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Chromatic and luminance contributions to a hyperacuity task.

Displacement thresholds with incremental chromatic and luminance edges were measured on different backgrounds. Above 3% luminance contrast, thresholds were always similar. At luminance contrasts below 3%, luminance edges could not be detected, but chromatic edges were still visible. At these low contrasts displacement thresholds for chromatic edges increased to a high level. We interpret these data in terms of multiple mechanisms; above 3% contrast a luminance mechanism determines thresholds, but when, at lower contrasts, chromatic mechanisms support detection, they also support the spatial task. Physiological data were consistent with the different mechanisms originating at the retinal ganglion cell level.

Animals↗

Acephalgic migraine. Fifteen years experience.

Sixty-one patients with acephalgic migraine have been seen and thoroughly evaluated at the USAF School of Aerospace Medicine over the past 15 years. Patient age ranged in years from 21 to 61, with the number of spells varying between 1 and 100 and lasting from 15 seconds to 3 hours. These phenomena were present for 2 weeks to 25 years. Ocular involvement was represented by scintillation, transient hemianopia, bilateral central scotomata, classic amaurosis fugax, diplopia, altitudinal field loss, tunnel vision; temporal crescent involvement, and several patients who developed a transient central scotoma in one eye with alterations in color perception. Other neurologic involvement occurred in 29%. Permanent neurologic deficit occurred in only one patient. Positive family history for migraine was present in only 24%. Headache is not a necessary feature of migraine attacks. One should consider migraine in any acute episodic neurologic disorder.

Adult↗

Assessment of visual functions following prenatal exposure to organic solvents.

Prenatal exposure to organic solvents has been previously associated with increased risk of color vision deficits and reduced visual acuity in young children. These findings prompted us to evaluate visual functioning in solvent-exposed infants using more sensitive non-invasive visual evoked potential (VEP) techniques. VEP techniques are described in the context of an ongoing prospective longitudinal cohort study of infants exposed to organic solvents in utero. VEPs are recorded via three active electrodes fitted over the occipital cortex while infants view changing visual stimuli. The sweep VEP is used to assess contrast detection and visual acuity by presenting sinusoidal gratings that "sweep" across a range of contrasts and spatial frequencies. Transient VEPs are used to assess responses to equiluminant chromatic- and luminance-modulated sinusoidal gratings presented in pattern onset-offset format. A single case study is presented showing abnormal chromatic responses and reduced contrast sensitivity in a 2.5-year-old boy following prenatal exposure to perchloroethylene (PCE). These VEP techniques therefore appear promising for the clinical assessment of visual toxicity in pediatric populations.

Child, Preschool↗

Visual dysfunction in workers exposed to a mixture of organic solvents.

The aim of this study was to investigate the relationship between the workers occupationally exposed to a mixture of organic solvents and their visual functions. Here the visual functions included color vision (CV), visual contrast sensitivity (CS) and visual evoked potentials (VEP). Test subjects were 182 workers at 53 furniture factories in the same industrial area of Japan. As control, a group consisted of 96 workers without exposure to any organic solvent was also tested. Exposure assessments were made both by the environmental concentration and biological monitoring. CV and CS tests were carried out for all the subjects. VEP was measured for 21 exposed subjects who were considered to have impaired CV and CS. In the results, the color confusion index (CCI) values of the exposed subjects were significantly higher than that of the age-matched controls (P<0.01). Their CS values were significantly lower than those in the controls at spatial frequencies of 6 and 12 cycles per degree (cpd) (P<0.01 and <0.05, respectively). A significant correlation between the concentration of urinary methylhippuric acid and contrast sensitivity was found by a multiple regression analysis (P<0.05). CCI showed a negative correlation at all spatial frequencies of CS in a simple regression analysis, no abnormal data were found by the VEP test in the exposed subjects who were found to have impaired CV and CS. The results suppose that a low concentration of the mixed organic solvents might affect the retina and optic nerve. However, it needs to be further researched if such an impact affects the Brodmann's areas of visual cortex in the brain.

Adult↗

Color discrimination impairment in workers exposed to mercury vapor.

