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The ocular fingings in 60 patients with homozygous sickle-cell disease over the age of 40 years have been described. Peripheral retinal vessel disease was common and appeared to increase with age. Retinitis proliferans was common among older patients in the group. Angioid streaks occurred in 13 (22 per cent) patients.
PURPOSE: There are few personal reports in the literature, by knowledgeable vision scientists, of the loss of binocular vision. This case is reported. CASE REPORT: This 68 year old retired pediatric ophthalmologist suffered an almost total loss of vision, OD, as a result of a sudden massive hemorrhage into the vitreous body from a bridging retinal vessel, which remained after repair of a spontaneous large horseshoe retinal tear. This caused significant problems with both remaining monocular vision, cognition, and space perception. It was surprisingly disabling. A diary is included. RESULT: The author now appreciates better: 1. that the overlap and cross compensation of monocular vision is quite significant; 2. that monocular depth perception may be impaired by any type of intervening optical media; 3. that a two dimensional world is very different and vastly inferior to a three dimensional world. COMMENT: Such problems are not ordinarily expected or described in these circumstances, but considering what is in the literature, they may be more common and serious than assumed by eye care professionals, and should be taken into consideration in rendering eye care in similar situations. Loss of binocular vision results in a significant handicap even when the vision remaining in the good dominant eye is normal. It is truly remarkable to this victim that so many mature patients are willing to accept this situation in the form of surgical or optical monovision to avoid spectacles for presbyopia.
Diabetes mellitus often results in diabetic retinopathy caused by pathological changes of the retinal vessel tree. Early detection of these changes can delay the disease. Image processing can reduce the workload of screeners and can play a central role in quality assurance tasks. Therefore we aimed at the refinement and development of image processing algorithms to improve the quality and cost effectiveness of screening and diagnosis of diabetic retinopathy. In order to support ophthalmologists in their routine and to enable the quantitative assessment of vascular changes in colour fundus photographs a multi-resolution approach was developed which segments the vessel tree efficiently and precisely into digital images of the retina. The vessel tracker aims at determining as correctly as possible the retinal vascular network captured on a digital image irrespective of its origin. In addition to the tracker, algorithms were developed to detect the optic disk, bright lesions such as cotton wools spots, and dark lesions such as haemorrhages. The following classification of veins and arteries identifies arteries in 78.4 % and veins in 66.5% correctly. This helps selecting conspicuous images from a great number of patients.
A case of septic occlusion of the retinal vessels causing severe endophthalmitis is presented. The documentation of the retinal involvement before development of the abscess with photography and fluorescein angiography is rather exceptional. Although pars plana vitrectomy saved the eye, the vision was lost because vascular occlusion caused a retinal tear with retinal detachment.
We applied real-time laser speckle flowgraphy (RLSFG) to quantitate the choroidal circulation. RLSFG was developed utilizing the laser speckle phenomenon. A diode laser, 830 nm in wavelength, serves as the light source. The quantitative index of blood flow velocity is represented as normalized blur (NB), or square blur rate (SBR). This method was applied to the posterior fundus of monkey and human eyes. While one measurement covers a fundus area of 1 mm x 1 mm, it is possible to measure a wider fundus area by montage. The wide color maps showed the architecture of choroidal vessels. It was possible to measure the choroidal blood flow in areas free of major retinal vessels. Application of the method to 3 eyes of retinal artery occlusion and 4 eyes of geographic choroiditis showed that the obtained SBR values in normal fundus is derived 25% from the retinal and 75% from the choroidal circulation. The findings show the potential value of RLSFG in quantitating the choroidal blood flow in situ.
