Behavioural and electrophysiological chromatic and achromatic contrast sensitivity in an achromatopsic patient (original) (raw)

A case study of cortical colour "blindness" with relatively intact achromatic discrimination

Journal of Neurology, Neurosurgery & Psychiatry, 1987

ofOxford and the Rivermead Rehabilitation Centre, Oxford, UK SUMMARY A patient is described whose most striking visual disorder was a grossly impaired ability to discriminate between different colours (hues) that were matched for brightness. In contrast his ability to discriminate between different neutral greys presented in the same fashion was much less abnormal, even though the greys were perceptually difficult. Although visual acuity was reduced and visual fields were constricted, and the patient's memory was moderately impaired, these associated symptoms could not themselves be the cause of his unusual colour vision. The patient had the symptoms of cerebral achromatopsia, and the relative preservation of his form vision (when his reduced acuity is taken into account) and his achromatic vision supports the view that the many different visual cortical areas recently demonstrated in the brains of monkeys, and presumed to exist in man, have a perceptual specialisation that matches their physiological differences. Cerebral achromatopsia is a severe disturbance of the perception of colour caused by cerebral cortical damage. The patient has great difficulty in discriminating between hues and commonly complains that the world looks drained of colour. Although the term achromatopsia implies that vision has become colourless, colours may still be perceived, albeit faintly (that is, they are desaturated). The condition contrasts sharply with other acquired disorders of colour vision where the primary fault is a disconnexion syndrome or a semantic disorder involving the use of colour words (see reference I for review) or an impaired ability to remember perceived colours for more than a few seconds.2 There are several reports which suggest that cerebral achromatopsia can appear without accompanying deficits in the perception of depth, form, acuity, movement or any other psychophysical dimension.34 However, the disturbances are often accompanied by apperceptive visual agnosia' and the cortical damage invariably involves

Form and motion from colour in cerebral achromatopsia

Experimental Brain Research, 1998

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 longand 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.

Pupillary responses to coloured and contourless displays in total cerebral achromatopsia

Brain, 2008

In two patients with total acquired cortical colour blindness and in six control subjects we studied the binocular pupillary response to a variety of sharply defined coloured and grey displays that either had the same mean luminance as the background (isoluminant) or were of greater mean luminance. Despite their complete inability to identify or to discriminate between colours the patients, like the control subjects, showed a pupillary response to the structured coloured displays, even when they were masked by dynamic luminance changes. However, and unlike the control subjects, the patients showed no pupillary response when the coloured displays lacked sharp chromatic borders, as in Gabors or Gaussians.The results indicate that although chromatic processing still occurs in cortical colour blindness its function is solely to give rise to the detection of sharp boundaries which, in their case, can provide the perception of shape but not hue. In accordance with this, the patients could no longer describe the isoluminant borderless figures, which were often totally invisible to them despite their strong chromatic contrast with the background.

Preserved Imagery for Colours in A Patient With Cerebral Achromatopsia

Cortex, 1997

We report the case of a patient who, after sequential bilateral strokes in the occipital regions sparing the primary visual cortex, developed a severe deficit of colour perception. At variance with other reports of acquired achromatopsic patients, she showed a perfectly vivid visual imagery for colours. These findings, together with similar data in domains other than colour processing, challenge the theories which posit that the same cognitive processes are involved in both the perception and the retrieval from memory of a given stimulus.

Cortical Color Blindness is Not “Blindsight for Color”

Consciousness and Cognition, 1998

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.

Chromatic edges, surfaces and constancies in cerebral achromatopsia

Neuropsychologia, 2004

We tested achromatopsic observer, MS, on a number of tasks to establish the extent to which he can process chromatic contour. Stimuli, specified in terms of cone-contrast, were presented in a three-choice oddity paradigm. First we show that MS is able to discriminate the magnitude of chromatic and luminance contrast, but performance is inferior to that of normal observers. Moreover, MS can discriminate isoluminant borders of different chromatic composition. These abilities are not the result of unintended luminance differences and are abolished when chromatic borders are masked by sharp luminance change. In simple displays, local cone-contrast signals can make a significant contribution to surface colour appearance in normal observers. In more complex displays, the perception of a surface's colour becomes largely independent of the local contrast to its background, via processes presumed to be similar to the edge integration and anchoring stages of Land's Retinex algorithm. We show that in simple displays the percepts of both MS and normal observers are dominated by local chromatic-contrast. But, although the percepts of normal observers change in line with the predictions of retinex theory in more complex displays, those of MS do not, remaining dominated by local contrast signals. We conclude that MS has lost the ability to perform edge integration and that this loss is closely related to his absence of colour experience.

The neurological basis of conscious color perception in a blind patient

Proceedings of the National Academy of Sciences, 1999

We have studied patient PB, who, after an electric shock that led to vascular insufficiency, became virtually blind, although he retained a capacity to see colors consciously. For our psychophysical studies, we used a simplified version of the Land experiments [Land, E. (1974) Proc. R. Inst. G. B. 47, 23-58] to learn whether color constancy mechanisms are intact in him, which amounts to learning whether he can assign a constant color to a surface in spite of changes in the precise wavelength composition of the light reflected from that surface. We supplemented our psychophysical studies with imaging ones, using functional magnetic resonance, to learn something about the location of areas that are active in his brain when he perceives colors. The psychophysical results suggested that color constancy mechanisms are severely defective in PB and that his color vision is wavelength-based. The imaging results showed that, when he viewed and recognized colors, significant increases in activity were restricted mainly to V1-V2. We conclude that a partly defective color system operating on its own in a severely damaged brain is able to mediate a conscious experience of color in the virtually total absence of other visual abilities.