Academic literature on the topic 'Disciform scar'

Purpose: To evaluate the proportion and reasons for ineligibility to re-register for extended health insurance at 5 years in patients diagnosed with neovascular age-related macular degeneration (AMD) and registered for extended health insurance. Methods: This retrospective study was performed in patients diagnosed with neovascular AMD and registered for extended health insurance with follow-up for at least 5 years. The criteria for re-registration for extended health insurance were determined along with the ineligibility for re-registration. Results: In total, 263 patients were included in the analysis. Of these, 148 (56.3%) did not satisfy the criteria for re-registration. No active treatment was performed in 98 patients during the last 6 months of the study period (no recurrence, 51 patients; additional treatment was not considered beneficial due to retinal damage even without disciform scar formation, 44 patients). Macular disciform scar formation was noted in 50 patients (33.8%). Older age (p = 0.013), poor visual acuity (p = 0.004), and retinal angiomatous proliferation (p < 0.001) were associated with ineligibility for re-registration due to severe retinal damage. Conclusions: Among the patients who were initially registered for extended health insurance, 56.3% failed to satisfy the re-registration criteria. The primary reason was advanced retinal damage. The results of this study provide useful information for patient education and to establish long-term treatment strategies.

Outer retinal tubulation (ORT) is a common finding in optical coherence tomography, which is usually associated with age-related macular degeneration. It is not clear are ORT appear as a sign of a degenerative process in the outer retinal layers or a way of photoreceptors survival. There are no data on the dynamics of ORT associated with angiogenesis inhibitors injections. This paper presents two clinical cases of dynamic observation of tubulation formation in age-related macular degeneration in the disciform scar stage and in the exudation stage after Aflibercept injections based on optical coherence tomography – angiography and scanning laser ophthalmoscopy. Key words: оuter retinal tabs, age-related macular degeneration, angiogenesis inhibitors.

We investigated the efficacy of monthly alternating injections of aflibercept and bevacizumab (MAAB) for maintenance treatment in patients with neovascular age-related macular degeneration (AMD) who showed improvement with the initial monthly injections but presented with rapid worsening after conversion to bimonthly injections. We included 72 patients with neovascular AMD who showed improvement with loading injections of aflibercept. For maintenance treatment, bevacizumab was administered every alternate month between the bimonthly aflibercept injections in 24 (33.3%) eyes showing worsening (MAAB group). The other eyes were treated with aflibercept (BiA group) bimonthly. Baseline low retinal thickness, thick choroid, and presence of intraretinal fluid were associated with worsening after extending the injection intervals. Visual improvement was lower in the MAAB group than in the BiA group, but the final visual outcomes were comparable. Additional bevacizumab stabilized the early fluctuation of retinal thickness, thus maintaining long-term visual stability without increasing the risk of geographic atrophy or disciform scar until the second year. Previously treated eyes or those with polypoidal choroidal vasculopathy responded less to the initial loading doses and showed worsening under the bimonthly regimen. MAAB was effective in preventing anatomical and functional deterioration when bimonthly aflibercept proved insufficient for the maintenance treatment of neovascular AMD.

ObjectivesTo analyze the choriocapillaris vessel density (CVD) of eyes at different stages of Age-related Macular Degeneration (AMD) with Optical Coherence Tomography Angiography (OCTA).MethodsThis is a prospective observational cross-sectional study on 21 age-matched healthy eyes and 84 eyes with AMD (i.e., early AMD, late AMD, Geographic Atrophy [GA], and disciform scar AMD). OCTA was used to automatically measure the CVD (%), on both the whole macula and the foveal area, in a layer going from 9 µm above to 30 µm below the Bruch’s membrane. Furthermore, in the GA subgroup, the extension of the Ellipsoid Zone (EZ) interruption and the area of macular chorio-retinal atrophy was analyzed.ResultsMacular CVD was significantly lower in the GA, late AMD and disciform scar AMD-subgroups compared to controls (respectively, p=0.0052; p&lt;0.0001; p=0.0003), whereas it did not significantly vary in the early AMD group (p=0.86). A significant difference between the early AMD and both the late AMD and the disciform scar AMD subgroups was also found (p=0.0009 and 0.0095, respectively). When comparing the foveal CVD of healthy and AMD eyes, a significant difference was found with every AMD subgroup (early AMD, p=0.011; GA, p&lt;0.0001; late AMD, p&lt;0.0001; disciform scar AMD, p&lt;0.0001). Furthermore, in the GA subgroup, the CVD had an inverse correlation with both the extension of the EZ-interruption (p=0.012) and with the calculated chorio-retinal atrophic area (p=0.009).ConclusionsOCTA could play a crucial role in the categorization of AMD, allowing for the evaluation of gradual flow impairment at different stages of the disease. Moreover, the detection of a decreased macular and foveal CVD may shed light on the pathogenesis of AMD.

