Extensive Macular Atrophy with Pseudodrusen-Like Appearance (EMAP)
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Extensive Macular Atrophy with Pseudodrusen-Like Appearance (EMAP) is a rare, bilateral retinal disorder characterized by (1) rapidly progressive macular atrophy that often expands preferentially along the vertical axis with polycyclic/multilobular borders, (2) diffuse pseudodrusen-like (subretinal drusenoid) deposits extending beyond the macula into the mid-periphery, and (3) peripheral paving-stone degeneration.[1][2] Compared with findings of typical age-related macular degeneration (AMD), EMAP is recognized earlier in life and may present with rod-predominant symptoms (e.g., nyctalopia/delayed dark adaptation).[3][4][5][6][7]
Disease Entity
Disease
EMAP was first described in 2009 as a distinct phenotype of bilateral macular atrophy associated with widespread pseudodrusen-like deposits and peripheral chorioretinal atrophy.[2] Although it shares features with AMD (particularly subretinal drusenoid deposits and atrophy), EMAP is characterized by a more vertically oriented distribution of atrophy and, in several cohorts, a relatively rapid progression of vision-related disability.[4][6][8] Several classification frameworks have been proposed, including a three-stage natural history based on the extent and topography of atrophy and a clustering-based clinical subtyping approach.[9][10]
A clustering-based study proposed four clinical subtypes:
- minimally atrophic (early disease with limited involvement)
- predominantly central (extensive macular atrophy with minimal peripheral changes)
- mixed (intermediate macular and peripheral involvement)
- predominantly peripheral (small macular atrophy with extensive peripheral degeneration).[9]
These subtypes are based on the relative extent of macular and peripheral involvement.
These subtypes are based on the relative extent of macular and peripheral involvement.
Etiology
The etiology remains uncertain. Available evidence suggests a multifactorial process, with proposed contributions from:
- Environmental/toxic exposures.[3]
- Systemic inflammation/complement pathway dysregulation.[6]
- Chronic autoimmune/inflammatory state: A Brazilian cohort reported a high frequency of prior rheumatic fever and prolonged benzathine penicillin prophylaxis among patients with EMAP, suggesting a possible regional immune-mediated association.[11] In contrast, in a screening study of patients with rheumatic fever-associated valvular disease, EMAP was uncommon (1.69%), indicating that additional genetic or environmental factors are likely required for disease expression.[12]
- Genetic factors are incompletely defined: Targeted testing in published cohorts has not consistently identified pathogenic variants in genes classically associated with inherited macular dystrophies (e.g., TIMP3, C1QTNF5). Furthermore, common AMD risk alleles may not fully explain the phenotype.[3][8]
Risk Factors
Reported associations include:
- Age: classically middle-aged at symptom onset, though later-onset presentations have been reported.[6][12][13]
- Sex: female predominance in some cohorts.[6][11][12]
- Family history of glaucoma and/or AMD.[6]
- Occupational or environmental toxic exposure and geographic clustering (ecologic associations; causality not established).[3]
- History of rheumatic fever and/or long-term benzathine penicillin exposure in some Brazilian cohorts.[11][12]
In a prospective RF-valvular cohort, subretinal drusenoid deposits were identified in 10.17% of patients overall and 18.37% of those aged ≥60 years. The presence of SDD was associated with older age, longer RF duration, and greater cumulative benzathine penicillin exposure.[12]
EMAP was not associated with several major AMD-related systemic risk factors, including cigarette smoking, hypertension, hypercholesterolemia, diabetes, BMI, and major cardiovascular disease, despite evidence of a systemic inflammatory/complement profile in EMAP cohorts; no significant association was found with family history of Alzheimer disease.[6]
General Pathology
Histopathologic data are limited; most descriptions are derived from multimodal imaging and functional testing. Reported clinicopathologic correlates include:
- Vertically predominant, polycyclic/multilobular macular atrophy that may be foveal-sparing in earlier stages.[1][2][8][10][14]
- Diffuse pseudodrusen-like (subretinal drusenoid) deposits extending beyond the macula (often appreciated on widefield imaging).[2][8]
- Peripheral paving-stone degeneration/peripheral chorioretinal atrophy in many cases.[1][2][8]
- OCT findings in some phenotypes include separation between the retinal pigment epithelium and Bruch’s membrane with hyperreflective material, consistent with basal laminar deposit–related changes reported in foveal-sparing or early disease.[7][14]
- Comparative multimodal imaging studies have reported differences in choriocapillaris and Bruch’s membrane profiles between EMAP and AMD-related geographic atrophy, though clinical utility is evolving.[15][16][17][18]
