning laser fluorescein angiograms. For estimation of retinal capillary density the area of the foveal avascular zone (FAZ) and the perifoveal intercapillary area (PIA) was quantified. 36 patients with NPG (mean age 57 (SD 13) years) and 21 healthy subjects (mean age 51 (13) years) were enrolled in the comparative study. RESULTS: In NPG patients the AVP (2.55 (1.1) seconds) was significantly prolonged (p<0.001) when compared with healthy subject data (AVP: 1.70 (0.39) seconds). No differences for arterial or venous diameter, FAZ, and PIA were observed in NPG patients compared with healthy subjects. FAZ, PIA, arterial and venous diameter were not correlated with visual field indices (except venous diameter with PSD, r=0.35 (p<0.05)) or cup to disc ratios. AVP was significantly correlated (p<0.05) with the size of the optic nerve head (r=-0.28), visual field indices (MD: r=-0.3; PSD: r=0.3; CPSD: r=0.3), and contrast sensitivity (r=-0.34). CONCLUSION: AVP times are significantly prolonged in NPG. The slowing of the retinal transit does not result from capillary dropout, or changes of peripapillary arterial or venous diameters with increased vascular resistance.

Blood Flow Velocity↗
PubMed2006

Inner retinal mechanisms engaged by retinal electrical stimulation.

PURPOSE: Retinal prosthetic devices are being developed to bypass degenerated retinal photoreceptors by directly activating retinal neurons with electrical stimulation. However, little is known about retinal activity during such stimulation. METHODS: Whole cell patch-clamp recordings were obtained from ganglion and bipolar cells in the salamander retinal slice preparation. A stimulating electrode was positioned at the vitreal surface of the slice. RESULTS: Brief pulses of cathodic current evoked transient inward currents in ganglion cells arising from action potentials. Longer pulses (>5 milliseconds) also evoked sustained inward currents in ganglion cells that appeared synaptic in origin because, unlike transient currents, sustained currents were blocked by inhibiting synaptic transmission with Cd2+. These synaptic currents reversed around ECl and were blocked by picrotoxin, strychnine, or both, suggesting they were mediated by GABAa/c and glycine receptors. Synaptic currents were also blocked by the NMDA antagonist MK801 and the KA/AMPA antagonist NBQX, suggesting that epiretinal stimulation evoked glutamate release from bipolar cells, which in turn stimulated the release of GABA and glycine from amacrine cells. Sustained currents were also evoked by epiretinal stimulation in bipolar cells. These currents reversed near ECl and were blocked by picrotoxin, suggesting they arose from GABAa/c receptors. CONCLUSIONS: Pulse duration is an important parameter for effective activation of the inner retina by epiretinal stimulation. Brief pulses evoke action potentials only in ganglion cells. However, longer pulses also evoke sustained synaptic currents by stimulating glutamate release from bipolar cell terminals, which, in turn, evokes the release of GABA and glycine from amacrine cells.

Action Potentials↗
PubMed2006

Refractile superficial retinal crystals and chronic retinal detachment: case report.

BACKGROUND: Few previous reports have described the presence of retinal refractile opacities at the macular area in patients presenting with longstanding peripheral retinal detachment. The exact nature of these opacities is unknown. CASE PRESENTATION: Two patients were referred with an abnormal appearance of refractile opacities in the macular area noted during routine examination. Both were found to have longstanding peripheral retinal detachments. Subretinal fluid analysis of one patient revealed the presence of multiple birefringent crystals. We hypothesise that these crystals are the origin of the refractile macular opacities noted. CONCLUSION: This report describes the rare presentation of asymptomatic peripheral retinal detachment by the detection of refractile macular opacities on routine examination. It highlights the importance of meticulous peripheral retinal examination in these cases. The article also describes the findings of the subretinal fluid analysis and discusses the possible hypothesis behind their appearance.

Adult↗
PubMed1995

Retinal circulation times in branch retinal vein occlusion.

To investigate the retinal hemodynamics in branch retinal vein occlusion (BRVO), we measured retinal circulation times using scanning laser ophthalmoscope (SLO) and studied their relationships with clinical findings. Arm-retina time (ART) and arteriovenous passage time (AVP) were measured in 30 eyes of 30 patients. Mean ART was 13.07 seconds. ART showed no difference in relation to sex and systemic diseases, but increased with age. Mean AVPs were 3.00 sec. and 3.39 sec. in superotemporal and inferotemporal BRVO, respectively. AVPs were delayed significantly in occluded branch of retinal veins. AVP was delayed three-fold when the area of capillary nonperfusion was over 6 disc area, but showed no difference according to the duration of disease or macular edema. These results suggest that SLO may be a useful tool for studying retinal hemodynamics in BRVO.

Adult↗
PubMed2005

[Posterior retinal hole secondary to a candida retinitis].

