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PubMed1988

A syndrome of multiple fundal anomalies in siblings with microcephaly without mental retardation.

Chorioretinal and retinal anomalies, among others, have been described in association with true autosomal recessive microcephaly. Accompanying hypertrophy of retinal pigment epithelium has been described in association with Gardner's syndrome. We present the cases of three siblings (two boys and one girl) with true autosomal recessive microcephaly without mental retardation and without associated systemic anomalies who showed hypertrophy of the retinal pigment epithelium similar to that described in Gardner's syndrome. In the boys, these spots were located on a background of fine variations in pigment, with scattered depigmented atrophic areas revealing the sclera in the peripheral and midperipheral fundus. Superadded white spots were located in front of the retinal vessels. The younger boy also had discrete patches of chorioretinal atrophy of 0.5 to 1 disc diameter. The girl, in addition to the hyperpigmented spots, had a diffuse area of chorioretinal atrophy. The anomalies described above suggest that congenital hypertrophy of the retinal pigment epithelium is not unique to Gardner's syndrome.

Abnormalities, Multiple↗

PubMed1996

Retinopathy in diabetic (KKA gamma) mice: diabetic microvascular changes to the retina in KKA gamma mice revealed by light and electron microscopy.

Pericytic changes in the retinal vessels of diabetic (KKA gamma) and control (C57BL) mice were studied by light and electron microscopy. An improved histochemical technique for alkaline phosphatase was used in the light microscopic study. In the control mice, a continuous pathway was identified extending from the retinal arterioles, via the superficial and deep retinal capillaries, to the retinal venules. The deep retinal capillaries formed networks and were localized within the deeper retinal layers; the retinal arterioles, superficial capillaries, and venules were present in the nerve fiber layer. Examination of KKA gamma mice, aged 16 to 28 weeks, revealed engorgement of the arterioles, hypertrophy of the pericytes (which contained numerous actin filaments) within the superficial retinal capillaries, and narrowing of the deep retinal capillaries. These microvascular changes indicate retinal hyperperfusion, local hypertension of the superficial retinal capillaries, adaptive hyperfunctional changes in the pericytes of these capillaries, and ischemia of the deep retinal capillaries. The pericytic changes observed in the diabetic capillaries contrasted sharply with previous reports; an explanation for this variance is suggested.

Alkaline Phosphatase↗

PubMedDate not supplied

Screening for retinopathy of prematurity: are a lid speculum and scleral indentation necessary?

We wanted to investigate the value of using a lid speculum and scleral indentation in performing binocular indirect ophthalmoscopy (BIO) in neonates at risk of retinopathy of prematurity (ROP). We performed a prospective masked comparison of BIO examinations using either a lid speculum and scleral indentation (SI) or no scleral indentation (NSI), in our neonatal intensive care unit. We did 57 consecutive BIO examinations of infants weighing less than 1500 g and/or having a gestational age of less than 32 weeks. With NSI, zone I ROP was reliably seen in 53 of 57 examinations; the superior, nasal, and temporal aspects of zone II were seen in 45 of 57 examinations; inferior zone II, in 22 of 57 examinations; and zone III in 1 of 57 examinations. SI facilitated complete peripheral fundus examination in all cases but had to be abandoned in two infants due to acute changes in oxygen saturation levels. Five infants developed threshold disease, and in two of them details of the active ROP ridge were missed with NSI. The gentle use of an eyelid speculum and globe rotation allows rapid and relatively atraumatic assessment of the peripheral fundus, even in babies who are being ventilated. Although threshold ROP may be diagnosed by observation of posterior retinal vessel dilation and tortuosity ("plus" disease), accurate grading of ROP is likely to require SI. In the absence of clearly developed "plus" disease, borderline or prethreshold disease may occasionally be missed using BIO with NSI. SI is necessary to examine the inferior midperipheral retinal vasculature (zone II) and the far peripheral temporal retina (zone III) and is associated with few complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Fundus Oculi↗

PubMed2006

Suppression of laser-induced choroidal neovascularization by subconjunctival injection of 9alpha-fluoromedroxyprogesterone acetate (FMPA), an anti-angiogenic agent, in rats.

