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The blood vessels that nourish the inner retina cast shadows on photoreceptors, creating "angioscotomas" in the visual field. We have found the representations of angioscotomas in striate cortex of the squirrel monkey. They were detected in 9 of 12 normal adult animals by staining flatmounts for cytochrome oxidase activity after enucleation of one eye. They appeared as thin profiles in layer 4C radiating from the blind spot representation. Angioscotomas can be regarded as a local form of amblyopia. After birth, when light strikes the retina, photoreceptors beneath blood vessels are denied normal visual stimulation. This deprivation induces remodeling of geniculocortical afferents in a distribution that corresponds to the retinal vascular tree. Angioscotoma representations were most obvious in monkeys with fine ocular dominance columns and were invisible in monkeys with large, well segregated columns. In monkeys without columns, their width corresponded faithfully to the inducing retinal shadow, making it possible to calculate the minimum shadow required to produce a cortical representation. The "amblyogenic threshold" was calculated as the fraction of the pupil area eclipsed to trigger remodeling of geniculocortical afferents. It was found to be constant over retinal eccentricity, vessel size, and shadow size. Ambliogenic shadows only three to four cones wide were sufficient to generate a cortical representation, testifying to the remarkable precision of the cortical map. The representations of retinal blood vessels separated by only 0.65 degrees were resolvable in the cortex, yielding an upper limit on cortical resolution of 340 microm in layer 4C.
OBJECTIVE: To validate a computer-based method for measuring the calibre of retinal blood vessels, and use it to determine the effects of ageing and arterial hypertension on the calibres of these vessels and on their ratio. METHODS: Digital eye fundus images covering a 50 degrees field and centred on the optic disc were obtained using a 540 nm filter. The boundaries of blood vessels crossing a series of circles concentric with the optic disc were located by an image analysis program; the calibres of vessels crossing the circles perpendicularly were determined automatically, the average arteriole and average vein calibres were calculated, and the arteriovenous ratio (AVR) was calculated as the ratio of these averages. The within-operator, between-operator and within-eye reliability of this method was investigated using images of 30 or 40 eyes; the effects of ageing on average vessel calibres and AVR using both eyes of each of 120 normotensive volunteers aged 10-69 years (60 males, 60 females); and the effects of arterial hypertension using a group of 54 hypertensive patients aged 50.9 +/- 13.9 years. RESULTS: Within-operator, between-operator and within-eye correlation coefficients for AVR were all better than 0.95, and the corresponding coefficients of variation were all better than 3%. The results of Bland Altman approach show a very good agreement. There were no significant differences between right and left eyes or between the sexes in either the normotensive or the hypertensive group. In the normotensive group, vein calibre was almost constant (111 +/- 6 microm), but arteriole calibre and AVR fell significantly from 96 +/- 6 microm and 0.870 +/- 0.046, respectively, in the second decade of life to 85 +/- 4 microm and 0.761 +/- 0.044 in the seventh decade. Arterial hypertension was not associated with changes in vein calibre, but was associated with decreases in arteriole calibre (from 91 +/- 7 microm among normotensive individuals to 84 +/- 2 microm) and AVR (from 0.816 +/- 0.056 to 0.755 +/- 0.027). Age significantly modulated the AVR-reducing influence of hypertension (P = 0.003). CONCLUSION: The proposed method of measuring retinal blood vessel calibres is reliable and precise (especially for the AVR). In this study, its results confirmed that increasing age and arterial hypertension are both associated with reductions in retinal arteriole calibre and AVR.
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PURPOSE: Several studies have investigated the changes in retinal vessel diameter during physiological stress or pathologic conditions. These studies were principally based on individual fundus photographs and as such did not allow the evaluation of vessel dynamics over time. The research objective was to detail the time course and amplitude changes in the diameter of arteries and veins across all retinal quadrants, during and after hyperoxic vascular stress. METHODS: The dynamics of changes in retinal vessel diameter were quantified with a retinal vessel analyzer, which digitizes fundus images in real time and simultaneously quantifies vessel diameter. The arterial and venous diameters within one disc diameter of the optic nerve head in each quadrant were studied. Twenty young adults participated in this study in which the vessel diameters were measured during successive phases of breathing either room air or pure oxygen. The oxygen saturation level (SaO(2)), end-tidal carbon dioxide (EtCO(2)), pulse rate (PR), respiratory rate (RR), and blood pressure (BP) were also monitored throughout testing. RESULTS: Breathing 100% O(2) caused an increase in SaO(2) and a decrease in the EtCO(2). All other systemic parameters measured (PR, RR, BP, and ocular perfusion pressure [OPP]) remained unchanged. However, the retinal veins and arteries constricted by approximately 14% and approximately 9% respectively, in all retinal quadrants. After experimental hyperoxia, inhalation of room air was associated with a progressive increase in the caliber of vessels toward their pretest size. The amplitude and overall profile of vessel reactivity to and recovery from hyperoxia was the same across retinal quadrants. CONCLUSIONS: These data indicate that, during systemic hyperoxic stress, the retinal vessels change in caliber uniformly across retinal quadrants in healthy young adults. This type of physiological vascular provocation could be used to investigate the quality of vascular regulation during aging and in vascular diseases of the eye.
