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Individual differences |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |
Visual processing in the brain goes through a series of processing stages. Destruction of the first visual cortical area, primary visual cortex (or V1 or striate cortex) leads to blindness in the part of the visual field that corresponds to the damaged cortical representation. The area of blindness - known as a scotoma - is in the visual field opposite the damaged hemisphere and can vary from a small area up to the entire hemifield.
Although individuals with damage to V1 are not consciously aware of stimuli presented in their blind field, Larry Weiskrantz and colleagues showed in the early 1970s that if forced to guess about whether a stimulus is present in their blind field, they do rather better than chance. This ability to detect stimuli that the individual is not aware of can extend to discrimination of the type of stimulus (for example, whether an 'X' or 'O' has been presented in the blind field), and has been dubbed blindsight.
It is not surprising from a neurological viewpoint that damage to V1 would lead to reports of blindness. Visual processing occurs in the brain in a hierarchical series of stages (with much crosstalk and feedback between areas). As V1 is the first cortical area in this hierarchy any damage to V1 severely limits visual information passing from retina, via the LGN and then V1, to higher cortical areas. However, the route from retina through V1 is not the only visual pathway into cortex (though it is by far the largest); it is commonly thought that the residual performance of people exhibiting blindsight is due to preserved pathways into extrastriate cortex that bypass V1. What is surprising is that activity in these extrastriate areas is apparently insufficient to support visual awareness in the absence of V1.
- Danckert, J. & Rossetti, Y. (2005). Blindsight in action: what can the different sub-types of blindsight tell us about the control of visually guided actions?. Neurosci Biobehav Rev 29 (7): 1035–1046.
- Stoerig, P. & Cowey, A. (1997). Blindsight in man and monkey. Brain 120: 535–559.
- Weiskrantz, L (1986). Blindsight: A case study and its implications, Oxford, Oxford University Press. ISBN: 0198521928.
- Danckert, J., Maruff, P., Kinsella, G., de Graaff, S., & Currie, J. (1998). Investigating form and colour perception in blindsight using an interference task: Neuroreport: An International Journal for the Rapid Communication of Research in Neuroscience Vol 9(13) Sep 1998, 2919-2925.
- Sahraie, A., Trevethan, C. T., MacLeod, M. J., Murray, A. D., Olson, J. A., & Weiskrantz, L. (2006). Increased sensitivity after repeated stimulation of residual spatial channels in blindsight: PNAS Proceedings of the National Academy of Sciences of the United States of America Vol 103(40) Oct 2006, 14971-14976.de:Rindenblindheit
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