CASE REPORT: We describe the case of a 36-year-old man with a history of intravenous heroin use, who was HIV negative. Left ocular examination disclosed a focal candida retinitis in the posterior pole associated with vitritis and moderate iritis. Treatment with fluconazole inactived the chorio-retinal lesion and resolved the vitritis, but developed an inner limiting membrane contraction over the macula. Two years later, vitreous traction produced a retinal hole that needed argon laser photocoagulation. DISCUSSION: Candida retinitis which penetrates into the vitreous cavity can produce retinal holes by vitreous traction over the lesion.

Adult↗
PubMed2001

[A case of central retinal vein occlusion followed by branch retinal artery occlusion].

BACKGROUND: The influence of retinal artery circulation on central retinal vein occlusion (CRVO) is not well known. CASE: A 73-year-old man with hypertension complained of transient visual loss in his left eye. At initial examination, ophthalmoscopy of his left eye showed mild dilatation and tortuosity of the retinal vein and a few dot hemorrhages. Fluorescein angiography disclosed normal arm-to-retina circulation time and no leakage of dye, but delayed retinal circulation time. These findings indicated venous stasis retinopathy of CRVO. In spite of intravenous infusion of prostaglandin E1 and vasodilative treatment, four days after initial examination, the patient's left eyeground showed complication of branch retinal artery occlusion (BRAO). A fibrinolytic agent was given intravenously, but four weeks later, his left eyeground developed typical hemorrhagic retinopathy. The hemodynamics of retrobulbar arterial circulation were investigated by color Doppler imaging. CONCLUSION: We report a case of venous stasis retinopathy of CRVO associated with BRAO, that developed hemorrhagic retinopathy despite treatment with prostaglandin E1 and other vasodilative agents. We think that arterial insufficiency might be responsible for the conversion from venous stasis retinopathy to hemorrhagic retinopathy of CRVO.

Aged↗
PubMed2001

Finding the retinal break in rhegmatogenous retinal detachment.

The development of subretinal fluid is governed by a limited number of anatomical factors and gravity. As a result, rhegmatogenous retinal detachments form in a predictable manner around the retinal break of their origin. The shape of the detachments points to the position of the break. The purpose of this review is to describe the characterstic contours of subretinal fluid in rhegmatogenous retinal detachments, and to highlight some rules and methodology which can help in the detection of the retinal break in phakic, psuedophakic and recurrent retinal detachments.

Cryosurgery↗
PubMed2005

[Characteristics of N-methyl-N-nitrosourea-induced retinal degeneration in animals and application for the therapy of human retinitis pigmentosa].

BACKGROUND: Retinitis pigmentosa(RP) is a human disease characterized by loss of photoreceptor cells, especially rods, leading to visual disturbance and eventually to blindness. Effective treatment for RP control is still unavailable. The establishment of reliable animal models is essential for a better understanding of this disease, and for the development of therapeutic intervention. Here we summarize the establishment of N-methyl-N-nitrosourea (MNU)-induced retinal degeneration in animals, and success in disease control using this model. RESULTS: Retinal damage induced by MNU was highly reproducible and involved photoreceptor cell loss. It was obvious in all animals at approximately 7 days following a single systemic administration of MNU to adult mice (60 mg/kg), rats (60-75 mg/kg), hamsters (90 mg/kg), shrews (65 mg/kg), and monkeys (40 mg/kg). Extensive investigation in the rats revealed that MNU-induced photoreceptor cell loss was due to apoptosis with a decrease of Bcl-2 protein, increase of Bax protein, and activation of caspase families. Therapeutic to control MNU-induced photoreceptor cell loss in rats was evaluated with caspase-3 inhibitor (Ac-DEVD-CHO), nicotinamide(NAM), and docosahexaenoic acid(DHA); 4,000ng Ac-DEVD-CHO injected intravitreally 0 and 10 h after MNU suppressed disease progression, 25-1,000 mg/kg NAM subcutaneously injected concurrently or subsequently to MNU reversed retinal damage, and dietary supplementation of 9.5% DHA counteracted photoreceptor cell loss. CONCLUSION: Although the mechanisms triggering pathogenesis and the apoptotic cascade may differ between animals and humans, MNU-induced retinal degeneration is caused by photoreceptor cell apoptosis. Thus, suppression of MNU-induced photoreceptor cell apoptosis in animals may provide therapeutic information for RP control in humans.

Animals↗
PubMedDate not supplied

[Immunopathologic study of retinal detachment with vitreo-retinal proliferation].