Polypoidal choroidal vasculopathy (PCV), characterized by aneurysmal polypoidal lesions in the choroidal vasculature, is a subtype of exudative age-related macular degeneration (AMD) which can cause permanent vision loss due to hemorrhage, exudation, macular edema, and disciform scar formation. Besides anti-vascular endothelial growth factor (anti-VEGF) therapy, photodynamic therapy (FDT) and combination therapies are currently being used in the treatment of PCV.

Age-related macular degeneration is basically evaluated as non-neovascular (dry) and neovascular (wet) type. Initial stages start with atrophy, drusen development in RPE-Bruch membrane level and pigmentary changes and in final stages may result in CNVM, disciform scar, and geographic atrophic changes. Visual acuity loss is more severe and faster in neovascular ARMD, late stages of geographic atrophy involving foveal center may also cause significant visual loss.

Retinal telangiectasia is a neuro-degenerative macular disease that is limited to juxtafoveal region in one or both eyes with capillary telangiectasia and focal retinal gliosis. Choroidal neovascularization (CNV) is one of the main complications that cause visual deterioration in retinal telangiectasia. When patients develop CNV, rapid visual deterioration with subretinal hemorrhage, cystoid macular edema, hard exudates, disciform scar, and retinocoroidal anastomosis may occur. In our review article we discussed CNV in retinal telangiectasia and current treatment approaches.

Purpose: To describe the multimodal imaging (MMI) features of subretinal drusenoid deposits (SDD) in Indian population. Methods: Patients diagnosed to have SDD from January 2016 to December 2018 at our tertiary care center were recruited. The diagnosis of SDD was made on the basis of MMI consisting of a combination of color fundus photography (CFP), optical coherence tomography (OCT), red-free (RF) imaging, blue autofluorescence (BAF), and near-infrared reflectance (NIR) imaging. The morphological type and distribution of SDD and the associated retinal lesions were reviewed. Results: Twenty-three patients with SDD were included. The mean age of the patients was 68.1 ± 12.2 years. SDD were noted in 77.8% of eyes clinically (n = 35/45) and could be detected in 100% of these eyes with OCT. The morphology of SDD was nodular in 65.7% of eyes (n = 23/35), reticular in 5.7% (n = 2/35), and mixed pattern in the remaining cases. BAF and NIR showed hyporeflective nodular lesions often with a target configuration. The location was commonly in the perifoveal area, mostly involving the superotemporal quadrant (74.3%, n = 26/35). Associated retinal lesions were type-3 neovascularization or retinal angiomatous proliferation in 17.1% (n = 6/35), disciform scar in 11.4% (n = 4/35), type-1 neovascularization in 8.5% (n = 3/35), and geographic atrophy in 5.7% (n = 2/35) of eyes. The mean subfoveal choroidal thickness was 186.2 ± 57.8 μm. Conclusion: SDD commonly have a nodular morphology and their identification often requires confirmations with OCT. Advanced age-related macular degeneration features are frequently present in eyes with SDD and the fellow eyes.

