Base color

Model & settings

Scotoma model

Vision loss severity50%

Perceptual severity curve Acquired dyschromatopsia Bilateral symmetry

Image simulation

Choose image Upload JPG/PNG (max 1200×1200). Simulated canvas next to original.

Research notes

Toxic optic neuropathy shares a common final pathway with LHON: selective injury of the papillomacular bundle (PMB) retinal ganglion cells, leading to bilateral — usually symmetric — cecocentral scotomas. The PMB's high mitochondrial density makes it uniquely vulnerable to agents that impair oxidative phosphorylation, folate/methionine cycling, or axonal transport. Methanol → formic acid → Complex IV block; ethambutol → chelates zinc/copper in mitochondrial complex and disrupts optic nerve axonal flow; tobacco-alcohol → cyanide + methanol synergy with B12 deficiency. Bilateral symmetry checkbox reflects the characteristic bilateral presentation distinguishing toxic ON from most ischemic or demyelinating types.

Swatches — Reference vs Toxic ON Cecocentral

Reference

HEX: — • RGB: — • xy: —

Toxic ON Sim

HEX: — • RGB: — • xy: —

ΔE (CIE76)

—

ΔE (CIEDE2000)

—

Deep preview

Reference

Simulated

Chromaticity (CIE xy)

Achromatic axis (to D65)

D65 white point: 0.313, 0.329

Image simulation

Simulations operate in linear sRGB for perceptual correctness. ΔE2000 implemented locally. Cecocentral scotoma is applied as a Gaussian radial mask centered at fixation, extended along the papillomacular bundle axis toward the blind spot. Diffuse depression applies global luminance attenuation approximating widespread RGC and fiber layer compromise. Dyschromatopsia desaturates along the red-green axis, reflecting the characteristic acquired color defect of PMB-type toxic optic neuropathy (similar axis to LHON). Use the bilateral symmetry checkbox to mirror the scotoma, reflecting the near-symmetric bilateral involvement that is the hallmark distinguishing toxic ON from most unilateral optic neuropathies.

Multi-condition comparison

Condition A

Condition B

Steps

Compare normal, Condition A and Condition B across multiple severities. If an image is loaded it will be processed into the grid, otherwise color swatches are shown.

Advanced mode

Scotoma radius (°)

Toxin class

Recovery profile

Clinical notes: Toxin class influences the scotoma morphology and severity. Mitochondrial toxins (methanol via formic acid; ethambutol chelating mitochondrial metals; linezolid inhibiting mitochondrial ribosome 23S-equivalent) produce predominantly PMB-type cecocentral scotomas with dyschromatopsia. Nutritional deficiency causes slowly progressive bilateral optic neuropathy; recovery with supplementation is typical if treated before optic atrophy is established. Tobacco-alcohol amblyopia combines cyanide (tobacco) with B12 depletion (alcohol), synergistically impairing optic nerve metabolism. Heavy metals impair axonal transport and mitochondrial function and are rare causes in occupational/environmental exposures.

Model assumptions & limits

Cecocentral scotoma is modeled as a symmetric Gaussian extending from the fixation point toward the physiological blind spot. Real toxic scotomas are often irregular and their horizontal elongation depends on the extent of PMB arc fiber damage.
Diffuse depression mode uses global luminance scaling. Real acute methanol poisoning severe cases produce near-complete field loss with subsequent tubular or fragmented fields during partial recovery.
Dyschromatopsia is applied as global red-green desaturation. In practice, color defects are spatially correlated with scotoma location and marginally worse at the scotoma center.
Bilateral symmetry is a simulation toggle; a small proportion of toxic ON cases are mildly asymmetric (especially early nutritional deficiency or unequal ethambutol dosing per eye blood supply).