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We experienced 2 females with systemic lupus erythematosus (SLE) who developed serous retinal detachment in the posterior pole of both eyes in its active phase. Fluorescein angiography showed multifocal pigment epithelial damages with fluorescein leakage into the subretinal space. However, retinal hemorrhages or cotton-wool spots typical of SLE were not observed in their courses.
Two types of anastomotic new vessels develop after retinal branch vein occlusions. In a previous article (Arch. Ophtal. (Paris), 1977, 8-9, pp. 507-522) the useful collateral vessels were described in the re-establishment of a better circulation in the territory of the occluded vein. The second part discusses new vessels: they are dangerous and useless. Their pathogenesis poses the problem of the relationship between hypoxia, ischaemia, revascularisation and vasoproliferation. Their prevention and treatment calls for laser photocoagulation of the ischaemic territory.
A 56-year-old myope developed a retinal detachment of the macular area and the temporal quadrants in his left eye that harbored a temporally-located pit of the optic nerve head. Under anesthesia a small peripheral retinal break was identified, and the retina was reattached successfully using cryotherapy and a limited scleral buckling procedure. Peripheral retinal breaks should be searched for in myopic eyes with optic pits and retinal detachments involving peripheral retinal quadrants.
Since the mid-1980s, the development of a therapeutic, computer-assisted laser photocoagulation system to treat retinal disorders has progressed under the guidance of Dr. Welch, the Marion E. Forsman Centennial Professor of Engineering, Department of Biomedical Engineering, the University of Texas at Austin. This paper reviews the development of the system, related research in eye movement and laser-tissue interaction, and system implementation and testing. While subsets of these topics have been reported in prior publications, this paper brings the entire evolutionary design of the system together. We also discuss other recent "spinoff" uses of the system technology that have not been reported elsewhere and describe the impact of the latest technical advances on the overall system design.
The murine VEGF gene is alternatively transcribed to yield the VEGF(120), VEGF(164), and VEGF(188) isoforms, which differ in their potential to bind to heparan sulfate and neuropilin-1 and to stimulate endothelial growth. Here, their role in retinal vascular development was studied in mice selectively expressing single isoforms. VEGF(164/164) mice were normal, healthy, and had normal retinal angiogenesis. In contrast, VEGF(120/120) mice exhibited severe defects in vascular outgrowth and patterning, whereas VEGF(188/188) mice displayed normal venular outgrowth but impaired arterial development. It is noteworthy that neuropilin-1, a receptor for VEGF(164), was predominantly expressed in retinal arterioles. These findings reveal distinct roles of the various VEGF isoforms in vascular patterning and arterial development in the retina.
We analyzed the vitreous findings in 62 patients (62 eyes) with major branch retinal vein occlusion to determine whether vitreous examination was useful in predicting the development of retinal or disk neovascularization, or both. In 18 eyes with no or partial posterior vitreous detachment and large areas of capillary nonperfusion (5 disk diameters or more), ten eyes (55.6%) eventually developed neovascularization. Only three of the remaining 44 eyes (6.8%) developed neovascularization. The probability of this development was greater in eyes with no partial posterior vitreous detachment at the initial vitreous examination (P = .0177, Cox's regression analysis), and in those with large areas of nonperfusion (P = .0097, Cox's regression analysis).
A series of 897 Nd:YAG laser posterior capsulotomies were reviewed for the complications of cystoid macular edema, retinal detachment, new onset of glaucoma, and worsened preexisting glaucoma. After Nd:YAG capsulotomy, 11 patients (1.23%; 95% confidence interval, 0.51% to 1.95%) developed cystoid macular edema and eight patients (0.89%; 95% confidence interval, 0.28% to 1.5%) developed a retinal detachment. The new onset of glaucoma was observed in seven patients (0.78%; 95% confidence interval, 0.20% to 1.36%). Five patients (0.56%; 95% confidence interval, 0.07% to 1.05%) with preexisting glaucoma had persistent worsening of their glaucoma. Most patients with a complication had no identifiable risk factors in common. The numbers of laser pulses and energy delivered were not risk factors. Retinal detachment and cystoid macular edema developed most often many months after capsulotomy and many months to years after the cataract surgery. Patients undergoing Nd:YAG laser capsulotomy therefore require ongoing medical observation to detect and treat these serious complications.
A 33-year-old woman underwent bone-marrow transplantation following radiation and chemotherapy for chronic myelocytic leukemia (CML); immunosuppressive therapy was continued for graft-versus-host disease. Five months after successful transplantation, she developed necrotizing retinitis in both eyes with rapid progression over the following weeks. Due to her immunosuppressed state the patient developed pneumonia and died. Postmortem evaluation of the retinal lesions in both eyes disclosed infection by Toxoplasma gondii, which was also found in the brain and myocardium. Multiple viable toxoplasmic cysts were observed at the transition zone from a necrotic to a normal retina. Additionally, cysts of Toxoplasma gondii a normal retina. Additionally, cysts of Toxoplasma gondii were seen in the adjacent intact retina and in areas of necrosis with almost complete absence of retinal or choroidal inflammation. Toxoplasmosis should therefore be considered along with fungi and viruses in the differential diagnosis of necrotizing retinochoroiditis in immunocompromised patients.
