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PubMed1975

[Typical retinitis pigmentosa with chronic progressive external ophthalmoplegia (author's transl)].

Report of a case of chronic progressive external ophthalmoplegia combined with retinitis pigmentosa, optic atrophy, marked attenuation of the retinal vessels, maculopathy, and complicated cataract. Visual fields and acuity were severely impaired. The ophthalmoplegia was histologically identified as ocular myopathy. In a review of 181 cases with CPEO the disease was found to be associated with retinitis pigmentosa in 7 per cent and with atypical pigmentary retinopathy in 36 per cent of the cases. A distinction of these two types of retinal dystrophy is justified by the clinical features and may indicate different hereditary patterns.

Adult↗
PubMed1992

Macular pucker after retinal detachment surgery.

To better understand postsurgical macular pucker in rhegmatogenous retinal detachment, we reviewed a consecutive series of 277 eyes in 268 patients in whom retinal detachment had spared the macular area and in whom no preretinal membrane with distortion of the retinal vessels had been present preoperatively. Postoperatively, 17 eyes (6.1%) developed obvious macular pucker; 260 eyes (93.9%) did not. Using the Mantel-Haenszel chi-square test, we found that patient age, preoperative vitreous hemorrhage, large retinal breaks of more than three disc diameters, and cryoapplication were significant precipitating factors of postoperative macular pucker. These findings are consistent with the view that dispersion of retinal pigment epithelial cells through the retinal break into the vitreous cavity is the major cause of this disorder. Minimal use of cryotherapy is recommended in treating elderly patients who have a large retinal break or a preoperative vitreous hemorrhage.

Adolescent↗
PubMedDate not supplied

[Clinical chorioretinal aspects of systemic immune vasculitis. I. General aspects].

The eye, due to its rich vascularity, is frequently involved, directly or not, in the systemic immune vascular pathology. For a better understanding of the ocular clinical syndrome, the paper discusses the etiologic and pathogenic factors, and their influence on the characteristics of chorioretinal changes. The etiologic factors are classified according to the predominance of the lesions of the choroidal or retinal vessels. The pathogeny of the chorioretinal changes is correlated with the histopathologic lesion (fibrinoid necrosis) and its involvement in the "choriocapillaris complex-brush membrane-EPR". Clinical chorioretinal syndrome, irrespective of its etiology, induces several retinal and choroidal changes having varied as a function of the evolution stage.

Chorioretinitis↗
PubMed1992

The retinal pigment epithelium induces fenestration of endothelial cells in vivo.

Rodent photoreceptor dystrophies are characterized by late stage ingrowth of retinal blood vessels into the retinal pigment epithelium (RPE) where they proliferate. Some of these vessels develop the fenestrated phenotype of the choriocapillaris (CC). To determine if development of fenestrae in these endothelial cells is a function of the duration of time the endothelial cell had been encapsulated by the RPE, we did an ultrastructural morphometric study of these vessels in urethane induced photoreceptor degeneration in Long-Evans rats. Retinas of animals aged 20, 24, 40 and 56 weeks were studied. The fraction of vessel profiles within the RPE that had fenestrated endothelial cells increased from 10% to 90% between 20 to 56 weeks. The average number of fenestrae per vessel increased approximately 25 fold between 20 and 24 weeks but stabilized after that, despite a decrease in the number of vessels present at 56 weeks. A large number of degenerated retinal vessel profiles were seen in the RPE at 40 weeks. These facts support the idea that the presence of the RPE induces endothelial cell fenestrae, and also show that a complex process of remodelling including proliferation and degeneration is occurring in these vessels. Analogies between the basic cell biology of neovascularization occurring in these rodent models and that of proliferative diabetic retinopathy and age-related macular degeneration are discussed.

Animals↗
PubMed2005

Altered retinal neovascularization in TNF receptor-deficient mice.

