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Biomedical subjects

A Cowey

Publications and source records attributed to A Cowey.

At least 73 records · Page 4Linked to original sources
PubMed1997

Temporal aspects of visual search studied by transcranial magnetic stimulation.

Transcranial magnetic stimulation was applied over the parietal visual cortex of subjects while they were performing 'pop-out' or conjunction visual search tasks in arrays containing eight distractors. Magnetic stimulation had no detrimental effect on the performance of pop-out search, but did significantly increase reaction times on conjunction search when stimulation was applied over the right parietal cortex 100 msec after the onset of the visual display for trials when the target was present. Target absent reaction times were elevated when stimulation was applied 160 msec after array onset. Stimulation had no effect on the number of errors made. The results suggest that a sub-region of the right parietal lobe is important for conjunction search but not for pre-attentive pop-out. The result from target present trials is consistent with timing data from studies of single cells in monkeys and the hypothesis that parietal areas generate a signal that projects back to extrastriate visual areas to enhance the processing of features in a restricted part of the visual field. The timing of the effect indicates that transcranial stimulation disrupts the mechanisms underlying the focal attention necessary for feature binding in conjunction search. The effects of TMS on target absent trials are interpreted in terms of fronto-parietal connections and the role of frontal cortex in decision-making. The results also highlight the efficacy of transcranial magnetic stimulation as a complement to other spatial and temporal imaging techniques.

Humans↗
PubMed1997

Visual detection in monkeys with blindsight.

Monkeys with unilateral striate cortical removal show residual visual abilities in their affected hemifield. To learn whether the monkeys, like patients with blindsight, lose the phenomenal representation of the visual stimuli they nevertheless respond to, we first studied their ability to localize a briefly presented target in either hemifield. By varying the luminance of the stimuli we determined their visual sensitivity, which was reduced by 0.3-1.5 log units in the impaired hemifield; suprathreshold stimuli yielded almost perfect performance. We then presented two tests designed to show whether the monkeys categorized visual stimuli in the impaired field in the same manner as they categorize them in the normal field. In the first test, they had to respond differently according to whether one or two lights were presented, with the relative position of the two stimuli in a pair being varied. Whenever one of the paired stimuli lay in the impaired hemifield, two of the three monkeys consistently ignored it, and responded as if it had been a single stimulus in the good field. In the second test, trials consisting of a single stimulus light were interleaved with blank trials. The monkey touched the position of the light or made a different response, indicating that no light had appeared. All three monkeys responded to a light of supra-threshold luminance presented in the impaired field as if it were a blank trial. These results suggest that monkeys with striate cortical destruction, like neurological patients with similar lesions, have blindsight rather than phenomenal vision when they have to detect brief static visual targets.

Animals↗
PubMed1997

Comparing the visual deficits of a motion blind patient with the visual deficits of monkeys with area MT removed.

The performance of a 'motion blind' patient on a series of tasks in which the perception of motion played an essential or no role was compared with that of a human subject with normal vision and with that of macaque monkeys in which cortical visual area MT had been removed and adjacent areas damaged. The patient experienced difficulties on those tasks in which the perception of motion was essential, but was unimpaired on those tasks that did not require it. Similarly, the tasks which the 'motion blind' patient found impossible or difficult were precisely those tasks on which monkeys lacking area MT performed poorly. Similarly, the tasks on which the patient performed well also presented no difficulties for the animals lacking cortical area MT. The close correlation between the pattern of visual perceptual impairments in the patient and monkeys indicates that the patient's inability to perceive most forms of visual movement is attributable to total loss of, or extensive damage to, a cortical visual area that is the human equivalent of area MT and perhaps its adjacent areas.

Adult↗
PubMed1997

Blindsight in man and monkey.

In man and monkey, absolute cortical blindness is caused by destruction of the optic radiations and/or the primary visual cortex. It is characterized by an absence of any conscious vision, but stimuli presented inside its borders may nevertheless be processed. This unconscious vision includes neuroendocrine, reflexive, indirect and forced-choice responses which are mediated by the visual subsystems that escape the direct cerebral damage and the Ensuring degeneration. While extrastriate cortical areas participate in the mediation of the forced-choice responses, a concomitant striate cortical activation does not seem to be necessary for blindsight. Whether the loss of phenomenal vision is a necessary consequence of striate cortical destruction and whether this structure is indispensable for conscious sight are much debated questions which need to be tackled experimentally.

Animals↗
PubMed1996

Imaging of radiocarbon-labelled tracer molecules in neural tissue using accelerator mass spectrometry.

