The vision of typhoon lengkieki.
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We report on two brain-damaged subjects who exhibit the uncommon pattern of loss of object color knowledge, but spared color perception and naming. The subject P.C.O., as in previously reported patients, is also impaired in processing other perceptual and functional properties of objects. I.O.C., in contrast, is the first subject on record to have impaired object color knowledge, but spared knowledge of object form, size and function. This pattern of performance is consistent with the view that semantic information about color and other perceptual properties of objects is grounded in modality-specific systems. Lesion analysis suggests that such grounding requires the integrity of the mesial temporal regions of the left hemisphere.
Six elderly patients with ocular involvement by Non-Hodgkin's lymphoma are reviewed. The characteristic clinical features were a history of fluctuating vision, findings of decreased colour vision, constricted visual fields, vitreous cells and subretinal infiltrates. Fluorescein angiography revealed pigment epithelial abnormalities and attenuated retinal vessels. Non-invasive investigations produced a definite diagnosis in two patients and a presumptive diagnosis in a further three. The ocular involvement was confirmed by vitreous cytology in only one patient: vitreous biopsies in three other patients yielded chronic inflammatory cells and no evidence of lymphoma. The condition responded poorly to steroids but well to radiotherapy.
A cheap, portable automated scorer for the Farnsworth-Munsell (FM) 100 hue test has been developed. It consists of a light pen, a series of omni-directional bar-codes attached to the reverse of the FM 100 hue caps and a small micro-computer. The print-out includes patient details, a linear histogram of the partial errors by cap position, indication of the peak error positions for congenital colour vision deficiencies and appropriate statistical analysis of the total error score. All the results are available within four minutes of completing the testing procedure.
Macular phototoxicity is known to occur with laser use, and there is evidence that the wavelength of the light used influences this effect. In this study, a computer based colour contrast sensitivity test was used to assess the immediate macular effects of photocoagulation of peripheral flat retinal holes in otherwise normal retinas, using blue-green (488 and 514 nm), yellow (577 nm), orange (595 nm) or red (647 nm) laser light. The laser aiming beam was not allowed to traverse the macula at any stage during treatment. No protan or deutan axis threshold changes were noted in the 17 patients tested irrespective of the laser wavelength used. Tritan axis sensitivity was significantly reduced one hour after treatment with the blue-green laser, but no tritan axis change was found after treatment with longer wavelength lasers. The effect was no longer present the day after treatment in the subjects tested. The results show that even peripheral retinal treatment with blue-green laser can cause acute macular phototoxicity.
A survey of van Gogh's work from 1886 to 1890 indicated that paintings with a yellow dominance were numerous, episodic, and multi-regional. His underlying illness, by his own admission, affected his life and work; furthermore, episodes of malnutrition, substance abuse, environmental exposure, and drug experimentation (all evident from correspondence) exacerbated his condition. Accordingly, we reviewed plausible agents that might have modified the artist's colour perception. Xanthopsia due to overdosage of digitalis or santonin is well documented elsewhere, but evidence of useage of either drug by van Gogh cannot be substantiated. It is unlikely that ageing of the human lens was an influence because of the artist's youth. Sunstroke is too restrictive to fit the multiplicity of regions and motifs. Hallucinations induced by absinthe, the popular liqueur of the period, may explain particular canvases but not the majority of 'high yellow' paintings. Van Gogh's proclivity for exaggerated colours and his embrance of yellow in particular are clear from his letters and, in contradistinction to chemical or physical insults modifying perception, artistic preference is the best working hypothesis to explain the yellow dominance in his palette.
