Biomedical subjects
Publications and source records attributed to V Walsh.
The colours we see reflect not only the light wavelengths presently being detected, but also those already received. To understand colour constancy therefore requires an understanding of adaptation in the visual system.
Monkeys with lesions of visual area V4 have deficits in colour constancy, but are able to discriminate hues and segment the spectrum in a categorical manner. To investigate the nature of the processing mechanisms subserving the spared functions we recorded occipital visual evoked potentials (VEPs) of normal monkeys and monkeys with bilateral lesions of area V4. The stimuli used to elicit the potentials were chromatic and achromatic gratings of low spatial frequency. The waveforms from the two groups of animals were similar in all respects. VEPs for the onset of a chromatic grating were negative-going, indicative of the activity of sustained units, as opposed to those elicited by offset or reversal of the grating which were positive-going. The amplitude of the chromatic, 12.5 Hz reversal VEP went through a minimum at isoluminance, in accord with low temporal resolution of colour processing. The VEP waveforms were identical in character from three weeks to approximately four years post-operatively. These data indicate that chromatic processing in areas V1 and V2 is normal after V4 lesions and, together with the behavioural evidence, that these areas are sufficient for some basic aspects of colour perception.
Monkeys with lesions of cortical visual area V4 were compared with unoperated monkeys in three experiments. In Expt. 1 they were tested for the reacquisition of a pre-operatively learned hue discrimination task. In Expt. 2, as a test of colour constancy, the monkeys were required to perform previously overlearned colour discrimination tasks when the amounts of red, green and blue light in the illuminant were changed. In Expt. 3 the animals were compared on the post-operative acquisition of hue, greyness and saturation discrimination tasks. The results of Expt. 1 showed that monkeys with V4 lesions can regain their pre-operative levels of performance on hue discrimination tasks. Expt. 2 showed that monkeys with V4 lesions have a colour constancy deficit. Expt. 3 reinforced the finding that the animals with V4 lesions could learn to perform fine hue discriminations but that their final, asymptotic performance was not as reliable as that of normal animals. The wavelength discrimination data are discussed within the context of recent electrophysiological findings that V4 is involved in selective attention to visual stimuli and the constancy data are interpreted as evidence that V4 is important for defining colour constancy thresholds but not for constructing the perceptual categories underlying constant colour perception.
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Monkeys with V4 lesions and unoperated controls were tested behaviourally for their perception of the colour categories red, green, blue and yellow. As expected, the monkeys with V4 lesions took longer to acquire the colour discriminations. However, the pattern of learning was the same in the two groups of animals. Both the lesioned and the control animals made more errors when the stimuli to be discriminated belonged to the same colour category than when they belonged to different categories and thus showed normal colour categorization. The results suggest that monkeys with V4 lesions perceive the colour spectrum according to the same fundamental perceptual categories as normal monkeys and humans, and thus support the view that, in the colour domain, the four basic perceptual categories are constructed by chromatic mechanisms operating earlier than visual area V4.
Monkeys with bilateral ablation of cortical visual area V4 were compared with unoperated controls for their ability to relearn postoperatively a series of preoperatively acquired two-choice visual discrimination problems. The animals with V4 lesions were impaired on relearning to discriminate between different shapes, and discrimination between identical shapes presented at different orientations was also impaired. Some of the deficits were consistent with disrupting the input to inferotemporal cortex, but discrimination of a subset of the stimuli is known to be unaffected by inferotemporal cortex lesions and could not be explained in the same way. To clarify the nature of the deficit, and to test the hypothesis that shapes differing in orientation are analyzed in the occipitoparietal processing pathway, animals with V4 lesions were also compared to normals on their ability to acquire a version of the landmark task. The V4 animals performed as well as the control animals on this task. The results suggest that V4 is important for the shape discrimination abilities that survive inferotemporal cortex lesions. The role of V4 in shape analysis is discussed in the light of recent evidence that V4 neurones are modulated by visual attention.
Eye tracking abnormalities have been proposed as a trait marker for schizophrenia on the basis of their familial prevalence and the consistency of tracking over time in clinically stable patients. However, few studies have examined stability through acute episodes of illness, and most studies have not analyzed changes in different forms of eye movements. Therefore, the authors examined eye tracking, clinical state, and neuroleptic dose during 4 consecutive weeks in nine recently hospitalized schizophrenic patients. For the patients and controls, qualitative ratings of pursuit accuracy remained relatively stable over time. In contrast, saccade frequency increased significantly, with a 57% increase in small saccades and a 77% reduction in larger saccades. In comparison with cross-sectional studies which have found no correlation between neuroleptic dose and tracking performance, a reduction in large saccades was strongly correlated with increase in neuroleptic dose. The findings suggest that pursuit accuracy may be a trait characteristic of schizophrenia, while the frequency and size of saccades are state dependent characteristics.
Physicians are aware of and support selected caries preventive techniques involving fluoride, particularly community water fluoridation, fluoridating school water supplies, and the prescription of dietary fluoride supplements. Physicians are generally less informed about the relative worth of other caries preventive measures. The role of the practicing physician in the provision of caries prevention methods is a very active one, with physicians prescribing fluoride supplements, counseling on diet, and providing oral hygiene education. Children would be better served in caries prevention if the interest and initiative of the medical practitioners were encouraged and current information was made available to them. These findings represent the preliminary analysis of a mailed survey to a stratified, systematic sample of 2,000 physicians who treat child patients in the nation.
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According to the magnocellular theory of dyslexia, otherwise intelligent children may fail to learn to read because of abnormalities in the magnocellular layers of the lateral geniculate nucleus (mLGN). If this were the case, one would predict that dyslexic subjects who show a deficit on low-level psychophysical tasks which tax the magnocellular system would also have deficits on higher-level visual tasks which do not rely on the properties of mLGN cells but depend upon the functioning of areas whose main inputs originate in the mLGN. In other words, magnocellular deficits should be traceable at later stages of visual processing. One area where such later processing is thought to occur is the posterior parietal cortex, damage to which impairs function on some classes of visual search. To test this hypothesis, we tested two groups of dyslexic subjects and a group of non-dyslexic controls on a range of visual search tasks. One group of dyslexic subjects had elevated motion coherence thresholds, a sign of deficits at the early levels (e.g. mLGN) of visual processing, and the other group had normal motion coherence thresholds. If the magnocellular deficits extended to the parietal cortex, it follows that the subjects with elevated motion coherence thresholds should have deficit in visual search, whereas those with normal motion coherence thresholds should not. The dyslexics with a motion coherence deficit were also impaired on serial visual search tasks but not on a parallel search. The dyslexics with normal motion coherence performance were unimpaired on visual search. The deficit was expressed as an elevation in reaction times, but there was no difference between the groups either in error rates or in the way the tasks were ranked according to difficulty. The results suggest that those dyslexics who have visual problems related to magnocellular functions also have visual-attentional problems related to the functions of areas such as the parietal cortex, which are dominated by inputs originating in the magnocellular LGN.
The brain areas involved in a task may change their contribution as one acquires expertise. An understanding of how this occurs relies on a good psychological theory of the processing requirements of a task and knowledge of which regions of the brain can perform the necessary component computations.