Pathophysiology
The mechanisms underlying these changes remain under investigation. Clinically, many patients report early dark-adaptation difficulty, and electrophysiology/microperimetry studies support rod-predominant dysfunction that may precede marked acuity loss.[5][7][19] Inflammation and complement pathway abnormalities have been reported at a cohort level (e.g., reduced CH50 and increased plasma C3), but these biomarkers are not diagnostic.[3][6] OCTA and high-resolution OCT studies suggest that choriocapillaris and Bruch’s membrane changes may extend beyond clinically apparent atrophy in EMAP.[15][16][18] The choriocapillaris is anatomically organized into independent lobules fed by terminal arterioles.[20] This architecture has been proposed as one possible contributor to the characteristic multilobular (polycyclic) lesion geometry seen in EMAP,[15][18] a vascular mechanism similarly proposed for the phenotypically overlapping diffuse-trickling geographic atrophy (GA).[21]
EMAP may share progression kinetics and lesion geometry features with diffuse-trickling geographic atrophy (DTGA), an AMD-associated GA phenotype characterized by earlier presentation, vertically elongated or lobular atrophy with fringed borders, rapid enlargement, and a thinner subfoveal choroid, while differing from non-DTGA AMD phenotypes.[17][18]
Primary Prevention
There is no proven strategy for primary prevention. Reported associations with occupational toxic exposure and geographic clustering should be interpreted cautiously; counseling should remain evidence-based and individualized.[3]
Diagnosis
History
Common history elements include:
- Progressive central vision loss and reading difficulty.
- Nyctalopia or dark adaptation difficulty (often early).[5][7]
- Paracentral scotomas or perceived visual field loss.[5][19]
- History of rheumatic fever and/or prolonged benzathine penicillin prophylaxis (particularly in Brazilian cohorts).[11][12]
Age at symptom onset may be earlier than typical AMD, but later-onset presentations have been reported.[12][13]
Age at symptom onset may be earlier than typical AMD, but later-onset presentations have been reported.[12][13]
Physical Examination
Examination typically includes best-corrected visual acuity, dilated fundus examination with attention to the distribution of pseudodrusen-like deposits, and careful peripheral evaluation for paving-stone degeneration. Widefield imaging is helpful to document extra-macular involvement.[1][2][8]
Signs
Common findings include:
- Bilateral, often symmetric macular atrophy with a larger vertical than horizontal axis and polycyclic/multilobular borders.[2][8][10]
- Diffuse pseudodrusen-like (subretinal drusenoid) deposits involving the posterior pole and extending into the mid-periphery.[2]
- Peripheral paving-stone degeneration/peripheral chorioretinal atrophy.[1][2][8]
- Foveal sparing in earlier stages in some eyes; functional deficits may be present despite preserved acuity[7][14][19]
- Subfoveal fibrosis or scarring in a subset of eyes (reported in association with worse visual acuity in some subtypes).[9][10]
- Temporal sparing: A relatively preserved region temporal to the macula (often appreciable on wide-field FAF) is reported as a consistent imaging sign of EMAP and may be helpful in differentiating EMAP from AMD-related geographic atrophy in the appropriate clinical context.[1]
While these signs are common, clinical presentation can vary from minimally atrophic disease to extensive macular and peripheral involvement. Four distinct clinical subtypes have been characterized: minimally atrophic (isolated macular atrophy without peripheral involvement), predominantly central (extensive macular atrophy with minimal peripheral changes), mixed (intermediate macular and peripheral involvement), and predominantly peripheral (limited macular atrophy with extensive peripheral degeneration).[9]
While these signs are common, clinical presentation can vary from minimally atrophic disease to extensive macular and peripheral involvement. Four distinct clinical subtypes have been characterized: minimally atrophic (isolated macular atrophy without peripheral involvement), predominantly central (extensive macular atrophy with minimal peripheral changes), mixed (intermediate macular and peripheral involvement), and predominantly peripheral (limited macular atrophy with extensive peripheral degeneration).[9]
Symptoms
- Photophobia or glare sensitivity may be reported.[1][2]
- Nyctalopia/dark adaptation difficulty.[5][7]
- Central visual acuity loss and metamorphopsia (if fovea involved).[2][4][10]
- Paracentral scotoma / field defects.[5][19]
Clinical Diagnosis
EMAP is a clinical diagnosis supported by multimodal imaging. Diagnostic criteria have been proposed and require the following features in both eyes:
Mandatory criteria (all must be present in both eyes):
- Diffuse subretinal drusenoid deposits and pseudodrusen-like deposits involving the posterior pole and mid-periphery on fundus examination and multimodal en face imaging.