PURPOSE: Tumor necrosis factor alpha (TNF-alpha) has been shown to play an integral role in inflammation, apoptosis, and angiogenesis. We induced retinopathy in tumor necrosis factor receptor-deficient mice (TNFR-) in order to examine the role TNF-alpha plays in the pathogenesis of retinopathy of prematurity. METHODS: On postnatal day (P) 7, TNFR-knockout mice and their congenic controls, B6129JF1 (B6129) mice, were exposed to 75% oxygen for up to 5 days and then allowed to recover in room air. Retinopathy was qualitatively assessed by examining fluorescein (FITC) angiography. Furthermore, retinal vascular changes were quantified by immunolabeling retinal vessels in cross sections with an anti-type IV collagen antibody. Disease pathology was quantified by counting preretinal neovascular nuclei. TUNEL analysis was performed to determine if TNFR-mice exhibited a reduced number of apoptotic cells after oxygen-induced retinopathy. RESULTS: FITC-perfused retinas qualitatively demonstrated similar degrees of vascular development and vaso-obliteration on P12 in the room air and hyperoxia-exposed TNFR- and B6129 mice. On P17, the hyperoxia-exposed TNFR- and B6129 mice qualitatively appeared to develop a similar degree of retinal neovascularization. However, FITC-perfused retinal flat mounts on P21 suggested that the hyperoxia-exposed TNFR-mice had a prolonged neovascular response compared to the hyperoxia-exposed B6129 mice. Type IV collagen staining revealed delayed development of the deep intraretinal vessels in the TNFR-room control mice and hyperoxia-exposed TNFR-mice, as compared with B6129 controls. On P17, the average number of preretinal nuclei was similar between the hyperoxia-exposed TNFR-mice and B6129 mice. However, on P21, the neovascularization in the B6129 mice had regressed (3.9 +/- 0.57, preretinal nuclei), whereas neovascularization in the TNFR-mice remained prominent (25.6 +/- 6.3, preretinal nuclei). On P21, the B6129 mice exhibited increased apoptosis in preretinal vascular tufts as compared with TNFR- mice. CONCLUSIONS: TNFR- mice had both an altered development of the intraretinal vessels and altered angiogenic response after hyperoxia. Therefore, absence of the TNF-alpha pathway appears to disrupt the local microenvironment promoting angiogenesis in the deep retinal vascular network, as well as altering tuft regression by modifying endothelial cell apoptosis.

Animals↗
PubMed1978

Hypoplasia of the optic nerve.

Premorbid ophthalmoscopic and histopathologic findings were correlated in a case of bilateral optic nerve hypoplasia in a 9-month-old infant with bilateral hydranencephaly. The double-ring sign was due to an extension of retina and retinal pigment epithelium (RPE) over the outer portion of the lamina cribrosa. The outer ring was the junction between sclera and lamina cribrosa, and the inner ring was the termination of the RPE. The center of the inner ring was the hypoplastic nerve head, which appeared whitish because of fibroglial tissue surrounding the central retinal vessels where they entered the optic nerve head. We speculate that an in utero vascular insult, after the third month of development, led to cystic cavitation of the anterior cerebral hemispheres, with subsequent retrograde degeneration of developing retinal ganglion cells.

Abnormalities, Multiple↗
PubMed1997

Outcome-based management of retinopathy of prematurity. Multicenter Trial of Cryotherapy for Retinopathy of prematurity Cooperative Group.

PURPOSE: A system is presented for sequentially computing the risk of progression of retinopathy of prematurity (ROP) for infants born weighing not more than 1250 gm. A personal computer program is used to monitor infants' risk of threshold ROP from first appearance of ROP, and the progression in severity is tracked with multiple logistic risk models developed from data in the Multicenter Trial of Cryotherapy for Retinopathy of Prematurity. METHODS: After entry of the infant's birth weight, gestational age, ethnicity, birth in the current hospital or elsewhere, single or multiple birth, and maturity zone of retinal vessels, risk of progression to threshold severity is calculated. New estimates of risk are computed at onset of ROP and prethreshold ROP (any zone I ROP, zone II stage 2+ or 3) according to the extent of retinal vascularization when ROP first appears, how rapidly ROP progresses, and how severe it is. When threshold ROP (8 total or 5 contiguous clock hours of stage 3+ in zone I or II) is reached,the system provides separate estimates of risk that the eye will have an unfavorable 3-month outcome if treated or not. RESULTS: Estimates of risk of progression to threshold disease among the 4099 patients in the Multicenter Trial of Cryotherapy for Retinopathy of Prematurity natural history study varied from less than 1% to more than 70%. For eyes with threshold disease, the risk of an unfavorable outcome at 3 months without treatment varied from less than 10% to more than 90%. CONCLUSION: This method of tracking identifies infants at high risk for severe ROP and poor structural outcome. It provides information about prognosis with a specificity heretofore impossible.

Algorithms↗
PubMed2004

The blood-retinal barriers system. Basic concepts and clinical evaluation.

Morphological studies demonstrating the presence in the retinal vessels of 'zonulae occludente' between the endothelial cells and physiological studies examining diffusion gradients in the vitreous after systemic or intravitreal administration of fluorescein, performed under the guidance of David Maurice, established the basis of the Blood-Retinal Barrier (BRB) concept. The BRB system is briefly reviewed as well as its role in health and disease. Regulation of the microenvironment of the retina is fundamental for appropriate retinal function and vision. The diffusional characteristics and transport functions of the BRB system may be evaluated and followed by vitreous fluorometry. Its clinical use has shown the importance of BRB alterations in a variety of retinal diseases but has been restricted by the lack of disease specificity. A recent development, the Retinal Leakage Analyzer, maps BRB alterations and has opened new perspectives for multimodal macula mapping and improved evaluation of newly available drugs that show promise for stabilizing the BRB.

