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Simulate fundus albipunctatus — a rare autosomal recessive stationary retinal dystrophy characterised by the accumulation of abundant, discrete white or yellow-white dots scattered across the mid-peripheral fundus at the level of the retinal pigment epithelium (RPE). The condition arises from loss-of-function mutations in the RDH5 gene (chromosome 12q13-q14), which encodes 11-cis retinol dehydrogenase — the enzyme responsible for the final oxidation step of 11-cis retinol to 11-cis retinal within the RPE visual cycle. Without functional RDH5, 11-cis retinal regeneration is severely delayed following photobleaching, leaving rod (and sometimes cone) photopigments in a prolonged bleached state that cannot be rapidly re-sensitised. This manifests clinically as marked nyctalopia (night blindness), abnormally prolonged dark adaptation (requiring up to 3 hours for rod threshold recovery versus 30–40 minutes in unaffected individuals), and the characteristic white dot deposits believed to represent accumulations of 11-cis retinyl esters and related visual cycle intermediates within RPE cells. Unlike retinitis pigmentosa, fundus albipunctatus follows a predominantly stationary course — daytime visual acuity, photopic colour vision, and visual fields are typically preserved throughout life. A subset of patients, however, develops a superimposed cone dystrophy variant with progressive central visual impairment. Model three phenotypic states: classic stationary scotopic impairment, the prolonged dark adaptation variant, and the rare progressive cone dystrophy form with central involvement. Inspect ΔE colour shift, CIE xy chromaticity, and image-level scotopic simulation. Advanced visual cycle, retinal dystrophy, and colour science research tool.

Fundus albipunctatus colour science simulation by Auric Artisan.

Base color
Disease variant & settings
Severity / scotopic impairment 50%
Image simulation
Upload JPG/PNG (max 1200 × 1200). See how a scene appears through the scotopic impairment, prolonged dark adaptation state, or progressive cone dystrophy variant of fundus albipunctatus.
Research notes
Fundus albipunctatus was first documented by Lauber in 1910, with the genetic basis established by Yamamoto et al. in 1999 who identified RDH5 as the causative gene. RDH5 catalyses the oxidation of 11-cis retinol to 11-cis retinal — the chromophore that combines with rod opsin (rhodopsin) and cone opsins — within the RPE visual cycle. Without functional RDH5, 11-cis retinyl esters accumulate in RPE cells, forming the characteristic funduscopic white dots (visible on fundus photography as discrete round lesions, 100–300 μm, sparing the fovea). The stationary nature distinguishes FA from progressive white dot syndromes — rod and cone ERG amplitudes, while markedly reduced in dark-adapted testing shortly after light adaptation, recover to near-normal values following 2–3 hours of complete darkness.
Swatches
Normal
HEX: — • RGB: — • xy: —
FA affected
HEX: — • RGB: — • xy: —
ΔE (CIE76)
ΔE (CIEDE2000)
Deep preview
Normal
FA (deep)
Chromaticity (CIE xy)
Scotopic impairment chromaticity shift
D65 white point: 0.313, 0.329
Image simulation
Multi-condition comparison
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Compare classic stationary, prolonged dark adaptation, and cone dystrophy variants across severity grades. Image simulation applies a scotopic channel reduction and optional central cone involvement profile to uploaded scenes.