BACKGROUND: Indocyanine green (ICG) angiography has been used to evaluate posterior uveitis in the clinical setting, despite the shortage of data on possible pathological correlates of observed findings. METHODS: We used both ICG angiography and fluorescein angiography to examine rats that developed a mild form of experimental autoimmune uveoretinitis (EAU) induced by immunization with interphotoreceptor retinoid-binding protein (IRBP). Angiography was performed on days 9, 10, 11 and 23 after IRBP immunization, and freshly enucleated eyes obtained on the same days were examined histopathologically by light microscopy and transmission electron microscopy. RESULTS: Diffuse dilatation and tortuosity of the retinal vessels was observed by both ICG and fluorescein angiography, with leakage from these vessels in focal areas in the periphery. In addition, deep hyperfluorescent spots in the central posterior pole, not associated with retinal vessels, were observed by ICG angiography only. These corresponded to Dalen-Fuchs-like nodules on funduscopy. On histopathological examination, eyes showed inflammatory cell infiltration around retinal vessels, disorganization of outer retinal layers, focal subretinal accumulations of cells (resembling Dalen-Fuchs nodules), and diffuse inflammatory cell infiltration in the choroid. Ultrastructural examination of a Dalen-Fuchs-like nodule revealed a mound of monocytes, appearing to contain phagosomes of lipofuscin and phospholipids, sandwiched between transformed retinal pigment epithelium (RPE) cells with disrupted apical processes and loss of basal interdigitation. CONCLUSION: These results suggest that ICG angiography may be useful in delineating certain abnormalities at the level of the RPE, in association with posterior ocular inflammation, that cannot be observed by fluorescein angiography alone.
The retinal vessel calibre responses to controlled stimulation of the autonomic nervous system were studied in 10 healthy subjects, using sustained isometric muscle contraction as stimulus. Each subject was studied twice using different mydriatic agents, (1) g.tropicamide 1% a parasympatholytic agent and (2) g. phenylephrine 10% a sympathetic agonist. In the tropicamide study, there was a mean arteriolar constriction of 8.1% (SEM 1.67, p less than 0.001) and venule constriction of 3.7% (SEM 0.85, p less than 0.001) with a mean rise in diastolic blood pressure of 27.4 mmHg (SEM 2.95, range: 13-45 mmHg). When g. phenylephrine 10% was used, there was a mean arteriolar constriction of 8.6% (SEM 1.68, p less than 0.001) and venule constriction of 4.8% (SEM 1.22, p less than 0.001) with a mean rise in diastolic blood pressure of 29.2 mmHg (SEM 2.56, range: 17-44 mmHg). There was no significant difference in retinal vessel calibre in the recovery phase compared to baseline phase (p greater than 0.05) or between the two mydriatic agents on vessel responses (p greater than 0.05). There was no correlation between the rise in diastolic blood pressure and the degree of retinal vessel constriction, during handgrip contraction in either study. This study has demonstrated a significant association between retinal vessel calibre and systemic autonomic nerve stimulation. The possible mechanisms for the retinal vessel constriction observed in this study are discussed.
