Blindsight

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This article is about the neurological phenomenon. For other uses, see Blindsight (disambiguation).

Blindsight is the ability of people who are cortically blind due to lesions in their striate cortex, also known as primary visual cortex or V1, to respond to visual stimuli that they do not consciously see.[1] The majority of studies on blindsight are conducted on patients who are blind on only one side of their visual field. Following the destruction of the striate cortex, patients are asked to detect, localize, and discriminate amongst visual stimuli that are presented to their blindside often in a forced-response or guessing situation, even though they cannot actually see the stimulus. Research shows a surprising amount of accuracy in the guesses of blind patients. This ability to guess, at levels significantly above chance, aspects of a visual stimulus, such as location, or type of movement without any conscious awareness of any stimuli is known as Type 1 blindsight. Type 2 blindsight occurs when patients claim to have a feeling that there has been a change within their blind area, for example, movement, but that it was not a visual percept.[2] This phenomenon challenges what we once believed to be true, that perceptions must enter consciousness to affect our behavior. Blindsight shows that our behavior can be guided by sensory information of which we are unaware. (Carlson, 2010) It 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.

Contents

History [edit]

We owe much of our current understanding of blindsight to early experiments on monkeys. One monkey in particular, Helen, could be considered the “star monkey in visual research” because she was the original blindsight subject. Helen was a macaque monkey that had been decorticated; specifically, her primary visual cortex (V1) was completely removed. This procedure had the expected results that Helen became blind as indicated by the typical test results for blindness. Nevertheless, under certain specific situations, Helen exhibited sighted behavior. Her pupils would dilate and she would blink at stimuli that threatened her eyes. Furthermore, under certain experimental conditions, she could detect a variety of visual stimuli, such as the presence and location of objects, as well as shape, pattern, orientation, motion, and color.[3][4][5] In many cases she was able to navigate her environment and interact with objects as if she was sighted.[6]

A similar phenomenon was also discovered in humans. Subjects who had suffered damage to their visual cortices due to accidents or strokes reported partial or total blindness. Nevertheless, when prompted they could “guess” with above-average accuracy about the presence and details of objects, much like the animal subjects. They could even catch objects tossed at them when prompted. Interestingly, the subjects never developed any kind of confidence in their abilities. Even when told of their successes, they would not begin to spontaneously make “guesses” about objects but instead still required prompting. Furthermore, blindsight subjects rarely express the amazement about their abilities sighted people would expect them to express.[7]

Describing Blindsight [edit]

Simply described, the brain contains several mechanisms involved in vision. Consider two systems in the brain which evolved at different times. The first that evolved is more primitive and resembles the visual system of animals such as fish and frogs. The second to evolve is more complex and is possessed by mammals. The second system seems to be the one that is responsible for our ability to perceive the world around us and the first system is devoted mainly to controlling eye movements and orienting our attention to sudden movements in our periphery. Patients with blindsight have damage to the second, “mammalian” visual system (the visual cortex of the brain and some of the nerve fibers that bring information to it from the eyes). (Carlson, 2010) This phenomenon shows that how, after the more complex visual system is damaged, people can use the primitive visual system of their brains to guide hand movements towards an object even though they can’t see what they are reaching for. Hence, visual information can control behavior without producing a conscious sensation.

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. Blindsight patients show awareness of single visual features, such as edges and motion, but cannot gain a holistic visual percept. This suggests that perceptual awareness is modular as well as the process of perceptual integration that unifies all information into a whole percept[5]. Therefore, object identification and object recognition are thought to be separate process and occur in different areas of the brain, working independently from one another. The modular theory of object perception and integration would account for the “hidden perception” experienced in blindsight patients. Research has shown that visual stimuli with the single visual features of sharp borders, sharp onset/offset times,[8] motion,[9] and low spacial frequency[10] contribute to, but are not strictly necessary for, an object’s salience in blindsight.

Theories of Causation [edit]

There are three theories for the explanation of blindsight. The first states that after damage to area V1, other branches of the optic nerve deliver visual information to the superior colliculus and several other areas, including parts of the cerebral cortex. These areas might control the blindsight responses, but still many people with damage to area V1 don’t show blindsight or only show it in certain parts of the visual field.

