Vilayanur S Ramachandran

The Emerging Mind

The Lecturer: Vilayanur S Ramachandran

Vilayanur S Ramachandran is Director of the Centre for Brain and Cognition and professor with the Psychology Department and the Neurosciences Programme at the University of California, San Diego. He is also Adjunct Professor of Biology at the Salk Institute.

He originally trained as a doctor and obtained an M.D. from Stanley Medical College, where he was awarded gold medals in pathology and clinical medicine. He also studied at Trinity College, Cambridge, where he was awarded a Ph.D. and was elected a senior Rouse-Ball Scholar.

He has received many honours and awards including a fellowship from All Souls College, Oxford. He is also a fellow of the Neurosciences Institute in La Jolla and a fellow of the Institute for Advanced Studies in Behavioural Sciences at Stanford.

He has lectured widely on art - as well as visual perception and the brain - and is a trustee of the San Diego Museum of Art. He has published over 120 papers in scientific journals, is Editor-in-chief of the Encyclopaedia of Human Behaviour and author of a popular book on neuroscience, Phantoms In The Brain.

Professor Ramachandran's work has concentrated on investigating phenomena such as phantom limbs, anosognosia or denial of paralysis, Capgras syndrome, and anorexia nervosa.

Although most of these conditions have been know since the turn of the century they have usually been treated as curiosities and there has been almost no experimental work on them. V.S. Ramachandran has brought them from the clinic to the laboratory and shown that an intensive study of these patients can often provide valuable new insights into the workings of the human brain.

Lecture 1: Phantoms in the Brain.

The history of mankind in the last three hundred years has been punctuated by major upheavals in human thought that we call scientific revolutions - upheavals that have profoundly affected the way in which we view ourselves and our place in the cosmos. First there was the Copernican revolution - the notion that far from being the centre of the universe, our planet is a mere speck of dust revolving around the sun. Then there was the Darwinian revolution culminating in the view that we are not angels but merely hairless apes, as Huxley once pointed out in this very room. And third there was Freud's discovery of the "unconscious" - the idea that even though we claim to be in charge of our destinies, most of our behaviour is governed by a cauldron of motives and emotions which we are barely conscious of. Your conscious life, in short, is nothing but an elaborate post-hoc rationalisation of things you really do for other reasons.

But now we are poised for the greatest revolution of all - understanding the human brain. This will surely be a turning point in the history of the human species for, unlike those earlier revolutions in science, this one is not about the outside world, not about cosmology or biology or physics, but about ourselves, about the very organ that made those earlier revolutions possible. And I want to emphasize that these insights into the human brain will have a profound impact not just on us scientists but also on the humanities, and indeed they may even help us bridge what CP Snow called the two cultures - science on the one hand and arts, philosophy and humanities on the other.

I would like to thank the BBC for inviting me to give the 2003 Reith lectures. I hope the lectures will appeal to a broad audience, fulfilling Lord Reith's original mission. Given the enormous amount of research on the brain, all I can do is to provide a very impressionistic survey rather than try to be comprehensive. Of course by doing this, I will be oversimplifying many of the issues involved and run the risk of annoying some of my specialist colleagues. But, as Lord Reith himself once said, "There are some people whom it is one's duty to offend!"

Although the lectures will cover a very wide spectrum of topics, there will be two recurring themes that run through all of them. The first broad theme is that by studying neurological syndromes that have been largely ignored as curiosities or mere anomalies we can sometimes acquire novel insights into the functions of the normal brain - how the normal brain works. The second theme is that many of the functions of the brain are best understood from an evolutionary vantage point.

The human brain, it has been said, is the most complexly organised structure in the universe and to appreciate this you just have to look at some numbers. The brain is made up of one hundred billion nerve cells or "neurons" which is the basic structural and functional units of the nervous system. Each neuron makes something like a thousand to ten thousand contacts with other neurons and these points of contact are called synapses where exchange of information occurs. And based on this information, someone has calculated that the number of possible permutations and combinations of brain activity, in other words the numbers of brain states, exceeds the number of elementary particles in the known universe.

Even though its common knowledge these days, it never ceases to amaze me that all the richness of our mental life - all our feelings, our emotions, our thoughts, our ambitions, our love life, our religious sentiments and even what each of us regards us his own intimate private self - is simply the activity of these little specks of jelly in your head, in your brain. There is nothing else.

Given the staggering complexity, where do you even begin? Well let's start with some basic anatomy. It's the 21st century and most people here have a rough idea what the brain looks like. It's got two mirror-image halves, called the cerebral hemispheres, so it looks like a walnut sitting on top of a stalk, called the brain stem, and each hemisphere is divided into four lobes, the frontal lobe, the parietal lobe, the occipital lobe and the temporal lobe. The occipital lobe in the back is concerned with vision. If it's damaged, you become blind. The temporal lobe is concerned with things like hearing, with emotions and certain aspects of perception. The parietal lobes of the brain are concerned with - at the sides of the head - they are concerned with creating a three-dimensional representation of the spatial layout of the external world, and also of your own body in that three-dimensional representation. And lastly the frontal lobes, in the front, are the most mysterious of all. They are concerned with some very enigmatic aspects of human mind and human behaviour such as your moral sense, your wisdom, your ambition and other activities of the mind which we know very little about.

Now there are several ways of studying the brain but my approach is to look at people who have had some sort of damage to a small part of the brain, or some change in a small part of the brain, and interestingly when you look at these people who have had a small lesion in a specific part of the brain, what you see is not an across-the-board reduction in all their cognitive capacities, not a blunting of their mind. What you see is often a highly selective loss of one specific function with other functions being preserved intact, and this gives you some confidence in asserting that that part of the brain is somehow involved in mediating that function.

You are going to see many examples of this in my lectures but just to give you a flavour for this kind of research, I'm just going to mention two or three of my favourite examples.

One of my favourites is prosopognosia, or face blindness. When there is damage to a structure called the fusiform gyrus in the temporal lobes on both sides of the brain, what you get is a patient who can no longer recognise people's faces. Now the patient isn't blind because he can still read a book and he's not psychotic or obviously mentally disturbed but he can no longer recognise faces by looking at people. Now that syndrome is very well known but there is another syndrome that is quite rare and that's what we call the Capgras Syndrome, and I'll give you an example of this. A patient I saw not long ago who had been in a car accident, had sustained a head injury and was in a coma for about a couple of weeks. Then he came out of this coma and he was quite intact neurologically when I examined him. But he had one profound delusion - he would look at his mother and say "Doctor, this woman looks exactly like my mother but she isn't, she is an imposter".

Now why would this happen? Now the important thing is this patient who I will call David is completely intact in other respects. Now to understand this disorder, you have to first realise that vision is not a simple process. When you open your eyes in the morning, it's all out there in front of you. It's easy to assume that it's effortless and instantaneous but in fact you have this distorted upside down image in your retina exciting the photoreceptors and the messages then go through the optic nerve to the brain and then they are analysed in thirty different visual areas, in the back of your brain. And then you finally after analysing all the individual features, you identify what you're looking at. Is it your mother, is it a snake, is it a pig, what is it? And that process of identification takes place in a place which we call the fusiform gyrus which as we have seen is damaged in patients with face blindness or prosopognosia.

So once the image is recognised, then the message goes to a structure called the amygdala which is sometimes called the gateway to the limbic system which is the emotional core of your brain, which allows you to gauge the emotional significance of what you are looking at. Is this a predator, is it a lion or a tiger? Is it a prey which I can chase? Is it a mate that I can chase? Or is it my departmental chairman I have to worry about, or is it a stranger who is not important to me, or something utterly trivial like a piece of driftwood? What is it?

Now what's happened in this patient? What we suggest is that maybe what's gone wrong is that the fusiform gyrus and all the visual areas are completely normal in this patient. That's why when he looks at his mother, he says "oh yeah, it looks like my mother", but the wire, to put it crudely, the wire that goes from the amygdala to the limbic system, to the emotional centres, is cut by the accident. So he looks at his mother and he says - "hey, it looks just like my mother, but if it's my mother why is it I don't experience this warm glow of affection (or terror, as the case may be). There's something strange here, this can't possibly be my mother, it's some other strange woman pretending to be my mother". It's the only interpretation that makes sense to his brain given the peculiar disconnection.

Now how do you test an outlandish idea like this? My student Bill Hirstein and I in La Jolla, and Haydn Ellis and Andrew Young here in England, did some very simple experiments measuring galvanic skin response which I'll talk about in detail in my last lecture, and we found - sure enough - there has been this disconnection between vision and emotion as predicted by our theory, just as we had thought. Now what's even more amazing is when David, this patient who when his mother said she's an imposter, an hour later his mother phones him and he picks up the phone and answers the phone and he says "mum, how are you, where are you?" Instantly he recognises her. There is no delusion. An hour later the mother walks into the room and he says "who are you? You look just like my mother but you're an imposter, you're not my mother". Now why does this happen? Well it turns out there's a separate pathway going from the auditory cortex in the superior temporal gyrus to the amygdala, and that pathway perhaps is not cut by the accident. That's why when he listens to his mother on the phone, he says "oh my god, this is my mum, where are you?" But when he sees her, the delusion kicks in immediately and he says "who are you"?

Now, there are many other twists to this story which I'm going to tell you about in my last lecture on neuropsychiatry, but I thought I'd just mention it briefly today because it's a lovely example of the sort of thing we do, of cognitive neuroscience in action.

Now we have talked about visual response to visual images, your emotional response to visual images. Obviously this response is vital for your survival but the existence of connections between visual brain centres and the limbic system or emotional core of the brain also raises another interesting question, and that is what is art? How does the brain response to beauty? Given that these connections are between vision and emotion, and art involves an aesthetic emotional response to visual images, surely these connections must be involved, and this is a topic I'll take up my lecture in Birmingham.

Now we've been talking about all these intricate connections in the brain, in the limbic system, in the visual centres, in the amygdala. An obvious question is the question of nature versus nurture. In other words, are these connections laid down by the genome in the foetus, or are they acquired in early infancy as the infant interacts with the world, the so-called nature/nurture debate. This takes me to the next syndrome I'd like to talk to you about and that is phantom limbs.

Everyone here knows what a phantom limb is. A patient has an arm amputated because there's a tumour, malignant tumour on the arm or there's been a car accident and the arm has to be amputated, but the patient continues to vividly feel the presence of that arm. Some of you here, this being England, would now about Lord Nelson who vividly felt a phantom arm. I'll tell you about an experiment we did on these patients. So we have a patient with a phantom left arm. His arm had been amputated above the left elbow so I had him sitting in my office blindfolded and I took a Q tip and touched different parts of the body and asked him what do you feel? I touched his shoulder and he said oh you're touching my shoulder. I touched his belly and he said oh you're touching my belly. I touched his chest and he said you're touching my chest - not surprising. But the amazing thing is when I touched his face, the left side of his face - remember his left arm is amputated so he has a phantom on the left side - when I touched his cheek he said oh my god doctor, you're touching my left thumb, my missing phantom thumb and he seemed as surprised as I was. Then I touched him on the upper lip and he said oh my god you're touching my phantom index finger, and then on his lower jaw and he said you're touching my phantom pinkie, my little finger.

So why does this happen? There was a complete map, a systematic map of the missing phantom hand on his face, draped on his face. So you have a medical mystery of sorts, the sort of mystery we saw with David, the patient with the Capgras syndrome, the sort of mystery that would have intrigued Sherlock Holmes, Conan Doyle or Berton Rouché. So what's going on?

To answer this question, you have to look at the anatomy of the brain again. The entire skin surface, touch signals, all the skin surface on the left side of the brain is mapped on to the right cerebral hemisphere on a vertical strip of cortical tissue called the post-central gyrus. Actually there are several maps but I'll simplify them and pretend there's only one map called the post-central gyrus. Now this a faithful representation of the entire body surface. It's almost as though you have a little person draped on the surface of the brain. It's called the Penfield homunculus, and for the most part it's continuous which is what you mean by a map, but there is one peculiarity and that is the representation of the face on this map on the surface of the brain is right next to the representation of the hand on this map, instead of being near the neck where it should be, so it's dislocated. Now nobody knows why, something to do with the phylogeny or the way in which the brain develops in early foetal life or in early infancy, but that's the way the map is.

So I realised that what's going on here is when you amputate the arm, the part of the cortex of the brain corresponding to the hand is not receiving any signals because you've removed the hand. So it's hungry for sensory input. So what happens is the sensory input from the face skin now invades the vacated territory corresponding to the missing hand, and that then is misinterpreted by higher centres in the brain and arising from the missing phantom hand. And that's why the patient says, every time you touch his face he says oh that's my phantom thumb you're touching, that's my phantom index finger, that's my phantom pinkie. In fact you can even put an ice cube on the face and the patient will say oh my thumb is ice cold. You can put a drop of hot water, in fact you put a drop of hot water and the water started trickling down the face, the patient will trace the trickle on his phantom with his normal hand following its path. On one occasion we had the patient raise his phantom and he was amazed to feel the trickle going uphill which is against the law of physics.

Now that's just a hypothesis but to test this idea, we used the brain imaging technique called MEG or magnetoencephalography which allows you to see which parts of the brain light up when you touch different parts of the body, and sure enough what we found was in this patient, Victor, unlike the normal brain when you touch his face, it activated not only the face area in the brain but also activated the hand region of the Penfield map in the brain. So there has obviously been this cross-wiring in the brain of this patient. And this is important because it allows you to link changes in brain anatomy, changes in brain maps, in the sensory map, with phenomenology, allows you to link physiology and psychology which is one of the goals of cognitive neuroscience, this discipline we're talking about.

The discovery also has broader implications. One of the things we were all taught as medical students is that connections in the brain are laid down in the foetus or in early infancy, and once they are laid down, there is nothing much you can do to change these connections in the adult and that's why when there's damage to the nervous system as in a stroke, there is such little recovery of function and why neurological ailments are so notoriously difficult to treat. What I am saying is that's wrong. In fact there's a tremendous amount of plasticity or malleability even in the adult brain, and you can demonstrate this in a five minute experiment in a patient with a phantom limb. Now how you go about harnessing this ability in the clinic may be to help patients recover from stroke or indeed from phantom limb pain is a question that we don't have time to go into but we can take up during discussions.

