About

Blue cone monochromacy (BCM) is an X-linked recessive condition where both L-cones (long-wavelength, ~564nm) and M-cones (medium-wavelength, ~534nm) are absent or non-functional. Affected individuals retain only S-cones (short-wavelength, ~420nm) and rod photoreceptors. This reduces color discrimination to roughly 1 dimension of hue - a narrow blue-yellow axis - with visual acuity typically between 20/60 and 20/200. Prevalence is approximately 1 in 100,000 males. Misdiagnosis as rod monochromacy or incomplete achromatopsia is common because standard Ishihara plates cannot distinguish BCM from other severe color vision deficiencies.

This simulator transforms pixel color data through the LMS cone response space, zeroing L and M channel contributions while preserving the S-cone signal and rod-mediated luminance. The severity parameter interpolates linearly between trichromatic and full BCM perception. Note: this tool approximates photopic BCM perception on a trichromatic display. It cannot replicate the reduced acuity, nystagmus, or photophobia that accompany the condition in vivo.

Formulas

The simulation converts each pixel from sRGB to the LMS cone response space, applies the BCM transformation matrix, then converts back. The sRGB to linear RGB conversion removes gamma encoding:

C_linear =

{

C_sRGB12.92 if C_sRGB ≤ 0.04045(C_sRGB + 0.0551.055)^2.4 otherwise

Linear RGB is then transformed to LMS cone response using the Hunt-Pointer-Estévez matrix:

LM=HS ⋅ R_linG_linB_lin

Where the Hunt-Pointer-Estévez matrix H is:

H = 0.40020.7076−0.0808−0.22631.16530.04570.00.00.9182

For BCM simulation, the L and M cone channels are replaced by a rod-mediated luminance estimate derived from the scotopic luminosity function. The rod response V′ is approximated from linear RGB:

V′ = 0.2126 ⋅ R_lin + 0.7152 ⋅ G_lin + 0.0722 ⋅ B_lin

The severity parameter t ∈ [0, 1] interpolates between original and simulated color:

C_out = (1 − t) ⋅ C_original + t ⋅ C_BCM

Where C_original is the original sRGB pixel value and C_BCM is the simulated BCM result. At t = 1, the output represents complete loss of L and M cone function.

Reference Data

Condition	Affected Cones	Functional Cones	Prevalence (Males)	Color Axis Remaining	Typical Acuity
Normal Trichromacy	None	L, M, S	-	3-dimensional	20/20
Protanopia	L	M, S	~1%	2-dimensional	20/20
Deuteranopia	M	L, S	~1%	2-dimensional	20/20
Tritanopia	S	L, M	~0.003%	2-dimensional	20/20
Blue Cone Monochromacy	L & M	S only	~0.001%	~1-dimensional	20/60 - 20/200
Rod Monochromacy	L, M, S	Rods only	~0.003%	0-dimensional	20/200+
Protanomaly	L (shifted)	L′, M, S	~1%	3-dimensional (reduced)	20/20
Deuteranomaly	M (shifted)	L, M′, S	~5%	3-dimensional (reduced)	20/20
Cone-Rod Dystrophy	All (progressive)	Variable	~0.01%	Degrades over time	Variable
Achromatopsia (complete)	L, M, S	Rods only	~0.003%	0-dimensional	20/200
S-Cone Syndrome	L & M (partial)	S dominant	Rare	~1-dimensional	20/100
OPN1LW/OPN1MW Deletion	L & M genes	S + Rods	Genetic variant	~1-dimensional	20/80 - 20/200
Cone Peak Sensitivity Wavelengths
S-cone (Blue)	420nm (range: 400 - 500nm)
M-cone (Green)	534nm (range: 450 - 630nm)
L-cone (Red)	564nm (range: 500 - 700nm)
Rod (Scotopic)	498nm (range: 400 - 600nm)

Frequently Asked Questions

Complete achromatopsia (rod monochromacy) involves loss of all three cone types. Individuals see only via rods, producing a purely achromatic (grayscale) percept with peak sensitivity at 498 nm. BCM retains functional S-cones, preserving a residual blue-yellow color axis. BCM patients can discriminate short-wavelength stimuli (~400-500 nm) from longer wavelengths, which rod monochromats cannot. BCM visual acuity is also typically slightly better (20/60-20/200 vs. 20/200+ for achromatopsia).

The S-cones have a spectral sensitivity centered at approximately 420 nm. Objects reflecting wavelengths in the 400-500 nm range will still produce differential S-cone excitation, yielding a perceived blue tint. A pure grayscale output would indicate rod monochromacy. The blue coloration in BCM simulation is physiologically accurate - it represents the residual chromatic channel that S-cones provide.

The simulation uses a rod luminance approximation based on the CIE scotopic luminosity function (V') to model rod contribution to perceived brightness. However, this is a photopic-range approximation rendered on a standard display. True mesopic and scotopic adaptation - where rod signals dominate - cannot be accurately simulated on a gamma-corrected sRGB monitor. The simulation best represents BCM perception under moderate indoor lighting.

Yes. The simulation maps the 3D sRGB gamut to a reduced subspace. Metamerism applies: multiple original colors can collapse to the same simulated output. However, the reverse is also possible in edge cases. Real BCM individuals may use subtle brightness cues or S-cone excitation differences that the simulation's matrix approximation cannot perfectly capture. The simulation is a population-average model, not an individual-specific one.

BCM results from mutations in the OPN1LW and OPN1MW genes on the X chromosome (Xq28), which encode L-cone and M-cone opsins respectively. The most common genotype involves deletion of the locus control region (LCR) or having only a single hybrid gene that produces a non-functional pigment. Severity varies with residual cone function: some patients retain trace L/M cone activity, producing an anomalous trichromacy under bright photopic conditions. The severity slider in this tool models this continuum from partial to complete L/M cone loss.

The Hunt-Pointer-Estévez (HPE) chromatic adaptation matrix is a standard transform for converting CIE XYZ to LMS cone fundamentals. It is widely used in color appearance models (CIECAM02). For CVD simulation, Brettel et al. (1997) and Viénot et al. (1999) validated similar LMS-based approaches against empirical color matching data from dichromats. The HPE matrix provides physiologically reasonable cone response estimates. Accuracy is limited primarily by the display gamut and the population-average nature of cone sensitivity functions.