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At least 19 recordsLinked to original sources

Occult choroidal neovascularization. Influence on visual outcome in patients with age-related macular degeneration. Macular Photocoagulation Study Group.

OBJECTIVE: To determine whether the presence of occult choroidal neovascularization (CNV) influenced the anatomic and visual acuity outcomes in a randomized clinical trial of krypton red laser photocoagulation to treat juxtafoveal neovascular lesions in age-related macular degeneration. DESIGN, SETTING, AND PATIENTS: The fluorescein angiograms obtained at the baseline examination at tertiary retinal referral centers between April 1, 1981, and December 31, 1987, as part of the Macular Photocoagulation Study (MPS) Age-Related Macular Degeneration Study-Krypton Laser were evaluated retrospectively at the MPS Fundus Photograph Reading Center by two senior readers independently (with open adjudication of any differences) from 1992 to 1994. Criteria for classifying classic and occult CNV by the MPS Group were established in 1989, 2 years after the last patient had been assigned randomly to treatment or observation in the krypton laser study. MAIN OUTCOME MEASURES: Treatment coverage of classic and occult CNV, persistent CNV, recurrent CNV, and visual acuity from scheduled follow-up examinations for up to 5 years were analyzed for the absence or presence of occult CNV at baseline. RESULTS: The number of eyes with classic CNV but not occult CNV, classic and occult CNV, and occult CNV but no classic CNV were almost identical for the eyes assigned randomly to treatment or observation. Classic CNV almost always was covered completely with intense laser treatment; nevertheless, recurrent CNV developed in more than half of these eyes within 1 year after initial laser treatment. In contrast, in more than half of the eyes with occult CNV, more than 50% of the occult CNV was not covered with heavy laser treatment. Laser treatment was clearly beneficial for eyes with classic CNV but no occult CNV and almost equivalent to no treatment for eyes with classic and occult CNV. The few eyes with occult CNV but no classic CNV precluded conclusions about the value of treatment in this subgroup. CONCLUSIONS: These results strengthen previous reports that laser treatment is beneficial for eyes with juxtafoveal choroidal neovascular lesions when classic CNV is present, even though CNV often recurs. Treatment of classic CNV alone in eyes with classic and occult CNV was not beneficial in this study. Distinguishing classic CNV from occult CNV can aid in the selection of patients who will benefit most from laser treatment.

Adult↗

Risk factors for choroidal neovascularization in the second eye of patients with juxtafoveal or subfoveal choroidal neovascularization secondary to age-related macular degeneration. Macular Photocoagulation Study Group.

OBJECTIVES: To verify and quantify previously reported risk factors for development of choroidal neovascularization (CNV) in the fellow eye of patients with 1 eye affected with CNV secondary to age-related macular degeneration, to examine the value of characteristics of the pericentral macula in the quantification of risk for developing CNV, and to explore whether the presence of occult CNV in the first eye affects the development of CNV in the fellow eye. DESIGN, PATIENTS, AND SETTING: Follow-up study of fellow eyes of 670 patients enrolled in multicenter, randomized clinical trials of laser photocoagulation of juxtafoveal or subfoveal CNV. MAIN OUTCOME MEASURE: Development of CNV. RESULTS: Three characteristics of the central macula of the fellow eye and 1 systemic factor were associated independently with an increased risk of developing CNV: the presence of 5 or more drusen (relative risk, 2.1; 95% confidence interval, 1.3-3.5), focal hyperpigmentation (relative risk, 2.0; 95% confidence interval, 1.4-2.9), 1 or more large drusen (relative risk, 1.5; 95% confidence interval 1.0-2.2), and definite systemic hypertension (relative risk, 1.7; 95% confidence interval, 1.2-2.4). Estimated 5-year incidence rates ranged from 7% for the subgroup with no risk factors to 87% for the subgroup with all 4 risk factors. Characteristics of the pericentral macula were not strongly associated with the development of CNV. The presence of occult CNV in the first eye affected had no influence on the development of CNV or on the type of CNV in the fellow eye. CONCLUSIONS: The prognosis of the fellow eye is affected strongly by characteristics of its central macula and by systemic hypertension. These factors should be considered when counseling patients with unilateral neovascular age-related macular degeneration and when targeting patients for preventive interventions.

