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We treated a young patient with unilateral gray-yellow subretinal lesions associated with bullous retinal detachment in the posterior pole. Angiography revealed the presence of multiple areas of subretinal pigment epithelial pooling of the dye. It is rare to find an association between acute inflammation of the retinal pigment epithelium and sensory retinal detachment.
OBJECTIVE: To investigate the clinical features of central retinal vein occlusion (CRVO) complicating exudative retinal detachment (ERD). METHODS: General health, vision, intraocular pressure, appearance of the fundus and fundus fluorescein angiography (FFA) and the results of ultrasound examination in cases with CRVO complicating ERD were analyzed. RESULTS: Eight patients were male and 7 patients were female. Age of those patients ranged from 18 to 42 years, averaged 25 years. Five cases combined with neovascular glaucoma. Initial vision ranged from 0.05 to light perception. There were notably edema and hemorrhage in the macular region. Extensive exudative appeared at the edge of edema and detachment region. The extent of retinal detachment was 2/12 - 5/12 quadrant at sitting position. No collateral vessels were found on the optic disk. FFA showed extensive blockage by the hemorrhages or capillary nonperfusion. CONCLUSIONS: ERD is a rare and severe complication of CRVO, which usually develops in young patients and combines with neovascular glaucoma. The appearance in fundus and FFA shows a characteristic features.
We have studied the adhesion of human CD4+ lymphocytes to cultured human retinal vascular endothelial cells (EC) and human retinal pigment epithelial cells (RPE), both of which comprise the cellular components of the blood-retina barrier. We have observed differences in the lymphocyte-RPE and the lymphocyte-EC interactions. Firstly, RPE cells were found to express high levels of the adhesion molecule ICAM-1 constitutively, whereas EC expressed ICAM-1 only after induction with IFN-gamma. In addition, lymphocyte binding to normal and minimally stimulated RPE (5 U/ml, 4 hr) was predominantly ICAM-1 dependent, but after maximal stimulation (500 U/ml, 4 days), increased lymphocyte adhesiveness included an ICAM-1-independent component, which was apparently not due to involvement of MHC class II or CD2 molecules. In contrast, binding of lymphocytes to unstimulated EC involved both an ICAM-1-dependent and an ICAM-1-independent mechanism, the latter being subject to inhibition by monoclonal antibody to CD2. Studies of adhesion at 4 indicated that no binding occurred to normal or stimulated RPE, but binding to EC was observed, albeit reduced to 50% of the 37 binding level, and this implies that the LFA-3/CD2 adhesion pathway may also be involved in lymphocyte binding to EC. Overall, the results indicate a functional difference between RPE and EC affecting T-cell adhesion, migration and activation at the blood-retinal barrier, which must be considered when devising therapies to prevent lymphocyte infiltration of the eye.
64 cases (66 eyes) of retinal detachment in which no breaks can be found were treated with pars plana vitrectomy, scleral buckling or encircling procedures. The selection of operation depended on the shape and size of retinal detachment, the position of peripheral retinal lattice degeneration, phakia or aphakia, traumatic situation and the appearance of proliferative vitreoretinopathy. The results showed that the detached retina was successfully reattached in 53 eyes (80.3%), 4 eyes were improved (6%), only 9 eyes failed (16.7%). The technic of operation and application are discussed. We consider that suitable active surgical treatment for this kind of cases is encouraging.
Posterior vitreous fluorescence was measured with a fluorophotometer 60 minutes after intravenous sodium fluorescein (14 mg/kg) in 6 patients (age range 30 to 54 years) with central retinal vein occlusion (CRVO). Plasma free fluorescein was measured at frequent intervals for 60 minutes. A permeability index (PI) was estimated by dividing the area under the vitreous fluorescence scan by the area under the plasma free fluorescein curve. Initially mean PI was 24.3 (range 12.6-31.6) and 2.1 (range 1.3-31.) cm s-1 X 10(-7) in affected and unaffected eyes respectively. After 6 to 12 months, PI in affected eyes approached the values in the unaffected eyes of 5 patients with mild CRVO but remained elevated in one patient who presented with severe (ischaemic) CRVO. In each patient qualitative changes in retinal appearances paralleled quantitative changes in PI. The effect of venous outflow obstruction on the blood-retinal barrier can be quantitated by fluorophotometry.
The authors present 26 cases (28 eyes) of rhegmatogenous retinal detachment, lasting more than 6 months, in which retinal telangiectasias appear in the periphery of the retina as a secondary phenomena, seemingly related to hypoxic factors. A comparison is made with a control group of 25 cases of longstanding retinal detachment taken at random in order to establish statistical differences. Considerations regarding their pathogenesis and their value as a prognostic sign are made.
