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PubMed1997

[Functions of the transforming growth factor-beta superfamily in eyes].

One human body is composed of 6 x 10(13) cells, and eyes are also composed of many cells of different functions. The cellular functions and intercellular interaction are regulated by many regulators including cytokines and growth factors to maintain the homeostasis. The transforming growth factor-beta (TGF-beta) superfamily, a large family of multifunctional factors, regulates various cellular functions, including cellular proliferation, migration, differentiation, apoptosis and extracellular matrix production. The TGF-beta superfamily contains about 30 multifunctional factors, and is divided into several families according to the sequence homology. The TGF-beta family, the activin family, and bone morphogenic proteins belong to the TGF-beta superfamily. TGF-beta superfamily members transduce signals through type I and type II serine/threonine type transmembrane receptors. The signals are transduced from receptors through nuclei by Smad family members, which are phosphorylated by the activated type I receptors and translocate from cytoplasm into nuclei. TGF-beta family members and the TGF-beta superfamily receptor family are expressed in ocular tissues including the cornea, ciliary epithelium, lens epithelium, retina, and blood vessels. This observation suggests the importance of the TGF-beta superfamily in eyes. Smad family members (Smad 1, Smad 2, Smad 3 and Smad 4) are expressed in the cultured retinal pigmant epithelial cell line (D407), in which TGF-beta and activin A stimulate the translocation of Smad 2, but not Smad 1 into nuclei, whereas bone morphogenetic protein (BMP) stimulates that of Smad 1, but not Smad 2. TGF-beta superfamily members play important roles in the pathogenesis of retinal neovascularization and in the wound healing process of corneal tissue. TGF-beta inhibits the endothelial functions, but, stimulates angiogenesis in vivo. TGF-beta is involved in the formation of abnormal connective tissue in corneal wound healing. In these processes, many cytokines and growth factors are involved, interacting with each other and forming networks. It is mandatory to clarify the networks to investigate molecular pathogenesis and new therapeutic agents.

Diabetic Retinopathy↗
PubMed1998

[Vascular endothelium-related factors and atherosclerosis/arteriosclerosis: serum hepatocyte growth factor as a possible indicator of vascular lesions].

To investigate the possible involvement of hepatocyte growth factor (HGF) with vascular lesions, we studied the relationship between serum HGF concentrations and the grades of retinal arteriosclerosis, coronary atherosclerosis proliferative changes in the retina of diabetic subjects, and activities of systemic vasculitis. Individuals with more advanced grades of retinal arteriosclerotic change showed higher serum HGF values (grade 0, 0.053 +/- 0.005 ng/ml ; grade 1, 0.144 +/- 0.022 ng/ml ; grade 2, 0.338 +/- 0.36 ng/ml ; grade 3, 0.526 +/- 0.051 ng/ml). The serum HGF concentration was increased in subjects with single- (0.200 +/- 0.012 ng/ml, double- (0.334 +/- 0.018 ng/ml) or triple- (0.379 +/- 0.022 ng/ml) vessel coronary heart diseases, compared with that in subjects with intact coronary arteries (0.112 +/- 0.008 ng/ml). Serum HGF in diabetes without retinopathy was lower than that in nondiabetic subjects (0.041 +/- 0.003 ng/ml vs 0.080 +/- 0.010 ng/ml, p < 0.05), but did not differ from that in other diabetic subjects with background retinopathy (0.058 +/- 0.007 ng/ml) or preproliferative retinopathy (0.048 +/- 0.010 ng/ml). Serum HGF was increased in patients with proliferative retinopathy without photocoagulation (0.213 +/- 0.025 ng/ml, p < 0.01), but not in those with photocoagulation (0.040 +/- 0.008 ng/ml). Serum HGF concentration was increased (p < 0.01) during the acute phase of Schönlein-Henoch purpura (0.31 +/- 0.15 ng/ml), a systemic vasculitis, but it returned to control levels during the remission phase (0.11 +/- 0.10 ng/ml). Increased serum HGF may be involved in the pathogenesis of arteriosclerosis/atherosclerosis, retinal neovascularization, or vasculitis, and measurement of serum HGF may be a useful test for predicting these vascular lesions.

Aged↗
PubMed1989

Cellular mechanisms of iris neovascularization secondary to retinal vein occlusion.