9alpha-Fluoromedroxyprogesterone acetate (FMPA) is a synthetic analog of medroxyprogesterone acetate (MPA). FMPA exhibited more potent anti-tumor and anti-angiogenic activities in some assay systems than the parent agent, MPA. Exudative age-related macular degeneration (AMD) is characterized by choroidal neovascularization (CNV). Anecortave acetate, an angiostatic steroid, is clinically efficacious in patients with exudative AMD. Betamethasone is an anti-angiogenic steroid. Therefore, we examined the effects of FMPA, anecortave acetate and betamethasone on laser-induced CNV in rats. Anecortave acetate and betamethasone were included as positive controls. Crypton laser was applied to the fundus in Brown Norway rats. Laser photocoagulations were performed in each eye between the major retinal vessels of the superior retina. Subconjunctival injection of FMPA, anecortave acetate or betamethasone was performed once just after the photocoagulation (on day 0). The incidence of CNV formation was evaluated by fluorescein angiography (FAG) on day 14. On the next day, examination of the retinal function was performed by electro retinogram (ERG). Subconjunctival injection of FMPA at doses of 300, 1000 and 3000 microg/eye dose-dependently inhibited the incidence of CNV formation. Significant differences were observed at doses of 1000 and 3000 microg/eye of FMPA as compared with the control group. Anecortave acetate and betamethasone significantly inhibited the incidence of CNV formation. FMPA at the doses used in this study did not affect the retinal function in rats, as determined by ERG. FMPA appeared to be effective in a rat model of CNV, so it was demonstrated that FMPA might be useful in the treatment of AMD.

Angiogenesis Inhibitors↗

PubMed2002

Benefits and complications of photodynamic therapy of papillary capillary hemangiomas.

OBJECTIVE: To evaluate the potential benefit and risks of photodynamic therapy (PDT) in the treatment of papillary capillary hemangioma. DESIGN: Prospective, noncomparative, interventional case series. PARTICIPANTS: Five patients with solitary capillary hemangioma on the temporal portion of the optic nerve presenting with exudative decompensation and decrease in visual acuity (VA). METHODS: All eyes received a standardized PDT treatment with 6 mg/kg body surface area verteporfin and application of 100 J/cm(2) light at 692 nm. One to three PDT courses were performed until resolution of exudation was achieved. A continuous follow-up was provided with documentation 1 week before and at 4 to 6 weeks, 3 months, and 12 months after the last treatment application. MAIN OUTCOME MEASURES: Functional parameters included best-refracted VA (Early Treatment Diabetic Retinopathy Study), and central scanning laser ophthalmoscope (SLO) scotometry and peripheral (automated perimetry) visual fields; anatomic parameters were presence of retinal edema or serous detachment (ophthalmoscopy) and tumor size (ultrasonography). RESULTS: Pretreatment VA levels ranged from 20/40 to 20/800; posttreatment levels ranged from 20/64 to 20/2000. Tumor regression with resolution of macular exudate and serous retinal detachment was obtained in all eyes. A decline in VA of 1, 3, and 10 lines, respectively, was documented in three patients. Complications included transient decompensation of vascular permeability, occlusion of retinal vessels, and ischemia of the optic nerve. CONCLUSIONS: PDT is successful in reducing tumor size and exudative activity. Vaso-occlusive effects at the level of the retina and optic nerve compromise the functional benefit. Parameters proven safe in choroidal neovascularization may be inappropriate in retinal capillary lesions of the optic nerve.

Adult↗

PubMed1996

Myelinated nerve fibers and retinal vascular abnormalities.

BACKGROUND/PURPOSE: Abnormal retinal vessels may develop in a region of myelinated nerve fibers, and these vessels may cause vitreous hemorrhages. METHODS: The clinical histories of seven patients with retinovascular abnormalities in a patch of myelinated nerve fibers are presented. None of the reported patients had other evidence of systemic disease. The cases were traced by a multicentric retrospective study. RESULTS: Retinal vascular abnormalities ranged from mild telangiectasis to frank neovascularization, with or without obstruction of the capillary network and signs of branch artery and vein occlusion. Age at diagnosis ranged from 15 to 68 years. Vitreous hemorrhages occurred in the four youngest patients and occurred at 15, 27, 27, and 43 years of age. Laser photocoagulation was applied in three patients and vitrectomy was performed in one. CONCLUSION: The authors' findings suggest that the abnormal structure of the myelinated nerve fibers and the thickened nerve fiber layer of the affected portions of retina may play a role in the onset of retinal vascular abnormalities and eventually cause telangiectasis, branch artery and vein occlusion, neovascularization, and vitreous hemorrhages. This suggestion is based on the absence of other causes of neovascularization or vitreous hemorrhage in all seven patients, and on the relatively young age of four of the patients with this association.

