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Seeing double: the role of meaning in alphanumeric-colour synaesthesia.

When PD, an alphanumeric-colour synaesthete, is shown black digits or letters, each grapheme elicits a highly specific colour, called a "photism" (e.g., a 2 induces green, a Z induces brown). Previous experiments showed that photisms interfere with video-colour naming when the photism colour and the video colour are incongruent. Here we used coloured ambiguous graphemes that could be interpreted as either digits or letters depending on context (e.g., an ambiguous grapheme was interpreted as a 2 if presented within a block of digit trials, but as a Z if presented within a block of letter trials). Ambiguous graphemes were presented in video colours that were either congruent or incongruent with PD's photisms. Crucially, what was a congruent trial in one context was an incongruent trial in the other context. PD's pattern of response times indicated that identical graphemes could induce differently coloured photisms depending on their interpretation. This suggests that the meaning of graphemes ultimately determines their synaesthetic colour.

Cognition↗

Synaesthetic photisms guide attention.

We evaluated whether synaesthetic colour experiences (i.e., photisms) guide or attract attention. An alphanumeric-colour synaesthete, J, and seven non-synaesthetes searched for target digits presented against backgrounds that were either congruent or incongruent with the colours of J's photisms for the target digits. For J, the slope of the search function for detecting the target digits on incongruent trials was shallower than the slope of the search function for detecting the target digits on congruent trials. In contrast, for the seven non-synaesthetes, the slopes of the search functions for detecting the target digits on congruent and incongruent trials were equivalent. These findings suggest that synaesthetic colour experiences influence the efficiency of visual search by guiding or attracting attention.

Attention↗

Achromatopsia, color vision, and cortex.

Brain damage can entirely abolish color vision in cases of complete achromatopsia. Other processes that depend on wavelength differences, however, can be retained. Form and motion defined by pure color differences can be perceived readily even when the colors themselves cannot be told apart. The loss of color vision in cerebral achromatopsia has been equated with the loss of a "color center" presumed indispensable for the phenomenal experience of hue. The "color center" has been assigned a role in the cortical construction of color, specifically in implementing the computations that underlie color constancy. Many features of the condition are consistent with this account. Other neurologic patients, however, retain conscious experience of hue, yet fail to disentangle the illuminant and the reflectance properties of surfaces. For them, color experience is determined by the wavelength composition of light reflected from a surface. If their wavelength-dependent vision is mediated by activity in early visual areas, then it is difficult to understand why these areas are unable to perform a similar role when they remain intact in achromatopsic observers. The prevalence of cells in the ventral visual areas of the monkey brain that code color and the further fractionation of color-related areas in human observers revealed by functional imaging suggest multiple color areas. Their different contributions are only just beginning to become apparent.

Brain Diseases↗

Beyond visual acuity: new and complementary tests of visual function.

Visual acuity is an essential component of the routine ophthalmic examination and the most common measure of visual function. There is increasing recognition, however, of the need to evaluate visual function beyond the limited extent afforded by visual acuity. The primary objective of this article is to introduce a variety of new and lesser-used techniques for measuring visual function that complement visual acuity assessment, each of which has been shown to detect visual dysfunction in patients with normal visual acuity.

Color Perception↗

Chromatic visual phenomenon caused by a subluxed intraocular lens.

A 74-year-old man developed an unusual chromatic aberration as a complication of cataract extraction surgery with posterior chamber intraocular lens implantation. The patient could see the location and color of one of the haptics of the dislocated lens. His symptoms resolved with miotic therapy.

Aged↗

A table of color distance scores for quantitative scoring of the Lanthony Desaturate color vision test.

The Lanthony Desaturate Panel D-15 (D-15d) color vision test is used in neurotoxicological testing to assess acquired color vision deficits. The original test design included a qualitative scoring method. Quantitative scoring requires mapping the colored objects used in the test into a color space describing perceptual distances. A table of these distances has previously been published for the saturated version of this color vision test, but not the desaturate test. This communication includes a table of color distances for the calculation of Bowman's Total Color Distance Score (TCDS) for the D-15d. This table should be useful for non-computerized scoring under field test conditions or for devising one's own computerized scoring methods using the tabulated color distances for a look-up table. Data analysis programs using SAS or Matlab are available from the author.

Color↗

Color discrimination in schizophrenia.