We developed an animal model that allows the early phases of iris neovascularization to be studied in detail. Three major retinal branch veins were occluded with the argon laser in five eyes of cynomolgus monkeys, after which the eyes were enucleated at various time intervals. We observed three phases of the neovascular process in the iris. The early phase was characterized by vessel dilation and intense uptake of tritiated thymidine in the vascular endothelial cells. In the intermediate phase, prominent new vessels, ectropion uveae, peripheral anterior synechiae, and elevated intraocular pressure developed. Also noted were a decrease in tritiated thymidine uptake of the endothelial cells, a remarkable increase in stromal cell tritiated thymidine activity, and the formation of a neovascular membrane in association with the anterior migration of stromal cells. The late phase was marked by a further reduction of tritiated thymidine uptake and regression of the neovascular membrane.

Animals↗
PubMed2007

Clinicopathological findings of retinal angiomatous proliferation.

BACKGROUND: Neovascular membranes obtained from surgical excision of neovascularization for retinal angiomatous proliferation (RAP) were examined histopathologically in an attempt to elucidate the pathogenic mechanism of RAP. METHODS: Nine eyes of eight patients (mean age, 79 +/- 6 years) who underwent neovascularization excision were studied. Three eyes had stage II with RPE detachment, six had stage III. Immunohistochemical studies were performed to identify von Willebrand factor, vascular endothelial factor (VEGF), CD68 and hypoxia inducible factors (HIF-1 alpha and HIF-2 alpha). RESULTS: Multiple soft drusen were present in the macular area in all patients. In one stage II eye, we observed intraretinal neovascularization as a VEGF-positive mass, CD68-positive macrophage migration and HIF expression. In another stage II eye, neovascularization had extended above the RPE, while VEGF-positive fibroblasts were observed below the RPE. Therefore, in stage II, neither angiographic nor histopathological examinations identified choroidal neovascularization. In one phase III eye, angiography demonstrated choroidal neovascularization and chorioretinal anastomosis. Histopathologically, chorio-retinal communication was observed in the region where the RPE was destroyed, and VEGF-positive neovascularization was also seen below the RPE. CONCLUSIONS: The findings of multiple drusen in elderly patients together with macrophage migration and HIF expression surrounding VEGF-positive retinal neovascularization suggest ischemic and inflammatory factors to be associated with the development and progression of RAP.

Aged↗
PubMed1980

Retinal and choroidal neovascularization in sickle cell disease.

Small vessel obstruction characterizes sickle cell disease and, when occurring in the peripheral retinal vessels, initiates a sequence of vascular events which may culminate in the development of proliferative sickle retinopathy (PSR). Repeated examinations of the retinal vasculature of patients with different genotypes of sickle cell disease over the last 10 years (Condon and Serjeant, 1972a, b, c; 1975; 1980a) have allowed observations on the natural history of PSR and on factors related to its development. Choroidal neovascularization has been a common complication of a trial of xenon arc photo-coagulation in PSR. Observations on the aetiology and natural history of both retinal and choroidal neovascularization are presented in this report.

Adolescent↗
PubMed1990

Selective neovascularization of the retinal pigment epithelium in rat photoreceptor degeneration in vivo.

Photoreceptor cell degeneration in rodents from a variety of causes results in neovascularization of the retinal pigment epithelium as a late stage phenomenon. Even though the vessels within the pigment epithelium arise from the retinal circulation, they can manifest the choroidal endothelial cell phenotype of fenestrated endothelial cells. In order to study the detailed cellular events which result in incorporation of retinal vessels within the retinal pigment epithelium, a morphological and morphometric analysis of the RPE and vasculature was performed in rats. Urethane, given subcutaneously to newborn rats, results in a photoreceptor degeneration but does not affect the RPE, choroid or inner retinal layers. Retinas were studied from rats of 8 to 24 weeks of age, the time period when vascularization of the RPE occurs. Loss of retinal vessels is first seen at 12 weeks, primarily in substantial dropout of vessel profiles in the outer plexiform layer (OPL) vessel bed. There is a gradient of loss from the OPL bed to the nerve fiber layer (NFL) bed and from the central to peripheral region. Total vessel density of the experimental retinas is greater than controls at 8 and 12 weeks. This occurs because there is marked loss of retinal thickness, due to photoreceptor degeneration, without a comparable loss of vessel profiles. The total retinal vessel density decreases from 8 to 20 weeks, and appears to stabilize at 20 and 24 weeks. Analysis of the separate vessel beds shows that this apparent stabilization is due to continued loss of vessels within the sensory retina, and increased presence of vascular profiles within the RPE. Total absence of the photoreceptor cell is necessary for incorporation of vessels within the RPE. Since new vessel profiles develop in the RPE but not the adjacent sensory retina, we speculate that the RPE may stimulate neovascularization of the RPE. A model of the cellular events leading to RPE neovascularization is proposed.