OBJECTIVE: To study color discrimination impairment in workers exposed to elemental mercury (Hg) vapor. SUBJECTS: Twenty-four male workers from a chloralkali plant exposed to Hg vapor, aged 42+/-9.8 years, duration of exposure 14.7+/-9.7 years, were examined. The 8h TWA air-borne Hg concentration in workplace was 59 microg/m(3); mean Hg urinary excretion (HgU) was 20.5+/-19.3 microg/g creatinine; mean Hg urinary excretion after the administration of a chelating agent, sodium 2,3-dimercapto-1-propane-sulfonate (DMPS), was 751.9+/-648 microg/48h. Twenty-four age- and gender-matched control subjects were compared. Visual acuity, alcohol intake, smoking habits, and history of diseases or drugs potentially influencing color vision were registered. METHODS: The Lanthony 15-Hue desaturated test (L-D15-d) was used to assess color vision. The results were expressed quantitatively as Bowman's Color Confusion Index (CCI), and qualitatively according to Verriest's classification of acquired dyschromatopsias. RESULTS: The CCI was significantly higher in the exposed group than in the control (mean CCI 1.15 versus 1.04; P=0.04). The proportion of subjects with errorless performance on the Lanthony test was significantly lower in the Hg exposed group compared to referents (52% versus 73%; P=0.035). The exposed group showed higher frequency of type III dyschromatopsias (blue-yellow confusion axis) in comparison with the control group (12.5% versus 8.3%), however, the difference did not reach statistical significance. Multiple regression did not show any significant relationship between the CCI, and age, alcohol consumption, or measures of exposure. CONCLUSION: In agreement with previous studies by Cavalleri et al. [Toxicol. Lett. 77 (1995) 351; Environ. Res. Sec. A 77 (1998) 173], the results of this study support the hypothesis that exposure to mercury vapor can induce sub-clinical color vision impairment. This effect was observed at an exposure level below the current biological limit for occupational exposure to mercury. This raises doubts on the actual protection afforded by this limit concerning the effect of mercury on color vision.

Adult↗

Color vision impairment in workers exposed to neurotoxic chemicals.

Recent research shows that occupational exposure to several solvents, metals and other industrial chemicals can impair color vision in exposed workers. Occupation-related color vision impairment usually results in blue-yellow color discrimination loss or, less frequently, a combination of blue-yellow and red-green loss. The eyes may be unequally involved, and the course is variable depending on exposure and other factors. The pathogenesis of occupational color vision loss has not been elucidated; it may be due to, e.g. a direct action of neurotoxins on receptors, possibly on the cone's membrane metabolism, and/or to an interference with neurotransmitters within the retina. Other possible pathogenetic mechanisms, such as a direct effect to the optic nerve, have also been suggested. Occupational color vision loss is usually sub-clinical, and workers are unaware of any deficit. It can be assessed using sensitive tests, such as the Farnsworth-Munsell 100 Hue (FM-100) or the Lanthony D-15 desaturated panel (D-15 d). The latter is the most widely used for studies in groups of exposed workers, and offers the possibility of a quantitative evaluation of the results by calculation of the Bowman's Color Confusion Index (CCI), or of the Vingrys' and King Smith's Confusion Index (CI). Other advantages of D-15 d are the possibility to perform the test directly at the workplace, and the reproducibility when performed in standardized conditions. In most cases, occupation-related color vision impairment is correlated to exposure levels, and has often been observed in workers exposed to environmental concentrations below the current occupational limit proposed by the ACGIH. Progression with increasing cumulative exposure has been reported, while reversibility is still discussed. Acquired color vision impairment related to occupational exposure to styrene, perchloroethylene (PCE), toluene, carbon disulfide, n-hexane, solvent mixtures, mercury and some other chemicals are discussed. Results show that color vision testing should be included in the evaluation of early neurotoxicity of chemicals in exposed workers. The D-15 d would be useful in the surveillance of workers exposed to solvents and other chemicals toxic to the visual system.

Animals↗

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↗

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↗

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↗

Tetrachromats.

Explore the source record for details and available documents.

Animals↗

A sensorimotor account of vision and visual consciousness.