Autoradiography is widely and successfully used to image the distribution of radiolabelled tracer molecules in biological samples. The method is, however, limited in resolution and sensitivity, especially for 14C. Here we describe a new method for imaging 14C-labelled tracers in sections of biological tissue. A highly focused beam of gallium ions bombards the tissue, which is eroded (sputtered) into constituent atoms, molecules and secondary ions. The 14C ions are detected in the secondary beam by the most sensitive method available, namely accelerator mass spectrometry. The specimen is scanned pixel by pixel (1 x 2 microm), generating an image in a manner analogous to scanning electron microscopy. The method can thus be regarded as a specialized form of scanning secondary ion mass spectrometry (SIMS), referred to here as SIAMS (ref. 2). We have used SIAMS to localize the neurotransmitter gamma-aminobutyric acid (GABA) in thin sections of cerebral cortex, and show that it can generate 14C images that are much improved on 14C autoradiography. A scan takes 10-20 min and reveals individual axons, neurons and glial cells at high sensitivity. In principle, the resolution could be increased by up to tenfold, and the method could be extended to some other nuclides.

Animals↗
PubMed1996

Impairment of the perception of second order motion but not first order motion in a patient with unilateral focal brain damage.

Unlike first order motion, which is based on spatiotemporal variations in luminance, second-order motion relies on spatiotemporal variation of attributes derived from luminance, such as contrast. Here we show that a patient with a small unilateral cortical lesion adjacent to human cortical area MT (V5) has an apparently permanent disorder in perceiving several forms of second-order but not first-order motion in his contralateral visual field. This result indicates that separate pathways for motion perception exist, either as divergent pathways from area MT or even from primary visual cortex, or as separate pathways from subcortical areas to extrastriate visual areas.

Adult↗
PubMed1996

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↗
PubMed1996

Contrast sensitivity in one-eyed subjects.

The effects of early monocular form deprivation on the developing mammalian visual system, and the anatomical and physiological consequences of early monocular enucleation, suggest that the remaining eye of human subjects who had the other eye removed early during development might be capable of supernormal performance. To test this inference, the achromatic contrast sensitivity of the remaining eye of subjects who had the other eye removed at different ages after birth was compared with that of normal subjects tested under monocular and binocular conditions. The results show that all subjects who had an eye removed during early development had a higher contrast sensitivity than the better eye of control subjects. Furthermore, the earlier in development that the eye was removed, the lower the spatial frequency at which contrast sensitivity is enhanced compared with measurements made in the better eye of control subjects, and the larger the range of spatial frequencies over which contrast sensitivity is supernormal.

Adolescent↗
PubMed1996

GABA immunopositive axons in the optic nerve and optic tract of macaque monkeys.

Using an antibody to gamma-aminobutyric acid (GABA), we examined the optic nerves and optic tracts from macaque monkeys at the light and electron microscopic levels to determine if there is a possible inhibitory projection from the retina to the brain. All of the monkeys (n = 5) had GABA immunopositive axons that were evenly distributed in their optic nerves. These immunopositive axons were slightly larger than the axons around them and comprised an average of 2.6% of the axons in the nerves. Thus, their estimated total was about 44,000 axons per nerve. In the optic tracts, the GABA immunopositive axons were not distributed evenly, but were concentrated mostly in the ventromedial part, indicating that this retinal pathway probably goes to a midbrain destination such as the superior colliculus. The present findings provide further evidence that there is a GABAergic retinal projection to the brain in primates with currently unknown physiological influences.

Animals↗
PubMed1996

Models of ganglion cell topography in the retina of macaque monkeys and their application to sensory cortical scaling.

We devised mathematical models of the topography of ganglion cells in the retina of macaque monkeys. The models consisted of a sum-of-three exponentials function fitted to measurements of ganglion cell density made on the nasal horizontal meridian, combined with known anisotropies across the horizontal and vertical meridians by means of elliptic interpolation to provide a full description of their density across the whole of the retinal surface. Integration using standard numerical techniques allowed the number of ganglion cells in arbitrary regions of the retina to be estimated. The topography of actual and effective total ganglion cell populations, and of primate alpha and gamma retinal ganglion cells, was modelled on previously published data. The models were used to test the hypothesis that the retinal projection to the striate cortex in macaque monkeys is peripherally scaled (i.e. merely reflects the eccentricity-dependent variation in density of ganglion cells in the retina) by comparing the cumulative proportion of ganglion cells with the cumulative proportion of cortical area as a function of eccentricity in the visual field. Discrepancies between the two curves indicated that the fovea and immediately surrounding retina are overrepresented in the striate cortex (i.e. there is more cortex per ganglion cell in and near the fovea than in the periphery), and the fact that the discrepancies persisted out to 25-50 degrees of eccentricity showed that the overrepresentation cannot be explained by the lateral displacement of foveal ganglion cells.

Animals↗
PubMed1996

The overrepresentation of the fovea and adjacent retina in the striate cortex and dorsal lateral geniculate nucleus of the macaque monkey.