Adolescent↗

PubMed1977

An unusual macular lesion associated with malaria.

A case of a young man afflicted with falciparum malaria is presented in which the primary ocular finding was a subpigment epithelial hemorrhage involving the macula. Previous reports in the literature concentrate on peripheral and central retinal hemorrhages, almost to the exclusion of choroidal vascular abnormalities. The value of this case lies in the recognition that the choroid can assume an important role in fundus abnormalities associated with malaria, probably on the basis of obstructive phenomena with subsequent ischemic degenerative changes, similar to the process which involves the retinal vessels and central nervous system.

Adult↗

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↗

PubMed1986

[Ocular hypotonia and retinal injuries in Steinert disease. Angiographic aspects].

The authors study ocular complications, mainly retinal, in three patients with myotonic dystrophy. The association of cataract, ocular hypotony, reticular or butterfly-shaped dystrophy of the macular pigmentary epithelium was observed in all cases. A bibliographical study regarding retinal lesions: clinical aspects (macular lesions and peripheral retinopathy), retinal functions (visual acuity, color sense, dark adaptation, electrophysiological examinations), histopathological aspects with proliferation of peripheral pigmentary epithelium, retinal and choroidal fibrohyalinosis. The authors report vitreous and retinal modifications (disc, macula, retinal vessels, peripheral retinopathy), evolutive aspects, electrophysiological anomalies in order to understand at best Steinert's ocular lesions.

Adult↗

PubMed1983

Permeability of abnormal blood-retinal barriers in rat phototoxic retinopathy: a clinicopathologic correlation study using fluorescent markers.

Phototoxic retinopathic rats were studied by vitreous fluorophotometry (VF) and histofluorescence microscopy using NaFl and FITC-Dextran molecules of selected molecular sizes as blood-retinal barrier permeability determinants. Retinopathic rats had significantly higher VF values than normal rats at a 35 mg/kg NaFl dosage; detectable levels were not obtained with 3.5 mg/kg NaFL nor with FITC-Dextrans. However, as demonstrated by histofluorescence microscopy, NaFl and FITC-Dex 3 molecules readily passed the abnormal BRB tissues to enter neural retina and vitreous space whereas FITC-Dex 20, 40, 70 and 150 molecules did not, except under certain circumstances. These studies indicate a barrier defect of both the retinal vessels and RPE is responsible for the in vivo demonstrated permeability abnormality.

Animals↗

PubMed1987

Color vision defects in sickle cell anemia.

The Farnsworth-Munsell 100-hue test was used to compare color vision in patients with sickle cell anemia, 20/20 visual acuity, and mild to severe peripheral retinopathy, but without posterior retinal vessel involvement, with matched normal controls. Patients with sickle cell anemia had significantly more blue-yellow and mixed color vision defects and significantly higher Farnsworth-Munsell 100-hue scores than did controls. There were no significant associations between color vision defects and the severity of peripheral retinal findings or the diameter of the foveal avascular zone. These results suggest that color vision defects may exist in patients with sickle cell anemia in the absence of ophthalmoscopic retinal changes in the posterior fundus.

Adult↗

PubMed1992

[Experimental study on earlier thrombogenic process in thrombin induced retinal venous obstruction in rabbit eye].

The purpose of this study was to morphologically investigate the thrombogenic process in the early stage of retinal venous obstruction development. Venous obstruction was induced by transadventitial instillation of thrombin (5 units) given to the rabbit retinal vessels via a sclerovitreous route. The changes were studied by ophthalmoscopy, fluorescence microscopy combined with an intravenously injected gelatin fluorescein preparation technique as well as light and electron microscopy. No ophthalmoscopic change was seen within 1 hr after thrombin instillation. Three hour after thrombin instillation, focal narrowing of retinal arterioles was found with intraluminal platelet aggregation and rouleaux formation of erythrocytes. On electron microscopy, a large number of monocytes was observed in the lumina and subendothelial space of a pericytic venule having a partial endothelial defect as well as monocyte adhesion to its luminal surface. At more than 6 hrs, subendothelial thrombi were observed in the venules without any endothelial lesion while no change was observed in the arterioles, capillaries and pericytic venules. These findings suggested the possibility of participation of the arteriolar lesion in the occurrence of retinal venous obstruction and the role of endothelial lesions caused by blood stasis in subendothelial thrombogenesis.

