BCM stems from mutations or deletions of the OPN1LW and OPN1MW genes, both on the X chromosome. As a recessive x-linked condition, BCM disproportionately affects males, unlike typical achromatopsia. Cerebral achromatopsia
Cerebral achromatopsia]is a form of acquired color blindness that is caused by damage to the cerebral cortex. Damage is most commonly localized to visual area V4 of the visual cortex (the major part of the colour center), which receives information from the parvocellular pathway involved in color processing. It is most frequently caused by physical trauma, hemorrhage or tumor tissue growth. If there is unilateral damage, a loss of color perception in only half of the visual field may result; this is known as hemiachromatopsia.. Cerebral achromats usually do not experience the other major symptoms of congenital achromatopsia, since photopic vision is still functions. Color agnosia involves having difficulty recognizing colors, while still being able to perceive them as measured by a color matching or categorizing task. Terminology
Monochromacy
  Complete lack of the perception of color in a subject, seeing only in black, white, and shades of grey. Hemeralopia
  Reduced visual capacity in bright light, i.e. day-blindness. Nystagmus
  Term to describe both normal and pathological conditions related to the oculomotor system. In the current context, it is a pathological condition involving an uncontrolled oscillatory movement of the eyes during which the amplitude of oscillation is quite noticeable and the frequency of the oscillation tends to be quite low. Photophobia
  Avoidance of bright light by those who have hemeralopia.
When as described; the condition is due to a saturation in the neural portion of the retina and not due to the absence of the photoreceptors per se.In general, the molecular pathomechanism of achromatopsia is either the inability to properly control or respond to altered levels of cGMP; particularly important in visual perception as its level controls the opening of cyclic nucleotide-gated ion channels (CNGs). Decreasing the concentration of cGMP results in closure of CNGs and resulting hyperpolarization and cessation of glutamate release. Native retinal CNGs are composed of 2 α- and 2 β-subunits, which are CNGA3 and CNGB3, respectively, in cone cells. When expressed alone, CNGB3 cannot produce functional channels, whereas this is not the case for CNGA3. Coassembly of CNGA3 and CNGB3 produces channels with altered membrane expression, ion permeability (Na+ vs. K+ and Ca2+), relative efficacy of cAMP/cGMP activation, decreased outward rectification, current flickering, and sensitivity to block by L-cis-diltiazem.Mutations tend to result in the loss of CNGB3 function or gain of function—often increased affinity for cGMP—of CNGA3. cGMP levels are controlled by the activity of the cone cell transducin, GNAT2. Mutations in GNAT2 tend to result in a truncated and, presumably, non-functional protein, thereby preventing alteration of cGMP levels by photons. There is a positive correlation between the severity of mutations in these proteins and the completeness of the achromatopsia phenotype.Molecular diagnosis can be established by identification of biallelic variants in the causative genes.