Aged↗

Age-related macular degeneration. Macular changes, prevalence and sex ratio. An epidemiological study of 1000 aged individuals.

An epidemiological ophthalmic investigation of 1000 individuals aged 60-80 years disclosed age-related macular degeneration (AMD), i.e. macular changes causing visual impairment in at least one eye with a prevalence of 12.2% of 924 individuals with both maculae examined. The prevalence increased with rising age for both sexes: age group 60-64 years: 2.3%, 65-69: 5.9%, 70-74: 12.1% and 75-80: 27.3%. No significant differences in prevalence rates of AMD were demonstrated between males and females in the respective age groups. About one half of the persons with AMD were affected in both eyes. No differences of AMD were found between right and left eyes. Findings of age related macular changes without visual impairment (AMCW) compared to AMD revealed far higher prevalences in the sixties and a smaller rise in the seventies (age group percentage in both sexes: 12.3, 18.0, 17.0 and 17.8%). No systematic prevalence differences were demonstrated between sexes. The collected data of AMD and AMCW might indicate a shift from AMCW to AMD in women, particularly aged 70-74 years and in men, particularly aged 75-80 years. Macular changes in total (AMD + AMCW) was found in 28.5% of the population (age group percentage 14.6, 23.8, 29.0 and 45.0%). No sex differences were found.

Age Factors↗

Foveal cone electroretinograms in strabismic amblyopia: comparison with juvenile macular degeneration, macular scars, and optic atrophy.

A hand-held stimulator-ophthalmoscope was used to elicit foveal cone electroretinograms (ERGs) from fifteen patients with strabismic amblyopia. The ERGs were in response to a 4 degrees stimulus visualized on the fundus and centred on the fovea throughout testing. Foveal cone ERGs from amblyopic eyes were normal in amplitude and normal in b-wave implicit time. Interocular differences in ERGs in patients with amblyopia were no greater than those in normal subjects. Patients with comparable visual acuity loss due to macular scars or juvenile hereditary macular degeneration had abnormal foveal cone ERGs, while patients with optic atrophy had normal responses. These findings support the idea that the defect in strabismic amblyopia does not involve a functional abnormality in the fovea distal to the ganglion cell layer.

Adolescent↗

Persistent and recurrent neovascularization after krypton laser photocoagulation for neovascular lesions of age-related macular degeneration. Macular Photocoagulation Study Group.

The persistence and recurrence of choroidal neovascularization after initial treatment with laser photocoagulation have been shown to be major contributors to loss of visual acuity. The 247 eyes assigned to krypton red laser photocoagulation in the Age-Related Macular Degeneration Study-Krypton Laser were examined to describe the incidence, timing, visual impact, and potential risk factors for persistence and recurrence. Persistent neovascularization detected within 6 weeks of initial treatment was observed in 32% of treated eyes, and recurrent neovascularization was estimated by life-table methods to develop in an additional 47% over a 5-year period. Both persistence and recurrence were accompanied by an increased frequency of severe visual loss. The persistence rate among eyes having 10% or more of the foveal side of the neovascular membrane not covered by treatment was twice as high as in eyes having more extensive coverage. Patients having a fellow eye with a neovascular membrane or scar, a fellow eye with 20 or more drusen in the central macula, or a fellow eye with nongeographic atrophy at initial visit had more recurrences than patients without these characteristics. Ophthalmologists treating similar lesions may be able to reduce persistent neovascularization and the associated visual loss by covering the entire lesion with treatment.

Age Factors↗

Persistent and recurrent neovascularization after laser photocoagulation for subfoveal choroidal neovascularization of age-related macular degeneration. Macular Photocoagulation Study Group.