Diabetic retinopathy (DR) still remains the leading cause of blindness in the working population of Japan and western world, though therapies such as retinal photocoagulation and vitrectomy can be remarkably effective when administered at an appropriate stage in the disease process. Consequently, there is a need for further investigation of the pathogenesis of DR to develop better therapy. DR is characterized by gradually progressive alterations in the retinal microvasculature, leading to three fundamental morbidities: 1. vascular hyperpermeability, 2. vascular occlusion, and 3. neovascularization. Recent studies have revealed that hyperglycemia causes several metabolic disorders which cause DR directly or indirectly through the abnormal expression of cytokines including vascular endothelial growth factor (VEGF). In this study, we performed precise tests of the correlation between intraocular VEGF and the three fundamental changes in the diabetic retina mentioned above. Ultrastructural study of the human retina revealed that two major pathways are responsible for hyperpermeability of diabetic retinal vessels, i.e., intercellular or paracellular transport (opening of the tight junctions) and intracellular or transcellular transport (caveolae, intracytoplasmic vesicles, and fenestration). All these pathways were induced by intravitreal injection of VEGF. The major trigger of VEGF overexpression is tissue ischemia caused by vascular occlusion. However, the retinas from the eyes with background DR revealed increased expression of VEGF without apparent incidence of vascular occlusion. We have identified accumulation of advanced glycation end products (AGEs) in these retinas, and found that AGEs are a major stimulus for VEGF overexpression in background DR. Retinal vascular occlusion was caused by thrombus formation primarily in the capillary vessels. Thrombi mainly consisted of fibrin, platelets, and leucocytes in the early stage of their formation, and glial cells and macrophages were also involved in the later stage. The blood coagulation process plays an important role in fibrin formation in thrombi. The expression of tissue factor (TF), an initiator of extrinsic blood coagulation, was upregulated by VEGF in retinal vascular endothelial cells (REC). In addition, AGEs were also thrombogenic through the induction of TF expression and suppression of the expression of prostacyclin stimulating factor (PSF), which stimulate prostacyclin synthesis in vascular endothelial cells. These findings suggest that AGEs, VEGF, and TF could interact in a vicious circle because AGEs and VEGF could induce retinal vascular occlusion which results in further increase in VEGF expression. Intravitreal injection of VEGF could induce retinal neovascularization. VEGF stimulates vascular endothelial cell proliferation by binding to a specific receptor named kinase insert domain-containing receptor/fetal liver kinase (KDR/FIk-1, KDR). AGEs and basic fibroblast growth factor (bFGF) induced expression of KDR in REC, and a transcription factor Sp 1 was involved in this process. Since the expression of KDR as well as VEGF was already upregulated in the retinas with background DR, VEGF appeared to start to induce the proliferative changes long before the actual onset of proliferative DR. These findings indicated that VEGF and its receptor system plays a pivotal role all through the disease process of DR. We considered that amelioration of the activated VEGF and its receptor system could lead to the development of new therapy for DR. We have developed two novel methods to prevent retinal neovascularization by inhibiting VEGF and its receptor system. 1. An insulin sensitizing agent (troglitazone) inhibited proliferation, migration, and in vitro tube formation by REC as well as oxygen-induced retinal neovascularization in a mouse model. Thus, glycemic control by troglitazone could reduce the incidence of neovascularization in diabetic eyes. 2. (ABSTRACT TRUNCATED)
Injection of the KOS strain of herpes simplex virus type 1 into the anterior chamber of one eye of a BALB/c mouse produces bilateral retinal inflammation which progresses in the contralateral eye to total retinal necrosis by day 10 post-inoculation. Although both immune and direct viral cytopathic effects have been proposed as causes of the initial infiltration, the precise mechanism(s) of the contralateral retinal necrosis remains uncertain. In this study, histopathological examination of the uninoculated eyes of HSV-1 injected BALB/c mice revealed the presence of vitreous traction against the internal limiting membrane of the retina which was associated with separation of the nerve fiber layer from the underlying ganglion cell layer. This separation resulted in avulsion of Mueller cell footplates and retinal vessels, hemorrhage into the schisis cavity and disruption of the underlying retinal architecture. The schisis began focally on day 8 or 9 post-inoculation, and the entire retina of most animals was involved by day 10 or 11. These results suggest that retinal schisis involving separation of the nerve fiber layer from the ganglion cell layer contributes to necrosis of the retina in the uninoculated contralateral eye.