It has been shown that dual trunk central retinal vein (CRV) occurs in 20.3 per cent of a normal population. Confirmatory evidence has been produced by the results of anatomical, histological and micro-dissection studies. Occlusion of the single trunk of such a vein in its retrolaminar, or intraneural part, would result in a venous occlusion affecting one-half of the retina similar to that of branch retinal vein occlusion (BRVO). Yet this should be regarded as a variation of CRVO. Visual prognosis seems to be better in hemi-central retinal venous occlusion than in total CRVO. The site of development of collateral gives a clue to the site of the occlusion. Therefore, it is suggested that hemi-CRVO is a distinct entity and should not be confused with so-called hemi-spherical vein occlusion which is a variation of BRVO.
Surgical procedures used today to treat retinal detachment with an inverted giant retinal tear have considerably improved. Vitrectomy associated with perfluorocarbon liquid injection has replaced old procedures necessary to unfold the inverted retinal flap. Seventeen patients were operated on with an anatomic success rate of 76% and an average follow up of fifteen months. The successive surgical stages (lensectomy, retinopexy, internal tamponade, circular scleral buckle) are discussed. Proliferative vitreoretinopathy is the maill postoperative complication explaining the high rate of reoperation (56%). In high myopia, a prophylactic circular scleral buckle of the fellow eye has become systematic.
93 eyes (93 patients) of complicated retinal detachment were treated with vitreo-retinal surgery. Among the series, 75 eyes were rhegmatogenous with PVR C3-D3 in 66 eyes (88.0%), while the remaining 18 eyes were traction induced. None of the cases had giant tears or complicating diabetes. On discharge from the hospital, the operation was effective in 62 cases (66.7%), in whom the retina was totally reattached or only a small amount of subretinal fluid remained. In a group of 40 eyes where the inert gas SF6 was used, the operation was effective in 30 cases (75.0%). 41 cases were followed up postoperatively for over 3 months, averaging 13.7 months, to find the operative results stable in 33 eyes (80.5%), with the visual acuity improved in 22 cases (66.7%), unchanged in 9 cases (27.3%), and decreased in 2 cases (6.0%). The operative procedures, the peeling of pre-retinal membrane, the effect of PVR severity on the operative results, and the promotion of operative efficacy by application of wide encircling buckle and inert gas tamponade were discussed.
The authors report a case of congenital arteriovenous communication of the retinal near the macula, associated with a central retinal vein occlusion. This occlusion only affected the inferior half-retina, especially the area surrounding the arteriovenous anastomoses. Laser photocoagulation was applied to areas of peripheral ischemia. After a 12 month follow-up, a marked decrease of visual acuity occurred, attributable to severe ischemia and edema in the posterior pole. An extension of the peripheral capillary non perfusion required additional laser treatment. We also observed the reduction in caliber of the arteriovenous anastomosis. The association of congenital arteriovenous communication and retinal vein occlusion is rare. The clinical and pathogenic features are discussed. Photocoagulation of extensive peripheral capillary occlusion is recommended in order to prevent neovascular complications.
Sixty-one patients (64 eyes) with central retinal artery occlusion (CRAO) and 41 patients (44 eyes) with branch retinal artery occlusion (BRAO) were studied in detail clinically to find out the pathogenesis of their ocular neovascularization (NV). Ocular NV was seen in 12 eyes (11 patients) with CRAO: iris NV was seen in all 12 eyes, angle NV was seen with neovascular glaucoma (NVG) in ten of them, and no NV was seen in BRAO. Nine of ten patients with CRAO associated with NVG were old, having severe carotid artery disease (CAD) and severe generalized atherosclerotic arterial disease; in the remaining patient, NVG was caused by diabetes mellitus. Severe CAD results in chronic ocular ischemia, which, in turn, produces NV of the iris and angle and NVG; the latter, combined with poor perfusion pressure in the central retinal artery (caused by severe CAD), results in CRAO. Our study showed little evidence that CRAO, per se, is responsible for ocular NV. Various evidence in support of this hypothesis is presented. Our study also showed that the only eyes to recover good vision were those with transient CRAO for up to 11/2 hours, and no treatment helped.
