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.
The terminal half-life of trimipramine has been variously reported to be as little as 8 hours (in plasma) and as long as 24 hours. In any case, the terminal half-life of trimipramine is described as shorter than that of other TCAs, which makes it ideal for use in the treatment of insomnia.Trimipramine is a racemic compound with two enantiomers. [1] CYP2C19 is responsible for the demethylation of (D)- and (L)-trimipramine to (D)- (L)-desmethyltrimipramine, respectively, and CYP2D6 is responsible for the 2-hydroxylation of (D)- and (L)-desmethyltrimipramine to (D)- and (L)-2-hydroxydesmethyltrimipramine, respectively. CYP2D6 also metabolizes (L)-trimipramine into (L)-2-hydroxytrimipramine. Chemistry
Trimipramine is a tricyclic compound, specifically a dibenzazepine, and possesses three rings fused together with a side chain attached in its chemical structure. Other dibenzazepine TCAs include imipramine, desipramine, and clomipramine. Trimipramine is a derivative of imipramine with a methyl group added to its side chain and is also known as 2-methylimipramine or β-methylimipramine. The tri- prefix in its name may allude to the fact that its side chain features three methyl groups. Trimipramine is a tertiary amine TCA, with its side chain-demethylated metabolite desmethyltrimipramine being a secondary amine. Other tertiary amine TCAs include amitriptyline, imipramine, clomipramine, dosulepin (dothiepin), and doxepin. The chemical name of trimipramine is 3-(10,11-dihydro-5H-dibenzo[b,f]azepin-5-yl)-N,N,2-trimethylpropan-1-amine and its free base form has a chemical formula of C20H26N2 with a molecular weight of 294.434 g/mol. The drug is used commercially as the maleate salt. The CAS Registry Number of the free base is 739-71-9 and of the maleate is 521-78-8. History
Trimipramine was developed by Rhône-Poulenc.