Base color

Distortion model & settings

Distortion type

Severity50%

Perceptual severity curve Multi-pass deep simulation

Image simulation

Choose image Upload JPG/PNG (max 1200 × 1200). See how a scene would appear during a neurological visual distortion episode.

Research notes

Neurological visual distortions arise from abnormal processing in the visual cortex and subcortical visual pathways. The most studied is migraine with aura, affecting approximately 25-30% of migraine patients. During an aura, a wave of cortical spreading depression (CSD) — a slow (2-5 mm/min) depolarisation wavefront followed by sustained neural suppression — propagates across primary visual cortex (V1). Because V1 is retinotopically organised, the CSD wave produces a moving visual disturbance: the scintillating scotoma (a crescent of flickering zigzag lines, the "fortification spectrum") followed by a region of visual field loss. The scintillation arises from hyperexcited neurons ahead of the CSD wavefront; the scotoma from suppressed neurons behind it. Motion smear and temporal persistence occur when saccadic suppression fails or when vestibulo-ocular reflex gain is abnormal (oscillopsia in nystagmus, vestibular disorders). Chromatic edge halos result from lateral inhibition breakdown in colour-opponent cortical circuits.

Swatches

Normal

HEX: — • RGB: — • xy: —

Distorted

HEX: — • RGB: — • xy: —

ΔE (CIE76)

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ΔE (CIEDE2000)

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Deep preview

Normal

Distorted (deep)

Chromaticity (CIE xy)

Distortion shift vector

D65 white point: 0.313, 0.329

Image simulation

Neurological distortion simulations model cortical visual processing anomalies (CSD aura, temporal persistence, lateral inhibition failure) in sRGB approximation. True neurological visual experiences are subjective, variable across patients, and dependent on individual cortical architecture. This tool approximates the perceptual distortion for educational and neuro-ophthalmological research. ΔE2000 implemented locally per Sharma et al. (2005). CSD wave model based on Dahlem & Chronicle (2004) reaction-diffusion framework. Not for clinical diagnosis — consult a neurologist for evaluation of visual aura or distortion symptoms.

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

Wave frequency (Hz)

Propagation speed

Halo spread (px)

Model notes: Cortical spreading depression (CSD) is modeled as a reaction-diffusion wavefront (FitzHugh-Nagumo) propagating across a retinotopic cortical map. The visual field distortion is computed by inverse-mapping the cortical CSD wave back to visual space using log-polar cortical magnification. Motion smear is modeled as a temporal integration kernel (exponential decay, τ ≈ 100-500 ms). Chromatic halos use a Laplacian-of-Gaussian edge detector with colour-opponent channel separation (L-M, S-(L+M)).

Model assumptions & limits

CSD wave is modeled as a 2D wavefront on a flat cortical surface — real V1 has sulcal folding that distorts propagation paths and creates discontinuities in the visual field scotoma.
Retinotopic mapping uses the conformal log-polar model (Schwartz, 1980) — actual cortical magnification varies individually by ±20%.
Motion smear assumes a simple exponential temporal integration kernel — real saccadic suppression and temporal masking involve complex interactions across multiple cortical areas (V1, MT/V5, FEF).
Chromatic halos are an approximation based on lateral inhibition failure in colour-opponent double-opponent cells — the actual neural mechanism is not fully understood.