PURPOSE: The author studied the retinal vasculature in patients with acquired immune deficiency syndrome (AIDS) by infusion of microspheres impregnated with fluorescent dye. METHODS: Experimental study of the structural integrity of the retinal microvasculature in 14 autopsy patients with AIDS was compared with age- and gender-matched control retinas. MATERIALS: Fourteen autopsy eyes from patients with AIDS, eight autopsy eyes from immunosuppressed control patients, and four autopsy eyes from nonimmunosuppressed control patients were studied. EXPERIMENTAL METHOD: The central retinal arteries of autopsy eyes were perfused with fluorescent microspheres of 10 and 200 nm in diameter. The retinas were dissected from the eyes and viewed by fluorescence microscopy. RESULTS: Vascular breaches permeable to 200-nm microspheres were discovered in eyes from patients with AIDS. Ruptured microaneurysms were identified at the center of retinal hemorrhages in 7 of 14 eyes from patients with AIDS and 5 of 8 immunosuppressed control eyes. Leakage around microaneurysms occurred even in the absence of hemorrhage and were more frequent in eyes from patients with AIDS (11/14) than in control eyes (3/12). Cotton wool patches were surrounded by tortuous retinal vessels and microaneurysms. CONCLUSIONS: Ruptured microaneurysms are a frequent cause of retinal hemorrhage in immunosuppressed patients. Breaches in microaneurysms occur even in the absence of hemorrhage. These breaches are often at least 200 nm in diameter, a size that is permissive to capsids and virions of cytomegalovirus (CMV). Ruptured and/or leaky microaneurysms are potential sources of CMV permeation of the blood-retinal barrier. Breaches of the retinal microvasculature are not specific to patients with AIDS and occur frequently in other immunosuppressed patients.
Transport of lactic acid and other monocarboxylates such as pyruvate and the ketone bodies through cellular membranes is facilitated by specific transport proteins. We used chicken polyclonal antibodies to the monocarboxylate transporters-1 and -2 to determine their cellular and subcellular distributions in rat retina, and we compared these distributions to those of the glucose transporters-1 and -3. Monocarboxylate transporter-1 was most highly expressed by the apical processes of retinal pigment epithelium that surround the outer segments of the photoreceptor cells. In contrast to glucose transporter-1, monocarboxylate transporter-1 was not detected on the basal membranes of pigment epithelium. The luminal and abluminal endothelial plasma membranes in retina also exhibited heavy labeling by antibody to monocarboxylate transporter-1. In addition, this transporter was associated with the Müller cell microvilli, the plasma membranes of the rod inner segments, and all retinal layers between the inner and external limiting membranes. Monocarboxylate transporter-2 was found to be abundantly expressed on the inner (basal) plasma membrane of Müller cells and by glial cell processes surrounding retinal microvessels. This transporter was also present in the plexiform and nuclear layers but was not detected beyond the external limiting membrane. Recent studies have shown that lactic acid transport is of particular importance at endothelial and epithelial barriers where membranes of adjoining cells are linked by tight junctions. Our results suggest that monocarboxylate transporter-1 functions to transport lactate between the retina and the blood, both at the retinal endothelium and the pigment epithelium. The location of monocarboxylate transporter-2 on glial foot processes surrounding retinal vessels suggests that this transporter is also important in blood-retinal lactate exchange. In addition, the abundance of these transporters in Müller cells and synaptic (plexiform) layers suggests that they function in lactate exchange between neurons and glia, supporting the notion that lactate plays a key role in neural metabolism.