Immunopathological studies were performed on biopsies or autopsies of pars plana samples from patients with retinal detachment, with or without vitreo-retinal proliferation. Immunoglobulins and complement deposits have been found in vitreo retinal proliferation, together with a deviant expression of HLA-DR and DQ antigens by pigmented epithelial cells of the ciliary body. Gamma interferon is able to induce this expression in vitro, and the inducing effect of this lymphokine and other mediators has been tested on pigment epithelium cultures. Cultured pigment epithelial cells expressed HLA-DR and DQ antigens after being stimulated by very low doses of gamma interferon. The precise target of this immune reaction is still impossible to determine, but its consequences could be the release of growth factors as FGF, which has been found at very high levels in pigmented and non pigmented cells of pars plana and ciliary processes. Our work asserts the existence of auto-immune phenomena in retinal detachment with vitreo-retinal proliferation as well as in proliferative diabetic retinopathy, their exact involvement remaining to determine.

HLA-DQ Antigens↗
PubMed1989

Pseudophakic retinal detachments. The relationships between retinal tears and the time following cataract surgery at which they occur.

The types and locations of retinal tears associated with 268 pseudophakic retinal detachments were studied as a function of the time at which they occurred following cataract surgery. Retinal detachments occurring more than two years following cataract extraction were significantly more likely to have their most posterior retinal break located at the posterior margin of the vitreous base than at or behind the equator. This distribution of tears was not observed in detachments occurring within six months of cataract surgery, with equatorial tears being significantly more common in early onset detachments than in those occurring after two years. The anterior tears which cause most retinal detachments long after cataract extraction are due to persistent chronic traction upon the vitreous base rather than to acute posterior vitreous detachment.

Aged↗
PubMed1984

Retinal telangiectasia, retinoschisis and retinal detachment.

A 32-year-old woman had progressive bilateral peripheral and central retinal telangiectasis with secondary exudative, nonrhegmatogenous, retinal detachment, and secondary retinoschisis. This is unique constellation of clinical findings, retinal telangiectasis itself being an uncommon disease, and usually occurring in young males, unilaterally. Theories for the etiology of this disease process are presented. The disease was successfully treated bilaterally with retinal cryopexy extensively applied to the retinal telangiectasis, both peripheral and paracentral, with both scleral buckling and drainage of copious amounts of thick subretinal exudation.

Adult↗
PubMed1988

Retinal pigment epithelial cells in culture produce retinal vascular mitogens.

Conditioned medium from human retinal pigment epithelial cells in culture significantly stimulated the proliferation of subcultured bovine retinal capillary endothelial cells, pericytes, and freshly isolated retinal microvessels. The vascular mitogenic activity enhanced that of retinal crude extract. No evidence emerged of an inhibitor of microvascular cellular proliferation produced by retinal pigment epithelial cells.

Animals↗
PubMed1986

Cell generation, death, and retinal growth in the development of the hamster retinal ganglion cell layer.

During the early postnatal period in the hamster, the retinal ganglion cell layer grows, establishes its central connections, and undergoes substantial cell loss. In this study, we describe the development of the retinal ganglion cell layer with particular attention to the creation of local specializations in cell density. Changes in the number and spatial distribution of cells identified by a single 3H thymidine injection were examined through the period of maximal cell loss (postnatal days 4-10) and at adulthood. The cells of the retinal ganglion cell layer are generated from embryonic day 10 to postnatal day 3. Overall, cell number in the ganglion cell layer increases by approximately 108,000 cells (223%) from postnatal day 1 to 5, because of continued migration of cells generated prenatally. Cell number decreases from postnatal day 5 to 10 (25%), coincident with the presence of degenerating cells. Cell type is correlated with day of generation: the largest cells, all having retinal ganglion cell morphology, are generated on embryonic days 10 and 11; intermediate-sized cells predominantly of ganglion cell morphology on embryonic day 12; and smaller cells of displaced amacrine or glial cell morphology thereafter. At adulthood, the hamster retina shows a streaklike elevation of cell density through central retina. However, at the time of maximal cell number (postnatal day 5), cell density is uniform across the retina. During the period of cell degeneration, cells are lost in greater relative numbers from the retinal periphery. This cell loss occurs principally from the first-generated cells (embryonic days 10 and 11), as shown by both changes in the distribution of labeled cells and by the spatial pattern of labeled degenerating cells. From postnatal day 10 to adulthood, relative cell density continues to decline in the periphery of the retina, thus suggesting that differential growth completes the production of the adult cell density distribution.

Animals↗
PubMed1988

Retinal projections to the superior colliculus and dorsal lateral geniculate nucleus in the tammar wallaby (Macropus eugenii): II. Topography after rotation of an eye prior to retinal innervation of the brain.

