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A peculiar dilation and tortuosity of small retinal vessels within the arcuate areas of the retinal nerve fiber layer occurred in a series of patients with acute malnutritional optic neuropathy ("tobacco-alcohol amblyopia"). These evanescent vascular abnormalities may be caused by arteriovenous shunting. They seem to be specific indicators of the early phase of this disease.
A new spontaneous mouse mutation named fierce (frc) is deleted for the nuclear receptor Nr2e1 gene (also known as Tlx, mouse homolog of Drosophila tailless). The fierce mutation is genetically and phenotypically similar to Nr2e1 targeted mutations previously studied on segregating genetic backgrounds. However, we have characterized the fierce brain, eye, and behavioural phenotypes on three defined genetic backgrounds (C57BL/6J, 129P3/JEms, and B6129F1). The data revealed many novel and background-dependent phenotypic characteristics. Whereas abnormalities in brain development, hypoplasia of cerebrum and olfactory lobes, were consistent on all three backgrounds, our novel finding of enlarged ventricles in 100% and overt hydrocephalus in up to 30% of fierce mice were unique to the C57BL/6J background. Developmental eye abnormalities were also background-dependent with B6129F1-frc mice having less severe thinning of optic layers and less affected electroretinogram responses. Impaired regression of hyaloid vessels was observed in all backgrounds. Furthermore, retinal vessels were deficient in size and number in 129P3/JEms-frc and B6129F1-frc mice but almost entirely absent in C57BL/6J-frc mice. We present the first standardized behavioural tests conducted on Nr2e1 mutant mice and show that C57BL/6J-frc and B6129F1-frc mice have deficits in sensorimotor assays and are hyperaggressive in both sexes and backgrounds. However, C57BL/6J-frc mice were significantly more aggressive than B6129F1-frc mice. Overall, this extensive characterization of the fierce mutation is essential to its application for the study of behavioural, and brain and eye developmental disorders. In addition, the background-dependent differences revealed will enable the identification of important genetic modifiers.
An eleven-year-old boy with systemic lupus erythematosus (SLE) developed severe bilateral lupus retinopathy when he was in active stage of SLE. The patient, who had suffered from SLE for 3 years, was admitted to our hospital because of high grade fever, systemic lymphadenopathy, leukopenia, elevation of erythrocyte sedimentation rate and hypocomplementemia. The dose of prednisolone was increased considering he was exacerbated of SLE, however, the convulsion as CNS lupus occurred to him. After the event he noted loss of vision in his bilateral eyes. The ophthalmologic examination revealed the lesions of cotton-wool spots, retinal vessel dilatations and diffuse occlusions of the retinal arterioles and venules which were compatible with lupus retinopathy. Although the coagulation time was normal, antiphospholipid antibodies were positive at the time of ocular involvement. Careful attention should be paid to the occurrence of lupus retinopathy when the patients with SLE developed in the active stage or CNS lupus, especially they have antiphospholipid antibodies.
The effects of timolol maleate on intraocular pressure (IOP) and the severity of retinopathy induced by exposure to 80% oxygen were studied in newborn Wistar rats. One drop of timolol maleate (0.25%) instilled in each eye twice a day for the first ten days of life substantially reduced intraocular pressure without significantly modifying arterial pressure. Forty percent of the ratlings treated in this way failed to develop oxygen-induced retinopathy (OIR) after exposure to 80% oxygen for the first five days of life; in the other 60% OIR was less severe than that seen in an identically oxygenated group that did not receive timolol. The authors hypothesize that the pharmacologically induced reduction in IOP may have attenuated the effects of the high concentrations of oxygen on the immature retinal vessels by improving the ocular perfusion pressure. The possibility that timolol maleate also exerts a direct action on the caliber of these vessels cannot be excluded.