Animals↗
PubMed1994

Retinal and choroidal neovascularization in a transgenic mouse model of sickle cell disease.

A complication of sickle cell disease is proliferative retinopathy. We investigated the eyes from a transgenic mouse model of sickle cell disease (alpha H beta S[beta MDD] type) to determine if pathological changes occurred in their retinas and choroids. One retina from each animal was processed by flat-embedding adenosine diphosphatase-reacted retinas in glycol methacrylate. The fellow eye from each animal was embedded whole in glycol methacrylate for histopathological analysis of all ocular structures. Retinal vascular occlusions resulted in nonperfused areas of retina and arterio-venous anastomoses. Intra- and extraretinal neovascularization was observed adjacent to nonperfused areas. Retinal pigmented lesions were formed by the migration of retinal pigment epithelial cells into sensory retina, often ensheathing choroidal neovascularization. The incidence of this bilateral chorioretinopathy was 30% in animals older than 15 months of age. The ocular histopathological changes we observed in the mouse model mimicked many aspects of human proliferative sickle cell retinopathy. Furthermore, this is the first genetically derived animal model for chorio-retinal neovascularization.

Anemia, Sickle Cell↗
PubMed2002

Blockade of nitric-oxide synthase reduces choroidal neovascularization.

Nitric oxide (NO) promotes retinal and choroidal neovascularization, although different isoforms of nitric-oxide synthetase (NOS) are critical in each. Deficiency of endothelial NOS (eNOS) suppresses retinal but not choroidal neovascularization, whereas deficiency of neuronal NOS (nNOS) or inducible NOS (iNOS) suppresses choroidal, but not retinal neovascularization. In this study, we investigated the effect of N(G)-monomethyl-L-arginine (L-NMMA), a nonspecific NOS inhibitor, in three models of ocular neovascularization. Oral administration of L-NMMA caused significant inhibition of choroidal neovascularization in mice with laser-induced rupture of Bruch's membrane and significantly inhibited subretinal neovascularization in transgenic mice with expression of vascular endothelial growth factor (VEGF) in photoreceptors (rho/VEGF mice) but did not inhibit retinal neovascularization in mice with ischemic retinopathy. By extensive mating among mice deficient in NOS isoforms, triple homozygous mutant mice deficient in all three NOS isoforms were produced. These mice had marked suppression of choroidal neovascularization at sites of rupture of Bruch's membrane and near-complete suppression of subretinal neovascularization in rho/VEGF mice but showed no difference in ischemia-induced retinal neovascularization compared with wild-type mice. These data indicate that NO is an important stimulator of choroidal neovascularization and that reduction of NO by pharmacologic or genetic means is a good treatment strategy. However, the situation is more complex for ischemia-induced retinal neovascularization for which NO produced in endothelial cells by eNOS is stimulatory, but NO produced in other retinal cells by iNOS and/or nNOS is inhibitory. Selective inhibitors of eNOS may be needed for treatment of retinal neovascularization.

Animals↗
PubMed1988

Neovascularization in central retinal vein occlusion: electroretinographic findings.

Electroretinograms (ERGs) were measured in 15 patients with central retinal vein occlusion (CRVO). Seven of the patients had neovascularization of the iris (NVI) at the time of testing, and two developed NVI within one month of testing; six did not have NVI or any other form of neovascularization (NV) and were no longer considered to be at risk for NV from their present occlusion. The ERGs were recorded as a function of the stimulus intensity and to a 30-Hz flickering stimulus. A Naka-Rushton-type function was fit to b-wave amplitudes, measured as a function of stimulus intensity, to evaluate changes in ERG amplitude and sensitivity. Compared with eyes in the no-NV group, eyes developing NVI had significantly reduced ERG sensitivity and amplitudes. The distributions of sensitivity values in these two groups did not overlap. All of the eyes with NV showed large a- and b-wave and 30-Hz implicit time delays, but only one eye had a b/a-wave amplitude ratio close to or less than 1. A comparison of ERG sensitivity, amplitude data, and flicker timing data with retinal fluorescein angiography in a two-alternative forced-choice analysis showed that ERG sensitivity and amplitude loss were better than retinal fluorescein angiography at discriminating eyes with CRVO and NVI from eyes with CRVO without NVI.