Animals↗

PubMed1977

Intraocular pressure and diabetic retinopathy.

Between intraocular pressure (I.O.P.) and the metabolic carbohydrate disturbance is a relationship: 1. diabetics frequently show primary open angle-galucoma; 2. as the diabetic retinopathy progresses towards stage III (Pr.), IOP decreases; 3. as diabetics exhibit dilatation of veins, increased blood viscosity, arteriolar narrowing and increased I.O.P. central retinal vessel disease with hemorrhages occurs redily; 4. capillary hemorrhages, periapaillary and macular oedema may be caused by increased oncotic pressure with acidosis of the blood; hyperglycemia with ketosis goes together with decreased I.O.P.; 5. only mild I.O.P.-rise may be considered as usefull to prevent hemorrhages by reducing retinal blood flow resulting subsequently from reduced uveal blood flow; 6. local application of glucocorticoids with permanent control of visual fields and I.O.P. should be a good additional treatment for diabetic retinopathy; unfortunately only very few cases are responsive to increase of I.O.P. by glucocorticoids; 7. it is important that prolactine levels in the blood are higher in the morning before the patient wakes up: this goes together with the morning I.O.P.-rise in glaucoma patients. Decreased activity of the hypophysis improves the diabetic retinopathy; this is contradictory to the beneficial effect of mild I.O.P.-rise.

Adult↗

PubMed2004

Histopathological abnormalities in ocular blood vessels of CADASIL patients.

PURPOSE: To assess histopathological findings in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). DESIGN: Case reports and histopathological evaluation of enucleated eyes. METHODS: Four eyes from two CADASIL patients were enucleated at autopsy and prepared for histopathological analysis using light and electron microscopy. RESULTS: Thickening of arterial walls with fibrosis, eosinophilic Periodic acid Schiff-positive basement membrane material and loss of vascular smooth muscle cells (VSMC) in the central retinal artery and its branches, the leptomeninges, the ocular adnexa, and the optic disk were observed. On electron microscopy, numerous deposits of granular, osmiophilic material in arterial walls as well as VSMC and pericyte degeneration were noted. In contrast to retinal vessels, the choroid was not affected. CONCLUSION: Our findings suggest a differential involvement of small blood vessels in CADASIL, depending on the angioarchitecture and support autopsy data of nervous tissue describing that loss of VSMCs is most pronounced in tissues depending on blood-tissue barriers.

Bruch Membrane↗

PubMed1998

In vivo delivery of phosphorothioate oligonucleotides into murine retina.

OBJECTIVES: To determine the fate of phosphorothioate oligonucleotides (S-ODNs), which are commonly used for antisense strategy, in murine retina in vivo with the use of fluorescein isothiocyanate (FITC)-labeled S-ODNs, and to evaluate our fusogenic liposome system that may facilitate the delivery of S-ODNs. METHODS: The FITC-labeled S-ODNs were encapsulated in liposomes, which were then coated with the envelope of inactivated hemagglutinating virus of Japan (HVJ; Sendai virus) by fusion (HVJ liposomes). Intravitreal injection of naked FITC-labeled S-ODNs or of the HVJ liposomes was done in ICR mice. After fixation, cryosections and flat-mounted retinas were prepared and examined by fluorescence microscopy. RESULTS: Injection of naked FITC-labeled S-ODNs at 3 micromol/L exhibited weak fluorescence in 13% of the cells in the ganglion cell layer. When the concentration was increased to 30 micromol/L, high fluorescence was seen in 59% of cells in the ganglion cell layer at this time. This fluorescence diminished within a day. In contrast, injection of HVJ liposomes containing FITC-labeled S-ODNs at 3 micromol/L resulted in high fluorescence in 44% of the cells in the ganglion cell layer at 1 hour, and this fluorescence lasted for up to 3 days. This treatment also resulted in high fluorescence within retinal vessel walls, and weak fluorescence in photoreceptor cells. CONCLUSIONS: Intravitreally injected S-ODNs were rapidly eliminated from neural retina, and the use of HVJ liposomes could improve the delivery of S-ODNs. This method may be a potentially useful system for the antisense-based therapies for retinal diseases.