- Macular findings meeting one of three scenarios:
- No evident macular atrophy on short-wavelength autofluorescence (SW-AF) but diffuse macular RPE-Bruch's membrane (RPE-BM) separation on OCT, OR
- Moderately hypoautofluorescent ("grayish") macular atrophy on SW-AF surrounded by RPE-BM separation on OCT, OR
- Moderately hypoautofluorescent ("grayish"), multilobular macular atrophy with vertical, leaf-shaped, or confluent configuration, together with temporal sparing.
- Negative genetic testing for known causes of inherited retinal diseases (IRDs).
Complementary Features (supportive but not mandatory):
Complementary Features (supportive but not mandatory):
- Peripheral pavingstone-like degeneration (well-defined, roundish patches of chorioretinal atrophy, most often inferotemporal).
- Rod and cone system dysfunction on full-field ERG (DA 0.01 ERG shows decreased b-wave amplitude; LA 30 Hz flicker shows implicit time delay disproportionate to amplitude reduction).
- Photopic negative response reduction, indicating early retinal ganglion cell dysfunction even with preserved visual acuity.[22]
Clinical Staging
| Stage | Symptoms | Multimodal imaging findings |
| Pre-EMAP (Stage 0) | None | Reticular pseudodrusen in the superior perifovea, with foveal sparing; early structural changes may precede overt atrophy |
| Initial EMAP (Stage I) | Nyctalopia and altered color perception | Widespread RPE–BrM separation with focal or diffuse EZ attenuation; absent or minimal patches of RPE atrophy |
| Intermediate EMAP (Stage II) | Nyctalopia, near vision difficulties, mild visual loss | Multiple patches of RPE atrophy (more prominent superiorly); limited foveal involvement (less than 1 optic disc diameter of atrophy) |
| Late EMAP (Stage III) | Severe visual loss | Extensive macular atrophy with foveal involvement (more than 1 optic disc of atrophy diameter) |
| + | Development of macular neovascularization at any stage | |
Because phenotypic overlap exists with AMD and inherited retinal diseases, the diagnosis should be supported by the overall pattern. In one study, both confirmed EMAP cases had received prior diagnoses of "dry AMD with geographic atrophy" before comprehensive multimodal imaging.[12] The presence of diffuse SDDs extending into mid-periphery, vertically oriented atrophy, temporal sparing, and earlier onset should prompt consideration of EMAP.
Diagnostic Procedures
Recommended evaluation typically includes:
- Color fundus photography and widefield imaging to document deposit distribution and peripheral changes.[3][13]
- Fundus autofluorescence (FAF)
- OCT
- Subretinal drusenoid deposits and outer retinal/RPE atrophy; in some phenotypes, RPE–BrM interface changes and features suggesting basal laminar deposits.[14]
- High-resolution OCT may identify Bruch’s membrane breaks and associated structural features, including basal laminar deposit debris in EMAP and hyperreflective pyramidal structures in AMD-related GA, which may help differentiate the two conditions in selected cases.[16]
- OCTA
- Near-infrared imaging/NIR-AF complements FAF assessment.[8]
- Visual function testing
- Microperimetry or perimetry to document scotomas/field loss and for longitudinal monitoring (particularly in research/advanced care settings).[8][19]
- Full-field ERG can show diffuse retinal dysfunction and may support the diagnosis when the phenotype is atypical.[5][22]
Laboratory Test
No laboratory test is required for routine diagnosis.