Biological Transport↗
PubMed1989

The retinal nerve fiber layer in normal eyes.

The retinal nerve fiber layer is different in normal and glaucomatous eyes. The authors used red-free photographs to examine the retinal nerve fiber layer in 234 normal eyes. The retinal nerve fiber layer was most visible in the inferior temporal arcade, followed by the superior temporal arcade, then by the temporal macular area, and finally the nasal area. This distribution was significantly (P less than 0.0001) correlated to (1) the configuration of the neuroretinal rim, which was significantly broadest at the inferior disc pole followed by the superior one, (2) the juxtapapillary caliber of the retinal vessels, which were significantly wider in the inferior temporal arcade than in the superior temporal arcade, and (3) the location of the foveola 0.53 +/- 0.34 mm inferior to the middle point of the vertical optic disc axis. The retinal nerve fiber layer decreased with age. No correlation occurred with sex or right or left eye. No localized retinal nerve fiber layer defects were seen. These features of the normal retinal nerve fiber layer are important for diagnosis of retinal nerve fiber layer changes secondary to optic nerve damage in the diseased eye.

Adolescent↗
PubMed1995

[A case of uncomplicated retinal astrocytoma].

A 45-year-old Japanese women whose left eye contained an elevated, whitish yellow, and multi-lobed mass of 1.5 disc diameters that extended out from the retina adjacent to the optic disc. Ultrasonography demonstrated high reflectivity corresponding to the lesion of the left eye. By fluorecein angiography the tumor showed autofluorescein, retinal vessel through the tumor in the venous phase, and in the late phase pronounced staining of the tumor. A scanning laser ophthalmoscope showed the surface in detail. A search of the literature revealed only 16 cases of uncomplicated retinal astrocytoma.

Astrocytoma↗
PubMedDate not supplied

Cone-rod dystrophy in the Guinea baboon.

Three stages of macular degeneration associated with diffuse cone-rod dystrophy have been described in a Guinea baboon (P papio) colony. Clinically, the affected animals displayed abnormal behavior associated with decreased vision. Ophthalmoscopically, the lesion in the macula was the only change observable in early cases; retinal vessel attenuation and optic disc pallor were seen only in the advanced cases. The hyperfluorescence of the maculae was the result of loss of pigment in the pigmented epithelium. Electrophysiology supported a cone-rod sequence of this retinal dystrophy. Histologic examination confirmed the theory that the dystrophy began in the cone outer segment but eventually involved all the photoreceptors.

Animals↗
PubMed2002

Tubedown-1 in remodeling of the developing vitreal vasculature in vivo and regulation of capillary outgrowth in vitro.

Tubedown-1 (tbdn-1) is a mammalian homologue of the N-terminal acetyltransferase subunit NAT1 of Saccharomyces cerevisiae and copurifies with an acetyltransferase activity. Tbdn-1 expression in endothelial cells becomes downregulated during the formation of capillary-like structures in vitro and is regulated in vivo in a manner which suggests a functional role in dampening blood vessel development. Here we show that tbdn-1 is expressed highly in the vitreal vascular network (tunica vasculosa lentis and vasa hyaloidea propria) during the pruning and remodeling phases of this transient structure. The vitreal blood vessels of mice harboring a targeted inactivation of TGF-beta2 fail to remodel and abnormally accumulate, a phenomenon reminiscent of the ocular pathology resembling persistent fetal vasculature (PFV) in humans. Since suppression of normal tbdn-1 expression has been previously observed in retinal vessel proliferation, we analyzed vitreal vascular changes and tbdn-1 expression in TGF-beta2(-/-) eyes. The nuclei of vitreal vessel endothelial cells in TGF-beta2(-/-) eyes express proliferating cell nuclear antigen (PCNA) and exhibit increased levels of active (P42/44)mitogen-activated protein kinase (phospho-(P42/44)MAPK), characteristics consistent with proliferative endothelial cells. In contrast to normal vitreal vessels, collagen IV expression exhibited a disorganized pattern in the TGF-beta2(-/-) vitreal vessels, suggesting vessel disorganization and possibly a breakdown of vessel basal laminae. Moreover, vitreal vessels of TGF-beta2(-/-) mice lack expression of pericyte markers (CD13, alpha smooth muscle actin) and show ultrastructural changes consistent with pericyte degeneration. The accumulating vitreal blood vessels of TGF-beta2(-/-) mice, while maintaining expression of the endothelial marker von Willebrand Factor, show a significant decrease in the expression of tbdn-1. We addressed the functional role of tbdn-1 in the regulation of vitreal blood vessels using an in vitro model of choroid-retina capillary outgrowth. Clones of the RF/6A fetal choroid-retina endothelial cell line showing suppression of tbdn-1 levels after overexpression of an antisense TBDN-1 cDNA display a significant increase in the formation of capillary-like structures in vitro compared with controls. These findings suggest that tbdn-1 inhibits capillary-like formation in vitro and may serve to dampen vitreal blood vessel formation preceding the regression of the vitreal vasculature during development. Our results also suggest that tbdn-1 may participate with TGF-beta2 in regulating normal development of the vitreal vasculature.