Variations in classic Leber hereditary optic neuropathy (LHON) include recovery of vision and association with other neurological abnormalities. Sixteen multi-generational Australian families originating from the United Kingdom with LHON were studied by the one examiner, using the same protocol. In particular, recovery of vision and other neurological abnormalities were noted. One very large family (Tas2) and one small family (Vic2) were found to have frequent recovery of vision (50% of patients). They both had the 14484 T to C mutation in their mitochondrial DNA (mtDNA). One apparently unique family (Qld1) was found to have frequent juvenile encephalopathy and peripheral neurological signs. They had the 4160 T to C and 14484 T to C mutations. The remaining 13 families rarely showed visual recovery or associated neurological abnormalities. They had the common 11778 G to A or the 3460 G to A mutations. Thus mitochondrial genotypes in LHON are associated with variable phenotypes.
A pilot echographic study was conducted to determine the incidence and severity of optic nerve swelling in acute 'idiopathic' optic neuritis and to examine cerebrospinal fluid dynamics in the subarachnoid space, employing the method of standardised echography and the '30 degrees test'. An attempt was made to correlate the degree of nerve swelling with the initial visual loss and with the rate and extent of recovery of vision. The visual function and echographic features of the optic nerve in 27 patients with the diagnosis of acute optic neuritis were assessed with standardised echography. A significant increase in nerve diameter was found in 74% of cases. There was a correlation between nerve swelling and the severity of initial visual loss. The authors conclude that standardised echography is a useful tool in the diagnosis of optic neuritis and may play a role in predicting the visual outcome.
The retina contains Na+K(+)-ATPase and carbonic anhydrase (CA), enzymes that regulate ion fluxes across cell membranes of photoreceptors. Since inhibition of retinal Na+K(+)-ATPase by digitalis impairs colour vision, we wanted to find out whether this also occurs after inhibition of CA. In a double-masked cross-over study with placebo, 14 male volunteers were given 50 mg q.i.d. of the CA inhibitor methazolamide for 2 weeks. A disturbance of colour discrimination was observed in 8 of the 14 subjects, in the classification phase of Lanthony New Color Test. The presence of the disturbance was not significantly correlated to the degree of acidosis or to other side-effects. Its mechanism could be interpreted as a specific effect of CA inhibition in the retina (or the visual cortex) calculated to more than 99.9%.
Automated colour vision testing in pseudophakes showed unexpected results. Chromatic discrimination sensitivity was measured in 22 diabetic pseudophakes with no retinopathy, 23 diabetic pseudophakes with background retinopathy and 34 non-diabetic pseudophakes. These results were compared with those in age-matched normal and diabetic phakic subjects, all of whom had good vision. The diabetics were also matched for retinopathy grading and duration of diabetes. In all three groups, red-green discrimination sensitivity was worse in the pseudophakes when compared with the corresponding phakic subjects (normals, p < 0.001; no retinopathy, p = 0.467; background retinopathy, p = 0.057). However, tritan vision was marginally worse in the normal pseudophake group but was better in the two diabetic pseudophake groups, when compared with phakic controls. This may be due to a reduction in tritan sensitivity in age-matched phakic controls from the effects of increased lens yellowing with age.
A prospective study was carried out to investigate acquired colour-vision deficits in diabetics using an automated, computer-controlled, cathode-ray-tube based test of chromatic contrast. Chromatic-contrast thresholds estimates were measured along both a red/ green (constant S-cone) confusion axis and a tritan (constant M/L-cone) confusion axis for 305 eyes of 305 diabetics. The diabetic data were partitioned into groups based on a clinical categorisation of retinopathy. The diabetic data were compared with both age-matched and 'lens-equated' control data obtained from a bank of 347 normal subjects. Further analysis of differences between diabetic-status groups was performed. Associations between chromatic contrast threshold estimates and age, duration of disease, and severity of both macular oedema and ischaemia were investigated. The diabetic group was found to have significantly reduced chromatic-contrast threshold estimates when compared with normal controls, even in the absence of retinopathy. This reduction in chromatic contrast was predominantly tritanopic in nature. Interestingly, no reduction in red/green chromatic-contrast threshold estimate was found in diabetics without retinopathy. The tritan deficit seen in diabetics without retinopathy was strongly correlated with duration of disease, but when adjustments were made to account for the effects of duration-dependent lens yellowing, the tritan deficit was no longer apparent. A correlation between both the severity of macular oedema and severity of ischaemia with chromatic-contrast loss was established. Acquired reductions in both red/green and tritan chromatic-contrast threshold estimates seen in diabetics are strongly correlated with the severity of retinopathy. The results provide evidence that the specific tritan deficits seen in diabetics can be explained by the effects of lens yellowing rather than by selective damage of the blue cone system as has been hypothesised by other groups. The results provide support for the potential use of automated CRT-based tests of colour vision in diabetic retinopathy screening protocols.
