Visual Cortex

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.

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


1) By Antonio Cruz/ABr (Agência Brasil.) [CC-BY-3.0-br (, via Wikimedia Commons


How are invisible colours possible?


Pharell Williams: ‘I could always visualize what I was hearing… Yeah, it was always like weird colors.’

To some people I am half colour blind even though I can see everything from blue to red like most people. For them it is odd that I can only see colours when they are directly presented to me. More than that, I can only see colours for which there are proper words. These people literally see black and white symbols in colour depending on which symbol it is. And the colours they see are sometimes those which I will never see in my life because they are invisible. Incredible? A journey through the visual brain shows how this feat is possible.

The first report of invisible colour perception came from Ramachandran and Hubbard (2001), then at San Diego. They briefly mentioned a man only known as S.S. who suffers from s-cone weakness, i.e. the cells in his eyes which are sensitive to blue are impaired. Therefore, he cannot see the full colour spectrum the way most people can.
S.S. also happens to be a grapheme-colour synaesthete, i.e. he literally sees a certain colour consistently when presented with, for example, a given number. However, these number-evoked colours were special. He described them as ‘weird’ or ‘extraspectral’. He had only ever seen them in his mind’s eye, never in the outside world.
Rather than being an isolated case, regular synaesthetes can see these so called ‘Martian’ colours as well  (Ramachandran & Hubbard, 2003). Furthermore, Oliver Sacks writes about a musician he calls Michael whose synaesthesia links musical keys with colours. Sacks writes that ‘some keys seem to have a strange hue which he can hardly describe, and which he has almost never seen in the world about him’ (2007, p. 182). Pharell Williams could be yet another case.
How can we make sense of this? To understand how the human brain can give rise to Martian colour perception, a quick tour through the visual brain is necessary. When light hits the eye, it is transformed into the electrochemical information currency of the brain. The information travels from the eyes directly to the back of the brain within about 100 milliseconds (a tenth of a second). Because this area in the back of the head is so well understood to be the primary target for visual information, it is simply called the primary visual cortex or V1 for short.
visual pathway

Note how information travels from the front to the back.

After some low level information processing in V1, information is passed on to other visual areas which are specialized in certain jobs, e.g. V5 processes motion, V4 processes colour, and grapheme areas process numbers and letters.
The brain’s left hemisphere. Grapheme area in green. Colour area in red.
When looking at where these different areas lie, one gets a sense for why motion-colour synaesthesia is not found while word/number-colour synaesthesia is so common. The human brain happens to be organised in such a way that V4 (colour) lies very close to the grapheme area. V5, on the other hand, is a lot farther. Research in the last decade (reviewed in Hubbard et al., 2011) has revealed that in synaesthetes colour and grapheme areas are unusually well connected and they show activation of the colour area just after the grapheme area responds when synaesthetes view graphemes.
Martian colours are thought to be so unusual because information has not taken the usual route (eye -> V1 -> V4) but instead went to a grapheme area first and then entered V4 (eye -> V1 -> grapheme area -> V4). Similarly, musically induced Martian colours may look so weird because auditory information recoded in V4 simply isn’t of the same quality as visual information which comes from V1.
So, colour perception appears not only determined by where information is processed but also by where it originates. A good lesson to remember whenever you try to localise function X in brain area Y: information origin matters.
Some people out there see things which are so unusual that there isn’t even a proper word for these experiences. To them I am not only half-colour blind (even though I do not suffer from s-cone weakness like S.S.). I am also unimaginative – as not just my eyes but also my imagination is limited to the colours of the rainbow, a subset of the colours which can be experienced. If you believe that the rainbow is complete, you may well be as colour blind as I am.

Hubbard, E.M., Brang, D., & Ramachandran, V.S. (2011). The cross-activation theory at 10 Journal of Neuropsychology, 5, 152-177 DOI: 10.1111/j.1748-6653.2011.02014.x
Ramachandran, V.S., & Hubbard, E.M. (2001). Psychophysical investigations into the neural basis of synaesthesia Proceedings of the Royal Society B, 268, 979-983 DOI: 10.1098/rspb.2000.1576

Ramachandran, V.S., Hubbard, E.M. (2003). The phenomenology of synaesthesia. Journal of Consciousness Studies, 10, 49-57.

Sacks, O. (2007). Musicophilia. New York: Vintage.

1) By kallerna (Own work) [CC-BY-SA-3.0 ( or GFDL (], via Wikimedia Commons
2) By Wiley (Wikimedia) [CC-BY-SA-3.0 (, via Wikimedia Commons
3) from Ramachandran, V.S., & Hubbard, E.M. (2001). Psychophysical investigations into the neural basis of synaesthesia. Proceedings of the Royal Society of London B, 268, p. 981.