Retinal projections to visual centers in a marsupial mammal, the tammar wallaby (Macropus eugenii), have been investigated after an eye rotation prior to retinal innervation of the brain. Retinal topography to the superior colliculus and dorsal lateral geniculate nucleus was mapped by using laser lesions of the retina and horseradish peroxidase histochemistry. Despite the change in orientation of optic axon outgrowth from the developing eye after rotation, retinal ganglion cells made orderly connections in the colliculus and geniculate according to their original retinal position within the eye and not their rotated position. Axons must have corrected their pathways at some point between the back of the eye and their targets. The optic chiasm was one such site. Optic axons from the rotated eye took an abnormal course at the caudal end of the chiasm. Growth of optic axons through aberrant pathways in the brain did not preclude specific innervation of targets. When by chance optic axons entered through the oculomotor nerve root they specifically innervated their correct visual centers, albeit in reduced density, and did not innervate inappropriate targets. These results support the idea of specific interactions between growing axons, the pathways they grow along, and their targets.

Animals↗
PubMed2002

Levobetaxolol-induced Up-regulation of retinal bFGF and CNTF mRNAs and preservation of retinal function against a photic-induced retinopathy.

Betaxolol (racemic), a beta-adrenoceptor antagonist that is used to lower intraocular pressure in the treatment of glaucoma, has been shown to protect inner retina cells from various insults. To determine if such protection could be afforded to retinal photoreceptors and retinal pigment epithelial cells (RPE), levobetaxolol (S-betaxolol) was evaluated in a photic-induced retinopathy model. Rats were dosed (IP) with vehicle or levobetaxolol (10 and 20 mg kg(-1)) 48, 24 and 0 hr prior to exposure for 6 hr to fluorescent blue light. The electroretinogram (ERG) and retinal morphology were assessed after a 3 week recovery period. Evaluation of the ERG demonstrated significant protection of retinal function in levobetaxolol (20 mg kg(-1))-dosed rats compared to vehicle-dosed rats. Similarly, the RPE and outer nuclear layer were significantly thicker in levobetaxolol (20 mg kg(-1))-dosed rats compared to vehicle-dosed rats. To elucidate potential mechanism(s) of the neuroprotective activity of levobetaxolol, bFGF and CNTF mRNA levels in normal rat retinas were evaluated 12 hr after a single i.p. injection. Northern blot analysis of levobetaxolol treated retinas demonstrated a 10-fold up-regulation of bFGF and a two-fold up-regulation of CNTF mRNA levels, trophic factors that have been shown to inhibit retinal degeneration in a number of species. These studies suggest that levobetaxolol can be used as a novel neuroprotective agent to ameliorate retinopathy.

Adrenergic beta-Antagonists↗
PubMed1999

A novel retinal degeneration locus identified by linkage and comparative mapping of canine early retinal degeneration.

Early retinal degeneration (erd) is an early onset progressive retinal atrophy, a hereditary canine retinal disease phenotypically similar to human retinitis pigmentosa (RP). In previous efforts to identify the erd locus, canine homologs of genes causally associated with RP in humans, such as opsin (RHO), the beta-subunit gene for cyclic GMP phosphodiesterase (PDE6B), and RDS/peripherin, were excluded. A genome-wide screen was undertaken on canine families segregating the erd disease. Analysis of over 150 canine-specific markers has localized erd to a single linkage group comprising two previously identified canine linkage groups, 20 and 26, corresponding to canine radiation hybrid groups RH.34-a and RH.40-a. Multipoint analysis places erd in the interval between marker FH2289 (distance 23.6 cM) and FH2407 (5.9 cM) with a lod score of 12.23. Although the erd linkage group has not been assigned to an identified canine chromosome, conserved synteny of this linkage group with human 12p13-q13 suggests several candidates for erd and identifies a novel retinal degeneration locus. The rapid progress now occurring in canine genetics will expedite identification of the genes and molecular mechanisms underlying the inherited traits and diseases that make the dog a unique asset for study of mammalian traits.

Animals↗
PubMed1985

Electrophysiological estimation of the function of different retinal zones in normal eyes and in retinal degenerations.

By means of electroretinographical responses from different areas of the retina (zonular ERGs) both healthy people and patients with central and peripheral retinal degenerations were examined. Responses were registered from three retinal areas (zones): central (red, green, and blue stimuli, 10 degrees in diameter, during adaptation of 20 lux); paramacular (a dim, blue, ringlike stimulus, 15 degrees inner and 50 degrees outer diameter, presented at the beginning of dark adaptation) and peripheral (very dim, blue ring stimulus of a 50 degree inner and 110 degrees outer diameter, after 3 min of dark adaptation). The data obtained by this method of stimulation give information about the function of stimulated retinal areas and provide new criteria for the function of the spectrally different photoreceptors responsible for intact color vision. Examples are presented that reveal the value of this method for the detection of congenital color vision defects and for the classification of different types of retinal degeneration. This method is shown to be highly effective and has many advantages over the common routine Ganzfeld ERG technique, especially in cases of unusual retinal degenerations.

Color↗