Blindsight
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Blindsight is a phenomenon in which people who are perceptually blind in a certain area of their visual field demonstrate some response to visual stimuli, without any qualitative experience ('qualia'). In Type 1 blindsight subjects have no awareness whatsoever of any stimuli, but yet are able to predict, at levels significantly above chance, aspects of a visual stimulus, such as location, or type of movement, often in a forced-response or guessing situation. Type 2 blindsight is when subjects have some awareness of, for example, movement within the blind area, but no visual percept, or quale. This may be caused by, for example, the person being aware of their eyes' tracking motion which will function normally. Blindsight is caused by injury to the part of the brain responsible for vision.
Pathophysiology
Visual processing in the brain goes through a series of 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, Lawrence Weiskrantz and colleagues showed in the early 1970s that if forced to guess about whether a stimulus is present in their blind field, some observers do better than chance. This ability to detect stimuli that the observer is not conscious of can extend to discrimination of the type of stimulus (for example, whether an 'X' or 'O' has been presented in the blind field). This general phenomenon has been dubbed "blindsight".
It is unsurprising from a neurological viewpoint that damage to V1 leads 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 the retina, via the LGN and then V1, to higher cortical areas. However, the route from the retina through V1 is not the only visual pathway into the 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 the 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.
Blindsight may be thought of as a converse of the form of anosognosia known as Anton's syndrome, in which there is full cortical blindness along with the confabulation of visual experience.
Notable medical fiction authors including Robin Cook write extensively on this condition <cite: Blindsight>. Other medical fiction authors include Tess Gerritsen; Brett Chatz; Patricia Cornwell and Michael Palmer.Template:ClarifymeTemplate:Specify
References
- 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&ndash, 1046. doi:10.1016/j.neubiorev.2005.02.001.
- Stoerig, P. & Cowey, A. (1997). "Blindsight in man and monkey". Brain. 120: 535&ndash, 559. doi:10.1093/brain/120.3.535.
- Weiskrantz, L (1986). Blindsight: A case study and its implications. Oxford, Oxford University Press. ISBN 0-19-852192-8.
- Leh, S.E., Mullen, K.T., and Ptito, A. (2006). "Absence of S-cone input in human blindsight". European Journal of Neuroscience. 24 (10): 2954–60. doi:10.1111/j.1460-9568.2006.05178.x.
- Leh, S.E., Johansen-Berg, H. and Ptito,A. (2006). "Unconscious vision: New insights into the neuronal correlate of blindsight using Diffusion Tractography". Brain. 129 (Pt7): 1822–32. doi:10.1093/brain/awl111.
- Ptito, A. and Leh, S.E. (2007). "Brain Mechanisms of Blindsight". Article invitée; Neuroscientist. 13 (5): 506–18.