Doctor of Philosophy (PhD)
BACKGROUND: The accumulation of abnormal extracellular deposits beneath the retinal pigment epithelium characterises the pathology of early age-related macular degeneration. However, the histopathological threshold at which age-related changes become early AMD is not defined, and the effect of each of the deposits (basal laminar deposit and membranous debris) on disease progression is poorly understood. Evidence suggests that macrophages play a key role in the development of AMD lesions, but the influence of basal laminar deposit (BLamD) and membranous debris on the recruitment and programming of local macrophages has not been explored. Although evidence also suggests that inflammation and innate immunity are involved in AMD, the significance of anti-retinal autoantibodies to disesase pathogenesis is not known. AIMS: (i) To determine the histopathological threshold that distinguishes normal ageing from early AMD; (ii) to determine the influence of BLamD and membranous debris on disease progression; (iii) to examine whether distinct early AMD phenotypes exist based on clinicopathological evidence; (iv) to determine the histopathological context in which Bruch’s membrane macrophages first found; (v) to examine the relationship between Bruch’s membrane macrophages and subclinical neovascularisation; (vi) to determine if the progressive accumulation of BLamD and membranous debris alters the immunophenotype of Bruch’s membrane macrophages and/or resident choroidal macrophages; (vii) to determine if the anti-retinal autoantibody profile differs significantly between normal individuals and those with early AMD, neovascular AMD or geographic atrophy; (viii) to examine whether baseline anti-retinal autoantibodies can predict progression to advanced AMD in individuals with early AMD; and (ix) to examine whether baseline anti-retinal autoantibodies can predict vision loss in individuals with neovascular AMD. METHODS:Clinicopathological studies were performed to correlate progressive accumulation of BLamD and membranous debris to fundus characteristics and visual acuity, as well as to sub-macular Bruch’s membrane macrophage count. Immunohistochemical studies were perfomed to determine whether the presence of BLamD and membranous debris altered the programming of Bruch’s membrane or resident choroidal macrophages. The presence of serum anti-retinal autoantibodies was determined by western blotting, and the association with disease progression examined in early and neovascular AMD. RESULTS: The presence of both basal linear deposit (BLinD) and a continuous layer of BLamD represents threshold early AMD histopathologically, which was seen clinically as a normal fundus in the majority of cases. Membranous debris accumulation appeared to influence the pathway of progression from early AMD to advanced AMD. Bruch’s membrane macrophages were first noted when a continuous layer of BLamD and clinical evidence of early AMD were present, and increased with the amount of membranous debris in eyes with thin BLamD. Eyes with subclinical CNV had high macrophage counts and there was some evidence of altered resident choroidal macrophage programming in the presence of BLamD and membranous debris. Serum anti-retinal autoantibodies were found in a higher proportion of early AMD participants compared with both controls and participants with neovascular AMD, and in a higher proportion of individuals with atrophic AMD compared to those with neovascular AMD. The presence of baseline anti-retinal autoantibodies in participants with early AMD was not associated with progression to advanced AMD. Participants with neovascular AMD lost more vision over 24 months if they had IgG autoantibodies at baseline compared to autoantibody negative participants. CONCLUSIONS: The finding that eyes with threshold early AMD appear clinically normal underscores the need to utilise more sophisticated tests to enable earlier disease detection. Clinicopathological evidence suggests two distinct early AMD phenotypes, which follow two pathways of AMD progression. Macrophage recruitment and programming may be altered by the presence of BLamD and membranous debris, highlighting the need to further characterise the biology of human resident choroidal macropahges. Anti-retinal autoantibodies can be found in both control and AMD sera, and future approaches that allow the examination of subtle changes in complex repertoires will determine whether they are involved in AMD disease pathogenesis.