Neuropsychiatric conditions that involve dopaminergic depletion have been associated with color discrimination deficits along the blue-hue (tritan, or short-wavelength-sensitive) axis. Because dopamine dysregulation may be a major factor in schizophrenia, we investigated color vision in this disorder. The performance of males with schizophrenia (SZ, n = 16) and normal male control subjects (CS, n = 14) was evaluated on five measures of color discrimination. SZ made more hue discrimination errors than CS, but no pattern emerged regarding a hue-specific axis of deficit. Dosage of anti-psychotic medication was not correlated with performance on hue discrimination. These results suggest that in medicated patients with schizophrenia, the dopaminergic disturbance, which may involve system hyperactivity, does not produce tritan-specific color deficits that have been observed in disorders involving dopaminergic hypoactivity.

Adult↗

Human colour discrimination based on a non-parvocellular pathway.

BACKGROUND: Traditionally, colour information is assumed to be carried by neural channels in the parvocellular pathway and to be encoded in an opponent manner, while other, non-parvocellular, spectrally non-opponent channels are thought to play no part in colour vision. But is the parvocellular pathway the only way that colours can be discriminated in human vision? We studied two patients with cerebral achromatopsia, who lack conscious colour perception but are nevertheless able to make use of colour information. In particular, we investigated whether, in these patients, colour discrimination is mediated by the parvocellular pathway. RESULTS: The achromatopsic patients carried out a forced-choice colour- and luminance-discrimination task, and showed clear evidence of unconscious colour processing, consistent with previous studies. We added different types of luminance noise to see when this unconscious colour information could be masked. The results of the colour-discrimination-with-noise and the brightness-non-additivity experiments showed a double-dissociation between patients. This indicates that, in one patient, unconscious colour discrimination may be subserved by a spectrally non-opponent mechanism, which does not have the characteristics of the parvocellular pathway and which is responsive to fast flicker. Spectral sensitivity, contrast sensitivity and motion perception experiments confirmed that this patient lacks a working opponent parvocellular system. The second achromatopsic patient showed evidence of a residual parvocellular system. CONCLUSIONS: Our results show that chromatic discrimination need not be mediated by neural mechanisms, the parvocellular system in particular, normally assumed to subserve conscious colour perception. Such discrimination may be mediated by a neural subsystem which responds to fast flicker, is spectrally non-opponent, and supports normal motion perception.

Aged↗

Now you see it, now you don't. Colour vision.

Studies of patients who are colour blind as a result of brain damage show that colour contributes much more to our perception of the visual world than merely the registration of hue.

Color Perception↗

Colour vision. Dalton's eyes and monkey genes.

Recent molecular genetic studies show how changes in the protein component of a visual pigment alters its absorbance; they also explain the abnormal colour vision of one of the great pioneers of visual science.

Animals↗

GCAP1 (Y99C) mutant is constitutively active in autosomal dominant cone dystrophy.

GCAP1 stimulates photoreceptor guanylate cyclase (GC) in bleached vertebrate photoreceptors when [Ca2+]free decreases but is inactivated when cytoplasmic [Ca2+]free increase after dark adaptation. A Y99C mutation in GCAP1 has recently been found to be associated with autosomal dominant cone dystrophy. We show that the GCAP1(Y99C) mutant and native GCAP1 are highly effective in stimulation of photoreceptor GC1. The Ca2+ sensitivity of the mutant GCAP1, however, is markedly altered, causing reduced but persistent stimulation of GC1 under physiological dark conditions. These results are consistent with a model in which enhanced GC activity in dark-adapted cones leads to elevated levels of cytoplasmic cGMP. Alterations in physiological cGMP levels are also associated with other retinal degenerations, including Leber's congenital amaurosis.

Adaptation, Physiological↗

Tetrachromats.

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Animals↗

MZ female twins discordant for X-linked diseases: a review.

The 20 reported cases of MZ female twins discordant for X-linked diseases are reviewed. In such twins the X-inactivation pattern is opposite skewing (abnormal allele inactivated in most cells of the normal twin, and normal allele inactivated in most cells of the affected twin) or skewing in one twin and random in the cotwin. The diseases involved map in two specific regions: Xq27-28 and Xp21. The only exceptions are Fabry's disease and Aicardi's syndrome, which map in Xq22 and Xp22 respectively. No concordant MZ female carrier twins, either normal or affected, have been described. Three main hypotheses have been proposed to explain such characteristics [2, 5, 14], but none is completely satisfactory. The constant discordance for X-linked diseases in MZ female twins has important consequences for genetic counselling.

Color Vision Defects↗