Cerebral achromatopsia

Cerebral achromatopsia is a type of color-blindness caused by damage to the cerebral cortex of the brain, rather than abnormalities in the cells of the eye's retina. It is often confused with congenital achromatopsia but underlying physiological deficits of the disorders are completely distinct.

The number of reported cases of cerebral achromatopsia are relatively few compared with other forms of color-vision loss. In addition, the severity of the color perception deficits along with other psychological effects vary between patients.

Cerebral achromatopsia differs from other forms of color blindness in subtle but important ways. It is a consequence of cortical damage that arises through ischemia or infarction of a specific area in the ventral occipitotemporal cortex of humans. This damage is almost always the result of injury or illness.

A 2005 study examined 92 case studies since 1970 in which cerebral lesions affected color vision. The severity and size of the visual field affected in cerebral achromatopsiacs vary from patient to patient.

The majority of cases in the 2005 study were the result of bilateral lesions in the ventral occipital cortex. It is unknown whether this was the result of bilateral lesions being more likely to produce color-loss symptoms, or if it was a sampling effect of patients with more severe brain trauma more often being admitted for treatment. In many of the cases examined, patients reported only partial loss of color vision. The locations of color vision loss can be restricted to one hemisphere or one quarter of the visual field. The term "hemiachromatopsia" has been used to denote patients who experience loss of color in only one hemisphere of the visual field. However, as applied to achromatopia resulting from brain trauma, the term is incomplete in characterizing the often-complex nature of the vision loss.

In still rarer cases, temporary ischemia of the associated ventral occipital cortex can result in transient achromatopsia. The condition has thus far been characterized only in stroke patients and provides further support for a color processing area.

In one case, a 78-year-old stroke victim had lost the ability to identify color, but was unaware of his deficit until doctors performed color discretion tests. Even when presented with this information, the patient believed he had retained his ability to perceive color even though the world around him appeared grey. He attributed this achromatism to "poor lighting" and it took several weeks for the patient to fully appreciate the extent of his disability. In addition, the characteristic comorbidity of prosopagnosia was present. After two months and frequent sessions with doctors, tests indicated his color had fully returned. The ischemia caused by lesions on the posterior cerebral arteries had subsided and follow up MRI scans indicated that blood flow had once again returned to the VOC.

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