Rhegmatogenous retinal detachments were created in one eye of each of six cynomolgus monkeys. Total vitrectomy alone was performed in the fellow eyes. The rate of disappearance of fluorescein sodium injected into the vitreous cavity was measured with kinetic vitreous fluorophotometry. Intravitreal 10(-4)M probenecid was used to inhibit active outward transport of fluorescein. In eyes with retinal detachment, the rate of fluorescein loss from the vitreous cavity was decreased 44% and 22% following intravitreal injection of 10(-4) and 10(-5)M furosemide (Lasix), respectively. Intravitreal 10(-4)M furosemide decreased the rate of fluorescein loss in fellow eyes by 35%. The rate of fluorescein loss via the anterior chamber accounted for only 1% to 8% of the total rate of vitreous fluorescein loss. Thus, it is concluded that intravitreal absorption across the retinal pigment epithelium.
OBJECTIVE: To determine the prevalence of cytomegalovirus (CMV) isolates resistant to ganciclovir sodium or foscarnet sodium at the time of diagnosis of CMV retinitis, prior to the initiation of therapy. DESIGN: Prospective epidemiologic study. SETTING: An acquired immunodeficiency syndrome ophthalmology clinic. PATIENTS: Patients with acquired immunodeficiency syndrome and newly diagnosed CMV retinitis. INTERVENTION: Culturing blood and urine samples for CMV and testing of all positive isolates for sensitivity to ganciclovir and foscarnet. MAIN OUTCOME MEASURE: Prevalence of the following: blood culture isolates resistant to ganciclovir (inhibitory concentration 50% [IC50] > 5.5 mumol/L) or foscarnet (IC50 > 400 mumol/L) and urine culture isolates resistant to ganciclovir or foscarnet. RESULTS: Forty-nine patients were enrolled during a 13-month period. Forty-four patients had blood culture samples that could be evaluated; of these, 66% were positive (59% of patients). Thirty-four patients had urine cultures that were evaluable; of these, 82% were positive (57% of patients). Overall, 78% of patients had either a urine or blood culture sample positive for CMV. No blood culture isolates were resistant to ganciclovir, and only 1 urine culture isolate (2% of patients) was resistant to ganciclovir. Three percent of blood culture isolates and 4% of urine culture isolates (2% and 2% of patients, respectively) were resistant to foscarnet. Overall, 4% of patients had either a blood or urine culture isolate resistant to foscarnet. CONCLUSION: Resistance to ganciclovir or foscarnet at the time of diagnosis of CMV retinitis is uncommon.
Mutations in the Drosophila retinal degeneration B (D-rdgB) gene cause light-enhanced retinal degeneration. Here, we report the isolation of the cDNA encoding human homologue of the D-rdgB and initial characterization of the gene products. Like D-rdgB, the human rdgB homologue (H-rdgB) is a transmembrane protein with the N-terminus sharing high homology to two closely related cytosolic proteins, phosphatidylinositol transfer protein (PITP) alpha and beta, indicating that rdgB like proteins belong to the family of PITP proteins. Using Northern and Western blotting, we demonstrated that the rdgB homologue is expressed in rat retina, olfactory bulb, and brain, but not in nonneuronal tissues. In the rat retina, immunoreactivity of the rdgB homologue was observed in photoreceptors and throughout the inner nuclear and plexiform layers; the strongest staining was in the inner plexiform layer. In the photoreceptor cells, the rdgB homologue was located primarily in the inner segment where sorting and traffic of membranes required for outer segment assembly take place. These data, together with recent findings showing PITPs as on important component of intracellular membrane traffic apparatus in mammalian cells, suggest that rdgB homologue may play a role in photoreceptor membrane renewal and in neurotransmitter release. Furthermore, using somatic hybrid cell hybridization and fluorescence in situ hybridization H-rdgB gene was mapped to human chromosome 11q13, a region known to contain several retinopathy loci, including Best disease and Bardet-Biedl syndrome I. Therefore, H-rdgB gene is an attractive candidate for several inherited retinal degenerative diseases.
Retinitis pigmentosa (RP) is the most frequent form of inherited retinopathy. RP is genetically heterogeneous with autosomal dominant, autosomal recessive and X-linked forms. Autosomal dominant retinitis pigmentosa (adRP) accounts for about 20-25% of all RP cases. At least ten adRP loci have so far been mapped. However, mutations causing adRP have been identified only in four retina-specific genes: RHO (encoding rhodopsin) in approximately 20% of adRP families, peripherin/RDS (3-5% of adRP) and recently RP1 (Pierce et al., 1999, Sulivan et al., 1999) and NRL gene. Only one mutation in the NRL gene causing adRP has so far been reported (Bessant et al., 1999). Here we report a novel mutation Pro51Leu in an adRP Spanish family supporting that mutation in NRL is the cause of adRP. A second missense mutation Gly122Glu has been observed in a simplex RP patient that may represent a sporadic case of retinitis pigmentosa. Hum Mutat 17:520, 2001.