Animals↗

PubMed2006

[Combined hamartoma of the retina and retinal pigment epithelium. Four case studies].

INTRODUCTION: Combined hamartoma of the retina and retinal pigment epithelium is a rare condition, characterized by a proliferation of the retinal pigmentary epithelium and retinal gliosis leading to a disorganization of the retina and papilla. This study aimed to demonstrate the advantages of early diagnosis and regular monitoring. OBSERVATIONS: We report a series of four children followed between 2001 and 2004 with combined hamartoma of the retina and retinal pigment epithelium, with age of diagnosis ranging from 3 months to 8 years. The main reason for consultation was reduction of vision. The clinical examination objectified the existence of a slightly grayish peripapillary formation with tortuous retinal vessels. This condition was confirmed by angiography with fluorescein in three cases and by optical coherence tomography (OCT) in one case. Progression showed the persistence of low vision in all four cases and the appearance of a neovascular membrane in one case. DISCUSSION: Combined hamartoma of the retina and retinal pigment epithelium is probably a congenital tumor whose pathogenesis has not yet been elucidated. The diagnosis is clinical and the patient can be thoroughly examined by retinal angiography and optical coherence tomography (OCT). In this disorder, it is important to eliminate retinoblastoma and malignant melanoma of the choroid, showing the advantage of radiological exploration. Progression is stationary; nevertheless a reduction in visual acuity can be related to an epiretinal membrane or a neovascular membrane. CONCLUSION: Knowledge of the clinical aspect is essential to differentiate this condition from the malignant retinal processes. This tumor can progress in spite of its benign character. Regular follow-up is essential and can improve the visual prognosis.

Child↗

PubMed2006

Ten-year incidence of retinal vein occlusion in an older population: the Blue Mountains Eye Study.

OBJECTIVE: To assess the 10-year incidence of retinal vein occlusion (RVO) and its predictors in an older population. METHODS: The Blue Mountains Eye Study examined 3654 residents aged 49 years and older (82.4% response) from 1992 to 1994, reexamined 2335 residents (75.1% of survivors) from 1997 to 1999, and reexamined 1952 residents (75.6% of survivors) from 2002 to 2004. Incident RVO was assessed from stereoscopic retinal photographs. Kaplan-Meier cumulative 10-year incidence was calculated. RESULTS: After excluding 47 residents with RVO at baseline and 171 residents with no photographs at either follow-up examination, 2346 residents were considered at risk of developing RVO. The cumulative 10-year incidence of RVO was 1.6%. Age was significantly associated with the incidence of RVO (P = .03, Mantel-Haenszel chi(2) test for trend). Factors predicting the incidence of RVO included mean arterial blood pressure (age-adjusted odds ratio [OR], 1.41 per 10-mm Hg increase), ocular perfusion pressure (OR, 1.71 per 10-mm Hg increase), obesity (OR, 2.16), and presence of retinal arteriolar wall signs (focal narrowing: OR, 3.37; arteriovenous nicking: OR, 4.09; and opacification: OR, 4.89). CONCLUSIONS: Older age (> or =70 years), increasing mean arterial blood pressure, and atherosclerotic retinal vessel signs were significant predictors of incident RVO.

Aged↗

PubMed1985

Massive peripheral retinal sclerosis. Correlation between light and scanning electron microscopic findings.

Peripheral retinal sclerosis (PRS) is especially massive in cases of high myopia and retinitis pigmentosa. The distribution and configuration of the sclerotic formations in nine such cases were studied and compared by light microscopy and SEM. Different aspects of the sclerotic structures are described. It is shown that no formations of PRS lie isolated within the degenerated retinal tissue as could be supposed by light microscopy. They are always in multiple contact to or originate from the vitreo-retinal border layer and/or peripheral retinal vessels. This leads to the supposition that these preexisting collagenous structures participate in some way in the formation of PRS.

Aged↗