The central part of the retina, which includes the fovea, is substantially overrepresented in the topographic map of the retina in the striate cortex. We tested whether this simply reflects the uneven distribution of ganglion cells in the retina in accordance with the "principle" of peripheral scaling, or whether there is additional expansion of the fovea and adjacent retina in the retinocortical projection. Wheatgerm agglutinated horseradish peroxidase was injected into the striate cortex of three rhesus macaque monkeys so as to surround the representation of the fovea at a mean eccentricity of 8.6 degrees, and the retinae were processed histochemically to stain the retrogradely and transneuronally labelled ganglion cells which projected topographically to the injection sites. This enabled regions of the striate cortex to be related precisely to corresponding regions of the dorsal lateral geniculate nucleus and retina. Mathematical models of the distribution of ganglion cells in the retina, clipped, three-dimensional computer reconstructions of the striate cortex and lateral geniculate nucleus, and counts of neurons in the latter, were used to calculate the proportion of neurons allocated to the marked perifoveal region at each stage of projection. This was used to calculate the relative allocation of neurons to the representation of the fovea and surrounding retina among the different stages of the visual pathway. The values obtained showed that the cortical representation of the perifovea was expanded two to three times more than could be accounted for on the basis of ganglion cell topography in the retina, and that the expansion occurred both between the retina and the thalamus, and between the thalamus and the cortex. These results are inconsistent with the idea that peripheral scaling is a general principle of sensory representation in the cortex. They could also explain why many visual thresholds, including hyperacuities, cannot be accounted for by peripheral factors such as ganglion cell density.

Animals↗
PubMed1996

Behavioural and electrophysiological chromatic and achromatic contrast sensitivity in an achromatopsic patient.

OBJECTIVES: In cases of incomplete achromatopsia it is unclear whether residual visual function is mediated by intact striate cortex or results from incomplete lesions to extrastriate cortical visual areas. A patient with complete cerebral achromatopsia was tested to establish the nature of his residual vision and to determine the integrity of striate cortex function. METHODS: Behavioural contrast sensitivity, using the method of adjustment, and averaged visually evoked cortical potentials were measured to sinusoidally modulated chromatic and achromatic gratings in an achromatopsic patient and a normal observer. Eye movements were measured in the patient using a Skalar infrared monitoring system. RESULTS: The patient's chromatic contrast sensitivity was normal, indicating that despite his dense colour blindness his occipital cortex still processed information about spatial variations in hue. His sensitivity to achromatic gratings was depressed particularly at high spatial frequencies, possibly because of his jerk nystagmus. These behavioural results were reinforced by the nature of visually evoked responses to chromatic and achromatic gratings, in which total colour blindness coexisted with an almost normal cortical potential to isoluminant chromatic gratings. CONCLUSIONS: The results show that information about chromatic contrast is present in some cortical areas, and coded in a colour-opponent fashion, in the absence of any perceptual experience of colour.

Adult↗
PubMed1995

Cerebral achromatopsia in monkeys.

In human cerebral achromatopsia, extrastriate cortical damage produces a severe or complete loss of colour vision, with relative sparing of non-chromatic vision. The critical lesion appears to be in a medial occipito-temporal area, occupying the lingual and caudal fusiform gyri; positron emission tomography has shown that this cortical region is one of several activated in normal human observers during colour vision tasks. Attempts to find an analogous 'colour centre' in the cortex of monkeys have not been successful. In particular, ablation of cortical area V4, sometimes thought on physiological grounds to be more involved in wavelength and colour coding than any other visual cortical area, produces only mild impairments in colour discrimination. In the present study we tested the colour vision of monkeys after cortical ablations that mainly or entirely spared area V4. One group of monkeys (group AT) received ablations in the temporal lobe anterior to area V4, and a second group (group MOT) received ablations in a medial occipito-temporal area roughly corresponding in cranial location to the lesion that produces human cerebral achromatopsia. The animals in group MOT showed no impairment of their colour vision. Group AT, in contrast, had a severe impairment in chromatic vision, with a relative sparing of non-chromatic vision. Their behaviour was indistinguishable from that of a human patient with total cerebral achromatopsia who had been tested on the same tasks. These results show that area V4 in macaque monkeys is not analogous, and probably not homologous, to the human colour centre. Instead, they suggest that the area of the monkey's brain corresponding to the colour area in the human brain is in the temporal cortex, anterior to area V4.

Animals↗
PubMed1995

Blindsight in monkeys.

Blindsight, the visually evoked voluntary responses of patients with striate cortical destruction that are demonstrated despite a phenomenal blindness, has attracted attention from neuroscientists and philosophers interested in problems of perceptual consciousness and its neuronal basis. It is assumed to be mediated by the numerous extra-geniculostriate cortical retinofugal pathways whose properties are studied primarily in monkeys. Like patients with blindsight, monkeys with lesions of the primary visual cortex can learn to detect, localize and distinguish between visual stimuli presented within their visual field defects. Although the patients deny seeing the stimuli they can nevertheless respond to (by forced-choice guessing) in their phenomenally blind fields, it is not known whether the monkeys experience the same absence of phenomenal vision. To determine whether they too have blindsight, or whether they actually see the stimuli in their field defects, monkeys who showed excellent detection in tasks where a visual stimulus was presented on every trial, albeit at different positions, were tested in a signal-detection task in which half the trials were blank trials, with no visual stimulus. They classified the visual stimuli presented in the field defect as blank trials, demonstrating, like patients, blindsight rather than degraded real vision.

Animals↗