Many current neurophysiological, psychophysical, and psychological approaches to vision rest on the idea that when we see, the brain produces an internal representation of the world. The activation of this internal representation is assumed to give rise to the experience of seeing. The problem with this kind of approach is that it leaves unexplained how the existence of such a detailed internal representation might produce visual consciousness. An alternative proposal is made here. We propose that seeing is a way of acting. It is a particular way of exploring the environment. Activity in internal representations does not generate the experience of seeing. The outside world serves as its own, external, representation. The experience of seeing occurs when the organism masters what we call the governing laws of sensorimotor contingency. The advantage of this approach is that it provides a natural and principled way of accounting for visual consciousness, and for the differences in the perceived quality of sensory experience in the different sensory modalities. Several lines of empirical evidence are brought forward in support of the theory, in particular: evidence from experiments in sensorimotor adaptation, visual "filling in," visual stability despite eye movements, change blindness, sensory substitution, and color perception.

Brain↗

Visual dysfunction with basal skull tumours.

Early detection of visual loss caused by tumours of the base of the skull is accomplished by systematic tests of the pregeniculate optic pathway. Even when central acuity is relatively preserved, a relative afferent pupillary defect and reduced color perception yield evidence of impaired optic nerve conduction. Although confrontation tests of the visual fields are useful screening techniques, unexplained symptoms should be pursued with static and kinetic perimetry. Patterns of optic nerve and chiasmal field loss and atrophy of the dis or retinal nerve fibers are imprecise guides to the location of basal skull tumours. Regardless of the pattern of visual field defect, unexplained progressive loss of vision demands intensive neuroradiologic study of the basal cisterns and skull.

Brain Neoplasms↗

Devic's neuromyelitis optica treated with intravenous gamma globulin (IVIG).

BACKGROUND: Devic's syndrome is a demyelinating disease of the spinal cord and optic nerves. It tends to have a poor prognosis, probably due to the occurrence of necrosis within lesions. There is no proven effective treatment although relapses are commonly treated with corticosteroids and people with recurrent attacks may be managed with chronic immune suppressing treatments. Intravenous gamma globulin (IVIG) and plasma exchange are reasonable treatment options because Devic's syndrome is believed to be antibody mediated. We report two patients of Devic's syndrome that stabilized following initiation of monthly IVIG. PATIENT 1: A 42-year-old woman with a 23 year history of Devic's syndrome continued to have frequent attacks of optic neuritis unresponsive to daily corticosteroids and azathioprine. Since initiation of monthly IVIG 5 1/2 years ago she has had no further definite attacks. She has also noted minimal improvement in color perception. PATIENT 2: A 58-year-old woman with a three year history of Devic's syndrome experienced five attacks during the first 16 months of disease. Monthly IVIG was associated with complete cessation of relapses and significantly improved neurological status over one year of treatment. CONCLUSIONS: Because active Devic's disease often results in severe, permanent neurological impairment, preventive intervention should be considered. These cases suggest that IVIG may be effective in preventing attacks and possibly in enhancing neurological recovery. Randomized controlled trials will be needed to confirm this and to determine optimal dosing and treatment duration.

Adult↗

Opponent-color detection threshold asymmetries may result from reduction of ganglion cell subpopulations.

Thresholds for psychophysically opposite stimuli--light and dark, or equiluminous red and green, or equiluminous blue and yellow--are usually nearly equal. This color threshold symmetry is sometimes violated in subjects who have optic nerve hypoplasia, a congenital loss of retinal ganglion cells. We describe a subject who has optic nerve hypoplasia, who exhibits large red-green and blue-yellow detection threshold asymmetries for equiluminous spots. Temporal and spatial integration for equiluminous red and green test spots also differed from normal; static perimetric thresholds for equiluminous green, blue, and yellow (but not red) spots lacked the normal "V" shaped minimum at the fovea. These asymmetries may relate to a developmental paucity of some ganglion cell subtypes. Optic nerve hypoplasia may allow the contributions to detection made by individual ganglion cell subtypes to be isolated psychophysically, in analogy to the study of cone spectral sensitivity in dichromats.

Adult↗

Molecular genetics of color-vision deficiencies.