In the last few years the progress made in producing an integrated automated retinal surgical laser system has grown tremendously. Two different techniques have been developed in parallel: an analog and a digital system. Both the analog and digital systems are capable of tracking the retina while precisely placing lesions in desired locations. However, each system has its unique advantages and disadvantages to an automated surgical system. Current work has been conducted to integrate these two techniques to take full advantage of their unique capabilities. The goal of this research is to successfully integrate the systems to provide a better retinal surgical treatment for those individuals affected by diabetes, retinal tears, and other eye disorders.
Dlx homeobox genes, the vertebrate homologs of Distal-less, play important roles in the development of the vertebrate forebrain, craniofacial structures and limbs. Members of the Dlx gene family are also expressed in retinal ganglion cells (RGC), amacrine and horizontal cells of the developing and postnatal retina. Expression begins at embryonic day 12.5 and is maintained until late embryogenesis for Dlx1, while Dlx2 expression extends to adulthood. We have assessed the retinal phenotype of the Dlx1/Dlx2 double knockout mouse, which dies at birth. The Dlx1/2 null retina displays a reduced ganglion cell layer (GCL), with loss of differentiated RGCs due to increased apoptosis, and corresponding thinning of the optic nerve. Ectopic expression of Crx, the cone and rod photoreceptor homeobox gene, in the GCL and neuroblastic layers of the mutants may signify altered cell fate of uncommitted RGC progenitors. However, amacrine and horizontal cell differentiation is relatively unaffected in the Dlx1/2 null retina. Herein, we propose a model whereby early-born RGCs are Dlx1 and Dlx2 independent, but Dlx function is necessary for terminal differentiation of late-born RGC progenitors.
(1) Ten patients (mean age 71) with fully developed central retinal venous occlusion were treated by isovolemic hemodilution over a period of four to six weeks. Hematocrit was lowered in steps to about 30% to improve retinal microcirculation. For two to four days, 500 ml whole blood were exchanged daily for about 250 ml hydroxyethyl starch and 250 ml plasma. The procedure was repeated every five to ten days whenever the hematocrit exceeded 35%. Visual acuity was considered to be improved when the patient could read at least two more lines on the test card. Four to six weeks after starting hemodilution therapy visual acuity had improved in seven patients, deteriorated in one, and was unchanged in two. In the follow-up study six months after treatment visual acuity, as compared to data before treatment, had improved in four patients, deteriorated in two and was unchanged in four. Three patients developed a neovascular glaucoma and had to undergo photocagulation treatment. (2) As expected, hemodilution failed to improve visual acuity in five patients who had had a complete central retinal arterial occlusion for more than four hours. (3) This is the first time that a beneficial effect of isovolemic hemodilution on visual acuity, probably mediated by an improvement in retinal blood flow, has been demonstrated in man. However, only in retinal tissue with at least minimal blood flow (venous but not arterial occlusion) can this method be effective. Except for severe anemia or thrombocytosis there are no absolute contraindications. No adverse side-effects were observed. To prevent neovascularization it is planned to use a combination of hemodilution and photocoagulation.
We have recently characterized a cytosolic aldehyde dehydrogenase from rat kidney that functions as a retinal dehydrogenase (RALDH) and have cloned the corresponding gene. RALDH catalyzes the oxidation of retinal to retinoic acid, which regulates cell growth and differentiation by activating retinoic acid receptors. In situ hybridization demonstrates that RALDH mRNA expression is prominent in kidney in 2-day-old rats, is detected in lung and in epithelia of several tissues, but is not found in liver tissue. Retinal dehydrogenase activity peaks in kidney at Day 2 after birth and decreases gradually until adulthood, correlating well with RALDH expression. Weaker activity is also detectable in lungs but not in liver. Notably, distribution patterns of RALDH in kidney tissues are dramatically altered during postnatal development (P). From P0 to P6, hybridization is essentially concentrated within the marginal nephrogenic zone of the cortex. Expression progresses to deeper cortical layers from P12 to P16 and is intense in the medulla at P42, and focal expression is still detectable in the cortex. Immunocytochemical localization of RALDH in neonatal kidney shows staining mostly in cortical zone convoluted tubules and in adult rat shows staining in segments of distal and proximal tubules. These data suggest an important role for RALDH in modulating retinoic acid levels in different cell types during rat kidney development. The changing patterns of RALDH expression mirror stages of nephron formation in the developing rat kidney, strongly suggesting a central role for RALDH and thus for retinoids in controlling kidney development.
During the embryonic development of the eye, a group of founder cells in the optic vesicle gives rise to multipotent progenitor cells that generate all the neurons and the Müller glia of the mature retina. In most vertebrates, a small group of retinal stem cells persists at the margin of the retina, near the junction with the ciliary epithelium. In fish and amphibians, the retinal stem cells continue to produce progenitors throughout life, adding new retina to the periphery of the existing retina as the eye grows. In birds the new retinal addition is more limited, and it is absent in those mammals that have been analyzed. Nevertheless, cells from the retinal periphery and ciliary body of mammals can be isolated and grown in vitro for extended periods. Methods for the study of both embryonic progenitors and adult retinal stem cells in vitro and in vivo have led to a better understanding of retinal development, allowed for the screening of factors important in retinal growth and differentiation, and enabled the development of methods to direct stem and progenitor cells to specific fates. These methods may ultimately lead to the development of strategies for retinal repair.