OK so we have seen that after our arm amputation, the patient's brain gets cross-wired. The face input now innervates the hand region of the brain. Now that happens because of amputation. It turns out that the same thing can happen because of a mutation, if there is something wrong with your genes. Instead of the brain modules remaining segregated, you get this accidental cross-wiring and then you get a curious condition called synesthesia, which we have now been studying. This is going to be a topic of my lecture in Oxford. Briefly it was described by Francis Galton or clearly documented by him in the 19th century. He pointed out that some people who are perfectly normal in other respects have one peculiar symptom, if you want to call it a symptom, and that is these people who are otherwise completely normal, they get their senses mixed up and that is every time they hear a particular tone they see a particular colour. So C sharp is red, F sharp is blue. Another tone might be indigo, OK? And this phenomenon, this mingling of senses is synesthesia. Galton pointed out also that it runs in families. We and others have confirmed this, including Simon Baron-Cohen.

Now, another aspect of this syndrome is whenever you hear a particular tone you see a particular colour. Some of these people also when they see numbers in black and white, like the number five or the number six or the number seven, what we call Arabic numerals - Indian numerals strictly speaking - when you see these numbers, every time you see a number it evokes a particular colour so 5 is always red, 6 is always green. It's always tinged green. 7 is always indigo, 8 is always yellow, so this again is another example of synesthesia and it's very common. We find it's about one in two hundred people have this so it's not as rare as people have thought it to be in the past.

Now why does this happen? Why does this mixing of signals occur? Well we, a student of mine, Ed Hubbard and I were looking at brain atlases, brain maps and we were struck by the fact that if you look at the fusiform gyrus, that's where the colour information is analysed. But amazingly the number area of the brain which represents visual graphemes of numbers, 5 6 7 8 and all of that, is right next to it also in the fusiform gyrus, almost touching it. So we said this can't be a coincidence. Maybe in some people there is some accidental cross-wiring. Just as after amputation we get cross-wiring between the face and the hand, in these people maybe there's a cross-wiring between the number and colour area in the fusiform gyrus. Of course the key difference is in the case of phantom limbs, it's the amputation that causes the reorganisation whereas in synesthesia given that it runs in families, we think it's caused by a gene or a set of genes which causes abnormal connections between adjacent brain regions, in this case between numbers and colours so every time he sees a specific number it evokes a particular colour.

First of all many neurologists, neuroscientists in the past, even though the phenomenon was described by Galton a hundred years ago, it's been regarded mainly as a curiosity. It sounds crazy. They're just crazy or they're just faking it to draw attention to themselves, or maybe it's childhood memories. You played with refrigerator magnets, 5 was red, 6 was blue, 7 was green. Now it never made much sense to me because why does it then run in families? You have to say maybe the same magnets were passed round. So first thing we wanted to show this is a real phenomenon, it's the person genuinely sees red when he sees 5. It's not just imagination or memory. How do you show that?

So we devised a simple display on the computer screen, a number of 5s scattered on the screen, black 5s, just black and white. Embedded among those 5s are a number of 2s and these 2s form a shape like a triangle, a hidden shape, a triangle or a square. Now when all of us here, any one of us normals or less gifted individuals, looks at this pattern, you see nothing. But when a synesthete looks at it, who sees numbers as colour, he sees the 5s as red and the 2s as green so he looks at it and he says my god, instantly the 2s pop out and he says oh they're forming a triangle, they're forming a square. And they are much better at doing this than normal people so it's a clinical test for discovering synesthetes.

Now, the fact that synesthetes are actually better at this than normal people suggests that they can't be crazy. If they're crazy, how come they're better at it? So this shows this is a genuine sensory phenomenon. It also shows that it can't be memory association or something cognitive or a metaphor because - if that were true, how come he's able to see the triangle or the square pop out from the background? OK we have shown that this phenomenon is real, we in La Joya and as well as Jeffrey Gray and Mike Morgan and others here in London have done experiments to test the idea there's actual cross-wiring in the brain and have shown that in fact there's activation of the fusiform gyrus in the colour area just showing numbers to these people.

But then the next question is OK, here are some people with some quirk in the brain. They see numbers as colours so what's the big deal, why should I care? Well now I'm going to show you that you're all synesthetes but you're in denial about it. So what I want you to do is I want you all to imagine two shapes in front of you. I wish I had a slide but of course this is radio. One of them imagine is a shattered piece of glass with jagged edges, the other is like an amoeba, it's got undulating curvy shapes. And one of them I'm going to call a bouba, and the other is kiki - which is which? Now the amazing thing is 98% of people will pick the shattered piece of glass with the jagged edges, and say oh that's a kiki, and the undulating amoeboid shape, oh that's a bouba, even though they have never seen the shape before.

Why does this happen? Well I suggest it happens - I am going to talk about this in detail in my Oxford lecture - because you're all synesthetes.

Now we have talked about several syndromes, phantom limb, synesthesia, Capgras syndrome and these are quite bizarre and we have tried to explain it in terms of neural circuitry in the brain but there is a syndrome that is even more bizarre, and this is pain asymbolia. I'll tell you about a patient I saw in Vellore in India about ten years ago. He was quite normal, intellectually normal, mentally quite lucid, alert, attentive, his memory was normal, perception, everything was fine except I took a needle and pricked him with a needle to determine the intact, not to be sadistic but to determine the intactness of his pain pathways, to determine his pain sensations, and every time I poked him, of course, all of you here would say, ouch. He started giggling, telling me doctor, I feel the pain but it doesn't hurt. It feels very funny, like a tickle and he would start laughing uncontrollably.

Here is the ultimate irony - a human being laughing in the face of pain. OK, why would the patient do this? Well, seeing this patient made me ask an even more basic question, why does anybody laugh? Why do all of you here laugh, OK? Now a martian ethologist watching all of you here would be very suprised every now and then. It is a species-specific trait, laughter. Every now and then all of you here stop what you're doing, shake your head, make this funny staccato rhythmic sound, hyena-like sound. Why do you do it? Now clearly laughter is hard-wired, it's a "universal" trait. You see it every society, every civilization, every culture, society, has some form of laughter and humour - except the Germans.

So this suggests strongly it's hard-wired in the brain and this raises an interesting question. Why did it evolve in the brain, OK, how did it evolve through natural selection? When you look at all jokes and humour across societies, the common denominator of all jokes and humour despite all the diversity is that you take a person along a garden path of expectation and at the very end you suddenly introduce au unexpected twist that entails a complete re-interpretation of all the previous facts. That's called a punch-line of the joke. Now obviously that is not sufficient for laughter because then every great scientific discovery or every "paradigm shift" would be funny, and my scientific colleagues wouldn't find it amusing if I said their discoveries were funny.

OK, the key ingredient here is, it's not merely sufficient that you introduce a re-interpretation but the re-interpretation, the new model you have come up with should be inconsequential, it should be of trivial consequence. It sounds a bit abstract so let me illustrate with a concrete example. Here is a portly gentleman walking along, he is trying to reach his destination, but before he does that he slips on a banana peel and falls. And then he breaks his head and blood spills out and obviously you are not going to laugh. You are going to rush to the telephone and call the ambulance. But imagine instead of that, he walks along, slips on the banana peel, falls, wipes off the goo from his face, looks around him everywhere, and and then gets up, then you start laughing. The reason is I claim is because now you know it's inconsequential, you say, oh it's no big deal, there's no real danger here. So what I'm arguing is, laughter is nature's false alarm. Why is this useful from an evolutionary standpoint? So what you are doing with this rhythmic stocatto sound of laughter is informing your kin who share your genes, don't waste your precious resources rushing to this person's aid, it's a false alarm everything is OK. OK, so it's nature's OK signal.

OK, now what does this got to do with my patient in Vellore? Let me explain. When we examined his brain, when we do the CT scan we found there was damage to the region called the insular cortex on the sides of the brain. The insular cortex receives pain signals from the viscera and from the skin. That's where you experience the raw sensation of pain but it turns out there are many layers to pain. It's not just a unitary thing. From the insular cortex the message goes to the amygdala, which we encountered earlier in the context of the Capgras syndrome and then to the rest of the limbic system, and especially the anterior cingulate, where you respond emotionally to the pain, to the agony of pain and take the appropriate action. So my idea was, maybe what's happened on this patient is, the insular cortex is normal. That's why he says, doctor I can feel the pain, but the message, the wire that goes from the insular to the rest of the limbic system and the anterior cingulate is cut.

Therefore you have the two key ingredients you need for laughter and humour, namely one part of the brain signalling a potential danger, my god there is something painful here, but the very next instant the anterior cingulate says but I'm not getting any signal. Big deal, there is no danger here, forget it, OK. So you got the two key ingredients and the patient starts laughing and giggling uncontrollably, OK. So it is a disconnection similar to what we saw with the Capgras patient.

So we have seen several syndromes here which suggest that you can look at neurological oddities, neurological syndrome and learn a great deal about the functions of the normal brain. I would like to conclude with a quotation from my previous book, Phantoms in the Brain, "There is something distinctly odd about a hairless, neotenous primate that has evolved into a species that can look back over its own shoulder to ponder its own origins. Odder still, the brain cannot only discover how other brains work but also ask questions about itself, who am I? What is the meaning of my existence, especially if you are from India? Why do I laugh? Why do I dream, why do I enjoy art, music and poetry? Does my mind consist entirely of the activity of neurons in my brain? If so, what scope is there for free will? It is the peculiar recursive quality of these questions as the brain struggles to understand itself that makes neurology so fascinating. The prospect of answering these questions in the next millennium is both exhilarating and disquieting, but it's surely the greatest adventure that our species has ever embarked upon."

So I hope you'll stay with me for all the remaining lectures, thank you very much.

Lecture 2: Synapses and the Self

Our ability to perceive the world around us seems so effortless that we tend to take it for granted. But just think of what's involved. You have two tiny upside down distorted images inside your eyeballs but what you see is a vivid three-dimensional world out there in front of you and this transformation is nothing short of a miracle. How does it come about?

One common fallacy is to assume there is an image inside your eyeball, the optical image, exciting photoreceptors on your retina and then that image is transmitted faithfully along a cable called the optic nerve and displayed on a screen called the visual cortex. Now this is obviously a logical fallacy because if you have a screen and an image displayed on a screen in the brain, then you need another little chap in there watching that image, and there is no little chap in your head. And if you think about it, that wouldn't solve the problem either because then you'd need another little guy in his head looking at the image in his brain and so on and so forth, and you get an endless regress of eyes and images and little people without really solving the problem of perception.

So the first thing you have to do to understand perception is to get rid of the idea of images in the brain and think instead of transforms or symbolic representations of objects and events in the external world. Just as little squiggles of ink, print or writing, or dots and dashes in the Morse code can symbolize or represent something even they don't physically resemble what they are representing, similarly the action of nerve cells in your brain, the patterns of firing, represent objects and events in the external world even though they don't in any way resemble what's out there in the world. Neuroscientists are like cryptographers trying to crack an alien script, an alien code, in this case the code used by the nervous system to represent objects and events in the external world.

So today's lecture will be about the process we call seeing - about how you become consciously aware of things around you. As in our last lecture, I'll begin by telling you about patients with strange visual defects and then explore the wider implications of these syndromes for understanding the nature of conscious experience, how the activity of mere specks of jelly in the visual areas of your brain gives rise to all the richness of your conscious experience, the redness of red, your ability to recognize a burglar or your lover, and how does that happen.

We primates are highly visual creatures and it turns out we have not just one visual area, the visual cortex, but thirty areas in the back of our brains which enable us to see, perceive the world. It's not clear why we need so many, why do you need thirty areas, why not just one area? But perhaps each of these areas is specialised for a different aspect of vision. For example, one area called V4 seems to be concerned mainly with processing colour information, seeing colours, whereas another area in the parietal lobe called MT or the middle temporal area is concerned mainly with seeing motion. How do we know this? Well the most striking evidence comes from patients with tiny lesions that damage just V4, the colour area, or just MT, the motion area.

So for example, when V4 is damaged on both sides of the brain, you end up with a syndrome called cortical colour blindness or achromatopsia, and patients with cortical achromatopsia see the world in shades of grey, like a black and white movie, but they have no problem reading a newspaper or recognising people's faces or seeing direction of movement. Conversely if MT, the middle temporal area is damaged, the patient becomes motion blind. She can still read books and see colours but can't tell you which direction something is moving or how fast.

For example there was a woman in Zurich who had this problem, she was terrified to cross the street because unlike of us here, she saw the cars on the street not as moving but as a series of static images as though lit by a strobe light in a discotheque. She couldn't tell how fast a car was approaching even though she could read its number plate or tell you what colour it was. Even pouring wine into a glass was an ordeal; you and I gauge the rate at which the wine level is rising and slow down appropriately but she can't do this - so the wine always overflows. All of these abilities that seem so simple and effortless to all of us normal people -- it's only when something goes wrong we realize how extraordinarily subtle the mechanisms of vision really are and how complex a process it really is.

Now even though the anatomy of these thirty "visual" areas, the "seeing areas" in the brain looks bewildering at first, there is an overall pattern which I will now describe. The message from the eyeball on the retina goes though the optic nerve and goes to two major visual centers in the brain. One of these I'll call it the old system, the old visual centre, it's the evolutionary ancient centre, the old pathway that's in the brain stem and it's called the superior colliculus. The second pathway goes to the cortex, the visual cortex in the back of the brain and it's called the new pathway. The new pathway in the cortex is doing most of what we usually think of as vision, like recognizing objects, consciously. The old pathway, on the other hand, is involved in locating objects in the visual field, so that you can orient to it, swivel your eyeballs towards it, rotate your head towards it. Thereby directing your high acuity central foveal region of the retina towards the object so then you can deploy the new visual pathway and then proceed to identify what the object is and then generate the appropriate behaviour for that object.

Let me now tell you now about an extraordinary neurological syndrome called Blindsight discovered by Larry Weiscrantz and Alan Cowey at Oxford. It's been known for more than a century that if the visual cortex which is part of the new visual pathway, if that's damaged you become blind. For example if the right visual cortex is damaged you're completely blind on the left side if you look straight everything to the left side of your nose, you're completely blind to.