BACKGROUND: The accumulation of abnormal extracellular deposits beneath the retinal pigment epithelium characterises the pathology of early age-related macular degeneration. However, the histopathological threshold at which age-related changes become early AMD is not defined, and the effect of each of the deposits (basal laminar deposit and membranous debris) on disease progression is poorly understood. Evidence suggests that macrophages play a key role in the development of AMD lesions, but the influence of basal laminar deposit (BLamD) and membranous debris on the recruitment and programming of local macrophages has not been explored. Although evidence also suggests that inflammation and innate immunity are involved in AMD, the significance of anti-retinal autoantibodies to disesase pathogenesis is not known. AIMS: (i) To determine the histopathological threshold that distinguishes normal ageing from early AMD; (ii) to determine the influence of BLamD and membranous debris on disease progression; (iii) to examine whether distinct early AMD phenotypes exist based on clinicopathological evidence; (iv) to determine the histopathological context in which Bruch’s membrane macrophages first found; (v) to examine the relationship between Bruch’s membrane macrophages and subclinical neovascularisation; (vi) to determine if the progressive accumulation of BLamD and membranous debris alters the immunophenotype of Bruch’s membrane macrophages and/or resident choroidal macrophages; (vii) to determine if the anti-retinal autoantibody profile differs significantly between normal individuals and those with early AMD, neovascular AMD or geographic atrophy; (viii) to examine whether baseline anti-retinal autoantibodies can predict progression to advanced AMD in individuals with early AMD; and (ix) to examine whether baseline anti-retinal autoantibodies can predict vision loss in individuals with neovascular AMD. METHODS:Clinicopathological studies were performed to correlate progressive accumulation of BLamD and membranous debris to fundus characteristics and visual acuity, as well as to sub-macular Bruch’s membrane macrophage count. Immunohistochemical studies were perfomed to determine whether the presence of BLamD and membranous debris altered the programming of Bruch’s membrane or resident choroidal macrophages. The presence of serum anti-retinal autoantibodies was determined by western blotting, and the association with disease progression examined in early and neovascular AMD. RESULTS: The presence of both basal linear deposit (BLinD) and a continuous layer of BLamD represents threshold early AMD histopathologically, which was seen clinically as a normal fundus in the majority of cases. Membranous debris accumulation appeared to influence the pathway of progression from early AMD to advanced AMD. Bruch’s membrane macrophages were first noted when a continuous layer of BLamD and clinical evidence of early AMD were present, and increased with the amount of membranous debris in eyes with thin BLamD. Eyes with subclinical CNV had high macrophage counts and there was some evidence of altered resident choroidal macrophage programming in the presence of BLamD and membranous debris. Serum anti-retinal autoantibodies were found in a higher proportion of early AMD participants compared with both controls and participants with neovascular AMD, and in a higher proportion of individuals with atrophic AMD compared to those with neovascular AMD. The presence of baseline anti-retinal autoantibodies in participants with early AMD was not associated with progression to advanced AMD. Participants with neovascular AMD lost more vision over 24 months if they had IgG autoantibodies at baseline compared to autoantibody negative participants. CONCLUSIONS: The finding that eyes with threshold early AMD appear clinically normal underscores the need to utilise more sophisticated tests to enable earlier disease detection. Clinicopathological evidence suggests two distinct early AMD phenotypes, which follow two pathways of AMD progression. Macrophage recruitment and programming may be altered by the presence of BLamD and membranous debris, highlighting the need to further characterise the biology of human resident choroidal macropahges. Anti-retinal autoantibodies can be found in both control and AMD sera, and future approaches that allow the examination of subtle changes in complex repertoires will determine whether they are involved in AMD disease pathogenesis.

Pathologic processes involving the retina or choroid can present with a wide variety of visual field defects. Usually visual field defects of retinal diseases directly correlate with the fundus findings. Visual field changes are often the result of damage to the retina or scarring but, in conjunction with other clinical findings, they may help narrow the differential diagnosis. Most of the macular lesions result in visual field defects that do not respect the vertical or horizontal midline. Occasionally inflammatory disorders result in visual field defects that do not directly correlate with the retinal findings. For example, patients with multiple evanescent white dot syndrome (MEWDS) may have an enlarged blind spot. Macular disorders can cause central or paracentral scotomas depending on the location of the lesion. Causes of macular pathology include drusen, atrophy from dry age-related macular degeneration (AMD), retinal hemorrhage, choroidal neovascular membrane, macular edema, macular hole, macular scar, pathologic myopia, and macular dystrophies of the retina or choroid. Central serous chorioretinopathy (CSCR) can show a relative defect that is anatomically correlated with the area of subretinal or sub RPE (retinal pigment epithelium) fluid accumulation. Residual pigmentary changes in inactive CSCR can also cause a relative depression in the corresponding visual field. Pathologic myopia can present with a variety of visual field defects depending on the retinal findings, such as posterior staphyloma or choroidal neovascular membrane. AMD may show nonspecific changes in the central or paracentral visual field that correlate with the structural damage to the retina and choroid. Geographic atrophy in dry AMD can cause a dense scotoma correlated with the pattern of the atrophy. Choroidal neovascular membranes can cause a depression in the correlating visual field due to edema or hemorrhage. Disciform scars in endstage AMD can also cause a dense scotoma. Macular holes may cause a small central scotoma. Pattern dystrophies are a family of disorders with a common pathology at the level of the RPE. Butterfly dystrophy, an autosomal dominant disorder, and Sjögren reticular dystrophy, an autosomal recessive disorder, are two examples of pattern dystrophies.