The interaction of infrared light with the human ocular fundus, particularly sub-retinal structures, was studied in vivo. Visible and infra-red wavelengths and a scanning laser ophthalmoscope were used to acquire digital images of the human fundus. The contrast and reflectance of selected retinal and sub-retinal features were computed for a series of wavelengths or modes of imaging. Near infrared light provides better visibility than visible light for sub-retinal features. Sub-retinal deposits appear light and thickened; the optic nerve head, retinal vessels, and choroidal vessels appear dark. Contrast and visibility of features increases with increasing wavelength from 795 to 895 nm. Optimizing the mode of imaging improves the visibility of some structures. This new quantitative basis for near infrared imaging techniques can be applied to a wide range of imaging modalities for the study of pathophysiology and treatment in diseases affecting the retinal pigment epithelium and Bruch's membrane, such as age-related macular degeneration.
Monkeys injected with monkey retinal tissue incorporated in Freunld's complete adjuvant developed ocular lesions characterized by choroiditic patches in the fundus periphery and sheathing of retinal vessels. Bovine retina, monkey choroid plexus, and guinea pig kidney were ineffective in this respect.
Rubeosis iridis was produced experimentally in rhesus monkey eyes, by means of occlusion of the major retinal vessels of the retina and persistent ocular hypotony. Clinically, rubeosis iridis was recognized 5 days after the procedure. Histopathologically, these vessels developed anteriorly to the iris surface and endothelial fenestrations showed evidence of iris neovascularization. Endothelial cells of the vessels projected toward the internal lumen and showed immaturity. Newly formed vessels originated from the stromal vessels in the iris. This method is an effective experimental model for the induction of rubeosis iridis.
OBJECTIVES: To compare grating visual acuity of eyes with varying severity of retinal residua of retinopathy of prematurity to grating visual acuity of eyes that did not have acute-phase retinopathy of prematurity, showed no ocular abnormalities on follow-up, and were from patients who passed neurodevelopmental screening questions. DESIGN: Monocular grating visual acuity was measured by means of the Teller acuity card procedure when children reached 1, 2, 3 1/2, and 4 1/2 years of age. PATIENTS: A total of 1398 children with birth weights less than 1251 g whose acute-phase retinopathy of prematurity was documented as part of the Multicenter Cryotherapy for Retinopathy of Prematurity Study and who participated in follow-up visual acuity testing. RESULTS: Eyes with no or mild residua of retinopathy of prematurity showed a mean visual acuity similar to that of the comparison group. Eyes in a subgroup with abnormally straightened temporal retinal vessels showed a mean visual acuity approximately 1 octave below that of the comparison group. Mean visual acuity scores from eyes with macular heterotopia ranged from 1 octave (at 1 year) to more than 2 octaves (at 4 1/2 years) below the mean visual acuity of the comparison group. Mean visual acuity scores for the few eyes in the retinal fold or partial detachment group that had quantifiable visual acuity were well below the means for the comparison group. CONCLUSIONS: Acute-phase retinopathy of prematurity that regresses without retinal residua produces no deficit in grating visual acuity between 1 and 4 1/2 years of age. In contrast, eyes with macular heterotopia show a visual acuity deficit, and the deficit is greater at older than at younger ages. Eyes with retinal fold or partial detachment that have measurable visual acuity show large visual acuity deficits at all ages.
Treatment with insulin-like growth factor I (IGF-I) is accompanied by mild generalized and reversible edema. These changes may be due to increased capillary permeability. Therefore, we studied the effects of subcutaneous IGF-I treatment in healthy subjects on capillary permeability of the skin and the retina. Eight healthy subjects were treated with saline or recombinant human IGF-I (rhIGF-I) (10 micrograms.kg-1.h-1 s.c.) in a randomized crossover fashion. Transcapillary diffusion of sodium fluorescein (NaF) was quantitated by video densitometry in the skin in all subjects on the 4th treatment day. In seven subjects, plasma penetration of NaF at the blood-retinal barrier was investigated using vitreous fluorometry (VF) on days 3 and 5. Fluorescent light intensities of the skin and plasma penetration determined by VF were significantly higher during the IGF-I treatment as compared with those during the control situation. In conclusion, IGF-I treatment at the above dose is accompanied by increased transcapillary diffusion of NaF in skin and in retinal vessels.