PURPOSE: For the first time noninvasive measurement of the myogenic response of retinal arterioles is possible by the use of the Retinal-Vessel-Analyzer (RVA). This study investigates the influence of age on retinal autoregulation. PATIENTS AND METHODS: In 40 healthy volunteers continuous measurement of a retinal arteriole over a 9-min period was performed. After a 3-min baseline measurement isometric exercise caused a rise in blood pressure of 15-30 mm Hg. During the last 3 minutes recovery was documented. Volunteers were split into a group of 20 younger (18-34 yrs.) and 20 older subjects (35-57 yrs.). For statistical analysis the Mann-Whitney test was used. RESULTS: All volunteers showed a rise in blood pressure. Significant differences in the blood-pressure rise were followed by a myogenic response of 1% up to 10% vasoconstriction. An individual autoregulation-curve was defined with negative gradient. Significant differences between the younger and the older volunteers can be identified by this methodology. CONCLUSION: Age has a significant influence on the myogenic response in human retinal arterioles. Age should be considered as a factor in clinical studies on retinal autoregulation.
A 4-year-old, neutered male domestic shorthair cat presented for evaluation of ataxia and visual deficits. Neurological examination revealed severe cerebellar ataxia with symmetrical hypermetria and spasticity, a coarse whole-body tremor, positional vertical nystagmus, and frequent loss of balance. A menace response was absent bilaterally, and the pupils were widely dilated in room light. A funduscopic examination revealed markedly attenuated to absent retinal vessels and pronounced tapetal hyperreflectivity, findings consistent with end-stage retinal degeneration. Blood work evaluation included retroviral testing, a complete blood count, serum biochemistry analysis, taurine levels, and toxoplasma immunoglobulin G and immunoglobulin M titers. All were within reference ranges. The patient was euthanized, and a necropsy was performed. Microscopically, lesions of the nervous system were confined to the cerebellum and were consistent with cerebellar cortical abiotrophy. Selective photoreceptor degeneration was seen on histopathological examination of the retina with a reduction in the number of rods and cones. The combination of clinical findings and histopathological lesions seen here has not been previously reported in the cat.
PURPOSE: A pilot study of human neural retinal transplantation was undertaken to investigate three major issues: whether a safe surgical procedure could be devised for transplantation of neural retinal tissue into the subretinal space, whether the transplant would be accepted in the subretinal space, and whether an improvement in vision could be achieved. METHODS: Eight patients with bare light perception (LP) vision due to retinitis pigmentosa (RP) and one patient with bare LP vision due to advanced neovascular age-related macular degeneration (AMD) received subretinal transplants of human fetal retinal microaggregate suspensions without postoperative systemic immunosuppression. The patient with AMD also received a fetal retinal sheet transplant. The ages of the patients ranged from 31 to 94 years (median, 55 years). The pre- and postoperative evaluations included visual function testing, detailed fundus examinations, fundus photography, fluorescein angiography, macular perimetry using a scanning laser ophthalmoscope (SLO), and full field and focal electroretinograms (ERGs). RESULTS: Three of the eight RP patients demonstrated possible improved light sensitivity during the initial months of follow-up. However, visual improvement disappeared between 3 and 13 months of follow-up. After transplantation, no subject showed any changes in the ERG recordings or SLO macular perimetry relative to their preoperative baseline. No patient experienced a retinal detachment, infection, or extensive bleeding. None of the patients developed retinal vasculitis or intraocular inflammation. In one RP patient, fluorescein angiography and fundus photography documented the formation and maturation of new host retinal vessels in the area of the transplant. CONCLUSIONS: Transplantation of fetal retinal photoreceptor suspensions into the subretinal space was achieved safely in nine subjects. Although a definite positive effect on visual function could not be demonstrated, the apparent high tolerance for graft tissue is promising for future efforts in the field of neural retinal transplantation.