The fetal alcohol syndrome (FAS) occurs in children born by alcoholic mothers. The syndrome consists of growth deficiency of prenatal onset, central nervous system effects with retarded mental and motor development and malformations of various organs, the most striking being the facial abnormities. There is a small head circumference and midfacial deformities. Typical eye features are telecanthus, epicanthus, short palpebral fissures, a flat nose bridge, ptosis, microphthalmus and strabismus. 30 children with FAS were examined for defects of the inner parts of the eyes. Malformations of the optic discs and retinal vessels were the most frequent findings, occurring in 16 children. Another five children had borderline findings. Nine had bilateral hypoplasia of the optic discs, eight of them also with changes of the retinal vessels, most often increased tortuousity. Four children showed bilateral optic atrophy. One of them also had highly tortuous retinal vessels. One girl had very tortuous retinal vessels without other findings in her fundi. One boy had pronounced malformations of both eyebulbs and another boy had bilateral changes of his eyeground structures. Various intraocular malformations were observed in 53% of the children with FAS.
PURPOSE: To evaluate whether the position of the central retinal vessel trunk exit on the lamina cribrosa spatially correlates with the location of parapapillary atrophy in glaucoma. METHODS: Color stereo optic disc photographs of 79 patients with primary or secondary open-angle glaucoma and 53 normal subjects were morphometrically evaluated. We determined the position of the central retinal vessel trunk exit on the lamina cribrosa surface and measured the area of parapapillary atrophy in four 90 degrees quadrants. RESULTS: After correction for normal values, the beta zone area of parapapillary atrophy in the glaucoma eyes was significantly larger, when measured in the disc quadrant most distant to the central retinal vessel trunk exit than as if measured in the quadrant containing the vessel trunk exit. CONCLUSIONS: Position of the central retinal vessel trunk exit on the lamina cribrosa influences the location of parapapillary atrophy in glaucoma. The longer the distance to the central retinal vessel trunk exit, the more enlarged is parapapillary atrophy.
OBJECTIVES: To investigate the morphological changes of retinal microcirculation in streptozotocin (STZ)-diabetic rats and the contribution of leukocyte to diabetic retinopathy (DR). METHODS: 12 male Wistar rats were randomly divided into normal control group, 3 month group and 6 month group of STZ-diabetic rats. Each group was perfused with 4% paraformaldehyde and fixed. Rat retina digest preparations were observed by light microscope, and the number of pericyte was counted. RESULTS: The decrease of pericytes in STZ-diabetic rats was remarkable compared with that of normal control at 6 months. At 6 months, STZ-diabetic rat retinal digest preparations showed that some of the capillaries were blocked by leukocytes. CONCLUSIONS: After injection of STZ in rats for 6 months, early morphological changes of DR were observed, and leukocytes played a potential role in the pathogenesis of DR.
We studied the distribution pattern of sodium fluorescein in human eyes microscopically. The ciliary body showed early and diffuse leakage, with staining of the basement membrane of the nonpigmented ciliary epithelium, indicating movement of fluorescein from the ciliary body into the aqueous humor. After five minutes the iris stroma stained with fluorescein, probably from the aqueous humor. The retinal vessels and retinal pigment epithelium were impermeable to fluorescein. Corresponding to the background fluorescence seen in fluorescein angiography, fluorescence was present in Bruch's membrane and in the stroma of the inner one third of the choroid. Drusen stained most intensely in areas of greatest PAS positively. Early fluorescence of the optic disk was the result of intravascular perfusion of the dye. Minimal diffusion of fluorescein from the fenestrated choroidal vessels across the border tissue of Elschnig into the peripheral optic nerve bundles was observed. Late fluorescene of the optic disk was due mainly to fluorescein staining of the lamina scleralis and glial columns.
We examined eight members of three generations of a family with a history of hereditary retinal degenerative disease. Four affected members have multiple whitish retinal dots resembling snowflakes. Other positive ocular findings in the four members with retinal flakes include myopia, cataract, fibrillary vitreous degeneration with occasional strands, attenuated retinal arterioles, sheathed retinal vessels, occlusion of small retinal vessels, white with and without pressure, annular macular pigment defects, and occasional spicules of pigment. Goldmann perimetry showed irregular annular scotomas in three patients. Electroretinographic response was extinguished in one and subnormal in three. Electro-oculography showed the light rise-to-dark trough ratio to be decreased in the affected patients. Based on results of vitreoretinal biomicroscopy, Goldmann perimetry, and visual electrodiagnostic testing, we suspect that snowflake degeneration may be just a variant of retinitis pigmentosa.