Another explanation to the phenomenon is that even though the majority of a person’s visual cortex may be damaged, tiny islands of healthy tissue remain. These islands aren’t large enough to provide conscious perception, but nevertheless enough for blindsight. (Kalat, 2009)

A third theory is that the information required to determine the distance to and velocity of an object in object space is determined by the lateral geniculate nucleus before the information is projected to the cerebral cortex. In the normal subject these signals are used to merge the information from the eyes into a three-dimensional representation (which includes the position and velocity of individual objects relative to the organism), extract a vergence signal to benefit the precision (previously auxiliary) optical system (POS), and extract a focus control signal for the lenses of the eyes. The stereoscopic information is attached to the object information passed to the cerebral cortex.[11]

Evidence of blindsight can be indirectly observed in children as young as two months, although there is difficulty in determining the type in a patient who is not old enough to answer questions.[12]

Case Study [edit]

In 2003, a patient known as TN lost use of his primary visual cortex, area V1. He had two successive strokes, which knocked out the region in both his left and right hemisphere. After his strokes, ordinary tests of TN’s sight turned up nothing. He could not even detect large objects moving right in front of his eyes. Researchers eventually began to notice that TN exhibited signs of blindsight and in 2008 decided to test their theory. They took TN into a hallway and asked him to walk through it without using the cane he always carried after having the strokes. TN was not aware at the time, but the researchers had placed various obstacles in the hallway to test if he could avoid them without conscious use of his sight. To the researchers' delight, he moved around every obstacle with ease, at one point even pressing himself up against the wall to squeeze past a trashcan placed in his way. After navigating through the hallway, TN reported that he was just walking the way he wanted to, not because he knew anything was there. (de Gelder, 2008)

Research [edit]

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.[13] 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).

Electrophysiological evidence from the late 1970s (de Monasterio, 1978; Marrocco & Li, 1977; Schiller & Malpeli, 1977) has shown that there no direct retinal input from S-cones to the superior colliculus, implying that the perception of color information should be impaired. However, recent evidence point to a pathway from S-cones to the superior colliculus, opposing de Monasterio’s previous research and supporting the idea that some chromatic processing mechanisms are intact in blindsight.[14][15]

Marco Tamietto & Beatrice de Gelder performed experiments linking emotion detection and blindsight. Patients shown images on their blind side of people expressing emotions correctly guessed the emotion most of the time. The movement of facial muscles used in smiling and frowning were measured and reacted in ways that matched the kind of emotion in the unseen image. Therefore, the emotions were recognized without involving conscious sight.

A recent study found that a young woman with a unilateral lesion of area V1 could scale her grasping movement as she reached out to pick up objects of different sizes placed in her blind field, even though she could not report the sizes of the objects.[16] Similarly, another patient with unilateral lesion of area V1 could avoid obstacles placed in his blind field when he reached toward a target that was visible in his intact visual field.[17] Even though he avoided the obstacles, he never reported seeing them.

Brain regions involved [edit]

Visual processing in the brain goes through a series of stages. Destruction of the primary visual 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. Visual processing occurs in the brain in a hierarchical series of stages (with much crosstalk and feedback between areas). 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.

To put it in a more complex way, recent physiological findings suggest that visual processing takes place along several independent, parallel pathways. One system processes information about shape, one about color, and one about movement, location and spatial organization. This information moves through an area of the brain called the lateral geniculate nucleus, located in the thalamus, and on to be processed in the primary visual cortex, area V1 (also known as the striate cortex because of its striped appearance). People with damage to V1 report no conscious vision, no visual imagery, and no visual images in their dreams. However, some of these people still experience the blindsight phenomenon. (Kalat, 2009)

The superior colliculus and prefrontal cortex also have a major role in awareness of a visual stimulus.[18]

Philosophical reception [edit]

Colin McGinn sees in the phenomenon of blindsight one reason for his thesis of a natural depth of consciousness.[19] Robert Nozick also joins McGinn in supporting this thesis.[20]

Notes [edit]