Heparin-induced extracorporeal LDL precipitation (HELP) eliminates selectively fibrinogen, LDL cholesterol, cholesterol, triglycerides and LP(a) from the blood plasma using extracorporeal circulation. The reduction of fibrinogen and LDL about 50% after only one procedure immediately improves the hemorrheological situation, which has so far not been achieved by any hemorrheologically active substance. Five patients (1 central retinal vein occlusion, 3 branch vein occlusions, 1 central arterial occlusion) ranging from 59-76 years underwent HELP treatment six times over a 5-week period. After the first HELP procedure the fibrinogen was lowered from 278 +/- 57.8 to 157 +/- 22.2 mg/dl and LDL from 162.2 +/- 58 to 82.4 +/- 32.5 mg/dl. Plasma viscosity decreased from 1.3 +/- 0.07 to 1.1 +/- 0.05 mPa/s. At the end of the treatment an increase in visual acuity of 3 or more lines and an improvement in the visual field was seen in all patients. Measurements of the arteriovenous passage time with laser scan video fluorescein angiography before and at the end of the therapy showed a significant decrease from 3.5 +/- 1.59 to 2.88 +/- 1.54 s (P < 0.05) without influencing the arm-retina time. This first clinical and hemorrheological data on the HELP procedure in retinal vessel occlusion demonstrate a promising regimen in the treatment of acute retinal microcirculatory diseases.
PURPOSE: Previous studies in humans have demonstrated that oxygen (O2) reduces retinal vessel caliber and blood flow, whereas carbon dioxide (CO2) usually has opposite effects. The influence of O2 and CO2 on choroidal circulation is not fully understood, however. This study was conducted to determine the effects of systemic hyperoxia and hypercapnia on global choroidal hemodynamics, as evaluated by pulsatile ocular blood flow (POBF) tonography. METHODS: In this experiment, 16 and 22 healthy volunteers breathed 100% O2 and carbogen, respectively. POBF and intraocular pressure (IOP) were measured twice with a UK OBF tonograph for each of the following conditions: in ambient room air breathing, after breathing pure O2 or carbogen through a face mask, and in ambient room air 10 minutes after mask removal. Heart rate (HR), hemoglobin oxygen saturation level (SaO2), and systemic arterial blood pressure (BP) were monitored throughout testing. The end-tidal CO2 (EtCO2) level and respiratory rate (RR) were also recorded during carbogen breathing. RESULTS: Results revealed that HR was reduced (P<0.004) and SaO2 was increased (P = 0.0001) by both oxygen and carbogen breathing. Systemic arterial BP remained stable throughout the experiment. EtCO2 was increased during carbogen breathing (P = 0.0001), whereas RR was reduced (P = 0.0175). IOP was significantly decreased during both phases of the experiment (P = 0.0001). Finally, POBF was not altered by pure O2 breathing, but it increased on average by 7.7% during carbogen breathing (P = 0.0222). CONCLUSIONS: The data obtained with POBF tonography indicate that the choroid reacts to increased blood CO2 concentration, but not to systemic hyperoxia, in a manner similar to that in retinal and brain vessels.
I have described the vascular changes after retinal branch vein occlusion and have shown progressive changes both in the large retinal vessels and in the capillary bed. The capillary reactions are comparable to those seen in central retinal vein occlusion. Retinal oedema due to capillary dilatation and leakage occurs in both conditions but, whereas this is generalized in central retinal vein occlusion, local changes occur in branch vein occlusion. Capillary closure also occurs in both conditions, but the neovascular response differs. In branch vein occlusion significant new vessel formation is restricted to the retina leading to recurrent vitreous haemorrhage. This contrasts with central retinal vein occlusion in which thrombotic glaucoma due to predominantly anterior segment neovascularization is the most serious cause of visual loss.