Electroretinography↗
PubMedDate not supplied

Neovascularization in experimental retinal venous obstruction in rabbits.

PURPOSE: To investigate the later pathohistological changes in experimental retinal venous obstruction in rabbits. METHODS: Experimental retinal venous obstruction was produced in retinal blood vessels of rabbits by trans-adventitial dropping of thrombin. Fundus observation was performed 3 months and 1 year thereafter. Retinal histological examinations were performed by fluorescein microscopy, light microscopy, and transmission electron microscopy. RESULTS: Vessels with a rete mirabile and arteriovenous anastomosis were observed after 3 months. On a flat gelatin-fluorescein preparation, regions with no perfusion, thought to be areas of vascular occlusion in the periphery, were observed extensively. Clear leakage of gelatin-added fluorescein was noted from vessels in the periphery, and minute neovascularization with a rete mirabile from these vessels was confirmed. Newly formed retinal vessels were also observed by transmission electron microscopy. The endothelial cells of these newly formed vessels had a large nucleus, a number of ribosomes, and thin basement membrane. Proliferative changes included glial cells that had penetrated into the basement membrane of ghost vessels. CONCLUSION: Our long-term observations confirmed that proliferative changes and neovascularization occurred in this model of retinal venous obstruction.

Animals↗
PubMed2002

Monitoring retinal function in neovascular maculopathy using multifocal electroretinography - early and long-term correlation with clinical findings.

PURPOSE: To objectively investigate and longitudinally monitor retinal function in patients with choroidal neovascularization (CNV) due to exudative age-related macular degeneration (AMD) and myopia using multifocal electroretinography (mfERG). METHODS: Patients with classic and occult subfoveal CNV secondary either to AMD or to myopia were enrolled in the study. The mfERGs were performed at the beginning of the study and every 3 months subsequently during a follow-up period of 15 months. In addition, standardized visual acuity testing, ophthalmologic examinations, color fundus photographs and fluorescein angiography were performed. The mfERG records were derived with the VERIS-System (Electro-Diagnostic Imaging, San Mateo, Calif., USA); 103 locations within the central 50 degrees in diameter were stimulated concurrently by means of the m-sequence technique. Fixation stability was monitored throughout the recording session with an infrared eye monitoring system (VERIS Refractor/Camera unit). The first-order response component was extracted for each stimulated retinal location. The response densities of the first-order kernel were evaluated as a function of eccentricity from the center (ring 1) to the periphery of the stimulated area (ring 6). The results were compared to those derived from age-matched normal control groups. For each patient mfERG responses measured on follow-up visits were compared to each other to evaluate and monitor changes in retinal function. These changes were tested for correlation with those observed in other clinical and electroretinographic findings. Statistical analysis was performed using the Pearson coefficient. RESULTS: Subfoveal neovascular maculopathy was associated with a reduction in response density most prominent within the central 5 degrees over the area affected by CNV detected either at the beginning of the study or at the follow-up recordings. During the follow-up period patients 1 and 4 showed stabilization or a slight increase in response densities over the neovascular lesion-complex and a corresponding stabilization or slight increase in visual acuity accompanied by a decrease in the activity of the neovascular lesion as determined by fluorescein angiography. Patient 2 revealed an increase in response density correlating with an increase in visual acuity and decrease in lesion size. In the contralateral eye of this patient the response density dropped in the area of new subfoveal CNV. In patient 3 continuous progression of the disease was documented by fluorescein angiography and visual acuity. It correlated well with a continuous decrease in retinal response densities during the follow-up. CONCLUSIONS: Objective monitoring of retinal function and correlation with morphological and psychophysical findings was at least in part possible in patients suffering from AMD and myopia. In all of four patients whose subfoveal CNV was documented by fluorescein angiography. Response densities were reduced particularly in the central 5 degrees and in visual acuity. The mfERG data showed a moderate to high statistical correlation with visual function as measured by visual acuity. On the other hand, the greatest linear dimension of the lesion size showed only a weak to moderate statistical correlation with both the response densities of the mfERG and the visual acuity. We conclude that the size of the CNV complex does not represent an accurate measure of retinal function in neovascular maculopathy. The good correlation of the mfERG data with visual acuity suggests that it may serve for objective assessment of retinal function, of the areas overlying the CNV. It shows potential as a valuable tool for longitudinal monitoring of AMD patients.

