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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.[1][2] 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. 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 (see occipital lobe). Evidence for it can be indirectly observed in children as young as two months, although it is difficult to determine the type in a person who is not old enough to answer questions.[3]


Technical details

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.[4] 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–Babinski syndrome, in which there is full cortical blindness along with the confabulation of visual experience.

Medical fiction author Robin Cook writes extensively on this condition.

Philosophical reception

Colin McGinn sees in the phenomenon of blindsight one reason for his thesis of a natural depth of consciousness.[5]


  1. ^ Carey, Benedict (December 22, 2008). "Blind, Yet Seeing: The Brain’s Subconscious Visual Sense". The New York Times (New York, NY). ISSN 0362-4331. Retrieved 2008-12-25. "The study, which included extensive brain imaging, is the most dramatic demonstration to date of so-called blindsight, the native ability to sense things using the brain’s primitive, subcortical — and entirely subconscious — visual system."  
  2. ^ Briggs, Helen (December 22, 2008). "Blind man navigates maze". BBC News (London, England). Retrieved 2008-12-25.  
  3. ^ Boyle NJ, Jones DH, Hamilton R, Spowart KM, Dutton GN.. Blindsight in children: does it exist and can it be used to help the child? Observations on a case series.. PMID 16174315.  
  4. ^ Weiskrantz, Lawrence (1986). Blindsight: A Case Study and Implications. Oxford University Press. ISBN 0-19-852192-8. OCLC 21677307.  
  5. ^ McGinn, Colin (1991). The Problem of Consciousness. Essays Towards a Resolution. Blackwell. ISBN 0-631-18803-7.


  • 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. doi:10.1016/j.neubiorev.2005.02.001.  
  • Stoerig, P. & Cowey, A. (1997). "Blindsight in man and monkey". Brain 120: 535–559. doi:10.1093/brain/120.3.535. PMID 9126063.  
  • 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. PMID 16714319.  
  • Ptito, A. and Leh, S.E. (2007). "Brain Mechanisms of Blindsight.". Article invitée; Neuroscientist 13 (5): 506–18. doi:10.1177/1073858407300598. PMID 17901259.  

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