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Heinz Schärli
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Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (1999) 11 (5): 502–510.
Published: 01 September 1999
Abstract
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It is well known that a lesion in the optic radiation or striate cortex leads to blind visual regions in the retinotopically corresponding portion of the visual field. However, various studies show that some subjects still perceive certain stimuli even when presented in the “blind” visual field. Such subjects either perceive stimuli abnormally or only certain aspects of them (residual vision) or, in some cases, deny perception altogether even though visual performance can be shown to be above chance (blindsight). Research on monkeys has suggested a variety of parallel extrastriate visual pathways that could bypass the striate cortex and mediate residual vision or blindsight. In the present study, we investigated a subject with perimetrically blind visual areas caused by bilateral brain damage. Black and white stimuli were presented at many locations in the intact and affected areas of the visual field. The subject's task was to state, using confidence levels, whether the target stimulus was black or white. The results revealed an area in the “blind” visual field in which the subject perceived a light flash when the experimental black stimulus was presented. We hypothesize that a spared region in the visual cortex most likely accounts for these findings.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (1999) 11 (1): 52–66.
Published: 01 January 1999
Abstract
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Brain damage in the visual system can lead to apparently blind visual areas. However, more elaborate testing indicates that some visual ability may still exist for specific stimuli in the otherwise blind regions. This phenomenon is called “blindsight” if subjects report no conscious awareness of visual stimuli but when forced to guess, nevertheless perform better than chance. It has mainly been suggested that secondary visual pathways are responsible for this phenomenon. However, no published study has clearly shown the neural mechanism responsible for blindsight. Furthermore, experimental artifacts may have been responsible for the appearance of the phenomenon in some subjects. In the present study, the visual fields of nine subjects were mapped and residual visual performance was examined in many areas using three different experimental procedures. Artifacts such as stray light or eye movements were well controlled. In addition, confidence ratings were required after each trial in the forced-choice tests. The results show that only one subject with a lesion in the optic radiation had blindsight in two discrete areas of the affected visual field. Spared optic radiation fibers of the main (primary) geniculo-striate visual pathway were most likely to account for this finding.