  1. ^ Celesia, G., G. (2010). Visual perception and awareness: a modular system. Journal of Psychophysiology 24(2), 62-67. doi: 10.1027/0269-8803/a000014
  2. ^ Weiskrantz, Lawrence (1997). Consciousness Lost and Found: A Neuropsychological Exploration. ISBN 0-19-852301-7. 
  3. ^ Humphrey, N. (1970). What the frog's eye tells the monkey's brain. Brain, Behavior, and Evolution , 3, 324-337.
  4. ^ Humphrey, N. (1974). Vision in a monkey without striate cortex: A case study. Perception , 3, 241-255.
  5. ^ Humphrey, N. (1992). A History of the Mind. New York: Simon & Schuster.
  6. ^ Holt, J. (2003). Blindsight & The Nature of Consciousness. New York: broadview press.
  7. ^ Humphrey, N. (2006). Seeing Red: A study in Consciousness. Cambridge: Belknap.
  8. ^ Alexander, I., Cowey, A. (2010). Edges, colour and awareness in blindsight. Consciousness and Cognition, 19, 520–533.
  9. ^ Ffytche, D.,H., Zeki, S. (2011). The primary visual cortex, and feedback to it, are not necessary for conscious vision. Brain, 134, 247-257. doi:10.1093/brain/awq305
  10. ^ Sahraiea, A., Hibbardb, P., B., Trevethana, C., T., Ritchiea, K., L., Weiskrantz, L. (2010). Consciousness of the first order in blindsight. PANS 107(49), 21217–21222.
  11. ^ Fulton, J. (2004) Processes in Biological Vision Section 7.4 http://neuronresearch.net/vision/pdf/7Dynamics.pdf/
  12. ^ Boyle NJ, Jones DH, Hamilton R, Spowart KM, Dutton GN. (2005). "Blindsight in children: does it exist and can it be used to help the child? Observations on a case series.". Developmental medicine and child neurology 47 (10): 699–702. doi:10.1017/S0012162205001428. PMID 16174315. 
  13. ^ Weiskrantz, Lawrence (1986). Blindsight: A Case Study and Implications. Oxford University Press. ISBN 0-19-852192-8. OCLC 21677307. 
  14. ^ Hall, N. J., Colby, C. L. (2009). Response to blue visual stimuli in the macaque superior colliculus. Society for Neuroscience, 756.
  15. ^ Garret, bob. Brain & behavior: an introduction to biological psychology. (2011). SAGE publications inc (3), 315-318.
  16. ^ Whitwell RL, Striemer CL, Nicolle DA, Goodale MA. (2011). "Grasping the non-conscious: preserved grip scaling to unseen objects for immediate but not delayed grasping following a unilateral lesion to primary visual cortex.". Vision Res. 51 (8): 908–24. doi:10.1016/j.visres.2011.02.005. PMID 21324336. 
  17. ^ Striemer CL, Chapman CS, Goodale MA. (2009). ""Real-time" obstacle avoidance in the absence of primary visual cortex.". Proc. Natl. Acad. Sci. USA. 106 (37): 15996–6001. doi:10.1073/pnas.0905549106. PMID 19805240. 
  18. ^ Hall, N. J., Colby, C. L. (2009). Response to blue visual stimuli in the macaque superior colliculus. Society for Neuroscience, 756. http://dx.doi.org/10.1016/j.concog.2010.01.008
  19. ^ McGinn, Colin (1991). The Problem of Consciousness. Essays Towards a Resolution. Blackwell. ISBN 0-631-18803-7.
  20. ^ Nozick, Robert (2001). Invariances: The Structure of the Objective World. Harvard University Press. ISBN 978-0-674-00631-7.

References [edit]

  • 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. PMID 16143169. 
  • Stoerig, P. & Cowey, A. (1997). "Blindsight in man and monkey". Brain 120 (3): 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. PMID 17156217. 
  • 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. 
  • Carlson, N. R. (2010). Physiology of behavior. (10th ed., pp. 4–5). Boston, MA: Pearson Education, Inc.
  • Collins, G. (2010, April 22). Blindsight: Seeing without knowing it [Web log message]. Retrieved from http://blogs.scientificamerican.com/observations/2010/04/22/blindsight-seeing-without-knowing-it/
  • de Gelder, B. (2010, April 27). Uncanny sight in the blind. Retrieved from http://www.scientificamerican.com/article.cfm?id=uncanny-sight-in-the-blind
  • Tamietto, M., de Gelder, B. (2010). Neural basis of the non-conscious perception of emotional signals. Nature reviews neuroscience 11, 697-709. doi:10.1038/nrn2889
  • de Gelder, B., Tamietto, M., & van Boxtel, G. (2008). Intact navigation skills after bilateral loss of striate cortex. Current Biology, 18th(24th), doi: 10.1016/j.cub.2008.11.002
  • Kalat, J. W. (2009). Biological psychology. (10th ed., pp. 169–170). Belmont, CA: Wadsworth.
  • Physorg. (2008, October 14). Retrieved from http://phys.org/news143222136.html
  • Ratey, J. J. (2002). A user's guide to the brain: Perception, attention, and the four theaters of the brain . (p. 99). New York, NY: Vintage Books.
  • De Monasterio, F. M. (1978). Properties of ganglion cells with atypical receptive-field organization in the retina of macaques. Neurophysiology 41, 1435–1449.
  • McIntosh, A., R., Rajah, M., N., Lobaugh, N., J. (1999). Interactions of prefrontal cortex in relation to awareness in sensory learning. Science 284, 1531-1533.

External links [edit]

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