OBJECTIVE: To determine the incidence and visual impact of and risk factors for persistent and recurrent neovascularization after laser photocoagulation of subfoveal choroidal neovascularization (CNV) in patients with age-related macular degeneration. DESIGN, PATIENTS, AND METHODS: The records of 189 eyes in the Subfoveal New CNV Study and 100 eyes in the Subfoveal Recurrent CNV Study assigned to laser photocoagulation were examined. Persistent CNV (detected within 6 weeks of treatment) and recurrent CNV (detected after 6 weeks) were defined angiographically by fluorescein leakage from the periphery of the treatment scar. Incidence was estimated using survival analysis methods. RESULTS: In both studies, persistent CNV was observed in approximately 13% of the eyes, and recurrent CNV was estimated to have developed by 3 years in an additional 35% of the eyes. In the New CNV Study, by 3 years, 36% of the eyes with persistent CNV had lost 6 or more lines of visual acuity as had 19% of the eyes with recurrent CNV and 27% of the eyes without persistence or recurrence. The presence of neovascular maculopathy in the fellow eye was associated with an increased risk for persistence or recurrence in the study eye. In the New CNV Study, partial coverage of the lesion with heavy laser treatment and/or runoff was associated with increased risk for persistence; less extensive natural scarring of the lesion at study entry was associated with increased risk for recurrence. CONCLUSIONS: Close to half of the eyes treated for subfoveal CNV have persistent or recurrent CNV within 3 years. There is a strong association between neovascular maculopathy in the fellow eye and the inability of laser photocoagulation to permanently obliterate signs of CNV from the study eye. Within these two studies, there was little additional damage to visual function resulting from persistent or recurrent neovascularization. There appears to be no reason to deviate from the protocol goal of covering the entire neovascular complex when treating eyes with subfoveal CNV.

Aged↗

Loculated fluid. A previously undescribed fluorescein angiographic finding in choroidal neovascularization associated with macular degeneration. Macular Photocoagulation Study Reading Center.

The Foveal Photocoagulation Study, a component of the Macular Photocoagulation Study, is designed to evaluate whether laser treatment can reduce the risk of severe visual loss in eyes with well-defined choroidal neovascular membranes associated with macular degeneration that extend through the foveal center. On one third of the 554 baseline angiograms of study patients enrolled in and whose eyes were graded in the study as of January 31, 1990, the Reading Center staff has noted an unusual pattern of hyperfluorescence in the late-transit frames that has not been described previously. This pattern, which we call "loculated fluid," consists of a well-demarcated area of hyperfluorescence that appears to represent pooling of fluorescein in a compartmentalized space anterior to the choroidal neovascular leakage. Although the loculated fluid may conform to a pattern of typical cystoid macular edema, it can also pool within an area deep to the sensory retina in a shape that does not bear any resemblance to cystoid macular edema. This pattern is important to recognize because it (1) should not be confused with the angiographic pattern or extent of choroidal neovascularization and (2) should be differentiated from a serous detachment or tear of the retinal pigment epithelium.

Body Fluids↗

Age-related macular degeneration.

Macular degeneration is now responsible for approximately 95% of blindness and partial sighted registrations in the UK. This review has been written specifically to make the general medical community of the UK aware of the prevalence and clinical manifestations of aged-related macular degeneration. The review encompasses the risk factors, the disabilities and problems experienced by suffers of the condition and current therapeutic options. Age related macular degeneration increases in prevalence in our community from 0% among people under 55 years old to 18.5% among those 85 years or older. There is a marked female preponderance. The exudative form of the disorder is commoner. Treatment remains supportive for most patients with macular degeneration although a minority will benefit from macular laser photocoagulation.

Aged↗

Oral zinc in macular degeneration.

Macular degeneration associated with age and drusen, an important cause of severe visual loss in older persons, is of unknown cause. The sensory retina and retinal pigment epithelium, which are cell layers in zinc, appear to be prominently involved in the disease process. Because zinc plays a role in the metabolic function of several important enzymes in the chorioretinal complex, we undertook a prospective, randomized, double-masked, placebo-controlled investigation of the effects of oral zinc administration on the visual acuity outcome in 151 subjects with drusen or macular degeneration. Although some eyes in the zinc-treated group lost vision, this group had significantly less visual loss than the placebo group after a follow-up of 12 to 24 months. This is the first controlled oral intervention study to show a positive, if limited, treatment effect in macular degeneration, a major public health problem. Because of the pilot nature of the study and the possible toxic effects and complications of oral zinc administration, widespread use of zinc in macular degeneration is not now warranted.

Administration, Oral↗

Molecular genetics of macular degeneration.