Although complement and inflammatory markers have been studied and may be abnormal in some cohorts, they are not validated diagnostic tests.[3] EMAP has been associated with abnormal erythrocyte sedimentation rate, reduced CH50, and increased plasma C3 levels.[6]
Genetic testing is not diagnostic but should be considered to exclude inherited retinal disease (particularly ABCA4, PRPH2, TIMP3, and C1QTNF5 variants).[8][13] Proposed diagnostic criteria do require negative genetic testing for known IRDs.[1]
Differential Diagnosis
Important differentials include:
- Geographic Atrophy secondary to AMD, including diffuse-trickling phenotype.[17][18]
- Key distinguishing features favoring EMAP: onset before age 55, nyctalopia/early rod dysfunction, and peripheral findings; namely pseudodrusen-like deposits extending to the mid-periphery with far-peripheral paving-stone degeneration.[5][17][18]
- Note: OCT and FAF features can overlap substantially between EMAP and DTGA.[17][18] Widefield imaging and careful review of the overall phenotype remain important.[1]
- Retinal dystrophies with macular atrophy (e.g., ABCA4-associated disease, pattern dystrophy/PRPH2, Sorsby fundus dystrophy/TIMP3, late-onset retinal degeneration/C1QTNF5).[3][8]
- Choroideremia and other chorioretinal atrophies (depending on distribution and family history)
- Central areolar choroidal dystrophy.
- Myopic macular degeneration (if high myopia is present).
- Toxic retinopathies (guided by exposure history).[3]
Management
General Treatment
There is no established disease-modifying therapy for EMAP. Management focuses on recognition, monitoring for complications (particularly MNV), and visual rehabilitation.[1][4]
Patients should be counseled regarding progressive atrophy and potential for substantial visual disability. Referral for low-vision services is appropriate as functional vision declines.
Clinical subtype and stage may inform counseling (e.g., predominantly central phenotypes and more advanced stages are more likely to have foveal involvement and worse acuity).[9][10]
Medical Therapy
MNV/CNV has been reported in EMAP.[9][13][23][24] Most lesions were Type 2 and predominantly subfoveal, and showed a favorable anatomical response to anti-VEGF therapy.[25]
No pharmacologic therapy has proven efficacy for slowing EMAP-related atrophy.
Complement inhibitors approved for geographic atrophy (pegcetacoplan, avacincaptad pegol) have not been studied in EMAP populations and should not be extrapolated without direct evidence.[1]
Medical Follow-up
Follow-up should be individualized (often every 3–12 months) based on symptoms, foveal status, and concern for neovascular complications.
OCT (±OCTA) to monitor for MNV and structural progression; FAF can document atrophy expansion over time.[4][8][17][25]
Complications
- Progressive macular atrophy with foveal involvement and profound central vision loss.[4][6][8][9][10]
- Central/paracentral scotomas and broader functional visual field loss.[5][19]
- Subfoveal fibrosis/scarring in some eyes (more common in the predominantly central subtype).[9][14]
- MNV/CNV, reported in a minority of eyes but clinically important because it may worsen vision and is associated with faster atrophy growth in affected eyes.[9][13][23][25][24]
Prognosis
EMAP is typically progressive and can lead to legal blindness. In the French national case-control study, many patients progressed to legal blindness within approximately 5–10 years.[6] Longitudinal series demonstrate fast atrophy expansion with corresponding declines in visual function.[4][8][10] Late-stage disease can show extensive involvement beyond the macula and severe disability by standard blindness criteria.[8]