When examining a patient named GY who had this type of visual deficit, one half of the visual field completely missing, where he was blind, Weizcrantz noticed something really strange. He showed the patient a little spot of light in the Blind region. Weiscrantz asked him "what do you see"? The patient said "nothing" and that's what you would expect given that he was blind but now he told the patient "I know you can't see it but please reach out and touch it" The patient said well that's very strange - he must have thought this is a very eccentric request. I mean, point to this thing which he can't see.

So the patient said, you know I can't, I can't see it how can I point to it? Weiscrantz said well just try anyway, take a guess. The patient then reaches out to touch the object and imagine the researcher's surprise when the patient reaches out and points to it accurately, points to the dot that he cannot consciously perceive. After hundreds of trials it became obvious that he could point accurately on 99% of trials even though he claimed on each trial that he was just guessing. He said he didn't know if he was getting it right or not. From his point of view it might as well have been an experiment on ESP. The staggering implication of this is that the patient was accurately able to point to an object that he denied being able to see. How is this possible? How do you explain his ability to infer the location of an invisible object and point to it accurately?

The answer is obvious. As I said GY has damage to his visual cortex - the new pathway - which is why he is blind. But remember he still has the other old pathway, the other pathway going through his brain stem and superior colliculus as a back-up. So even though the message from the eyes and optic nerves doesn't reach the visual cortex, given that the visual cortex is damaged, they take the parallel route to the superior colliculus which allows him to locate the object in space and the message then gets relayed to higher brain centres in the parietal lobes that guide the hand movement accurately to point to the invisible object! It's as if even though GY the person, the human being is oblivious to what's going on, there's another unconscious zombie trapped in him who can guide the hand movement with uncanny accuracy.

This explanation suggests that only the new pathway is conscious - events in the old pathway, going though the colliculus and guiding the hand movement can occur without you the person being conscious of it! Why? Why should one pathway alone or its computational style perhaps lead to conscious awareness, whereas neurons in a parallel part of the brain, the old pathway can carry out even complex computations without being conscious. Why should any brain event be associated with conscious awareness given the "existence proof" that the old pathway through the colliculus can do its job perfectly well without being conscious? Why can't the rest of the brain do without consciousness? Why can't it all be blindsight in other words?

We can't answer this question directly yet but as scientists the best we can do is to establish correlations and try and home in on the answer. We can make a list of all brain events that reach consciousness and a list of those brain events that don't. We can then compare the two lists and ask, is there a common denominator in each list that distinguishes it from the other? Is it only certain styles of computation that lead to consciousness? Or perhaps certain anatomical locations that are linked to being conscious? That's a tractable empirical question and once we have tackled that, it might get us closer to answering what the function of consciousness might be, if any, and why it evolved.

Now I should add that the blindsight syndrome in GY seemed so bizarre, when it was first discovered that it was greeted with scepticism and some of my colleagues don't believe that it even exists. Well partly this is because the syndrome is very rare but also partly because it seems to violate common sense. How can you point to something you don't see? But actually that's not a good reason for rejecting it because in a sense we all suffer from blindsight. Now that sounds cryptic so let me explain that.

Imagine you are driving your car and having a lively animated intimate conversation with your friend sitting next to you. Your attention is entirely on the conversation, it's what you're conscious of. But in parallel you are negotiating traffic, avoiding the pavement, avoiding pedestrians, not running red lights and performing all these very complex elaborate computations without being really conscious of any of it unless something strange happens, like you see an actual zebra instead of just a zebra crossing! So in a sense you are not any different from GY all of you here, you have "blindsight" for driving and negotiating traffic. What we see in GY is simply an especially florid version of blindsight unmasked by disease, but his predicament is not fundamentally different from yours and mine.

Intriguingly you cannot imagine the converse scenario. Paying conscious attention to driving and negotiating traffic while unconsciously having a creative conversation with your friend. This may sound trivial but it is a thought experiment and it is already telling you something valuable, that computations involved in the meaningful use of language require consciousness but those involved in driving, however complicated, don't involve consciousness.

I believe this approach to consciousness will take us a long way toward answering the riddle of what consciousness buys you and why it evolved. My own philosophical position about consciousness accords with the view proposed by the first Reith lecturer, Bertrand Russell, there is no separate "mind stuff" and "physical stuff" in the universe, the two are one in the same, the formal term for this is neutral monism.

So we have talked about the messages in the new visual pathway. But now let us turn to the other pathway, the old pathway which goes to the colliculus, mediates blindsight. That projects to the parietal lobe in the sides of the brain. The parietal lobes are concerned with creating a three dimensional representation, a symbolic representation of the special lay-out of the external world so the ability that we call spatial navigation, avoiding bumping into things, dodging a missile that's hurled at you, catching something that's thrown at you all of these abilities depend crucially on the parietal lobes.

Now when the right parietal lobe is damaged, you get a fascinating syndrome, called neglect, in a sense the converse of blindsight. The patient can no longer move his eyes towards the object, which is looming towards him and he can no longer reach out and point to it or grab it. Now bear in mind he isn't blind to events on the left side of the world because if you draw his attention he can see it perfectly clearly and he'll identify it, he'll tell you what it is. So he's not blind. So you can think of neglect, I think the best description of it is, it's an indifference to the left side of the world. That's why you call it neglect.

If he's eating from a plate of food, he'll eat only from the right side of the plate and completely leave the left side of the plate uneaten. Then you draw his attention he will say "Oh my God, that's a nice avocado" and he'll take it. So when you draw his attention he can see it but otherwise he ignores it. If he is shaving he will only shave from the right side of his face, or if she's a woman only apply make-up on the right side of the face and that looks quite bizarre, as you can imagine.

Now as I said neglect is caused by damage to the right hemisphere. The patient is also usually paralysed on the left side because the right hemisphere of the brain controls the left side of the body. I wondered if it would be possible to "cure" neglect? Can you treat this patient, making him pay attention to the left side of the world he's ignoring?

So I hit on the idea of using a mirror, as in the case of phantom limbs in my previous lecture. So all I did was I had the patient sitting on a chair and then I stood to the right side of the patient and held a mirror like that so that when the patient rotated his head to the right he would be looking directly into the mirror that I was holding on his right side.

Now the question is, how does he react to this? Obviously he is not neglecting the right side, he's only neglecting the left side of the world so clearly he can see the mirror but he's going to see the reflection of the left side of the world inside the mirror. The question is how is he going to react to that? Well one possibility is he's going to say: "Hey my God, that is a reflection. There's a whole left side of the world that I have been ignoring, let me pay attention" and turn around and pay attention -- in which case you have cured neglect instantly with a mirror. Or he could say, "Well look the reflection is on my right side, so the objects are on my left but hey, left doesn't exist in my universe I'm supposed to neglect it so I'll just ignore it" so he ignores the reflection. What happens?

Well what happened actually as often happens in science - neither! OK? I stood on her right, so she is sitting here in her wheelchair I was sitting, standing on her right side, holding up a mirror, she looked inside the mirror, and on her left side was my student standing with a pen, holding a pen. And I asked the patient what do you see? What am I holding? The patient says, oh you're holding a mirror. I said, how do you know? She said well I can see my reflection in and it's cracked on the top -- which is true.

And I said, what do you see in the mirror? She said oh I see your student John, he's holding a pen. I said, OK I would now like you to use your right hand - remember her right hand is not paralysed - to reach out, grab the pen and then write your name on the pad that's on your lap. Now of course you try this on a normal person and actually I have tried it on a normal colleague. You know you just reach, you know you see the reflection in the mirror of the person holding the pen, you turn to the left, grab the pen and write your name on the pad. What did the patient do?

It's absolutely astonishing. The patient looked in the mirror, reaches out into the mirror for the reflection, bang, bang, bang, starts clawing the surface of the mirror, or on some occasions reaches behind the mirror trying to grab the reflection sometime yanking my tie, grabbing my belt buckle, remember I was holding the mirror on the patient's right side. And I said, what are you doing Mrs D, the patient's name?

The patient said, oh I am trying to reaching for the pen. I said, no, no, no I don't mean the reflection, I mean the real pen where is the real pen? The patient says: "The real pen is inside the mirror, Doctor," or on another occasion: " The pen is behind the darn mirror, Doctor." OK? Now this is absolutely astonishing because we have tried this on a three year old child so the child is sitting here on a chair, you hold the mirror on the right side of the child and you have an assistant holding a candy and you tell the child reach out, reach and grab the candy. The child realizes this is some kind of game, giggles and reaches correctly for the candy on the left side and takes it. Even a chimpanzee can do this, doesn't get confused a mirror image for a real object but the older and wiser Mrs D - seventy years of experience with mirrors - reaches straight into the mirror, bang, bang, bang. Why does this happen? We call it "mirror agnosia" or " looking glass syndrome" in honour of Alice who actually walked into the mirror thinking it was a real world. Why does it happen?

Well I think what happens is this patient's brain is saying, speaking metaphorically, look that's a mirror, I know it's a mirror, that's a reflection, therefore the object is on my left but left doesn't exist in my universe. Therefore the object must be inside the mirror, however absurd it seems to all of you chaps, and therefore I'll reach into the mirror, bang, bang, bang. All of that abstract knowledge about the laws of optics and mirrors is now distorted to accommodate this strange new sensory world that the patient finds herself trapped in.

Now I'll turn to another disorder which is also caused by damage to the right parietal and that is even more extraordinary. It's called denial or anosognosia. Remember most of these patients with right parietal damage also have some damage to the internal capsule so they are completely paralyzed on the left side of the body. It's what you mean by a stroke, this complete paralysis of the left side of the body, and most of them complain about this as indeed they should. They say when am I going to get better, my arm doesn't work. But a subset of them, a small percentage of them will vehemently deny that their left arm is paralyzed, and these are patients who don't have any neglect. They'll say doctor, it's moving fine. Why does this happen?

It's not clear but it is only seen when the right parietal is damaged, rarely seen when the left parietal is damaged and that gives out a clue. It tells you that the denial syndrome has something to do with hemispheric specialization. The manner in which the two cerebral hemispheres deal with the external world, especially the manner in which they deal with discrepancies in sensory input and discrepancies in beliefs. Specifically I would like to suggest when confronted with a discrepancy, the left hemisphere's coping style is to smooth over the discrepancy, pretend it doesn't exist and forge ahead. The right hemisphere's coping style is the exact opposite. It's highly sensitive to discrepancies so I call it the anomaly detector.

Now imagine a patient with a right hemisphere stroke left side paralyzed. The patient is sending a command to move the arm, he is getting a visual signal saying it is not moving so there is a discrepancy. His right hemisphere is damaged, his left hemisphere goes about its job of denial and confabulation smoothing over the discrepancy and saying, all is fine, don't worry. On the other hand, if the left hemisphere is damaged and the right side is paralyzed the right hemisphere is functioning fine, notices the discrepancy between the motor command and the lack of visual feedback and says, my god you are paralyzed. This was an outlandish idea but it's now been tested with brain imaging experiments and shown to be essentially correct.

Now this syndrome is quite bizarre - a person denying that he or she is paralyzed - but what we found about seven or eight years ago something even more amazing. Some of these patients will deny that another patient is paralyzed so the patient is sitting here. We saw the patient, another patient sitting in a wheelchair - I'll call him patient B - and I've told patient B move your arm. Patient B of course is paralyzed, doesn't move. And then I ask my patient - is that patient moving his arm? And the patient says yes of course he is moving his arm. He is engaging in denial of other people's disabilities.

Now at first this didn't make any sense to me then I came across some studies by Giaccomo Rizzollati, experiments done on monkeys. If you record from parts of the frontal lobes which are concerned with motor commands you find there are cells which fire when the monkey performs certain specific movements, like one cell will fire when the monkey reaches out and grabs a peanut, another cell will fire when the monkey pulls something, yet another cell when the monkey pushes something. That's well known. These are motor command neurons. But Rizzollati found that some of these neurons will also fire when the monkey watches another monkey performing the same action, so you find a peanut-grabbing neuron which fires when the monkey grabs a peanut. When the monkey watches another monkey grab a peanut, it fires. It's quite extraordinary because the visual image of somebody else grabbing the peanut is utterly different so you have to do this internal mental transformation to do that computation and for that neuron to fire and Rizzollati calls these mirror neurons. Another name for them is monkey-see monkey-do neurons and these neurons I think are the ones that are damaged in these patients.

Because think about what's involved in your judging somebody else's movements. Maybe you need to do a virtual reality internal simulation of what that person is doing, and that may involve the activity of these very same neurons, these mirror neurons. So these mirror neurons, instead of being some kind of curiosity, hold important implications for understanding many aspects of human nature like how do you read somebody else's movements, their intentions, their actions. Many aspects of what you called a theory of other minds, a sophisticated theory of other people's behaviour. We think it is this system of neurons that is damaged in these patients. The patient can therefore no longer construct an internal model of somebody else's actions.

I also want to argue that these neurons may have played an important role in human evolution and I am going to talk about this at length in my Oxford lecture on the emergence of language and abstract thinking, because think about it. One of the hallmarks of our species is what we call culture. And culture depends crucially on imitation of your parents, of your teachers and the imitation of complex skills may require the participation of mirror neurons. So what I'm arguing is somewhere around 50,000 years ago maybe the mirror neurons system became sufficiently sophisticated that there was an explosive evolution of this ability to mime complex actions, in turn leading to cultural transmission of information which is what characterises us humans.

Now let me conclude by emphasising once again that although the studies on patients are intriguing in themselves, our real agenda here is to understand in terms of brain function, us normal humans, how our brains work, the whole spectrum of abilities that we call human nature, whether it is body image or culture or language or abstract thinking and I hope to convince you that such a deeper understanding of the brain will have a profound impact not just on the sciences but on the humanities as well. Lofty questions about the mind are fascinating to ask, philosophers have been asking them for three millennia both in India where I am from and here in the West - but it is only in the brain that we can eventually hope to find the answers.

Thank you very much.

Lecture 3: The Artful Brain

In this lecture - which is the most speculative one in the series of five - I'd like to take up one of the most ancient questions in philosophy, psychology and anthropology, namely what is art? When Picasso said: "Art is the lie that reveals the truth" what exactly did he mean?