Macular degeneration is a leading cause of blindness that affects the aged population. The complexity of the molecular basis of macular disease is now beginning to be elucidated with the identification of disease-causing genes. For example, mutations in the ABCR gene, (recently identified in cones as well) which codes for retinal rod-specific ABCR protein is responsible for Stargardt macular dystrophy/fundus flavimaculatus, an autosomal recessive macular dystrophy with juvenile onset, which accounts for 7% of human retinal degenerative diseases. The gene mutant in X-linked juvenile retinoschisis, XLRS1, is the first macular dystrophy gene to be isolated by positional cloning. Mutations in the peripherin/RDS gene have been shown to be associated with a variety of distinct forms of macular degenerations. The tissue inhibitor of metalloproteinase 3 (TIMP3) is implicated in autosomal dominant Sorsby fundus dystrophy. Best vitelliform macular dystrophy was mapped to 11q12-q13. The cloned gene product is the protein bestrophin, which is a retinal specific gene expressed in the RPE and possibly involved in the metabolism and transport of polyunsaturated fatty acids. The cloning of genes for rare heritable forms of macular degeneration will increase our understanding of the basic pathogenesis of the disease process. In the future this should also allow us to test the hypothesis that the coincidence of subclinical mutations in a number of genes involved in the formation and function of the macula can be responsible for cases of age-related macula-degeneration which is by far the most common form of these macular disorders.

Eye Proteins↗

Macular degeneration.

Macular degeneration is a term that describes a large group of conditions that are collectively the most common cause of irreversible vision loss in the developed world. Approximately one in three people will be affected to some degree by the time they reach 75 years of age. Many forms of macular degeneration have a significant genetic component, and a large amount of progress has recently been made in understanding the genes involved. In the future, genetic testing may allow specific preventive treatments to be delivered to individuals at risk, decades before the disease would ordinarily become manifest.

Age Factors↗

Reorganization of visual processing in macular degeneration.

Macular degeneration (MD), the leading cause of visual impairment in the developed world, damages the central retina, often obliterating foveal vision and severely disrupting everyday tasks such as reading, driving, and face recognition. In such cases, the macular damage eliminates the normal retinal input to a large region of visual cortex, comprising tens of square centimeters of surface area in each hemisphere, which is normally responsive only to foveal stimuli. Using functional magnetic resonance imaging, we asked whether this deprived cortex simply becomes inactive in subjects with MD, or whether it takes on new functional properties. In two adult MD subjects with extensive bilateral central retinal lesions, we found that parts of visual cortex (including primary visual cortex) that normally respond only to central visual stimuli are strongly activated by peripheral stimuli. Such activation was not observed (1) with visual stimuli presented to the position of the former fovea and (2) in control subjects with visual stimuli presented to corresponding parts of peripheral retina. These results demonstrate large-scale reorganization of visual processing in MD and will likely prove important in any effort to develop new strategies for rehabilitation of MD subjects.

Fovea Centralis↗

Defective cone photoreceptor cytoskeleton, alignment, feedback, and energetics can lead to energy depletion in macular degeneration.