This study was undertaken to evaluate the optic disc changes in eyes with non-glaucomatous optic nerve damage. The intra- and parapapillary region was evaluated morphometrically in 106 eyes of 56 patients with simple optic nerve atrophy (SONA) and in 107 normal eyes of 57 subjects. Colour stereo optic disc diapositives were used. Only one randomly chosen eye per subject and patient was taken for statistical analysis. Characteristics of SONA were: decreased visibility of the parapapillary retinal nerve fibers, diminished retinal vessel diameter, and area with pallor larger than area with cupping. Size and form of the optic disc, neuroretinal rim, peripapillary scleral ring, and zone Alpha and Beta of the parapillary chorioretinal atrophy were not significantly different. Also, distinctness of a tesselated fundus, frequency of optic disc haemorrhages and frequency of bared circumlinear or bared cilioretinal vessels did not differ significantly. These morphologic features are helpful in the diagnosis and differential diagnosis of SONA.
138 diabetic retinopathy patients with good fluorescein angiograms of the macular areas were studied. Areas of capillary nonperfusion (CNP) were surrounded by other capillary abnormalities and were often based on a larger retinal vessel. A satistically highly significant anatomical relationship was found between CNP and neovascularization. In addition, the frequency of neovascularization increased with the increase in size of CNP.
PURPOSE: This study investigates the effect of smoking on retinal blood flow and autoregulation in smokers with and without diabetes. METHODS: Eleven patients with diabetes mellitus and ten control subjects were investigated. Laser Doppler velocimetry and retinal photography were used to measure retinal blood flow; vascular autoregulation was assessed with 60% oxygen breathing. These procedures were performed before and after smoking. RESULTS: Both groups demonstrated a significant increase in heart rate and systolic and diastolic blood pressure (P < 0.01). In both groups, smoking caused a significant decrease in retinal blood flow: 9.6% +/- 12% in the control group (P < 0.05) and 16.4% +/- 13.8% in the diabetic group (P < 0.01). The pre-smoking oxygen reactivity was comparable in both groups (P = 0.5); 27.9% +/- 3.3% and 32.0% +/- 5.0% in the control and diabetic groups, respectively. After smoking, oxygen reactivity was reduced significantly in the control group to 9.6% +/- 4.0% (P = 0.002) and eliminated in the patients with diabetes. CONCLUSIONS: This study shows that smoking reduces retinal blood flow and the ability of the retinal vessels to autoregulate to hyperoxia; these effects are likely to be due to the vasoconstrictive effect of nicotine, which is mediated through activation of the sympathetic system. Smoking has been shown previously to increase the level of carboxyhemoglobin, thereby reducing the oxygen-carrying capacity of blood, which, when associated with the reduced blood flow shown in the current study, may reduce retinal oxygen delivery. Hypoxia is a major factor in the progression of diabetic retinopathy; therefore, smoking may exert a detrimental influence, which may be compounded further by the additional effect smoking has on autoregulation.
Our current surgical treatment for threshold retinopathy of prematurity (ROP) is based upon three concepts which emerged from morphologic and biochemical study of 250 pairs of whole eye donations obtained over a ten year period. 1) Spindle cells normally migrate and canalize to form inner retinal vessels, but when stressed, spindle cells secrete angiogenic factors. The clinical implication is that transretinal cryotherapy to the avascular retina is efficacious because it obliterates spindle cells. The number and timing of cryosessions are determined by the migration and kinetics of spindle cells. 2) Myofibroblasts originate from the shunt, are the major cellular component of extraretinal fibrovascular proliferation (EFP), and contract to produce retinal distortion and detachment. The clinical implication is that a second transretinal cryotherapy session should obliterate the shunt and the EFP, and should eliminate the source of retinal traction. 3) Anterior ocular growth occurs exponentially during the period when ROP develops and is treated. The clinical implication is that a prophylactic scleral buckle supports the fixed surface area of the developing retina while the choroid and sclera enlarge anteriorly. Retinal distortion produces misaligned photoreceptors, and retinal detachment results in rapid retinal death.