As we saw in my previous lectures neuroscientists have made some headway in understanding the neural basis of psychological phenomena like body image, how you construct your body image, or visual perception. But can the same be said of art - given that art obviously originates in the brain?

In particular what I'd like to do is raise the question: "Are there such things as artistic universals?"

Now let me add a note of caution before I begin. When I speak of artistic universals I am not denying the enormous role played by culture. Obviously culture plays a tremendous role, otherwise you wouldn't have different artistic styles - but it doesn't follow that art is completely idiosyncratic and arbitrary either or that there are no universal laws.

Let me put it somewhat differently. Let's assume that 90% of the variance you see in art is driven by cultural diversity or - more cynically - by just the auctioneer's hammer, and only 10% by universal laws that are common to all brains. The culturally driven 90% is what most people already study - it's called art history. As a scientist what I am interested in is the 10% that is universal - not in the endless variations imposed by cultures. The advantage that I and other scientists have today is that unlike we can now test our conjectures by directly studying the brain empirically. There's even a new name for this discipline. My colleague Semir Zeki calls it Neuro-aesthetics - just to annoy the philosophers.

I recently started reading about the history of ideas on art - especially Victorian reactions to Indian art - and it makes fascinating reading.

For example if you go to Southern India, you look at the famous Chola bronze of the goddess Parvati dating back to the 12th century. For Indian eyes, she is supposed to represent the very epitome of feminine sensuality, grace, poise, dignity, everything that's good about being a woman. And she's of course also very voluptuous

Pic. The Goddess Parvati

But the Victorian Englishmen who first encountered these sculptures were appalled by Parvati, partly because they were prudish, but partly also just because of just plain ignorance.

They complained that the breasts were way too big, the hips were too big and the waist was too narrow. It didn't look anything like a real woman - it wasn't realistic - it was primitive art. And they said the same thing about the voluptuous nymphs of Kajuraho - even about Rajastani and Mogul miniature paintings. They said look these paintings don't have perspective, they're all distorted.

They were judging Indian art using the standards of Western art - especially classical Greek art and Renaissance art where realism is strongly emphasized.

But obviously this is a fallacy. Anyone here today will tell you art has nothing to do with realism. It is not about creating a realistic replica of what's out there in the world.

I can take a five dollar camera, aim it at one of you here, take a photograph. It's very realistic but you wouldn't give me a penny for it. In fact art is about the exact opposite. It's about deliberate hyperbole, exaggeration, in fact even distortion in order to create pleasing effects in the brain.

But obviously that can't be the whole story. You can't just take an image and randomly distort it and call it art - although many people in La Jolla where I come from do precisely that. The distortion has to be lawful. The question then becomes: What kinds of distortion are effective? What are the laws?

So one day I was sitting in a temple in India when I was on a sabbatical and in a whimsical frame of mind I just jotted down what I think of as the universal laws of art, the ten laws of art which cut across cultural boundaries. Given our time limits, I'm going to just tell you four or five of my ten laws - the rest are on the BBC Website, so you can go look it up.

Professor Ramachandran's suggested 10 universal laws of art:

1. Peak shift

2. Grouping

3. Contrast

4. Isolation

5. Perception problem solving

6. Symmetry

7. Abhorrence of coincidence/generic viewpoint

8. Repetition, rhythm and orderliness

9. Balance

10. Metaphor

The first law, I call peak shift and to illustrate this I'll use a hypothetical example from animal behaviour, from rat psychology.

Imagine you're training a rat to discriminate a square from a rectangle. So every time it sees a particular rectangle you give it a piece of cheese. When it sees a square you don't give it anything. Very soon it learns that the rectangle means food, it starts liking the rectangle - although you're not supposed to say that if you're a behaviourist. And it starts going towards the rectangle because it prefers the rectangle to the square.

But now the amazing thing is if you take a longer skinnier rectangle and show it to the rat, it actually prefers the longer skinnier rectangle to the original rectangle that you taught it. And you say: Well that's kind of stupid. Why does it prefer a longer skinnier rectangle rather than the one you originally showed it? Well it's not stupid at all because what the rat is learning is a rule - Rectangularity. And of course therefore if you make it longer and skinnier, it's even more rectangular. So it says: "Wow! What a rectangle!" and it goes towards that rectangle.

Now you say: Well, what's that got to do with art?

Well let's think about caricature. What do you do in a caricature? Supposing you want to produce a caricature of Maggie Thatcher or a caricature of Nixon, what do you do? You take Nixon's face and you say: What's special about his face? What makes him different from other people. So what you do is you take the mathematical average of all male faces and you subtract it from Nixon's face. And you get the big bulbous nose and the shaggy eyebrows. And then you amplify it. And then you get an image that looks even more like Nixon than Nixon himself. Now if you do it just right you get great portraiture, even a Rembrandt. But if you overdo it you get caricature, it looks comical. But it still looks even more like Nixon than the original Nixon. So you're behaving exactly like that rat.

But what's it got to do with the rest of art. Let's go back to the Chola bronze of Parvati. Let's talk about Indian art. Well the same principle applies. How does the artist convey the very epitome of feminine sensuality? What he does is simply take the average female form, subtract the average male form - you're going to get big breasts, big hips and a narrow waist. And then amplify it, amplify the difference. And you don't say: "My God, it's anatomically incorrect". You say: "Wow! What a sexy goddess!"

But that's not all there is to it because how do you bring in dignity, poise, grace?

Well what you do is something quite clever, what the Chola bronze artist does is something quite clever. There are some postures that are forbidden to a male. I can't stand like that even if I want to. But a woman can do it effortlessly. So what he does is he goes into an abstract space I call "posture space", and then subtracts the average male posture from the female and then exaggerates the feminine posture - and then you get elegant triple flexion - or tribhanga - pose, where the head is tilted one way, the body is tilted exactly the opposite way, and the hips again the other way. And again you don't say: "My God, that's anatomically inappropriate. Nobody can stand like that." You say: "My God! It's gorgeous. It's beautiful! It's a celestial goddess". So the image is extremely evocative and it's an example of the peak shift principle in Indian art.

OK, this is all about faces and caricatures and bodies and Chola bronzes. That seems quite reasonable, but what about the rest of art? What about abstract art? What about Picasso. What about semi-abstract art? What about impressionism, what about Cubism? Van Gogh? Monet? Henry Moore? How can my ideas even begin to approach some of those artistic styles?

To answer this question, you need to go and look at ethology, especially the work of Niko Tinbergen at Oxford more than fifty years ago. And he was doing some very elegant experiments on seagull chicks.

As soon as the herring-gull chick hatches, it looks at its mother. The mother has a long yellow beak with a red spot on it. And the chick starts pecking at the red spot, begging for food. The mother then regurgitates half-digested food into the chick's gaping mouth, the chick swallows the food and is happy. Then Tinbergen asked himself: "How does the chick know as soon as it's hatched who's mother? Why doesn't it beg for food from a person who is passing by or a pig?"

And he found that you don't need a mother.

You can take a dead seagull, pluck its beak away and wave the disembodied beak in front of the chick and the chick will beg just as much for food, pecking at this disembodied beak. And you say: "Well that's kind of stupid - why does the chick confuse the scientist waving a beak for a mother seagull?"

Well the answer again is it's not stupid at all. Actually if you think about it, the goal of vision is to do as little processing or computation as you need to do for the job on hand, in this case for recognizing mother. And through millions of years of evolution, the chick has acquired the wisdom that the only time it will see this long thing with a red spot is when there's a mother attached to it. After all it is never going to see in nature a mutant pig with a beak or a malicious ethologist waving a beak in front of it. So it can take advantage of the statistical redundancy in nature and say: "Long yellow thing with a red spot IS mother. Let me forget about everything else and I'll simplify the processing and save a lot of computational labour by just looking for that."

That's fine. But what Tinbergen found next is that you don't need even a beak. He took a long yellow stick with three red stripes, which doesn't look anything like a beak - and that's important. And he waved it in front of the chicks and the chicks go berserk. They actually peck at this long thing with the three red stripes more than they would for a real beak. They prefer it to a real beak - even though it doesn't resemble a beak. It's as though he has stumbled on a superbeak or what I call an ultrabeak.

Why does this happen?

We don't know exactly why, but obviously there are neural circuits in the visual pathways of the chick's brain that are specialized for detecting beaks as soon as the chick hatches. They fire when seeing the beak. Perhaps because of the way they are wired up, they may actually respond more powerfully to the stick with the three stripes than to a real beak. Maybe the neurons' receptive field embodies a rule such as "The more red contour the better," and it's more effective in driving the neuron, even though the stick doesn't look like a beak to you and me - or maybe even to the chick. And a message from this beak-detecting neuron now goes to the emotional limbic centres in the chick's brain giving it a big jolt and saying: "Wow, what a super beak!" and the chick is absolutely mesmerized.

Well now what's this got to do with art, you're wondering?

Well this brings me to my punch line of about art. What I'm suggesting is if those seagulls had an art gallery, they would hang this long stick with the three red stripes on the wall, they would worship it, pay millions of dollars for it, call it a Picasso, but not understand why - why am I mesmerized by this damn thing even though it doesn't resemble anything? That's what all of you are doing when you are buying contemporary art. You are behaving exactly like those gull chicks.

In other words human artists through trial and error, through intuition, through genius have discovered the figural primitives of our perceptual grammar. They are tapping into these and creating for your brain the equivalent of the long stick with the three stripes for the chick's brain. And what you end up with is a Henry Moore or a Picasso.

The advantage of these ideas is you can test them experimentally. You can actually record from cells in the brain which sort of fire when you show it a face in the fusiform gyrus. Now some of them will fire only to a particular view of a face. But higher up you've got neurons which respond to any view of a given face. And I'm predicting that if you present a Cubist portrait of a monkey face - where you present two views of a monkey's face in the same place - that cell will be hyper-activated. Just as the long stick with the three red stripes hyper-activates the beak-detecting neurons in the chick's brain, this Cubist portrait of a monkey face will hyper-activate these face-detecting neurons in the monkey brain - and the monkey says: "Wow! What a face". So what you have here is in fact a neural explanation for Picasso, for Cubism.

I've told you about one law so far - peak shift and the idea of ultra-normal stimuli. We have borrowed insights from ethology, neurophysiology, rat psychology to account for why people like non-realistic art.

The second law is more familiar to all of you. It's called Grouping.

Many of you may have seen those famous puzzle pictures, like Richard Gregory's Dalmatian dog. You just see a bunch of splotches when you first look at it but you sense you visual brain trying to solve a perceptual problem, trying to make sense of this chaos. And then after a few seconds, or maybe actually several seconds - 30 or 40 seconds - suddenly everything clicks in place and you group all the correct fragments together, and lo and behold you see a Dalmatian dog.

Richard Gregory's Dalmatian

Richard Gregory's Dalmatian

You can almost sense your brain groping for a solution to the perceptual riddle and as soon as you successfully group the correct fragments together to see the dog, what I suggest is a message gets sent from the visual centres of the brain to the limbic-emotional brain centres of the brain giving it a jolt and saying: "AHA, there is a dog" or "AHA, there is a face".

The Dalmatian dog example is very important because it reminds us that vision is an extraordinarily complex and sophisticated process. And even looking at a simple scene involves a complex hierarchy, a stage by stage processing. At each stage in the hierarchy of processing, when a partial solution is achieved - "Hey it looks a bit dog-like right here" - there is a reward signal "AHA", a partial "AHA", and a small bias is sent back to earlier stages to facilitate the further binding of the features of the dog. And through such progressive bootstrapping the final dog clicks in place to create the final big "AHA!" Vision has much more in common with problem solving - more like a twenty questions game - than we usually realize.

The grouping principle is widely used in both Indian and in Western art - and even in fashion design. For example you go to Harrods, and you pick out a scarf with red splotches on it. Then you often match it with a skirt which has got some red splotches on it. Now what's this all about? Is it just hype, is it just marketing? Or is it telling you something very deep about how the brain is organized? I'm going to argue it is telling you something very deep, something to do with the way the brain evolved.

Vision evolved mainly to discover objects and to defeat camouflage. You don't realize this when you look around you and you see clearly defined objects.

But imagine your primate ancestors scurrying up in the treetops trying to detect a lion seen behind fluttering green foliage. What you get inside the eyeball on the retina is just a bunch of yellow lion fragments obscured by all the leaves. But the brain says - so to speak - "What's the likelihood that all these different yellow fragments are exactly the same yellow simply by chance? Zero. They must all belong to one object, so let me link them together, glue them together. Oh my God, it's a lion - let me out of here!" And as soon as you glue them together, a signal gets sent to the limbic system saying: "AHA, there's something object-like, pay attention here".

So there's an arousal, and an attention which then titillates the limbic system, and you pay attention and you dodge the lion.

And such "AHAs" are created, I maintain, at every stage in the visual hierarchy as partial object-like entities are discovered that draw your interest and attention. What the artist tries to do is to generate as many of these "AHA" signals in as many visual areas as possible by more optimally exciting these areas with his paintings or sculptures than you could achieve with natural visual scenes or realistic images. Not a bad definition of art if you think about it.

That takes me to the third law - the law of perceptual problem solving or visual peekaboo. Now what do I mean by that?

As anyone knows a nude seen behind a diaphanous veil is much more alluring and tantalizing than a full-colour Playboy photo or a Chippendale pinup - or a Page Three girl, is that what you call it? Why?

As I said our brains evolved in highly camouflaged environments. Imagine you are chasing your mate through dense fog. Then you want every stage in the process - every partial glimpse of her - to be pleasing enough to prompt further visual search - so you don't give up the search prematurely in frustration. In other words, the wiring of your visual centres to your emotional centres ensures that the very act of searching for the solution is pleasing, just as struggling with a jigsaw puzzle is pleasing long before the final "AHA". Once again it's about generating as many "AHAs" as possible in your brain.

The fourth law is the law of isolation or understatement.

You all know that a simple outline doodle by Picasso or a nude by Rodin or Klimt can be much more evocative than a full colour photo of a woman. Similarly the cartoon-like outline drawings of bulls in the Lascaux Caves are much more powerful and evocative of the animal than a National Geographic photograph of a bull. Hence the famous aphorism in art: "Less is more".