Macular degeneration (MD) is a puzzling disease characterized by disturbance, and then complete loss, of fine detailed vision in the central macular region of the human retina, as a result of disturbed function and then death of photoreceptor cells. This review describes a possible pathomechanism for MD that involves a causal relationship between mutated genes, altered photoreceptor cytoskeletal proteins, defective cone photoreceptor alignment, and disturbed visual feedback mechanisms that leads to energy depletion and apoptosis of macular cone photoreceptors. MD may be associated with mutations in genes encoding certain photoreceptor proteins (ATP-binding cassette transporter retina, retinitis pigmentosa GTPase regulator, retinal degeneration slow/peripherin) that are components of, or interact with, microtubule-containing cytoskeletal systems at the connecting cilium of rods and cones and at the multiple incisures of rod outer segments (OSs). Vertebrate photoreceptors are directionally sensitive: the longitudinal axis of each cell is actively aligned towards the entrance pupil of the eye, and the cells are most sensitive to light travelling along this axis (as in the Stiles-Crawford effect). The mechanisms responsible for photoreceptor alignment involve movements made by photoreceptors in response to the direction of incident light, using their cytoskeletons. A model is proposed for photoreceptor alignment whereby light absorption in the OS causes fast membrane and slower cytoplasmic changes that spread from the OS to the inner segment myoid, where they activate feedback-controlled motor functions by cytoskeletal elements (microtubules and microfilaments) to produce a differential local bending that adjusts photoreceptor orientation. The fovea at the center of the human macula has specialized features that enable it to provide uniquely high visual acuity, if its cones are accurately aligned. Accordingly, it is proposed that some gene defects in MD cause disturbances at photoreceptor connecting cilia that lead to gradual defects in photoreceptor alignment; misalignment of central macular cones will be initially perceived as blurring, distortions, and decreased acuity of central vision. Although photoreceptors throughout the retina use their cytoskeletons for alignment, the accurate alignment of foveal cones is particularly important because their signals contain fine resolution information that is used in visual feedback systems, e.g., for adjusting accommodation and eye movements. Vision involves multiple feedback loops that are interdependent, e.g., the accuracy of alignment of foveal cones influences how effectively changes in accommodation bring images into focus, and the state of accommodation in turn influences how light entering the eye is projected onto foveal cones. It is proposed that in MD gene defects that disturb the cytoskeleton and alignment of photoreceptors lead to a disturbance in the normal signalling within these feedback systems, causing the mechanisms controlling the alignment of cones in the center of the macula to become progressively more disturbed and the cells to unnecessarily expend energy. These disturbances can lead to local energy depletion within the metabolically fragile central macular cones that trigger them to die, producing central areas of blindness. If this line of reasoning is correct, it may be possible to treat the local energy depletion within macular cones in MD by energy supplementation.

Cytoskeleton↗

Relationship of drusen and abnormalities of the retinal pigment epithelium to the prognosis of neovascular macular degeneration. The Macular Photocoagulation Study Group.

We graded macular features of 127 fellow eyes of participants in the Macular Photocoagulation Study who had an extrafoveal choroidal neovascular membrane secondary to age-related macular degeneration in the first eye and no initial evidence of the neovascular form of age-related macular degeneration in the fellow eye. Our aims were to determine the relationship of drusen characteristics and retinal pigment epithelial abnormalities to the risk of subsequent development of neovascularization in the fellow eye and the risk of subsequent development of recurrent neovascular membranes after photocoagulation in the first eye. Regression analysis demonstrated that the presence of large drusen and focal hyperpigmentation of the retinal pigment epithelium were independent risk factors for the subsequent development of neovascularization in the fellow eye (relative risk, 2.4 and 2.5, respectively). Only 10% of eyes with no large drusen or any retinal pigment epithelial hyperpigmentation compared with 58% of eyes with both large drusen and retinal pigment epithelial hyperpigmentation developed neovascularization in the fellow eye within 5 years. Using multivariate Cox regression analysis, we noted that the risk of developing recurrent neovascular membranes in the first eye was significantly increased when large drusen (relative risk, 2.8) were noted in the fellow eye at the time of laser treatment in the first eye. Fundus features in the fellow eye appear to help identify patients at high risk of developing visual loss from recurrent neovascular membranes following laser treatment in the first eye and from development of a neovascular membrane in the fellow eye.

Aging↗

[Vitelline macular degeneration and Best's macular degeneration are the same disease (author's transl)].

In 1905 F. Best had discovered infantile macular degeneration with dominant transmission, later named after him. From Best's pedigree 19 members could be examined by us. Besides the usual examination-methods, EOG, ERG, Fluorescein-Angiography and Chromato-Ophthalmoscopy were applied. In this way the characteristic findings of vitelline macular degeneration could be demonstrated. 7 family-members were typically affected according to their ages. 2 of them were found to be carriers with normal macula; they had however a pathological EOG. The question, if the diagnosis of Best's macular degeneration should be used further in the system of the hereditary macular degenerations or whether it is indeed the same disease as vitelline macular degeneration, is discussed. Best's macular degeneration and vitelline macular degeneration are synonymous. We recommend, that the term vitelline macular degeneration ought to be used intead of Best's macular degeneration. It remains F. Best's merit, that this disease has been recognised and des

Adolescent↗