PURPOSE: Previous results suggest that retinal neurons are infected early during murine cytomegalovirus (MCMV) infection of the inner retina. The purposes of this study were to identify which retinal neurons are infected and to determine the routes by which MCMV spreads in the retina. METHODS: Immunosuppressed (IS) BALB/c mice were inoculated with 5 x 10(3) PFU of MCMV (k181) through the supraciliary route. Injected eyes were collected at several times after inoculation, sectioned, and examined by electron microscopy and by staining for retinal cell antigens and for MCMV early (EA) or late (LA) antigen. RESULTS: MCMV-infected cells were observed in the choroid and RPE by day 3 after infection (PI) and in the inner retina beginning at day 5 PI. At this time, many horizontal and bipolar cells were MCMV-antigen-positive but only rare MCMV-infected amacrine cells (glycine positive or gamma-aminobutyric acid [GABA] positive) or MCMV-infected ganglion cells (NF positive) were observed in the inner retina. At day 10 PI, most virus-infected cells were glial fibrillary acidic protein (GFAP)- and GABA-positive glia. Virions were observed by electron microscopy in the choroid, RPE, and inner nuclear layer of the retina. Although virions were observed in the endothelium of the retinal vessels and the nearby retinal cells, the endothelial cell lining of the retinal vessels remained intact. Both apoptotic cells and necrotic cells were seen in the inner retina. CONCLUSIONS: In the inner retina, horizontal and bipolar cells were the early (< or = day 7 PI) targets of MCMV infection. Virus spread from the RPE and the photoreceptor layer to the inner retina through infected Muller cells and within the inner retina horizontally through infected horizontal cells.
Vitreous haemorrhage can be caused by a disruption of normal retinal vessels, bleeding from diseased retinal vessels, bleeding from abnormal new vessels or extension of haemorrhage through the retina from other sources. In the elderly, vitreous haemorrhage usually occurs spontaneously and only occurs occasionally as a result of trauma. Appropriate management of vitreous haemorrhage is dependent on the most likely cause in a particular patient. As always, an accurate medical history with a careful clinical examination, static and dynamic ultrasonography performed by an experienced examiner, results of other laboratory tests and an understanding of the common causes of vitreous haemorrhage in each age group is essential to come to a 'best guess' diagnosis as to the cause of the vitreous haemorrhage and thus guide the physician toward the appropriate management. Immediate surgical removal of blood if indicated, as well as improving the vision gives the added benefit of allowing a full examination of the underlying retina. For those in whom surgical removal of blood is not recommended, a careful and frequent follow-up with serial B-scan ultrasound allows the 'best guess' diagnosis to be confirmed at each visit, until such time as the vitreous haemorrhage resolves sufficiently to allow a full and proper examination of the retina. Where there is a confirmed retinal tear, retinal detachment or other fundal pathology these are treated appropriately with laser or surgery (vitrectomy). Preventative measures are dependent on the underlying cause of vitreous haemorrhage. Some of the underlying causes such as posterior vitreous detachment cannot be prevented. In others, such as retinal vein occlusion, measures may need to be taken so as to reduce the risk of a similar event in the same or fellow eye and to reduce the risk of potentially life-threatening associated systemic conditions such as a stroke or myocardial infarction.
Acute hypertension, induced either by intravenous injection of metaraminol bitartrate (Aramine), infusion of isotonic saline into the common carotid artery, or a combination of both procedures did not in the rhesus monkey lead to breakdown of the blood-retinal barrier. Whereas the cerebral vasculature was made permeable to blood-borne dye at carotid pressure above 160 mm Hg, the retinal blood vessels were intact even at pressures as high as 310 mm Hg. Hypertensive blood-brain barrier opening was associated with neurologic defects and brain edema. The results indicate that the retina is more resistant to acute hypertension than is the brain. The greater resistance in the retina may be due to the high number of contractile, perivascular mural cells counteracting increased intravascular hydrostatic pressure. An alternative or supplementary explanation is that choroidal and retinal blood vessels are better protected from surges in blood pressure than are brain blood vessels. Differences between the innervation of brain and ocular blood vessels could account for this.
Two (5.4%) of 37 patients with retinopathy of prematurity were noted to have zone I vascularization of the retina in at least one eye. Three eyes in the two patients showed plus disease with nonflorid stage 3 ridge formation and extraretinal fibrovascular proliferation. Two of the three eyes were not treated and rapidly progressed to total retinal detachment and blindness. The third eye was treated with cryotherapy and this was followed by resolution of the plus disease. Although the treated eye did not develop dragging of the retinal vessels or retinal detachment, it is unfortunately blind.