The normal X-chromosome-linked color-vision gene array is composed of a single long-wave-sensitive (L-) pigment gene followed by one or more middle-wave-sensitive (M-) pigment genes. The expression of these genes to form L- or M-cones is controlled by the proximal promoter and by the locus control region. The high degree of homology between the L- and M-pigment genes predisposed them to unequal recombination, leading to gene deletion or the formation of L/M hybrid genes that explain the majority of the common red-green color-vision deficiencies. Hybrid genes encode a variety of L-like or M-like pigments. Analysis of the gene order in arrays of normal and deutan subjects indicates that only the two most proximal genes of the array contribute to the color-vision phenotype. This is supported by the observation that only the first two genes of the array are expressed in the human retina. The severity of the color-vision defect is roughly related to the difference in absorption maxima (lambda(max)) between the photopigments encoded by the first two genes of the array. A single amino acid polymorphism (Ser180Ala) in the L pigment accounts for the subtle difference in normal color vision and influences the severity of red-green color-vision deficiency. Blue-cone monochromacy is a rare disorder that involves absence of L- and M-cone function. It is caused either by deletion of a critical region that regulates expression of the L/M gene array, or by mutations that inactivate the L- and M-pigment genes. Total color blindness is another rare disease that involves complete absence of all cone function. A number of mutants in the genes encoding the cone-specific alpha- and beta-subunits of the cGMP-gated cation channel as well as in the alpha-subunit of transducin have been implicated in this disorder.

Animals↗

Multifocal electroretinogram in trichromat and dichromat observers under cone isolating conditions.

The aim of this study was to obtain information about single cone class driven activity in the inner and outer retina in humans. We examined outer retinal activity with the multifocal electroretinogram (mfERG) and inner retinal activity using multifocal oscillatory potentials (mfOPs). A standard (black-white) stimulus was used, as well as stimuli aimed at isolating a single photoreceptor class. The results of 10 trichromats were compared to those of 2 protanopes and 2 deuteranopes. At both retinal layers we find that trichromats show cone isolating response amplitudes that reflect the expected number of cones and that single- gene dichromats have a similar total number of functioning cones as trichromats. The ratio of the responses of the L- and M-cones is slightly smaller for the mfOPs than for the mfERGs. The results indicate that there are major changes in the gain of retinal signals after the inner plexiform layer.

Adult↗

Effect of foveal tritanopia on reaction times to chromatic stimuli.

To investigate the effect of foveal inhomogeneities on sensitivity to chromatic stimuli, we measured simple reaction times (RTs) and detection thresholds to temporally and spatially blurred isoluminant stimuli at retinal eccentricities from 0 deg to 8 deg. Three color-normal subjects participated. Contrast gain was derived from the slope of the RT versus contrast function. With a Gaussian spatial distribution (S.D. = 0.5 deg) and modulation between white (CIE x, y, L = 0.31, 0.316, 12.5 cd x m(-2)) and blue (MBDKL 90 deg), gain was maximal at about 2-deg eccentricity and declined by approximately 1 log unit towards the center and the periphery. The red (0 deg) and green (180 deg) cardinal axes showed maximum gain in the center, whilst the yellow (270 deg) data were intermediate. Although the spatial extent of the Gaussian spot was much larger than the S-cone free zone, we wished to determine whether foveal tritanopia was responsible for the marked drop in sensitivity to the 90-deg stimulus. To align the color vector along a tritan line, we used a smaller disk (0.3 deg) with a blurred edge and measured detection threshold, rotating the vector until minimum central sensitivity was obtained. Other workers have used transient tritanopia or minimally distinct border to similar effect. By repeating this at different locations in color space, a group of vectors were obtained. These converged near to the S-cone co-punctal point, evidence that they lay along tritan confusion lines. These threshold findings were then confirmed using the RT-derived contrast gain function. The tritan vectors were less pronounced as stimulus size increased. With the vector optimized to produce foveal tritanopia, the RT gain versus eccentricity functions for the 90-deg and 270-deg stimuli both fell markedly in the center and periphery, and sensitivity peaked at about 3-deg eccentricity. There are some similarities between these findings and the underlying photoreceptor distributions. As a result, there is a greater difference in gain between red-green and blue-yellow systems in the center than in the near periphery. We conclude that the RT versus contrast function is a sensitive index of foveal opponency.

Color Perception↗