Aged↗
PubMed2005

Exacerbation of retinal degeneration and choroidal neovascularization induced by subretinal injection of Matrigel in CCL2/MCP-1-deficient mice.

This study presents a mouse model for human age-related macular degeneration (AMD) as characterized by subretinal deposit and choroidal neovascularization. Matrigel, a basement membrane extract, solidifies after implantation in tissue and can stimulate local angiogenesis. This study demonstrates the induction of neovascularization and focal retinal degeneration following subretinal Matrigel injection in mice. In senescent mice, the normal functioning of CC chemokine CCL2/MCP-1 and its receptor CCR2 confers protection against age-related retinal degeneration, a disease that shares many similar features with human AMD. Our data shows that CCL2-deficient mice develop more severe disease as compared to the wild-type controls. These findings suggest that Matrigel subretinal injection could be used to generate AMD-like pathological changes. The data support the previously proposed role of CCL2 in AMD pathogenesis.

Animals↗
PubMed1989

Neovascularization of the optic disc associated with obstruction of the central retinal artery.

Neovascularization of the optic disc (NVD) has, to the authors' knowledge, rarely been reported in association with acute obstruction of the central retinal artery (CRAO). The authors recently retrospectively reviewed 168 cases of CRAO. In this group, NVD developed in three patients soon after their CRAO, an occurrence rate of 1.8%. Rubeosis iridis also developed in two of these three patients. Although all three patients had either atherosclerotic carotid artery disease, diabetes mellitus, or both, in none of the cases was there clinical evidence implicating these diseases as the direct cause for the NVD. All three eyes received panretinal laser photocoagulation, with eventual resolution of the new vessels.

Adult↗
PubMedDate not supplied

[Functional diagnostics of retinal ischemia: Muller cells and neovascularization of the retina in diabetic retinopathy].

Electrography was made for 58 patients (110 eyes) with proliferative diabetic retinopathy distinguished by neovascularization. Fluorescence angiography and electroretinography were dynamically made for 1-1.5 years in 18 patients with preproliferative diabetic retinopathy. The hyperfunction of Muller cells with an increasing glial index, which was detected earlier by us in progressing retinal ischemia, was also observed in retinal neovascularization. The regular monitoring of the dynamics of electroretinogram (ERG, made several times) makes it possible to evaluate in each separate case a degree of neovascularization risk. When the value of the glial index abruptly drops in a patient, who had earlier regular increases in the index value, there is a high probability of a fast development of retinal neovascularization. Regular ERG examinations are advisable for the evaluation of a neovascularization risk.

Diabetic Retinopathy↗
PubMed2003

Retinochoroidal collateral veins protect against anterior segment neovascularization after central retinal vein occlusion.

OBJECTIVE: To test the hypothesis that retinochoroidal collateral veins (RCVs), or alternatively, retinociliary or optociliary shunts/collaterals/veins or opticociliary anastomoses, act protectively against the development of anterior segment neovascularization (ASN) following central retinal vein occlusion (CRVO). DESIGN: Case-control retrospective medical record review of patients with CRVO. PATIENTS: We identified 107 patients with CRVO, of whom 34 had developed ASN, by reviewing their medical records. After applying exclusion criteria, a case group and an age-, sex-, and visual acuity-matched control group were selected. We analyzed these groups for the presence or absence of RCVs and noted the time course involved in their development. MAIN OUTCOME MEASURES: Anterior segment neovascularization (including neovascularization of the iris and/or anterior chamber angle), neovascular glaucoma, and RCV development. RESULTS: Only 1 (5.4%) of 19 individuals who developed ASN did so in the presence of RCVs. In contrast, 11 (57.9%) of 19 individuals in the control group developed RCVs. Statistical analysis revealed that patients who developed ASN were roughly 25 times less likely to have had RCVs than individuals who never developed ASN (odds ratio = 24.74; P =.001). CONCLUSION: Retinochoroidal collateral veins are negatively associated with ASN post-CRVO and may function in a protective manner against such an outcome.

Aged↗
PubMed1999

[Knobby-like choroidal neovascularization accompanied with retinal pigment epithelial detachment].