Rat retinae were dissociated to yield intact microvessels 7 to 42 microm in diameter. These were loaded with fura-2 AM and single fragments anchored down in a recording bath. Intracellular Ca(2+) levels from 20- to 30-microm sections of vessel were estimated by microfluorimetry. The vessels studied were identified as metarterioles and arterioles. Only the microvascular smooth muscle cells loaded with fura-2 AM and changes in the fluorescence signal were confined to these cells: Endothelial cells did not make any contribution to the fluorescence signal nor did they contribute to the actions of the drugs. Caffeine (10 mM) or elevated K(+) (100 mM) produced a transient rise in cell Ca(2+) in the larger vessels (diameters >18 microm) but had no effect on smaller vessels (diameters <18 microm). Rises in cell Ca(2+) were accompanied by a rapid ( approximately 2 s to peak) contraction followed by relaxation. Caffeine and K(+) responses were blocked by ryanodine (10 microM) and nifedipine (1 microM), respectively. In all the vessels tested, vasopressin (arginine, 10 nM) elicited a transient increase in cell Ca(2+) and a constriction, irrespective of the diameter of the vessel. All vessels tested also responded to endothelin-1 (1-10 nM) through an Et(A) receptor to produce a transient rise in cell Ca(2+) followed by a plateau phase of elevated Ca(2+) and a constriction. In contrast to the transient effects of vasopressin, caffeine, and K(+), the cell Ca(2+) remained elevated (>30 min) on washing out the endothelin and the vessel failed to relax. These results demonstrate heterogeneity between smaller and larger retinal vessels with regard to Ca(2+) mobilisation and homogeneity with respect to the actions of vasoactive peptides.
Early electrophysiological changes following acute retinal ischaemia were studied by recording single or multiunit retinal ganglion cells and the electroretinogram (ERG) in barbiturate anaesthetized cats. Retinal ischaemia was initiated photochemically by platelet aggregation in retinal vessels which had been irradiated with monochromatic green light following an intravenous injection of Rose Bengal dye. No physiologically active ganglion cells were found within, or close to, the irradiated sites with chorioretinal oedema. On the other hand, in the areas 5-20 degrees away from the irradiation sites, ganglion cells had abnormally raised spontaneous (background) firing which obscured visually driven firing. The retinal areas where no physiologically active ganglion cells were found showed histopathological changes which are similar to those described for glutamate-induced retinal damage. Retinal areas where depolarized retinal ganglion cells were located, however, showed only minor vacuolation of the ganglion cell fibre layer. Early global electrophysiological changes following photochemically induced retinal vascular lesion were consistent with those predicted from the findings in the single cell study. Vascular lesions produced with high irradiation energy (10-30 J), which promote extensive chorioretinal oedema, resulted in gradual loss of visually responsive ganglion cells. Lesions produced by low-energy irradiation (2 J), causing slight narrowing of the blood columns in the vessels, on the other hand, resulted in significant increases in the amplitude and the implicit time of the ERG b-wave and the background firing of multiunit retinal ganglion cells. Electrophysiological changes associated with mild retinal ischaemia are analogous to physiological effects associated with exogenous glutamate or blockade of glutamate uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
Retinal vessel changes were experimentally investigated by a combination of color fundus photography, fluorescein angiography, and histologic studies in beagles that were fed a 30% galactose diet for up to 66 months. Previously, we have described the appearance of pericyte ghosts, microaneurysms, acellular capillaries, and intraretinal hemorrhages in dogs fed a galactose diet for up to 36 months. These disorders were similar to those observed in humans with background diabetic retinopathy. We report herein that dogs fed galactose for 48 to 60 months experience retinal changes associated with the chronic occlusion of capillary beds and subsequent ischemia of the retina. These changes included the appearance of broad areas of nonperfusion, soft exudates (cytoid bodies), intraretinal microvascular abnormalities, occluded arterioles, preretinal and intravitreal hemorrhages, and apparent new vessel growth around the optic disc. The present study clearly demonstrates that the galactose-fed dog is an animal model in which advanced retinal changes develop, and these changes are similar to those associated with preproliferative human diabetic retinopathy.