Cases reported "Color Vision Defects"

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1/5. Complete sparing of high-contrast color input to motion perception in cortical color blindness.

    It is widely held that color and motion are processed by separate parallel pathways in the visual system, but this view is difficult to reconcile with the fact that motion can be detected in equiluminant stimuli that are defined by color alone. To examine the relationship between color and motion, we tested three patients who had lost their color vision following cortical damage (central achromatopsia). Despite their profound loss in the subjective experience of color and their inability to detect the motion of faint colors, all three subjects showed surprisingly strong responses to high-contrast, moving color stimuli--equal in all respects to the performance of subjects with normal color vision. The pathway from opponent-color detectors in the retina to the motion analysis areas must therefore be independent of the damaged color centers in the occipitotemporal area. It is probably also independent of the motion analysis area MT/V5, because the contribution of color to motion detection in these patients is much stronger than the color response of monkey area MT.
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2/5. Attentional capture by colour and motion in cerebral achromatopsia.

    Cerebral achromatopsia is a rare condition in which damage to the ventromedial occipital area of the cortex results in the loss of colour experience. Nevertheless, cortically colour-blind patients can still use wavelength variation to perceive form and motion. In a series of six experiments we examined whether colour could also direct exogenous attention in an achromatopsic observer. We employed the colour singleton paradigm, the phi motion effect, and the correspondence process to assess attentional modulation. Although colour singletons failed to capture attention, a motion signal, based solely on chromatic information, was able to direct attention in the patient. We then show that the effect is abolished when the chromatic contours of stimuli are masked with simultaneous luminance contrast. We argue that the motion effect is dependent on chromatic contrast mediated via intact colour-opponent mechanisms. The results are taken as further evidence for the processing of wavelength variation in achromatopsia despite the absence of colour experience.
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3/5. A human visual disorder resembling area V4 dysfunction in the monkey.

    We surveyed a broad range of visual functions in a man who complained of abnormal color experience and inability to recognize faces following bilateral damage in the visual cortex. A lesion in his right visual cortex caused complete left visual field loss. A lesion in his left visual cortex, located entirely below the calcarine fissure, affected the vision in his remaining hemifield, the right one. Psychophysical testing showed severely defective color vision and pattern processing, but relatively normal luminance contrast detection thresholds. The finding of normal spatial contrast sensitivity and static stereopsis did not resemble a parvocellular defect of the type described in the monkey. The abilities to detect global coherent motion among noise, structure from motion and dynamic stereopsis, and to pursue moving targets showed normal motion processing at several levels. Together with normal flicker perception, these results excluded magnocellular or MT-like defects. Altogether, the findings mimic area V4 dysfunction.
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keywords = motion
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4/5. Cortical color blindness is not "blindsight for color".

    Cortical color blindness, or cerebral achromatopsia, has been likened by some authors to "blindsight" for color or an instance of "covert" processing of color. Recently, it has been shown that, although such patients are unable to identify or discriminate hue differences, they nevertheless show a striking ability to process wavelength differences, which can result in preserved sensitivity to chromatic contrast and motion in equiluminant displays. Moreover, visually evoked cortical potentials can still be elicited in response to chromatic stimuli. We suggest that these demonstrations reveal intact residual processes rather than the operation of covert processes, where proficient performance is accompanied by a denial of phenomenal awareness. We sought evidence for such covert processes by conducting appropriate tests on achromatopsic subject M.S. An "indirect" test entailing measurement of reaction times for letter identification failed to reveal covert color processes. In contrast, in a forced choice oddity task for color, M.S. was unable to verbally indicate the position of the different color, but was surprisingly adept at making an appropriate eye movement to its location. This "direct" test thus revealed the possible covert use of chromatic differences.
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5/5. Form and motion from colour in cerebral achromatopsia.

    patients with cerebral achromatopsia, resulting from damage to ventromedial occipital cortex, cannot chromatically order, or discriminate, hue. Nevertheless, their chromatic contrast sensitivity can be indistinguishable from that of normal observers. A possible contributor to the detectability of chromatic gratings is the subadditive nature of certain colour combination such that mixtures of, for example, red and green (yielding yellow) appear dimmer than expected from the simple addition of luminances. This subadditivity is believed to reflect colour-opponent interactions between the outputs of long- and medium-wavelength cones. We performed a first-order compensation for such subadditivity in chromatic gratings and demonstrated that their detection was still not abolished in an achromatopsic patient. In addition, we used a two-alternative forced-choice procedure with an achromatopsic patient, who was required to judge the apparent relative velocity of two drifting gratings with different degrees of compensation for subadditivity. It is well known that isoluminant gratings, constructed by adding a red and green sinusoidal grating of identical peak luminances in antiphase, appear to drift substantially slower than an achromatic grating with the same velocity. Adding 2f luminance compensation to an isoluminant grating of spatial frequency f, resulted in an identical minimum of perceived velocity at a compensation contrast of 5% in both achromatopsics and normal observers. Furthermore, while compensation for subadditivity did not substantially compromise grating detection at low contrasts, such correction severely affected motion detection. Saccadic eye movement accuracy and latency were also measured to uncompensated chromatic, compensated chromatic and achromatic targets. We conclude first that subadditivity, resulting from colour-opponent P-channel processes, influences motion judgements. The ability to extract motion from chromatic differences alone is little, if at all, different in achromatopsic and normal vision. Second, the paradoxical detection of sinusoidally modulated chromatic gratings in achromatopsic patients is not merely a result of subadditivity. Third, saccadic latency, but not accuracy, to chromatic targets is affected by luminance compensation. Finally, and more generally, wavelength processing continues to contribute to several aspects of visual processing even when colour is not perceived.
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