PURPOSE: To evaluate the clinical features of knobby choroidal neovascularization (CNV) which was detected using indocyanine green (ICG) angiography and the association between knobby CNV and idiopathic polypoidal choroidal vasculopathy (IPCV). METHOD: We studied 164 eyes with retinal pigment epithelial detachment (PED) accompanied with CNV. These patients were older than 50 years. We detected knobby CNV in 96 eyes of 164 PED eyes (58.5%). Knobby CNV was defined as follows: knobbed blood vessels were observed from the early phase and remained hyperfluorescent through the ICG angiography. We classified 3 groups on the basis of the types of vessels with knobby CNV: group I, multiple isolated knobby CNVs without continuous vessels (24 eyes); group II, knobby dilatations in some parts of CNV (45 eyes); group III, network vessels ending in multiple aneurysmal swelling as in IPCV (27 eyes). RESULT: We found knobby CNV in only 20% of eyes with serous PED, but about 70% in neovascular, serosanguineous, and hemorrhagic PED. The ratio of each group showed no distinction statistically. Knobby CNV mostly appeared in macular areas, and was frequently accompanied with subretinal or subpigment epithelial hemorrhage. Subretinal reddishorange lesions were seen in 50% of group I, 60% of group II, and 89% of group III. Knobby CNV showed occult CNV in fluorescein angiography. In late phase ICG angiography, knobby CNV leaked ICG. New lesions occurred in all groups. CONCLUSION: We think that knobby CNV is a common finding in subpigment epithelial neovascularization, and that IPCV vascular lesion is one type of subpigment epithelial neovascularization.

Aged↗
PubMed2000

Retinitis pigmentosa associated with peripheral sea fan neovascularization.

PURPOSE: To describe a case with retinitis pigmentosa associated with sea fan type retinal neovascularization. METHODS: Complete ocular examination including fluorescein angiography was performed in a 9-year-old girl. RESULTS: Ophthalmoscopically, in addition to arteriolar narrowing and bone corpuscular pigmentation of both retinae, a vascular lesion with surrounding intraretinal exudation was noted in the upper equatorial region of the right eye. On fluorescein angiography, the lesion stained in the form of a sea fan neovascularization. CONCLUSION: Sea fan type of neovascularization can be seen in association with retinitis pigmentosa. Fluorescein angiography is important in identifying the exact nature of such a lesion.

Child↗
PubMed2002

Influence of photodynamic therapy in choroidal neovascularization on focal retinal function assessed with the multifocal electroretinogram and perimetry.

PURPOSE: To study the influence of photodynamic therapy (PDT) on retinal function in patients with a predominantly classic choroidal neovascular membrane. DESIGN: Comparative observational study. PARTICIPANTS: Sixteen eyes with a choroidal neovascular membrane eligible for PDT were included. METHODS: Visual acuity, multifocal electroretinogram (MF-ERG, Electrodiagnostic Imaging, San Mateo, CA) recordings and visual fields (Octopus d32) were obtained before PDT with Visudyne, Novartis AG, Basel, Switzerland, and at follow-up 2 weeks to 3 months later. MAIN OUTCOME MEASURES: Visual acuity as well as peak-to-peak amplitudes, peak latencies, and focal differences in the scalar product of the two MF-ERG recordings were analyzed. Mean deviation, loss variance, and the absolute difference in sensitivity in the fields obtained were also analyzed. RESULTS: After PDT, mean visual acuity stabilized or improved in 13 eyes. Except for two eyes with a predominantly parafoveolar choroidal neovascular membrane, the MF-ERG contribution from the central 4 degrees was reduced below the normal level. Although it improved slightly after PDT, it remained below the normal range. In the central 7.5 degrees, retinal sensitivity increased by up to 80 dB and within the paracentral 7.5 degrees to 15 degrees, it increased by up to 183 dB in 13 eyes. CONCLUSIONS: Consistent with the results of the treatment of age-related macular degeneration with photodynamic therapy (TAP) study, PDT can lead to stabilization of visual acuity. Improvement in parafoveal function can be demonstrated in the central visual field, as well as in MF-ERG recordings, even in patients whose visual acuity remains stable. Therefore, the MF-ERG and central perimetry may aid the assessment of retinal function in treatment trials of patients with age-related macular degeneration.

Choroidal Neovascularization↗