But why should this be so? Isn't it the exact opposite of the first law, the idea of hyperbole, of trying to excite as many "AHAs" as possible? A pinup or a Page Three girl after all has much more information. It's going to excite many more areas in your brain, many more neurons, so why isn't it more beautiful?

The way out of this paradox is to consider another visual phenomenon, called Attention. It's a well-known fact that you can't have two overlapping patterns of neural activity simultaneously. Even though you've got one hundred billion nerve cells, you can't have two overlapping patterns. In other words, there is a bottleneck of attention. You can only allocate your attentional resources to one thing at a time.

Well when you look at a Page Three girl, the main information about her sinuous soft contours is conveyed by her outline. Her skin tone, hair colour after all is no different from anyone sitting here. It's irrelevant to her beauty as a nude. So in the realistic photo you have all this irrelevant information cluttering the picture and distracting your attention away from where it's needed critically - to her contours and outlines. By leaving all this out in a doodle or sketch the artist is saving your brain a lot of trouble. And this is especially true if the artist has also added some peak shifts to the outline to create an "ultra nude" or a "super nude".

What's the evidence for all this? Of course you can test it by doing brain imaging experiments comparing neural responses to outline sketches and caricatures versus full-colour photos. But there's also very striking neurological evidence from children with autism. Some of these children have what's called the savant syndrome. Even though they are retarded in many respects, they have one preserved island of extraordinary talent.

For example, a seven-year-old autistic child Nadia had exceptional artistic skills. She was quite retarded mentally, could barely talk, yet she could produce the most amazing drawings of horses and roosters and other animals. A horse drawn by Nadia would almost leap out at you from the canvas. Contrast this with the lifeless, two-dimensional, tadpole-like sketches drawn by most normal eight or nine-year-olds - or even normal adults.

So we have another paradox. How can this retarded child produce a drawing that is so incredibly beautiful? The answer, I maintain, is the principle of isolation.

In Nadia perhaps many or even most of her brain modules are damaged because of her autism, but there is a spared island of cortical tissue in the right parietal. So her brain spontaneously allocates all her attentional resources to the one module that's still functioning, her right parietal. Now it turns out that the right parietal is the part of your brain that's concerned with your sense of artistic proportion. We know this because when it's damaged in stroke, for example, in an adult, you lose your artistic sense. You produce drawings that are often excessively detailed but lack the vital essence of the picture you're trying to depict. You lose your sense of artistic proportion. Conversely, since everything else is damaged in Nadia's brain she allocates all her attention to this brain module - so she has a hyper-functioning art module in her brain. Hence the beautiful renderings of horses and roosters.

Another example, equally striking. Dr Miller, University of California, has studied patients who start developing rapidly progressing dementia in middle age, a form of dementia called the fronto-temporal dementia, affecting frontal lobes and temporal lobes, but sparing the parietal lobe. And guess what happens. These patients suddenly start producing the most amazingly beautiful paintings and drawings - not all of them but some of them - even though they had never had any artistic talent before the onset of their dementia. Again, it's the isolation principle at work. With all other modules in the brain not working the patient develops a hyper-functioning right parietal. There are even reports from Alan Snyder in Australia that you can temporarily paralyze parts of the brain in normal volunteers - all of us less gifted people here. Imagine just zapping bits of your brain and unleashing hidden talents. If that happens, it will truly be a brave new world.

We don't have time to talk about all my other laws in detail. But I'll just mention the last law on my list - and in many ways the most important, yet the most elusive: Visual Metaphor. You all know what a metaphor is in literature as when you say it's the East and Juliet is the sun. But you can do the same thing in visual art - both in Western art and in Indian art. For example, when you look at the Chola bronze of the dancing Shiva or Nataraja with multiple arms you are not meant to take the multiple arms literally or call it a multi-armed monstrosity like the Victorian art critic, Sir George Birdwood, did. Funnily enough he didn't think that angels sprouting wings were monstrosities - although I can tell you as a medical man you can have multiple arms, but wings on scapulae are anatomically impossible!

The multiple arms are meant to symbolize multiple divine attributes of God and the ring of fire that Nataraja dances in - indeed his dance itself - is a metaphor of the dance of the Cosmos and of the cyclical nature of creation and destruction, an idea championed by the late Fred Hoyle. Most great works or art - be it Western or Indian - are pregnant with metaphor and have many layers of meaning.

Everyone knows that metaphors are important yet we have no idea why. Why not just say: "Juliet is radiant and warm" instead of saying: "Juliet is the sun"? What is the neural basis for metaphor? We don't know but I'll have a stab at this question next week in my Oxford lecture on synesthesia.

With that I conclude my lecture on Neuro-aesthetics. Have we understood the neural basis of art? Of course not. We have barely scratched the surface. But I hope the "laws of art" I've discussed might give you some hints about the general form of a future theory of art.

The solution to the problem of aesthetics, I believe, lies in a more thorough understanding of the connections between the 30 visual centres in your brain and the emotional limbic structures. And once we have achieved a clear understanding of these connections, we will be closer to bridging the huge gulf that separates C.P. Snow's two cultures - science on the one hand and Arts, philosophy and humanities on the other.

We could be at the dawning of a new age where specialisation becomes old-fashioned and a new 21st century version of the Renaissance man is born.

Lecture 4: Purple Numbers and Sharp Cheese

In the 19th century, the Victorian scientist Francis Galton, who was a cousin of Charles Darwin, noticed something very peculiar. He found that certain people in the normal population who were otherwise perfectly normal had a certain peculiarity and that is every time they heard a specific tone, they would experience a specific colour. For example, C sharp might be red, F sharp might be blue, another tone might be indigo. And this curious mingling of the senses was called synesthesia. Some of these people also see colours when they see numbers. Every time they see a black and white number like the number five printed on a white page, or a white five on a black page for that matter, they would see it tinged red so five might be red, six would be green, seven would be indigo, eight would be yellow and so on and so forth. Galton also pointed out this condition runs in families and more recently Simon Baron Cohen in Cambridge has confirmed this, that it does indeed run in families.

Now I think it's fair to say that even though people have known about synesthesia for over a hundred years, it's been by and large recorded as a curiosity by mainstream neuroscience and psychology but what I'd like to do today in fact is suggest that anomalies can be extremely important in science. If you know which anomaly to pick, you can completely change the direction of your research and generate what you would call scientific revolutions. But first let's look at the most common explanations that have been proposed to account for synesthesia and in fact there are four of these. The first explanation is the most obvious and that is that they're just crazy! Now the second explanation is maybe they're just acid junkies or pot heads, they've just been on drugs. Now this is not an entirely inappropriate criticism because synesthesia is more common among people who use LSD but to me that makes it more interesting, not less interesting. Why should some chemicals cause synesthesia, if indeed they do?

The third idea is that maybe these people are just remembering childhood memories. For example maybe they were playing with refrigerator magnets and five was red and six was blue and seven was green, and for some reason they're stuck with these memories but this never made much sense to me because why would it then run in families? You'd have to say they're passing the same magnets down, or the propensity to play with magnets runs in families or something like that. Anyway it didn't make much sense but it's something you have to bear in mind. The fourth explanation is more subtle and it invokes sensory metaphors. If you look at our ordinary language, it's replete with synesthetic metaphors, cross-sensory metaphors such as for example if you said cheddar cheese is sharp. Well cheese isn't sharp, you can take a piece of cheese and rub it on your skin, it's actually soft. So why do you say it's sharp? Well you say oh no no, what I mean is it tastes sharp, it's a metaphor. But this is circular - why do you use a tactile adjective, touch you know sharp, for a taste sensation?

Now the problem with this explanation is that in science you can never explain one mystery with another mystery. Saying that synesthesia is just a metaphor doesn't explain a damn thing because we don't know what a metaphor is or how it's represented in the brain. And indeed as we go along, what I'd like to do is to turn it upside down and suggest the very opposite, that synesthesia is a sensory phenomenon whose neural basis you can discover in the brain and that in turn can give you an experimental foothold for understanding more elusive aspects of the mind such as what is a metaphor, so why has it been ignored? There's an important lesson here in the history of science. And I think in general it's fair to say that for a curious phenomenon, an anomaly to make it into mainstream science and have an impact, it has to fulfil three criteria, and that is first you have to show it's a real phenomenon. Second, you have to have a candidate mechanism that explains what it might be. And third it has to have broad implications. What's a big deal? So what, who cares? So for example if you take telepathy, OK telepathy has vast implications if true so the third criterion is fulfilled but the first criterion is not fulfilled, it's not repeatable. We don't even know if it's true, it's probably bogus. Another example would be bacterial transformation. If you take one species of bacteria - pneumococcus - and you incubate it with another species of bacterium, the second species actually becomes transformed into the first species and you can do this just extracting the chemical, the DNA, and then use that to induce the transformation and this was reliably repeatable. Many times it was repeated as published in a prestigious journal but people ignored it. OK why did they ignore it? Because nobody could think of a candidate mechanism. How can you possibly encode heredity in a chemical until Watson and Crick came along, described the double helical structure of DNA, described the genetic code and then people started accepting it, and recognised the importance of bacterial transformation.

So I'd like to do the same thing with synesthesia. First of all I'd like to show it's real, it's not bogus. Second, suggest candidate mechanisms, what's going on in the brain. And third, so what - why should I care? So I'm going to argue in fact synesthesia has very broad implications. It might tell you about things like metaphor and how language evolved in the brain, maybe even the emergence of abstract thought that us humans, human beings are very good at.

So first we need to show synesthesia is a real phenomenon. What we did was essentially develop a clinical test for discovering closet synesthetes, and how do you do that? First of all we found two synesthetes and these people saw numbers as colour, for example five as red and two as green, so we produced a computerised display on the screen which had a random jumble of fives on the screen and embedded among these fives are a number of twos, and the twos are arranged to form a shape like a triangle or a square or a circle. Now when you and I, anybody here in the audience who is not a synesthete looks at this display, it takes several seconds, as much as twenty or thirty seconds before you say oh I see all the twos, they are arranged to form a triangle or a square. Now when we showed this sample display to the two synesthetes, they immediately or very quickly saw the triangle or the square because the numbers are actually coloured for them, they see them conspicuously popping up from the background so this demolishes the idea that they're just crazy because if they're crazy, how come they're better at it than all of you normals? It also suggests that it's a genuine sensory effect because if it's just a memory association or something high level, how come they actually see the triangle? So we know the phenomenon is real and using this test and other similar tests, we are able to show that it's much more common than people have assumed in the past. In fact people have claimed that it's one in ten thousand. We find it's one in two hundred, probably two or three of you here in the audience who don't want to admit it.

So next what causes synesthesia? Well my students and I, especially Ed Hubbard, he and I were looking at brain atlases and we found if you look at a structure called the fusiform gyrus in the temporal lobes of the brain, it turns out that the fusiform gyrus has the colour area V4 which is described by Semir Zeki. This is the area which processes colour information but we were struck by the fact that the number area of the brain which represents visual numbers as shown by brain imaging studies, that number area is right next to it, almost touching the colour area of the brain so we said this can't be a coincidence, how come the most common type of synesthesia is number/colour and the number area and colour area are almost touching each other right next to each other in the same part of the brain? Maybe what's going on is these people have some accidental cross-talk, or cross-wiring, just as in my experiments on phantom limbs in my London lecture I showed that the face area becomes cross-wired with the hand area in the cortex, except in this case it happens not because of amputation but because of some genetic change in the brain. And now we've done imaging experiments on people with synesthesia and showed that if you show just black and white numbers, they get activation in the colour area.

Now the next question is why does this cross-wiring or cross-activation occur? Well remember I said it runs in families. Well this suggests there's a gene or set of genes involved. What might this gene be doing, this bad gene? Well one possibility is we are all born with excess connections in the brain. In the foetus there are many more redundant connections than you need and then you prune away the excess connections to produce the modular architecture characteristic of the adult brain, like Michelangelo chipped away everything that doesn't look like David to produce David. That's how you generate a brain. So I think what's happened in these people is that gene is defective and therefore there's defective pruing so there's cross-activation between adjacent areas of the brain - or there could be some kind of chemical imbalance that produced cross-activation between adjacent parts of the brain that are normally only loosely connected and this produces a hyperconnectivity between these parts of the brain.

Now what we found next was even more amazing. Take the same two synesthetes. Instead of showing them Arabic numbers- actually I should call them Indian numbers but it doesn't matter - Indian/Arabic numbers, you show them Roman numbers, Roman V which looks like a V or a 6. Guess what happens? They say oh I know it's a five but it doesn't look coloured, it's black and white so Roman numbers don't give colours. Now what does that prove? It's very important because it shows it's not the numerical concept that drives the colour but the visual appearance of the Indian/Arabic number and it fits with what I'm saying because the fusiform gyrus represents the visual appearance of numbers and letters and things like that, not the abstract concept of sequence or ordinality.

Where does that occur, the abstract idea of number? We don't know but a good guess is angular gyrus in the left hemisphere. We know that because when that's damaged in patients they can no longer - they're fluent in conversation, they are intelligent and all of that but they can't do even simple arithmetic. You say what's seventeen minus three, he'll say oh is it nine? Gets it completely wrong. So we think that abstract number concepts are represented in the angular gyrus and remember this chap's cross-wiring, is in the fusiform gyrus but in the visual appearance of a number and the colour.

Now, however, we then found this is not true of all synesthetes. All synesthetes are not made equal. We then ran into other synesthetes where it's not merely a number that evokes colour but even days of the week evoke colours. Monday is red, Tuesday is indigo, Wednesday is blue, months of the year evoke colour, December is yellow, January is red, February is indigo. No wonder people thought they were crazy! But remember, if you're a clinician you know when somebody sounds crazy it usually means you're not smart enough to figure it out. He isn't crazy. What do calendars, what do days of the week, months of the year and numbers have in common? What they all have in common is the abstract idea of sequence or ordinality. So what I am claiming is that's represented in the angular gyrus, higher up in the TPO junction, temporal parietal occipital junction in the vicinity of the angular gyrus, and guess what? The next colour area in the sequence is higher up in the general vicinity of the TPO junction, not far from the angular gyrus so what I'm arguing is - in these people the cross-wiring is higher up in the angular gyrus. Then you get a higher synesthete, so if the faulty gene is selectively expressed in the fusiform gyrus, lower at an earlier stage in processing, you get a lower synesthete driven by the visual appearance. If it's expressed selectively higher up in the vicinity of the angular gyrus, you get a higher synesthete driven by the numerical concept rather than by the visual appearance.

