How blind people see

Blind people have revolutionised our view on vision. Biology text books still teach us that vision functions roughly as light hitting the eyes where special cells – rods and cones – turn it into neural signals. These travel to the back of the head, the visual cortex, for brain processing leading to something we experience as ‘seeing’. Some blind people have offered a completely new picture. They see without visual cortex. They see without rods or cones. They see without experiencing ‘seeing’.

Stevie Wonder

Wearing sunglasses might impair vision – in the blind.

The visual cortex lies right at the back of the head and it is – as the name suggests – responsible for vision. If you lose it, you can’t see anymore. This happened to a partially blind patient only known by his initials DB, a man brought to scientific fame in 1974 by an article in the journal Brain. In it, Lawrence Weiskrantz and colleagues describe how DB is asked to say whether he is presented an X or an O in an area of his visual field where he is blind. DB performs more than 80% correct despite only guessing.
What happened when DB was told about his visual abilities? ‘[H]e expressed surprise and insisted several times that he thought he was just “guessing.” [H]e was openly astonished’ (p. 721). This phenomenon has been termed blind-sight and it is very unlike normal vision. It is usually much worse but there are exceptions. For example, DB is actually better at ‘blind-seeing’ very faint lines compared to his intact visual field or normal people’s vision (Trevethan et al., 2007). This rules out all sorts of concerns about blindsight such as the suggestions that DB might be lying or falsely describing degraded vision as no vision at all. Unusually good performance can hardly be faked.
If blind-sight is possible without visual awareness or visual cortex, is it also possible without the eye’s rods and cones which turn light into neural signals? Interestingly, yes. Back in 1995 a team led by Charles Czeisler reported an unusual finding in three blind people whose eyes were damaged due to various diseases. When a bright light was shone in their face, they had less melatonin – a hormone related to the sleep cycle – in their blood. Probably a little known cell type – called intrinsically photosensitive retinal ganglion cells – turned light into neural signals and generally helps us synchronize our sleep-wake cycle with the day-night cycle.
A new article by Vandewalle and collagues shows what the potential of this newly discovered cell type is. They tested three blind people with eye damage and simply asked ‘is there a light or not?’ If a light was on for ten seconds, all three ‘guessed’ significantly differently from chance. This is remarkable as these people reported not seeing anything, electrical brain potentials following light flashes were curiously absent and their eyes were undoubtedly damaged.
When looked at together, these phenomena offer a new picture of the visual system. In the text-books you see a linear picture roughly like this:
light –> rods/cones in the eye –> visual cortex –> rest of brain
A new model is needed because a remarkable range of behaviours can still be performed when the middle elements of this account are removed. Instead of a linear picture we need a collection of parallel pathways all using light to influence the brain. The blind-sight pathway proves that circumventing the visual cortex is possible. People without rods/cones prove that not even these cells are needed to make use of light.
And now imagine that vision is one of the best-understood systems in the brain. If even vision can offer such surprises it is difficult to imagine what other brain systems hide below the surface. However, going ‘below the surface’ also comes with a considerable cost. Ask blind people what they see and they simply say ‘nothing’. Their residual abilities are hidden from them. It takes careful psychological testing to make them aware of what they can do.
So, how do blind people see? Some of them see without even knowing it.

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Czeisler CA, Shanahan TL, Klerman EB, Martens H, Brotman DJ, Emens JS, Klein T, & Rizzo JF 3rd (1995). Suppression of melatonin secretion in some blind patients by exposure to bright light. The New England journal of medicine, 332 (1), 6-11 PMID: 7990870

Trevethan CT, Sahraie A, & Weiskrantz L (2007). Can blindsight be superior to ‘sighted-sight’? Cognition, 103 (3), 491-501 PMID: 16764848

Vandewalle G, Collignon O, Hull JT, Daneault V, Albouy G, Lepore F, Phillips C, Doyon J, Czeisler CA, Dumont M, Lockley SW, & Carrier J (2013). Blue Light Stimulates Cognitive Brain Activity in Visually Blind Individuals. Journal of cognitive neuroscience PMID: 23859643

Weiskrantz L, Warrington EK, Sanders MD, & Marshall J (1974). Visual capacity in the hemianopic field following a restricted occipital ablation. Brain : a journal of neurology, 97 (4), 709-28 PMID: 4434190
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Figures:

1) By Antonio Cruz/ABr (Agência Brasil.) [CC-BY-3.0-br (http://creativecommons.org/licenses/by/3.0/br/deed.en)%5D, via Wikimedia Commons

ResearchBlogging.org

3 comments

  1. “The blind-sight pathway proves that circumventing the visual cortex is possible.”

    I’m not sure that’s true. One explanation for blindsight is that the connectivity of the visual cortex is damaged, which prevents visual information from reaching consciousness, but visual processing itself may be partially intact. The information is there, they just can’t access it directly. It would be more accurate to say that blindsight proves that the brain has a way to access visual information that is hidden from consciousness

    Given that the circadian rhythm has a big influence on our cognitive functioning, I’m not surprised that people with damaged eyes are still able to tell light from darkness to a certain extent. In that case, it’s not implausible at all that this information goes somewhere else than the visual cortex. But being able to tell an X from an O is another matter entirely. You definitely need your visual cortex for that.

    1. Hi LTK,

      thanks for your comment. I am not aware of the connectivity theory of blindsight. Thanks for pointing it out.

      I take issue with your comment “But being able to tell an X from an O is another matter entirely. You definitely need your visual cortex for that.” Research in monkeys (Cowey & Stoerig, 1995, 1997) has put this matter to rest. The monkeys had their primary visual cortex removed (this was histollogically verified) and can still localise targets in their blind field even though they classify them as ‘not a light’. If by visual cortex, you mean V1, monkey research on blindsight does not support your point.

      Furthermore, concerning humans directly, in his 2004 review Alan Cowey (p. 580) writes that ‘many patients with blindsight have now been structurally imaged by MRI, and in some of them—most notably the much studied GY—there is not a shred of evidence that striate cortex is spared in the region corresponding to the huge field defect.’ Furthermore, ‘there is even evidence from functional neuroimaging (fMRI) that where there is spared striate cortex [i.e. primary visual cortex (RK)] it is not activated by visual stimuli that elicit blindsight in parts of the visual field corresponding to absent parts of striate cortex.’

      Cowey, A. (2004). Fact, artefact, and myth about blindsight. The Quarterly Journal of Experimental Psychology, 57A (4), 577-609.
      Cowey, A., & Stoerig, P. (1995). Blindsight in monkeys. Nature, 373, 247–249.
      Cowey, A., & Stoerig, P. (1997). Visual detection in monkeys with blindsight. Neuropsychologia, 35, 929–939.

      1. Fascinating! I wish I could give you the correct source for the theory that blindsight is related to connectivity, but I only remember it from one of the lectures in my BSc. Anyway, I’m glad to be proven wrong, because it means the brain is even more amazing than I thought. Thanks!

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