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Cortical Visual Loss
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Most dyschromatopsic patients are aware of their color problems. They complain of trouble matching clothes, distinguishing money, and perceiving traffic lights (69). On testing, achromatopsic patients cannot name colors shown to them, while dyschromatopsic patients may be able to name broad color categories like red or yellow. They fail on finer distinctions (e.g., crimson or scarlet), but not all healthy patients have those in their verbal repertoire. One could use the pseudo-isochromatic plates designed to detect congenital red-green defects (70, 71) but with caution, as some achromatopsic patients can still see the color boundaries between the numbers and the background, particularly if the cards are held at a distance (62, 71–73). The best tests require the patient to sort color chips by either their hue (e.g., red versus green), as done with the Farnsworth-Munsell 100 Hue (Figure 20.6) or D-15 tests, or their saturation (e.g., pink versus red), as with the Sahlgren Saturation Test (74). In contrast, they can see lightness normally (63, 72, 73, 75). Cerebral achromatopsia affects all colors (63), with simply an accentuation of our normal tritan-like tendencies to struggle more with blue-yellow hues (76). In those who show recovery, color after-images may still reveal subtle anomalies (65).
Achromatopsia
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
As is more relevant to this book about acquired conditions, it is also possible to be born with typical color vision but then lose it later in life due to brain damage. When severe colorblindness exists due to damage to the brain's cerebral cortex, it is called cerebral achromatopsia. In a person with cerebral achromatopsia, their eyes may be no different from a typical person's eyes. That is, the wavelengths of light are entering into their eyes, are turned into signals by the cone cells of the retina, and are sent into the brain. But the brain has forgotten how to turn those signals into perceptions of color. Because of this, these people typically lose the ability to even imagine colors (see Aphantasia), but there are exceptions (Bartolomeo et al., 1997).
Vision and Higher Cortical Function
Published in Andrei I. Holodny, Functional Neuroimaging, 2019
Sonia Gill, John Ulmer, Edgar A. DeYoe
The ventrally directed stream extends from the occipital lobe into inferotemporal cortex (Fig. 4). At mid-level stages of this stream, there is a complex of visual areas whose boundaries and homology with monkey areas have been controversial (22). The areas labeled here as V4/VO are associated with color and form processing and are located in the posterior fusiform gyrus or anterior lingual gyrus in humans (23,24). Damage to this region can cause cerebral achromatopsia characterized by a loss of color vision with sparing of visual acuity (23,24). Just anterior to V4/VO is the “fusiform face area.” Complex patterns, especially faces are analyzed here (25), and damage to this region can cause face agnosia (prosopagnosia). More generally, lesions near this same region, potentially involving the lateral occipital (LO) complex or other inferotemporal visual areas, produce visual object agnosias (26,27). Injury to this region in the dominant hemisphere can result in the inability to recognize words (alexia) (28,29), which is the written word analogue to visual object agnosia.
Erythropsia and Chromatopsia: Case Study and Brief Review
Published in Neuro-Ophthalmology, 2021
Michael S. Vaphiades, Brendan D. Grondines, Christine A. Curcio
Cerebral achromatopsia is a rare central nervous system disorder where the colour is completely drained from an object. It arises from impaired cortical processing rather than from damage to the retina or optic nerves.6,7 These patients see the world as “drained of colour,” “dirty,” or in shades of black and white. It can involve the entire visual field or just one hemifield, and loss of colour vision may be partial (dyschromatopsia) or complete. These patients typically have a lesion affecting the lingual and/or fusiform gyri on the inferior occipital surface and most cases involve bilateral lesions, but unilateral lesions (often associated with hemiachromatopsia) occur as well.7
Neuro-ophthalmology of movement disorders
Published in Expert Review of Ophthalmology, 2018
Creutzfeldt-Jakob disease (CJD) is a prion disease manifested by rapidly progressive cerebellar ataxia, cognitive decline, myoclonus, rigidity and a variety of other behavioral and motor abnormalities. Ocular signs are common in CJD and include visual hallucinations, ocular ataxia, oculomotor apraxia, cerebral achromatopsia, Anton syndrome (cortical blindness), slow saccades, and supranuclear gaze palsy [63,64].