OK next question - why did this gene survive?

One in two hundred people have this peculiarity of seeing coloured numbers and it's completely useless so why hasn't it vanished from the population and I'm going to suggest it's a bit like sickle cell anaemia - there's a hidden agenda. These genes are doing something else important. What? Well one of the odd facts about synesthesia which been known for a long time and again been ignored, is the fact that synesthesia is much more common among artists, poets, novelists, you know flaky types! So now why is it much more common? Well one view is that - in fact according to one study it's seven times more common among artists poets and novelists and the reason is what do artists, poets and novelists all have in common? Just think about it. What they all have in common is they're very good at metaphor, namely linking seemingly unrelated concepts in their brain, such as if you say "out out brief candle", so it's life, why do you call it a candle? Is it because life is like a long white thing? Obviously not. You don't take the metaphor literally, although schizophrenics do and we won't go into that. So why do you that? Well it's brief like a candle, it can be snuffed out like a candle, it illumines like a candle very briefly. Your brain makes all the right links and Shakespeare of course was a master of doing this. Now imagine one further assumption - if this gene is expressed more diffusely instead of being just expressed in the fusiform or in the angular, if it's expressed in the fusiform you get a lower synesthete, in the angular gyrus TPO junction you get a higher synesthete. If it's expressed everywhere you get greater hyperconnectivity throughout the brain making you more prone to metaphor, links seemingly unrelated things because after all concepts are also represented in brain maps. This may be seem counter-intuitive but after all a number, there's nothing more abstract than a number. You can have five pigs, five donkeys, five chairs - it's fiveness - and that's represented in a fairly small region namely the angular gyrus so it's possible that concepts are also represented in brain maps and these people have excess connections so they can make these associations much more fluidly and effortlessly than all of us less-gifted people.

Now, remember I said the third thing you have to do in science is show that this is not just some quirk. It has vast implications. Well what implications does synesthesia have? I'm going to show all of you that synesthesia is not just a quirk in some people's brain. All of you here are synesthetes, and I'm going to do an experiment. I want all of you to imagine in front of you, to visualise in front of you a bulbous amoeboid shape which looks a bit, has lots of curves on it, undulating curves. And right next to it imagine a jagged, like a piece of shattered glass with jagged shapes. And just for fun, I'm going to tell you this is Martian alphabet. Just as in English alphabet, A is a, B is b, you've got each shape with the particular sound, this is Martian alphabet and one of these shapes is kiki and the other is booba, and I want you to tell me which is which. How many of you think the bulbous shape is the kiki, raise your hands? Well there's one mutation there. In fact what you find is if you do this experiment, 98% of people say the jagged shape, the shattered glass is kiki, and the bulbous amoeboid shape is a booba. Now why is that? You never learnt Martian and nobody here is a Martian. The answer is you're all synesthetes but you're in denial about it. And I'll explain. Look at the kiki and look at the sound kiki. They both share one property, the kiki visual shape has a sharp inflexion and the sound kiki represented in your auditory cortex, in the hearing centres in the brain also has a sharp sudden inflexion of the sound and the brain performs a cross-modal synesthetic abstraction saying the only thing they have in common is the property of jaggedness. Let me extract that property, that's why they're both kiki. So what? Well I'll explain.

We have taken the same patterns I have just told you about, the booba/kiki, and shown them to patients who have damage, very small lesion in the angular gyrus of the left hemisphere and guess what? If you show them these two shapes and ask them to associate kiki with the two shapes, kiki and booba, they're random and by the way we don't use just these two shapes. We have a whole set of them and they cannot do this cross-modal associations even though they're fluent in conversation, they're intelligent, they seem normal in other respects. This makes perfect sense because the angular gyrus is strategically located at the crossroads between the parietal lobe (concerned with touch and propriaception) the temporal lobe (concerned with hearing), occipital lobe> (concerned with vision) so it is strategically placed to allow a convergence of different sense modalities to create abstract modality-free representations of things around you. Now think of what this involves. Think of the jagged shape and the sound, kiki. They have nothing in common. One is photons hitting the retina in parallel, and the other is a sharp sound hitting the hair cells sequentially but the brain abstracts the common denominator saying - but jaggedness is common, or the property of undulation is common, so what you're seeing here in the angular gyrus is the beginnings of a property that we call abstraction that us human beings excel in. And another point I'd like to make is why did this ability evolve in humans in the first place, cross-modal abstraction? Well it turns out if you look at lower mammals, compare them with monkeys, then compare them with the great apes and then with humans, there's a progressive enlargement of the TPO junction and angular gyrus, almost an explosive development and it's especially large in us humans. Why? Well I think this ability evolved because imagine your ancestors scurrying up on the treetops trying to grab branches, jumping from branch to branch, they've got a visual horizontal branch and then they have to adjust the angle of the arm and the fingers so that the proprioceptive map has to match the horizontality of the visual appearance and that's why the angular gyrus became larger and larger. But once you develop this ability to engage in cross-modal abstraction, that structure in turn became an exaptation for other types of abstraction that us humans excel in, be it metaphor or any other type of abstraction, so that's the claim being made here.

Now finally I would like to turn to language, how did language evolve? This has always been a very controversial topic and the question is look, here we have this amazing ability called language with all the nesting of clauses, this hierarchical structure of language, this recursive embedding of clauses, our enormous lexicon and it's an extraordinarily sophisticated mechanism. How could it possibly have evolved through the blind workings of chance through natural selection? How did we evolve from the grunts and howls and groans of our ape-like ancestors to all the sophistication of a Shakespeare or a George Bush? Now there have been several theories about this. Alfred Russell Wallace said the mechanism is so complicated it couldn't have evolved through natural selection. It was done by god, divine intervention. Maybe he's right but we can't test it so let's throw it away. Next theory was by Chomsky. Chomsky said actually something quite similar although he doesn't use the word god. He said this mechanism is so sophisticated and elaborate it couldn't have emerged through natural selection, through the blind workings of chance but god knows what happens if you pack one hundred billion nerve cells in such a tiny space, you may get new laws of physics emerging. Aha, that's how you explain language so he almost says it's a miracle although he doesn't use the word miracle. Now even if that's true we can't test it so let's throw it away. So then what actually happened? How did language evolve? I suggest the clue, the vital clue comes from the booba/kiki example, from synesthesia and I'd like to replace this idea with what I call the synesthetic boot-strapping theory of language origins, and I'll get to that in a minute.

So the next idea is Pinker's idea and his idea is look there's no big mystery here. You're seeing the final result of evolution, of language but you don't know what the intermediate steps are so it always looks mysterious but of course it evolved through natural selection even though we don't know what the steps were. Now I think he's right but he doesn't go far enough because as a biologist, we want the devils and the details. We want to know what those intermediate steps are, not merely that it could have happened through natural selection. Of course it happened through natural selection. There is nothing else so let's take the lexicon, words. How did we evolve such a wonderful huge repertoire of words, thousands of words? Did our ancestral hominoids sit near the fireplace and say, let's look at that. OK, everybody call it an axe, say everybody axe. Of course not! I mean you do that in kindergarten but that's not what they did. If they didn't do that, what did they do? Well what I'm arguing is that the booba/kiki example provides the clue. It shows there is a pre-existing translation between the visual appearance of the object represented in the fusiform gyrus and the auditory representation in the auditory cortex. In other words there's already a synesthetic cross-modal abstraction going on, a pre-existing translation if you like between the visual appearance and the auditory representation. Now admittedly this is a very small bias, but that's all you need in evolution to get it started and then you can start embellishing it.

But that's only part of the story, part one. Part two, I'm going to argue, there's also a pre-existing built-in cross-activation. Just as there is between visual and auditory, the booba/kiki effect, there's also between visual in the fusiform and the motor brocas area in the front of the brain that controls the sequence of activations of muscles of vocalisation, phonation and articulation - lips, tongue and mouth. How do I know that? Well let's take an example. Let's take the example of something tiny, say teeny weeny, un peu, diminutive - look at what my lips are doing. The amazing thing is they're actually physically mimicking the visual appearance of the object - versus enormous, large. We're actually physically mimicking the visual appearance of the object so what I'm arguing is that also again a pre-existing bias to map certain visual shapes onto certain sounds in the motor maps in the brocas area.

Lastly, the third factor - I think there's also a pre-existing cross-activation between the hand area and the mouth area because they are right next to each other in the Penfield motor map in the brain and let me give you an example, and I got scooped. Charles Darwin first described this. What he showed was when people cut with a pair of scissors you clench and unclench your jaws unconsciously as if to echo or mimic the movements of the fingers. He didn't explain why but I'd like to give it a name. I call it synkinesia - and that's because the hand and mouth areas are right next to each other and maybe there is some spill-over of signals. Now so what? Well, imagine your ancestral hominids evolving a system of gestures for communication, and this would have been important because vocalisation, you can't engage them in your hunting. Now the right hemisphere produces guttural emotional utterances along with the anterior singular. Now your mouth and tongue are already, there's a pre-existing translation of the visual symbols into mouth lip and tongue movements. Combine that with guttural utterances coming from the right hemisphere and anterior cingulate, what do you get? You get the first words, you get proto-words.

So now you've got three things in place - hand to mouth, mouth in brocas area to visual appearance in the fusiform and auditory cortex, and auditory to visual, the booba/kiki effect. Each of these is a small effect but acting together there's a synergistic boot-strapping effect going on and an avalanche effect, culminating in the emergence of language. Finally you say well what about the hierarchical structure of syntax? How do you explain that? Well I think like when you say he knows that I know that he knows that I know that I had an affair with his wife. How do you do this hierarchic embedding in language? Well partly I think that comes from semantics, from the region of the TPO where I said you'd engage in abstraction and I already explained how abstraction might have evolved, so partly abstraction feeds into syntactic structure, but partly from tool use. Early hominids were very good at tool use and especially what I call the sub-assembly technique in tool use where you take a piece of flint, make it into a head - step one. Then you haft it onto a handle - step two, and then the whole thing becomes one entity which is then used to hit you the subject, you hit the object. You do something to the object and this bears a certain operational analogy with the embedding of noun clauses. So what I'm arguing is what evolved for tool use in the hand area is now exapted and assimilated in the brocas area to be used in syntactic hierarchic embedding. So now look, each of these has a small bias but acting in conjunction they culminate in language. It's very different from Steve Pinker's idea which is that language is a specific adaptation which evolved step by step for the sole purpose of communication. What I'm arguing here is no, it's the fortuitous synergistic combination of a number of mechanisms which evolved for other purposes initially and then became assimilated into the mechanism that we call language. This often happens in evolution but it's a style of thinking that has yet to permeate neurology and psychology and it's very odd that neurologists don't usually think of evolution given that nothing in biology makes any sense except in the light of evolution as Dobzhansky once said.

So let me summarise what we've done. We begin with a disorder that's been known for a century but treated as a curiosity. And then we showed that the phenomenon is real, what the underlying brain mechanisms might be, and lastly spelt out what the broader implications of this curious phenomenon might be. So what have we done here with synesthesia? Let's take a look. One day we might be able to clone the gene or genes, because if you find a large enough family you might be able to do this. Then we can go on to the brain anatomy and say look, it's expressed in the fusiform gyrus and you get lower synesthesia. You go to angular gyrus you get higher synesthesia. If it's expressed all over you get artsy types! Then from the brain anatomy you go to detailed perceptual psychophysics. Either the pop-out effect, you know the 2s against the 5s which you can measure, and then finally all the way to understanding abstract thought and how it might have emerged, metaphor, Shakespeare, even the evolution of language - all of this in this one little quirk that people used to call synesthesia. So I agree wholeheartedly with what Huxley said in the last century just across the road here at the University Museum, contrary to Benjamin Disraeli's views and the views of Bishop Wilberforce. We are not angels, we are merely sophisticated apes. Yet we feel like angels trapped inside the bodies of beasts, craving transcendence and all the time trying to spread our wings and fly off, and it's really a very odd predicament to be in, if you think about it.

Thank you!

Lecture 5: Neuroscience - the New Philosophy

The main theme of our lectures so far has been the idea that the study of patients with neurological disorders has implications far beyond the confines of medical neurology, implications even for the humanities, for philosophy, maybe even for aesthetics and art. Today I'd like to continue this theme and take up the challenge of mental illness. The boundary between neurology and psychiatry is becoming increasingly blurred and it's only a matter of time before psychiatry becomes just another branch of neurology. I'll also touch on a few philosophical issues like free will and the nature of self.

Now if you look at ideas on mental illness, there've been traditionally two different approaches to mental illness. The first one tries to identify chemical imbalances, changes in transmitters and receptors in the brain - and attempts to correct these changes using drugs. And this approach has revolutionised psychiatry. It's been phenomenally successful. Patients who used to be put in straight jackets or locked up can now lead relatively normal lives. The second approach we can loosely characterise as the so-called Freudian approach. It assumes that most mental illness arises from your upbringing - maybe your mother. In this lecture what I'd like to do is propose a third approach which is radically different from either of these but in a sense complements them.

My point is if you really want to understand the origins of mental illness it's not enough to merely say that some transmitter has changed in the brain. You want to know how the change in the transmitter produces the bizarre symptoms that it does - why patients have those specific symptoms which you see and why the symptoms are different for different types of mental illness. That's our agenda here. And what I'd like to do is to try and explain the symptoms you see in mental illness in terms of the known function and the known anatomy and neural structures in the brain. And that will be the goal of this lecture. And I'll suggest that many of these symptoms and disorders will seem less bizarre when viewed from an evolutionary standpoint, that is from a Darwinian perspective. So let's give this discipline a new name - and I'd like to call this discipline evolutionary neuro-psychiatry.

Let's take the classic example of what people think of as a purely mental disorder, psychological disturbance - hysteria. Now I'm using the word here in the strictly medical sense, not somebody becoming hysterical and shouting and screaming. In the strictly medical sense, the word means that here is a patient who suddenly develops a paralysis of an arm or a leg, but if you examine this patient neurologically there are no deficits, brain MR scan reveals that the brain is apparently completely normal, there are no identifiable lesions, there's no damage. So the symptoms are dismissed as being purely psychological in origin.