Recent studies have suggested that advanced glycation end products (AGEs) are involved in the development of diabetic complications. To assess the pathogenic role of AGEs and vascular endothelial growth factor (VEGF) in the development of retinal neovascularization in diabetic retinopathy, we investigated the effect of AGEs on induction of VEGF by retinal Muller cells and measured AGE and VEGF concentrations in the vitreous of patients with proliferative diabetic retinopathy (PDR) and nondiabetic patients. The expression of VEGF mRNA and the production of VEGF protein by cultured Muller cells were enhanced by the presence of AGEs. The vitreous concentrations of AGEs and VEGF were both elevated in patients with PDR compared with patients without diabetes (P < 0.01). There was a moderate positive correlation between the levels of crossline and VEGF (r=0.698, P < 0.01). Elevation of AGEs in the vitreous may promote intraocular neovascularization in diabetic retinopathy through production of VEGF from Muller cells.
We studied the morphogenesis and the membrane skeleton in the retinal pigment epithelium during chicken embryogenesis and in culture, by using immunofluorescence and electron microscopy. During embryogenesis two distinct membrane skeletal structures were formed, an apical and a basolateral one. The former was seen in the apical surface already in the 10-day-old embryos. It was comprised of ankyrin and alpha-fodrin and showed a codistribution with Na+,K(+)-ATPase and an as yet uncharacterized cadherin-like molecule. The basolateral membrane skeleton was seen in the lateral walls already in the 10-day-old embryos, and later, between the 13th and 17th embryonic days, it also appeared at the basal membrane, coincidentally with the formation of the basal infoldings. It consisted of ankyrin and alpha-fodrin, but did not codistribute with any of the integral membrane proteins studied (Na+,K(+)-ATPase and cadherins). In culture, the retinal pigment epithelial cells retained their polarized morphology. Compared with the situation in vivo, however, there was a distinct translocation of the membrane skeletal components fodrin and ankyrin from the apical surface to the lateral walls, accompanied by a similar redistribution of Na+,K(+)-ATPase and the cadherin-like molecule. The results suggest that (1) there is, in the retinal pigment epithelium, an apical Na+,K(+)-ATPase-membrane skeleton structure stabilized by contacts between the retinal pigment epithelium and the neural retina, possibly mediated by a cadherin-like molecule, and that (2) there is another fodrin/ankyrin-based membrane skeleton in the basolateral walls that is important for the maintenance of the extensive folding of these surface areas.
The authors report three patients with systemic lupus erythematosus (S.L.E.) who developed primary retinal vasculitis. All patients showed evidence of four American Rheumatism Association diagnostic criteria for S.L.E. The first case consisted of a woman with retinal central vein occlusion. Auto-immunization against retinal S antigen was present. She improved under heparin therapy. In the second case, a young girl had chronic optic disk vasculitis for seven years. In the third case, retinal arterial occlusive disease was present with optic nerve involvement. The differential diagnosis with multiple sclerosis is discussed. S.L.E. is considered as autoimmune disease where circulating immune complexes play a major role in the pathogenesis. The ocular complications are probably a manifestation of the widespread systemic disease in patients without arterial hypertension. The authors summarize the ocular findings in S.L.E.: venous obstruction, constriction of retinal arteries, capillary vasculitis and disc neuritis. In some cases, there may be the first manifestations of the disease.
A case is reported of a 35-year-old male with established acquired immune deficiency syndrome who developed cytomegalovirus retinitis. When intravenous treatment with ganciclovir had to be withdrawn because of toxicity, one eye was treated successfully by intravitreal injections of the drug. After 15 weeks of intravitreal treatment this eye developed endophthalmitis.
We present a murine model of trilateral retinoblastoma. Ocular retinoblastoma and central nervous system tumors are observed in a line of mice formed by the transgenic expression of SV40 T-antigen. An oncogenic protein known to bind to the retinoblastoma gene product (p105-Rb) is specifically expressed within retinal cells in this model. All animals that carry this genetic alteration develop multifocal retinal tumors. Midbrain tumors are observed in 15% of ocular tumor-bearing animals, and these arise ventral to the cerebral aqueduct at the level of the pineal gland. Both ocular and central nervous system neoplasms are heritable in heterozygous offspring through 10 sequential generations of breeding. Retinal tumors display the gross appearance, invasive properties, light and electron microscopic features, and immunohistochemical staining characteristics of human retinoblastoma. The light and electron microscopic characteristics as well as immunocytochemical features of undifferentiated midline central nervous system neoplasms further correlate with human trilateral retinoblastoma. We postulate an alternative mechanism of retinoblastoma tumorigenesis that involves functional inactivation of retinoblastoma protein locally in the face of an intact retinoblastoma gene locus.