Using anterograde tracing with HRP and antibodies (ABs) against neurofilaments, we show that regrowth of retinal ganglion cell (RGC) axons in the lizard Gallotia galloti commences only 2 months after optic nerve transection (ONS) and continues over at least 9 months. This is unusually long when compared to RGC axon regeneration in fish or amphibians. Following ONS, lizard RGCs up-regulate the immediate early gene C-JUN for 9 months or longer, indicating their reactive state. In keeping with the in vivo data, axon outgrowth from lizard retinal explants is increased above control levels from 6 weeks, reaches its maximum as late as 3 months, and remains elevated for at least 1 year after ONS. By means of BrdU incorporation assays and antiproliferating cell nuclear antigen immunohistochemistry, we show that the late axon outgrowth is not derived from new RGCs that might have arisen in reaction to ONS: no labeled cells were detected in lizard retinas at 0.5, 1, 1.5, 3, 6, and 12 months after ONS. Conversely, numbers of RGCs undergoing apoptosis were too low to be detectable in TUNEL assays at any time after ONS. These results demonstrate that retinal axon regeneration in G. galloti is due to axon regrowth from the resident population of RGCs, which remain in a reactive state over an extended time interval. Neurogenesis does not appear to be involved in RGC axon regrowth in G. galloti.
Pineal gland N-acetyltransferase (NAT) activity and pineal and serum levels of melatonin declined linearly in albino rats acutely exposed to different intensities of red light (600 nm or higher; low, 140 microW/cm2; moderate, 690 microW/cm2; high, 1200 microW/cm2) during the middle of the night. The high intensity red light was as effective as white light (780 microW/cm2) in suppressing NAT activity and pineal and circulating melatonin. Red-light-inhibited nighttime NAT activity and suppressed nocturnal melatonin levels in both retinally degenerate and normal rats. Pretreatment with the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 (10 mg/kg intraperitoneally) completely prevented the red-light-induced inhibition of nighttime melatonin synthesis. Magnesium chloride (300 mg/kg intraperitoneally) reduced the inhibitory effects of low and moderate intensities of red light but was ineffective when high red-light intensity was used. However, both agents failed to antagonize the suppression of nighttime melatonin synthesis elicted by the exposure to white light. Since retinally degenerate and retinally normal animals respond in the same way to both red-light and pharmacological intervention with the NMDA receptor blocker MK-801, the findings indicate that the activation of central hypothalamic NMDA receptors might mediate the photic inhibition of nocturnal melatonin synthesis in the pineal gland elicited by the exposure to red light at night. Red-light-induced suppression of nocturnal melatonin synthesis possibly can be used to investigate the biochemical mechanisms by which light entrains melatonin synthesis and to study the pharmacological and physiological effects of endogenous and synthetic agents that antagonize the NMDA receptor response.
The retinas from a 68-year-old man with autosomal dominant retinitis pigmentosa caused by the threonine-17-methionine rhodopsin mutation were studied. Patients with this mutation have a characteristic clinical phenotype that shows intra- and interfamilial consistency. The retinas were examined by light and electron microscopy, including immunocytochemistry with markers for rods, cones, the retinal pigment epithelium, the interphotoreceptor matrix and Müller cells, and the results were correlated with those from visual function tests performed fourteen months before death. Grossly, both retinas had heavy deposits of bone spicule-like pigmentation inferiorly, but the superior retinas showed much less pigmentation. The maculas contained no rods and an incomplete monolayer of cone somata, consistent with the patient's severely reduced central vision. The inferior retinas contained no rods and rare cone somata, correlating with an absolute scotoma in the superior field. The superior retinas had near-normal-appearing rods and cones in the far periphery and a gradient from the midperipheral to central retina of progressively shortened outer segments and loss of photoreceptors, consistent with the patient's reduced rod and cone electroretinograms and retained rod and cone sensitivities in the inferior peripheral field by perimetry. Immunocytochemistry with rod-specific markers was qualitatively normal in the superior mid to far peripheral retina. Electron microscopic immunogold labeling with anti-rhodopsin revealed similar densities of gold particles over rod outer segments of the RP and a normal donor retina. Degenerate photoreceptors in the superior equatorial region of the RP retina had short outer segments, and some rods had surface labeling with anti-rhodopsin of the inner segments, somata and synapses. The results indicate regional retinal differences of disease severity in this genotype and that rods in the superior peripheral retina have normal morphology despite the presence of the mutant allele. To the authors' knowledge, this is the first detailed study of rod photoreceptors in the retina of an RP patient with a rhodopsin mutation.