But recent brain-imaging studies using PET scans and functional Magnetic Resonance imaging have dramatically changed our understanding of hysteria. Using PET scans and NMR, we can now find what parts of the brain are active or inactive, for example when a patient does some specific action or some mental process. And you can find out what parts of the brain light up when he does it - for example when you do arithmetic, mental arithmetic, what part of the brain lights up? (It's usually the left angular gyrus, it turns out). Or when I prick you with a needle and there's pain, what part of the brain lights up, what are the pathways involved? And this tells you that that particular pathway that's lighting up is somehow involved in mediating that function.

If I take anyone of you here and ask you to wiggle your finger and I do a PET scan to see what parts of the brain light up (and Kornhuber and Libet actually did this some decades ago) what I find is that two areas light up in the brain. One is called the motor cortex, which is actually sending messages to execute the appropriate sequence of muscle twitches to wiggle your finger. But also another area in front of it called the pre-frontal cortex that prepares you to move your finger. So there's an initial area which prepares you to move your finger and then there's the motor cortex that executes the motor programmes to make you wiggle your finger.

OK, fine. But what if you now try this experiment on an hysterical patient, who's hysterically paralysed? He says his arm isn't moving but there are no neurological abnormalities. What if you did a PET scan in his brain and you asked him to move his so-called paralysed arm. He says, No I can't do it. You say, Try anyway - and do a PET scan. And this was done by Chris Frith and Frackowiak and Peter Halligan and John Marshall and others. And what they found was when a person with hysterical paralysis tries to move his arm, again the pre-motor area lights up. And this means he's not faking it. He's intending to move the arm. But in addition to that there's another area that lights up. And that is the anterior cingular and the ventromedial frontal lobes, parts of the frontal cortex. This means he has every intention of moving it, but the anterior cingular and parts of the frontal lobes are inhibiting or vetoing this attempt to move the arm in the hysterical patient. And this makes sense because the anterior cingular and parts of the frontal lobes are intimately linked to the limbic emotional centres in the brain. And we know that hysteria originates from some emotional trauma that's somehow preventing him from moving his arm - and his arm is paralysed.

So we've talked about hysterical patients with hysterical paralysis. Now let's go back to normals and do a PET scan when you're voluntarily moving your finger using your free will. A second to three-fourths of a second prior to moving your finger, I get the EEG potential and it's called the Readiness Potential. It's as though the brain events are kicking in a second prior to your actual finger movement, even though your conscious intention of moving the finger coincides almost exactly with the wiggle of the finger. Why? Why is the mental sensation of willing the finger delayed by a second, coming a second after the brain events kick in as monitored by the EEG? What might the evolutionary rationale be?

The answer is, I think, that there is an inevitable neural delay before the signal arising in the brain cascades through the brain and the message arrives to wiggle you finger. There's going to be a delay because of neural processing - just like the satellite interviews on TV which you've all been watching. So natural selection has ensured that the subjective sensation of wiling is delayed deliberately to coincide not with the onset of the brain commands but with the actual execution of the command by your finger, so that you feel you're moving it.

And this in turn is telling you something important. It's telling you that the subjective sensations that accompany brain events must have an evolutionary purpose, for if it had no purpose and merely accompanied brain events - like so many philosophers believe (this is called epiphenomenalism) - in other words the subjective sensation of willing is like a shadow that moves with you as you walk but is not causal in making you move, if that's correct then why would evolution bother delaying the signal so that it coincides with your finger movement?

So you see the amazing paradox is that on the one hand the experiment shows that free will is illusory, right? It can't be causing the brain events because the events kick in a second earlier. But on the other hand it has to have some function because if it didn't have a function, why would evolution bother delaying it? But if it does have a function, what could it be other than moving the finger? So maybe our very notion of causation requires a radical revision here as happened in quantum physics. OK, enough of free will. It's all philosophy!

I'd now like to remind you of a syndrome we discussed in my first lecture, the Capgras delusion. So, the patient has been in a head injury, say a car accident. He seems quite normal in most respects, neurologically intact, but suddenly starts saying his mother is an impostor. She's some other woman pretending to be my mother. Now why would this happen, especially after a head injury? Now remember, he's quite normal in all other respects.

Well, it turns out in this patient the wire that goes from the visual areas to the emotional core of the brain, the limbic system and the amygdala, that's been cut by the accident. So he looks at the mother and since the visual areas in the brain concerned with recognising faces is not damaged, he says, Hey it looks just like my mother. But then there is no emotion because that wire taking that information to the emotional centres is cut. So he says, If this is my mother how come I don't experience any emotions? This must be some other strange woman. She's an impostor. Well, how do you test this?

It turns out you can measure the gut-level emotional reaction that someone has to a visual stimulus - or any stimulus - by measuring the extent to which they sweat. Believe it or not, all of you here - if I show you something exciting, emotionally important, you start sweating to dissipate the heat that you're going to generate from exercise, from action. And I can measure the sweating by putting two electrodes in your skin, changes in skin resistance - and if skin resistance falls, this is called the Galvanic Skin Response. So every time anyone of you here looks at tables and chairs, there's no Galvanic Skin Response because you don't get emotionally aroused if you look at a table or a chair. If you look at strangers there's no Galvanic Skin Response. But if you look at lions and tigers and - as it turns out - if you look at your mother, you get a huge, big Galvanic Skin Response. And you don't have to be Jewish, either. Anybody here, looking at your mother, you get a huge, big Galvanic Skin Response when you look at your mother.

Well, what happens to the patient? We've tried this on patients. The patient looks at chairs and tables, nothing happens. But then we show him a picture of his mother on the screen, no Galvanic Skin Response. It's flat - supporting our idea that there's been a disconnection between vision and emotion.

Now the Capgras delusion is bizarre enough, but I'll tell you about an even more bizarre disorder. This is called the Cotard's syndrome, in which the patient starts claiming he is dead. I suggested that this is a bit like Capgras except that instead of vision alone being disconnected from the emotional centres in the brain, all the senses, everything, gets disconnected from the emotional centres. So that nothing he looks at in the world makes any sense, has any emotional significance to this person, whether he sees it or touches it or looks at it. Nothing has any emotional impact. And the only way this patient can interpret this complete emotional desolation is to say, Oh, I'm dead, doctor. However bizarre it seems to you, it's the only interpretation that makes sense to him.

Now Capgras and Cotard are both rare syndromes. But there's another disorder, a sort of mini-Cotard's that's much more commonly seen in clinical practice (those of you here who are psychiatrists know this, or psychologists). It's called Derealisation and Depersonalisation. It's seen in acute anxiety, panic attacks, depression and other dissociative states. Suddenly the world seems completely unreal - like a dream. Or you may feel that you are not real - Doctor, I feel like a zombie. Why does this happen? As I said, it's quite common.

I think it involves the same circuits as Capgras and Cotard's. You've all heard of the phrase, playing possum. An opossum when chased by a predator suddenly loses all muscle tone and plays dead. Why? This is because any movement by the possum will encourage the predatory behaviour of the carnivore - and carnivores also avoid dead infected food. So playing dead is very adaptive for the possum.

Following the lead of Martin Roth and Sierra and Berrios, I suggested Derealisation and Depersonalisation and other dissociative states are an example of playing possum in the emotional realm. And I'll explain. It's an evolutionary adaptive mechanism. Remember the story of Livingstone being mauled by a lion.

Dr. Livingston, (picture courtesy of John Murray, Publishers)

He saw his arm being ripped off but felt no pain or even fear. He felt like he was detached from it all, watching it all happen. The same thing happens, by the way, to soldiers in battle or sometimes even to women being raped. During such dire emergencies, the anterior cingular in the brain, part of the frontal lobes, becomes extremely active. This inhibits or temporarily shuts down your amygdala and other limbic emotional centres, so you suppress potentially disabling emotions like anxiety and fear - temporarily. But at the same time, the anterior cingular makes you extremely alert and vigilant so you can take the appropriate action.

Now of course in an emergency this combination of shutting down emotions and being hyper-vigilant at the same time is useful, keeping you out of harm's way. It's best to do nothing than engage in some sort of erratic behaviour. But what if the same mechanism is accidentally triggered by chemical imbalances or brain disease, when there is no emergency. You look at the world, you're intensely alert, hyper-vigilant, but it's completely devoid of emotional meaning because you've shut down your limbic system. And there are only two ways for you to interpret this dilemma. Either you say the world isn't real - and that's called Derealisation. Or you say, I'm not real, I feel empty - and that's called Depersonalisation.

Epileptic seizures originating in this part of the brain can also produce these dreamy states of Deralisation and Depersonalisation. And, intriguingly, we know that during the actual seizure when the patient is experiencing Derealisation, you can obtain a Galvanic Skin Response and there's no response to anything. But once he comes out of the seizure, fine, he's normal. And all of this supports the hypothesis that I'm proposing.

OK, finally let's talk about another disorder, the one that jumps into people's minds when they think of madness - namely schizophrenia. These are patients who have bizarre symptoms. They hallucinate, often hearing voices. They become delusional, thinking they're Napoleon - or George Bush. Or they're convinced the CIA has planted devices in their brain to control their thoughts and actions. Or that aliens are controlling them.

Psycho-pharmacology has revolutionised our ability to treat schizophrenia, but the question remains: why do they behave the way they do? I'd like to speculate on this based on some work we've done on anosognosia (denial of illness) - which you see in right-hemisphere lesions - and some very clever speculations by Chris Frith and Sarah Blakemore. Their idea is that unlike normal people, the schizophrenic can't tell the difference between his own internally-generated images and thoughts versus perceptions that are evoked by real things outside.

If anyone of you here conjures up a mental picture of a clown in front of you, you don't confuse it with reality partly because your brain has access to the internal command you gave. You're expecting to visualise a clown, that's why you see it and you don't hallucinate. But if the mechanism in your brain that does this becomes faulty, then all of a sudden you can't tell the difference between a clown you're imagining and a clown you're actually seeing there. In other words, you hallucinate. You can't tell the difference between fantasy and reality.

Similarly, you and I momentarily entertain the thought it would be nice to be Napoleon. But in a schizophrenic this momentary thought becomes a full-blown delusion instead of being vetoed by reality.

What about the other symptoms of schizophrenia - the fact that aliens are controlling you? When you move your finger voluntarily, you know you sent the command, the motor centres in the brain sent the command. So you experience willing the movement. You don't say, Oh the finger moved on its own. But if the mechanism that performs this comparison is flawed, you no longer experience YOU willing the movement. So you come up with this bizarre interpretation. You say your movements are controlled by aliens or brain implants - and of course that's what paranoid schizophrenics do. How do you test a theory like this?

I want you all now to try an experiment. I mean that. I want you to try an experiment on yourselves. Using your right index finger - all of you try it - tap repeatedly your left index finger, keeping your left index finger steady and inactive. So you're all tapping your left index finger using your right index finger - left index finger is perfectly steady. Now you'll feel the tapping only on the left finger, very little on the right finger. OK, how many of you feel that? Yes, raise your hands. OK, 99 per cent of you. There are a few mutants, but we won't pursue that.

Now why is that? That's because the brain has sent a command from the left hemisphere to the right hand saying, Move. So the brain knows, it's tipped off the sensory areas of the brain, saying, Look you're going to move your right finger up and down so it's going to get some touch signals. But ignore them. It's not important. On the other hand, the left hand is perfectly steady so you feel the sensation only on the left finger, even though the tactile input is exactly the same.

Now try it the other way. Hold the right finger steady. Tap with the left finger. And you should now feel it mostly on the right, not on the left. Now the prediction is, if a schizophrenic tries this experiment, since he does not know the difference between internally generated actions and externally generated sensory stimuli, he will feel the sensations equally in both the fingers. It's a five-minute experiment - nobody's ever tried it.

Another prediction. I can come here and tickle anyone of you and you start laughing. Now interestingly, you can't tickle yourself. Try as hard as you want, you cannot tickle yourself. That's because your brain knows you're sending the command. Prediction: a schizophrenic should be able to tickle himself.

OK, it's time to conclude now. I hope that I've convinced you that even though the behaviour of many patients with mental illness seems bizarre, we can now begin to make sense of the symptoms using our knowledge of basic brain mechanisms. You can think of mental illness as disturbances of consciousness and of self, two words that conceal depths of ignorance. Let me try to summarise in the remaining five or ten minutes what my own view of consciousness is. There are really two problems here - the problem of the subjective sensations or qualia (а term for subjective sensations) and the problem of the self. The problem of qualia is the more difficult one.

The question is how does the flux of ions in little bits of jelly in my brain give rise to the redness of red, the flavour of marmite or mattar paneer, or wine. Matter and mind seem so utterly unlike each other. Well one way out of this dilemma is to think of them really as two different ways of describing the world, each of which is complete in itself. Just as we can describe light as made up of particles or waves - and there's no point in asking which is correct, because they're both correct and yet utterly unlike each other. And the same may be true of mental events and physical events in the brain.

But what about the self? The last remaining great mystery in science, it's something that everybody's interested in - and especially if you're from India, like me. Now obviously self and qualia are two sides of the same coin. You can't have free-floating sensations or qualia with no-one to experience it and you can't have a self completely devoid of sensory experiences, memories or emotions. For example as we saw in Cotard's syndrome, sensations and perceptions lose all their significance and meaning - and this leads to a dissolution of self.

What exactly do people mean when they speak of the self? Its defining characteristics are fourfold. First of all, continuity. You've a sense of time, a sense of past, a sense of future. There seems to be a thread running through your personality, through your mind. Second, closely related is the idea of unity or coherence of self. In spite of the diversity of sensory experiences, memories, beliefs and thoughts, you experience yourself as one person, as a unity.

So there's continuity, there's unity. And then there's the sense of embodiment or ownership - yourself as anchored to your body. And fourth is a sense of agency, what we call free will, your sense of being in charge of your own destiny. I moved my finger.