Prognostic factors:
- Clinical subtype: Predominantly central cases have significantly worse baseline visual acuity compared to predominantly peripheral and mixed subtypes. Foveal atrophy and fibrosis are significantly more common in predominantly central disease.[9]
- Foveal sparing: Eyes with earlier-stage disease (foveal sparing) generally maintain better central vision until later stages, though microperimetry demonstrates functional deficits that may not be captured by visual acuity testing alone.[19]
Global Variants
Although initially described in France, EMAP has since been reported in multiple regions, including Italy/Europe, Japan, and Brazil.[2][5][8][11][13][18]
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 Antropoli A, Bianco L, Romano F, et al. Extensive macular atrophy with pseudodrusen-like appearance (EMAP) clinical characteristics, diagnostic criteria, and insights from allied inherited retinal diseases and age-related macular degeneration. Prog Retin Eye Res. 2025;104:101320. doi:10.1016/j.preteyeres.2024.101320
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 Hamel CP, Meunier I, Arndt C, et al. Extensive Macular Atrophy with Pseudodrusen-like Appearance: A New Clinical Entity. Am J Ophthalmol. 2009;147(4):609-620. doi:10.1016/j.ajo.2008.10.022
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 Douillard A, Picot MC, Delcourt C, et al. Dietary, environmental, and genetic risk factors of Extensive Macular Atrophy with Pseudodrusen, a severe bilateral macular atrophy of middle-aged patients. Sci Rep. 2018;8(1):6840. doi:10.1038/s41598-018-25003-9
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 Romano F, Airaldi M, Cozzi M, et al. Progression of Atrophy and Visual Outcomes in Extensive Macular Atrophy with Pseudodrusen-like Appearance. Ophthalmol Sci. 2021;1(1):100016. doi:10.1016/j.xops.2021.100016
- ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 5.8 5.9 Watanabe SES, Quercia AZF, Sacai PY. Electrophysiological findings in extensive macular atrophy with pseudodrusen. Doc Ophthalmol. 2023;147(2):121-130. doi:10.1007/s10633-023-09941-y
- ↑ 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 Douillard A, Picot MC, Delcourt C, et al. Clinical Characteristics and Risk Factors of Extensive Macular Atrophy with Pseudodrusen. Ophthalmology. 2016;123(9):1865-1873. doi:10.1016/j.ophtha.2016.05.018
- ↑ 7.0 7.1 7.2 7.3 7.4 7.5 Romano F, Cozzi M, Casati S, et al. UNVEILING THE HIDDEN: EARLY MANIFESTATIONS OF EXTENSIVE MACULAR ATROPHY WITH PSEUDODRUSEN-LIKE APPEARANCE. Retin Cases Brief Rep. 2025;19(1):119-124. doi:10.1097/ICB.0000000000001513
- ↑ 8.00 8.01 8.02 8.03 8.04 8.05 8.06 8.07 8.08 8.09 8.10 8.11 8.12 8.13 8.14 8.15 8.16 Antropoli A, Bianco L, Condroyer C, et al. Extensive Macular Atrophy with Pseudodrusen-like appearance. Ophthalmology. 2024;131(10):1175-1184. doi:10.1016/j.ophtha.2024.04.001
- ↑ 9.00 9.01 9.02 9.03 9.04 9.05 9.06 9.07 9.08 9.09 9.10 Battaglia Parodi M, Antropoli A, Saladino A, et al. Clinical and Clustering-Based Subtyping of Extensive Macular Atrophy With Pseudodrusen-Like Appearance (EMAP). Transl Vis Sci Technol. 2025;14(12):26. doi:10.1167/tvst.14.12.26
- ↑ 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 Romano F, Cozzi M, Monteduro D, et al. NATURAL COURSE AND CLASSIFICATION OF EXTENSIVE MACULAR ATROPHY WITH PSEUDODRUSEN-LIKE APPEARANCE. Retina. 2023;43(3):402-411. doi:10.1097/IAE.0000000000003683
- ↑ 11.0 11.1 11.2 11.3 11.4 Moreira-Neto CA, Schmidt Andujar RA, Chao JCT, et al. Rheumatic fever and long-term use of benzathine penicillin as possible risk factors for extensive macular atrophy with pseudodrusen in a Brazilian cohort. Int J Retina Vitr. 2024;10(1):75. doi:10.1186/s40942-024-00592-y
