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It differs from other forms of colour-blindness in subtle but important ways. It is a consequence of cortical damage in lingual and fusiform gyri, near the base of the brain (ventro-medial occipital lobe). This damage is almost always the result of injury or illness. Because of the location of the tissues whose damage is associated with cerebral achromatopsia and the requirement that it be damaged in both hemispheres of the brain, complete cerebral achromatopsia is very rare.
Patients with cerebral achromatopsia deny having any experience of colour when asked and fail standard clinical assessments like the Farnsworth-Munsell 100-hue test (a test of colour ordering with no naming requirements). Patients may often not notice their loss of colour vision and merely describe the world they see as being drab. The critical difference between cerebral achromatopsics and people with other forms of colour blindness is that cerebral achromatopsics retain the ability to perceive chromatic borders. For example, they see a red square on a green background effortlessly even when the red and green are equally bright. There are various ways of ruling out a role for unintended luminance differences in accounting for this, e.g. random luminance masking. It even appears that cerebral achromatopsics can discriminate contrasts on the basis of colour direction, but they can't use these contrasts to compare the colour of surfaces that do not adjoin directly. It has been suggestsed that cerebral achromatopsia might best be seen as a failure in specific colour-constancy mechanisms.
Cerebral achromatopsia illustrates the way in which chomatic information can be used to achieve many goals, only one of which is the perception of surface colour, and that those different goals may be met by distinct pathways within the visual system.
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