PURPOSE: To determine whether differences in luminance contrast and colour contrast are factors in failing to identify American Optical pseudoisochromatic plates (AOPP). METHODS: We studied two groups of subjects. In 20 normal test subjects with no errors on the AOPP we used cross-polarising filters to darken and then gradually increase perceived luminance of the AOPP until these normal subjects correctly identified the plate. In a second group, to evaluate the relationship between a luminance contrast sensitivity score using Arden plates and AOPP identification, we tested 37 non-colour-deficient subjects who missed zero to five of the AOPP of low colour and luminance contrast (plates 9-12, 15). RESULTS: Using the cross-polarising filters, we found five plates that required more light to identify (plates 9-12, 15). In the second experiment, we found a significant relationship between the number missed of these five AOPP plates and a decrease in contrast sensitivity (r = 0.91, p < 0.001, Spearman correlation coefficient). CONCLUSION: Errors in AOPP colour plate detection may be due to loss of ability to perceive colour contrast and possibly luminance contrast.
The cone dystrophies are a heterogeneous group of inherited disorders that result in dysfunction of the cone photoreceptors and sometimes their post-receptoral pathways. The major clinical features of cone dystrophy are photophobia, reduced visual acuity and abnormal colour vision. Ganzfeld electroretinography shows reduced or absent cone responses. On the basis of their natural history, the cone dystrophies may be broadly divided into two groups: stationary and progressive cone dystrophies. The stationary cone dystrophies have received more attention, and subsequently our knowledge of their molecular genetic, psychophysical and clinical characteristics is better developed. Various methods of classification have been proposed for the progressive cone dystrophies, but none is entirely satisfactory, largely because the underlying disease mechanisms are poorly understood. Multidisciplinary studies involving clinical assessment, molecular genetics, electrophysiology and psychophysics should lead to an improved understanding of the pathogenesis of these disorders.
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A heterogeneous group of neurological disorders known as the spinocerebellar ataxias (SCA) are characterized by degeneration of the cerebellum, spinal cord and brainstem. We describe linkage analysis in four unusual SCA families revealing a distinct disease locus on chromosome 3p14-21.1. The disease in these families is distinguished from other forms of SCA by concomitant retinal degeneration. Initial visual problems leading to blindness, disabling ataxia and anticipation are seen in all kindreds. The anticipation in these families suggests a dynamic mutation at this locus. Eventual molecular characterization of this disease may provide valuable insights into the processes of both neural and retinal degeneration.
We describe a compelling demonstration of large-scale developmental reorganization in the human visual pathways. The developmental reorganization was observed in rod monochromats, a rare group of congenitally colorblind individuals who virtually lack cone photoreceptor function. Normal controls had a cortical region, spanning several square centimeters, that responded to signals initiated in the all-cone foveola but was inactive under rod viewing conditions; in rod monochromats this cortical region responded powerfully to rod-initiated signals. The measurements trace a causal pathway that begins with a genetic anomaly that directly influences sensory cells and ultimately results in a substantial central reorganization.
Three centuries of experimentation in optics, psychophysics and biochemistry established the dependence of color vision on three kinds of light-absorbing molecules, or pigments, in the cone cells of the retina. The author has isolated the genes that encode the pigments and has identified genetic anomalies that lead to color blindness.