Acetyltransferases↗
PubMed1991

Blood-retina barrier permeability in diabetes during acute ACE-inhibition.

We assessed the acute effect of ACE-inhibition (captopril) on blood-retina barrier (BRB) permeability in 10 hypertensive insulin-dependent diabetic patients with background retinopathy in a double-masked placebo controlled cross-over study. All patients underwent ophthalmological examination, fundus photography, fluorescein angiography, vitreous fluorometry, and continuous blood pressure recording within 3 h of the drug/placebo administration. The decrease in mean arterial blood pressure, from placebo treatment 149/92 +/- 17/7 to captopril treatment 132/83 +/- 14/7 mmHg (mean +/- SD), P less than 0.01 was not accompanied by a significant decrease in BRB permeability, which was 2.51 (1.24-9.15) with placebo and 3.02 (1.25-13.93).10(-7) cm/s during captopril treatment (geometric mean and-range), NS. Our study suggests that abnormal leakage through the BRB in hypertensive insulin-dependent diabetic patients with background retinopathy is caused predominantly by structural changes in the retinal vessels whereas hydrostatic forces play a minor role.

Adult↗
PubMed1986

Experimental chloroquine retinopathy.

Chloroquine retinopathy was produced experimentally in the eye of the albino corydoras (one of the tropical fish) by daily administration of chloroquine (0.1 mg per os). The enucleated eyes were examined from the 14th day to 3 months after the beginning of drug administration under light and electron microscopy. The first change of retina was the appearance of membraneous cytoplasmic body (MCB) in the cytoplasm of ganglion, amacrine, bipolar and horizontal cells. MCB might be degenerated lysosome. They showed lamellar figures or crystalline lattice-like structures. Secondarily, these MCB appeared in the inner segments of photoreceptor cells. The outer segments of rod cells disappeared, and then those of cone cells. Although photoreceptor cells were diminished in number in advanced degeneration, the cells of inner nuclear layer and ganglion cells were maintained in number. The presence of MCB dose not mean death of cells. The retinal pigment epithelial cells contained MCB in its cytoplasm only in severe degenerative cases, and did not show other remarkable changes. MCB also appeared in the cytoplasm of pericytes of retinal vessels. Chloroquine is considered to damage directly photoreceptor cells most severely.

Animals↗
PubMed2001

[Age-related contractility of retinal arterioles during pure oxygen breathing].

BACKGROUND: Pure oxygen breathing is a non-invasive method to test the contractility of retinal arterioles. The normal response curve of this provocation method was tested using the Retinal Vessel Analyzer (RVA). Statistical analysis between groups was performed with th Man-Whitney test, correlations were tested with Pearsons' linear function. METHODS: After a 3-min baseline measurement 32 healthy volunteers breathed 100% oxygen for 5 min. The diameter of an retinal arteriole was measured continuously during this provocation by the RVA. Volunteers were separated into four groups according age. RESULTS: All four groups reacted to pure oxygen breathing with significant vasoconstriction of the retinal arteriole: in the youngest group (20-29 years) the reduction was 14.6 +/- 5.2% and the three older age groups 9.4 +/- 5.2%, 4.6 +/- 2.7%, and 2.8 +/- 3.3%. The correlation between vasoconstriction and age was r = 0.73. CONCLUSIONS: Pure oxygen breathing is an easily performed method with minimal invasiveness to the patient. However, the age-correlated response curve must be kept in mind for the clinical use of this method.

Administration, Inhalation↗
PubMedDate not supplied

The abortive form of Bourneville-Pringle syndrome.

BACKGROUND/METHODS: To present a 26-year-old woman affected by the abortive form of Bourneville-Pringle syndrome. To our knowledge, this disease is unusual since only very few cases have been reported in the scientific literature at this time. RESULTS/CONCLUSIONS: Visual acuity was 20/20 in both eyes. No relevant ocular abnormalities were observed excepting two retinal hamartomas, a smaller one in the nasal midperiphery of the right eye and a larger one located along the super-temporal retinal vessels of the left eye. Classical signs of Bourneville-Pringle disease, such as mental retardation and epilepsy, were absent whereas a slight facial adenoma sebaceum and renal cysts represented the solely systemic manifestations of the disease. This case report confirms that retinal phakomata are a typical manifestation of Tuberous Sclerosis, even in the absence of a detected involvement of the brain.

Adult↗