- ↑ 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8 Cassavia Junior ASF, Bellanda V, Audi LO, et al. Assessing the prevalence of extensive macular atrophy with pseudodrusen-like appearance in patients with rheumatic fever-associated valvular heart disease: a cross-sectional study. Int J Retina Vitr. 2026;12(1):31. doi:10.1186/s40942-026-00805-6
- ↑ 13.0 13.1 13.2 13.3 13.4 13.5 13.6 13.7 13.8 Sato S, Morimoto T, Fujikado T, Tanaka S, Tsujikawa M, Nishida K. Extensive Macular Atrophy with Pseudodrusen in a Japanese Patient Evaluated by Wide-Field OCTA. Case Rep Ophthalmol. 2022;13(3):847-854. doi:10.1159/000526970
- ↑ 14.0 14.1 14.2 14.3 14.4 Fragiotta S, Parravano M, Sacconi R, et al. A COMMON FINDING IN FOVEAL-SPARING EXTENSIVE MACULAR ATROPHY WITH PSEUDODRUSEN IMPLICATES BASAL LAMINAR DEPOSITS. Retina. 2022;42(7):1319-1329. doi:10.1097/IAE.0000000000003463
- ↑ 15.0 15.1 15.2 15.3 Quarta A, Corradetti G, Romano F, et al. Distinct Profiles of Choriocapillaris Involvement in Extensive Macular Atrophy With Pseudodrusen-Like Appearance and Geographic Atrophy. Invest Ophthalmol Vis Sci. 2025;66(14):64. doi:10.1167/iovs.66.14.64
- ↑ 16.0 16.1 16.2 Quarta A, Alhelaly M, Romano F, et al. High-Resolution OCT Profiling of Bruch’s Membrane in Extensive Macular Atrophy With Pseudodrusen-Like Appearance and Geographic Atrophy. Invest Ophthalmol Vis Sci. 2026;67(2):12. doi:10.1167/iovs.67.2.12
- ↑ 17.0 17.1 17.2 17.3 17.4 17.5 17.6 Bianco L, Antropoli A, Arrigo A, et al. FUNDUS AUTOFLUORESCENCE IN EXTENSIVE MACULAR ATROPHY WITH PSEUDODRUSEN AND DIFFUSE TRICKLING GEOGRAPHIC ATROPHY. Retina. 2023;43(5):755-761. doi:10.1097/IAE.0000000000003733
- ↑ 18.0 18.1 18.2 18.3 18.4 18.5 18.6 18.7 Antropoli A, Arrigo A, Bianco L, et al. Quantitative multimodal imaging of extensive macular atrophy with pseudodrusen and geographic atrophy with diffuse trickling pattern. Sci Rep. 2023;13(1):1822. doi:10.1038/s41598-023-28906-4
- ↑ 19.0 19.1 19.2 19.3 19.4 19.5 19.6 Romano F, Boon CJF, Invernizzi A, et al. CORRELATION BETWEEN MICROPERIMETRY AND IMAGING IN EXTENSIVE MACULAR ATROPHY WITH PSEUDODRUSEN-LIKE APPEARANCE. Retina. 2024;44(2):246-254. doi:10.1097/IAE.0000000000003951
- ↑ Torczynski E, Tso MO. The architecture of the choriocapillaris at the posterior pole. Am J Ophthalmol. 1976;81(4):428-440. doi:10.1016/0002-9394(76)90298-1
- ↑ Fleckenstein M, Schmitz-Valckenberg S, Lindner M, et al. The "diffuse-trickling" fundus autofluorescence phenotype in geographic atrophy. Invest Ophthalmol Vis Sci. 2014;55(5):2911-2920. Published 2014 May 2. doi:10.1167/iovs.13-13409
- ↑ 22.0 22.1 Watanabe SES, Quercia AZF, De Assis GPSM, Borges ML, Sacai PY. Ganglion cell function loss in extensive macular atrophy with pseudodrusen. Int Ophthalmol. 2025;45(1):338. doi:10.1007/s10792-025-03713-0
- ↑ 23.0 23.1 Kamami-Levy C, Querques G, Rostaqui O, Blanco-Garavito R, Souied EH. Choroidal neovascularization associated with extensive macular atrophy with pseudodrusen-like appearance. J Fr Ophtalmol. 2014;37(10):780-786. doi:10.1016/j.jfo.2014.06.003
- ↑ 24.0 24.1 Romano D, Colombo L, Maltese P, Bertelli M, Rossetti LM. BRUCH MEMBRANE RUPTURE AND CHOROIDAL NEOVASCULARIZATION COMPLICATING EXTENSIVE MACULAR ATROPHY WITH PSEUDODRUSEN-LIKE APPEARANCE: A CASE REPORT. Retin Cases Brief Rep. 2023;17(5):557-561. doi:10.1097/ICB.0000000000001236
- ↑ 25.0 25.1 25.2 Trinco A, Antropoli A, Bianco L, et al. INCIDENCE, CHARACTERISTICS, AND OUTCOMES OF MACULAR NEOVASCULARIZATION IN EXTENSIVE MACULAR ATROPHY WITH PSEUDODRUSEN-LIKE APPEARANCE. Retina. 2025;45(9):1689-1700. doi:10.1097/IAE.0000000000004506