Systolic hypertension was induced in rhesus monkeys by obstructing the thoracic aorta and by ocular sympathectomy obtained with the retrobulbar injection of 6-hydroxydopamine. During the late phase of fluorescein angiography, fluorescein leaked from the choroidal circulation into the retina. The retinal vessels did not leak fluorescein. The effect was not permanent since fluorescein did not leak into the retina after the blood pressure returned to normal.
Transconjunctival cryocoagulation was performed on 38 eyes of 21 premature infants. The eyes were in stages 2-4 of retinopathy of prematurity. In stage 2 cryocoagulation was performed only if there were hemorrhages and/or a dilatation of the retinal vessels or (once) a rubeosis iridis. Cryocoagulation in stage 2, often considered superfluous, was effective in every case, but in stage 3 it was ineffective in many cases.
A diagnostic tools' set was worked out for the digital analysis of eye-fundus images; it comprises a retinophot and a digital camera adapted to it as well as a computer system and a special soft. A new mathematical model of a fragment of the ocular main microcirculation vessel and the below related global diagnostic parameters of the vascular system were elaborated: mean diameter, deviation from linearity, image acutance, fluctuations' amplitude for thickness and route, and sinuosity of thickness and route. The system of eye-fundus image processing provides for precising a nature of changes in vascular thickness along the route and for assessing the local diameter by using the vascular profile; it can also be used for determining the angle of vessels' branching. A set of expert diagnostic etalons was set up for vascular pathologies of the eye fundus and an appropriate database was created. The advantages of the designed system are: the possibility to use it comprehensively in clinical practice, less time needed to make and to analyze the eye-fundus images, a higher accuracy in determining the local vascular diameter, the possibility to perform simultaneously an analysis of diagnostic signs of retinal vessels on the basis of using a radically new approach towards assessing the vascular system ("tracing-type isolation of segments"), a higher diagnostic efficiency, the possibility to perform the differential diagnosis and the capability of preserving data without any limitations by volume and store duration time.
A 22-year-old man had X-linked retinoschisis with extensive vascular sheathing in the posterior pole and dendritic opacified retinal vessels in the periphery. Detailed fluorescein angiographic studies were performed. In the far periphery areas of capillary nonperfusion were seen. Sluggish circulation was present in the majority of dendritic opacified vessels in the areas of schisis. Late staining of the disc and posterior arteries and veins was noted. Scattered intraretinal fluorescein leakage was present even in clinically nonschitic retina, which suggests that the vascular changes may precede the retinoschisis. The patient's half-brother also had X-linked retinoschisis, but the schisis and the vascular changes were much less prominent. Although the retinal vascular changes with X-linked retinoschisis are similar to those seen with the Favre-Goldmann syndrome, a differentiation of the two diseases can be made by family studies, the presence or absence of nyctalopia, examination of the macular areas, measurement of dark adaptation, and electroretinogram determinations.
Hyperglycemia can result in key biochemical reactions that may contribute to thickening of basement membranes, dysfunction of pericytes and endothelial cells, and closure of retinal vessels. The Diabetes Control and Complications Trial has proved the value of good glycemic control in preventing retinopathy and/or delaying its progression. The primary care physician has a crucial role in translating these results into practice. Recognition and management of other risk factors, such as proteinuria, smoking, and hypertension, are easily done in the primary care setting. Also, appropriate referral to an ophthalmologist for retinal evaluation and treatment is both necessary and cost effective in reducing the burden of this devastating complication of diabetes.