Now as we've seen in my lectures so far, these different aspects of self can be differentially disturbed in brain disease, which leads me to believe that the self really isn't one thing, but many. Just like love or happiness, we have one word but it's actually lumping together many different phenomena. For example, if I stimulate your right parietal cortex with an electrode (you're conscious and awake) you will momentarily feel that you are floating near the ceiling watching your own body down below. You have an out-of-the-body experience. The embodiment of self is abandoned. One of the axiomatic foundations of your Self is temporarily abandoned. And this is true of each of those aspects of self I was talking about. They can be selectively affected in brain disease.

Keeping this in mind, I see three ways in which the problem of self might be tackled by neuroscience. First, maybe the problem of self is a straightforward empirical problem. Maybe there is a single, very elegant, Pythagorean Aha! solution to the problem, just like DNA base-pairing was a solution to the riddle of heredity. I think this is unlikely, but I could be wrong.

Second, given my earlier remarks about the self, the notion of the self as being defined by a set of attributes - embodiment, agency, unity, continuity - maybe we will succeed in explaining each of these attributes individually in terms of what's going on in the brain. Then the problem of what is the self will vanish or recede into the background.

Third, maybe the solution to the problem of the self won't be a straightforward empirical one. It may instead require a radical shift in perspective, the sort of thing that Einstein did when he rejected the assumption that things can move at arbitrarily high velocities. When we finally achieve such a shift in perspective, we may be in for a big surprise and find that the answer was staring at us all along. I don't want to sound like a New Age guru, but there are curious parallels between this idea and the Hindu philosophical view that there is no essential difference between self and others or that the self is an illusion.

Now I have no clue what the solution to the problem of self is, what the shift in perspective might be. If I did I would dash off a paper to Nature today, and overnight I'd be the most famous scientist alive. But just for fun let me have a crack at it, at what the solution might look like.

Our brains were essentially model-making machines. We need to construct useful, virtual reality simulations of the world that we can act on. Within the simulation, we need also to construct models of other people's minds because we're intensely social creatures, us primates. We need to do this so we can predict their behaviour. We are, after all, the Machiavellian primate. For example, you want to know was what he did a wilful action. In that case he might repeat it. Or was it involuntary in which case it's quite benign. Indeed evolution may have given us the skill even before self-awareness emerged in the brain. But then once this mechanism is in place, you can also apply it to the particular creature who happens to occupy this particular body, called Ramachandran.

At a very rudimentary level this is what happens each time a new-born baby mimics your behaviour. Stick your tongue out next time you see a new-born-baby and the baby will stick its tongue out, mimicking your behaviour, instantly dissolving the boundary, the arbitrary barrier between self and others. And we even know that this is carried out by a specific group of neurons in the brain, in your frontal lobes, called the mirror neurons. The bonus from this might be self-awareness.

With this I'd like to conclude this whole series of lectures. As I said in my first lecture, my goal was not to give you a complete survey of our knowledge of the brain. That would take fifty hours, not five. But I hope I've succeeded in conveying to you the sense of excitement that my colleagues and I experience each time we try to tackle one of these problems, whether you're talking about hysteria, phantom limbs, free will, the meaning of art, denial, or neglect or any one of these syndromes which we talked about in earlier lectures. Second, I hope I've convinced you that by studying these strange cases and asking the right questions, we neuroscientists can begin to answer some of those lofty questions that thinking people have been preoccupied with since the dawn of history. What is free will? What is body image? What is the self? Who am I? - questions that until recently were the province of philosophy.

No enterprise is more vital for the wellbeing and survival of the human race. This is just as true now as it was in the past. Remember that politics, colonialism, imperialism and war also originate in the human brain.

Thank you.

Brain Glossary

You can use our interactive brain to help you follow the lecture

http://www.bbc.co.uk/science/humanbody/body/interactives/organs/brainmap/

We would like to thank the Society for Neuroscience for their premission to reproduce this glossary. Some ammendations have been made.

A

Acetylcholine: A neurotransmitter in both the brain, where it may help regulate memory, and in the peripheral nervous system, where it controls the actions of skeletal and smooth muscle.

Action Potential: This occurs when a neuron is activated and temporarily reverses the electrical state of its interior membrane from negative to positive. This electrical charge travels along the axon to the neuron's terminal where it triggers or inhibits the release of a neurotransmitter and then disappears.

Adrenal Cortex: An endocrine organ that secretes corticosteroids for metabolic functions: aldosterone for sodium retention in the kidneys, androgens for male sexual development, and estrogens for female sexual development.

Adrenal Medulla: An endocrine organ that secretes epinephrine and norepinephrine for the activation of the sympathetic nervous system.

Affective Psychosis: A psychiatric disease relating to mood states. It is generally characterized by depression unrelated to events in the life of the patient, which alternates with periods of normal mood or with periods of excessive, inappropriate euphoria and mania.

Agonist: A neurotransmitter, a drug or other molecule that stimulates receptors to produce a desired reaction.

Amino Acid Transmitters: The most prevalent neurotransmitters in the brain, these include glutamate and aspartate, which have excitatory actions, and glycine and gamma-amino butyric acid (GABA) which have inhibitory actions.

Amygdala: A structure in the forebrain that is an important component of the limbic system.

Androgens: Sex steroid hormones, including testosterone, found in higher levels in males than females. They are responsible for male sexual maturation.

Anosognosia: A syndrome in which a person with a paralysed limb claims it is still functioning. One of Professor Ramachandran's patients, who had suffered a stroke which had paralysed the left side of her body, refused to accept that her arm couldn't move. Even though lucid in every other aspect (including awareness of the fact that she had suffered a stroke) she claimed her left arm was carrying out tasks even though clearly it wasn't. Anosognosia means denial of illness. An explanation may involve close analysis of the different roles of the left and right hemispheres of the brain.

Antagonist: A drug or other molecule that blocks receptors. Antagonists inhibit the effects of agonists.

Aphasia: Disturbance in language comprehension or production, often as a result of a stroke.

Auditory Nerve: A bundle of nerve fibers extending from the cochlea of the ear to the brain, which contains two branches: the cochlear nerve that transmits sound information and the vestibular nerve that relays information related to balance.

Autonomic Nervous System: A part of the peripheral nervous system responsible for regulating the activity of internal organs. It includes the sympathetic and parasympathetic nervous systems.

Axon: The fiberlike extension of a neuron by which the cell sends information to target cells.

B

Basal Ganglia: Clusters of neurons, which include the caudate nucleus, putamen, globus pallidus and substantia nigra, that are located deep in the brain and play an important role in movement. Cell death in the substantia nigra contributes to Parkinsonian signs.

Blindsight: Some patients who are effectively blind because of brain damage can carry out tasks which appear to be impossible unless they can see the objects. For instance they can reach out and grasp an object, accurately describe whether a stick is vertical or horizontal, or post a letter through a narrow slot . The explanation appears to be that visual information travels along two pathways in the brain. If only one is damaged, a patient may lose the ability to see an object but still be aware of its location and orientation.

Blindspots: Blindspots can be produced by a variety of factors. In fact everyone has a small blindspot in each eye caused by the area of the retina which connects to the optic nerve. To test this, visit our Mindgames section. These blindspots are often filled in by the brain using information based on the surrounding visual image. In some cases, patients report seeing unrelated images in their blindspots. One reported seeing cartoon characters. This phenomenon may involve other pathways in the brain.

Brainstem: The major route by which the forebrain sends information to and receives information from the spinal cord and peripheral nerves. It controls, among other things, respiration and regulation of heart rhythms.

Broca's Area: The brain region located in the frontal lobe of the left hemisphere that is important for the production of speech.

C

Capgras' delusion: A rare syndrome in which the patient is convinced that close relatives usually parents, spouse, children or siblings are impostors. It may be caused by damage to the connections between the areas of the brain dealing with face recognition and emotional response. A sufferer might recognise the faces of his loved ones but not feel the emotional reaction normally associated with the experience.

Catecholamines: The neurotransmitters dopamine, epinephrine and norepinephrine that are active both in the brain and the peripheral sympathetic nervous system. These three molecules have certain structural similarities and are part of a larger class of neurotransmitters known as monoamines.

Cerebral Cortex: The outermost layer of the cerebral hemispheres of the brain. It is responsible for all forms of conscious experience, including perception, emotion, thought and planning.

Cerebral Hemispheres: The two specialized halves of the brain. The left hemisphere is specialized for speech, writing, language and calculation; the right hemisphere is specialized for spatial abilities, face recognition in vision and some aspects of music perception and production.

Cerebrospinal Fluid: A liquid found within the ventricles of the brain and the central canal of the spinal cord.

Cholecystokinin: A hormone released from the lining of the stomach during the early stages of digestion which acts as a powerful suppressant of normal eating. It also is found in the brain.

Circadian Rhythm: A cycle of behavior or physiological change lasting approximately 24 hours.

Classical Conditioning: Learning in which a stimulus that naturally produces a specific response (unconditioned stimulus) is repeatedly paired with a neutral stimulus (conditioned stimulus). As a result, the conditioned stimulus can become able to evoke a response similar to that of the unconditioned stimulus.

Cochlea: A snail-shaped, fluid-filled organ of the inner ear responsible for transducing motion into neurotransmission to produce an auditory sensation.

Cognition: The process or processes by which an organism gains knowledge of or becomes aware of events or objects in its environment and uses that knowledge for comprehension and problem-solving.

Cone: A primary receptor cell for vision located in the retina. It is sensitive to color and used primarily for daytime vision.

Cornea: A thin, curved transparent membrane on the surface of the front of the eye. It begins the focusing process for vision.

Corpus Callosum: The large bundle of nerve fibers linking the left and right cerebral hemispheres.

Cortisol: A hormone manufactured by the adrenal cortex. In humans, it is secreted in greatest quantities before dawn, readying the body for the activities of the coming day.

Cotard's syndrome: A disorder in which a patient asserts that he is dead, claiming to smell rotting flesh or worms crawling over his skin. It may be an exaggerated form of Capgras' delusion, in which not just one sensory area (ie face recognition) but all of them are cut off from the limbic system. This would lead to a complete lack of emotional contact with the world.

D

Dendrite: A tree-like extension of the neuron cell body. Along with the cell body, it receives information from other neurons.

Dopamine: A catecholamine neurotransmitter known to have multiple functions depending on where it acts. Dopamine-containing neurons in the substantia nigra of the brainstem project to the caudate nucleus and are destroyed in Parkinson's victims. Dopamine is thought to regulate emotional responses, and play a role in schizophrenia and cocaine abuse.

Dorsal Horn: An area of the spinal cord where many nerve fibers from peripheral pain receptors meet other ascending nerve fibers.

E

Endocrine Organ: An organ that secretes a hormone directly into the bloodstream to regulate cellular activity of certain other organs.

Endorphins: Neurotransmitters produced in the brain that generate cellular and behavioral effects like those of morphine.

Epinephrine: A hormone, released by the adrenal medulla and the brain, that acts with norepinephrine to activate the sympathetic division of the autonomic nervous system. Sometimes called adrenaline.

Estrogens: A group of sex hormones found more abundantly in females than males. They are responsible for female sexual maturation and other functions.

Evoked Potentials: A measure of the brain's electrical activity in response to sensory stimuli. This is obtained by placing electrodes on the surface of the scalp (or more rarely, inside the head), repeatedly administering a stimulus, and then using a computer to average the results.

Excitation: A change in the electrical state of a neuron that is associated with an enhanced probability of action potentials.

F

Follicle-Stimulating Hormone: A hormone released by the pituitary gland. It stimulates the production of sperm in the male and growth of the follicle (which produces the egg) in the female.

Forebrain: The largest division of the brain, which includes the cerebral cortex and basal ganglia. It is credited with the highest intellectual functions.

Frontal Lobe: One of the four divisions (parietal, temporal, occipital) of each hemisphere of the cerebral cortex. It has a role in controlling movement and associating the functions of other cortical areas.

G

Gamma-Amino Butyric Acid (GABA): An amino acid transmitter in the brain whose primary function is to inhibit the firing of neurons.

Glia : Specialized cells that nourish and support neurons.

Glutamate: An amino acid neurotransmitter that acts to excite neurons. Glutamate probably stimulates N-methyl-D-aspartate (NMDA) receptors that have been implicated in activities ranging from learning and memory to development and specification of nerve contacts in a developing animal. Stimulation of NMDA receptors may promote beneficial changes, while overstimulation may be the cause of nerve cell damage or death in neurological trauma and stroke.

Gonad: Primary sex gland: testis in the male and ovary in the female.

Growth Cone: A distinctive structure at the growing end of most axons. It is the site where new material is added to the axon.

H

Hippocampus: A seahorse-shaped structure located within the brain and considered an important part of the limbic system. It functions in learning, memory and emotion.

Hormones: Chemical messengers secreted by endocrine glands to regulate the activity of target cells. They play a role in sexual development, calcium and bone metabolism, growth and many other activities.

Hypothalamus: A complex brain structure composed of many nuclei with various functions. These include regulating the activities of internal organs, monitoring information from the autonomic nervous system and controlling the pituitary gland.

I

Immediate Memory: A phase of memory that is extremely short-lived, with information stored only for a few seconds. It also is known as short-term and working memory.

Inhibition: In reference to neurons, it is a synaptic message that prevents the recipient cell from firing.

Ions: Electrically charged atoms or molecules.

Iris: A circular diaphragm that contains the muscles which alter the amount of light that enters the eye by dilating or constricting the pupil. It has an opening in its center.

J

K

Korsakoff's Syndrome: A disease associated with chronic alcoholism, resulting from a deficiency of vitamin B-1. Patients sustain damage to part of the thalamus and cerebellum. Symptoms include inflammation of nerves, muttering delirium, insomnia, illusions and hallucinations and a lasting amnesia.

L

Limbic System: A group of brain structures - including the amygdala, hippocampus, septum and basal ganglia - that work to help regulate emotion, memory and certain aspects of movement.

Long-Term Memory: The final phase of memory in which information storage may last from hours to a lifetime.

M

Mania: A mental disorder characterized by excessive excitement. A form of psychosis with exalted feelings, delusions of grandeur, elevated mood, psychomotor overactivity and overproduction of ideas.

Melatonin: Produced from serotonin, melatonin is released by the pineal gland into the bloodstream. It affects physiological changes related to time and lighting cycles.

Memory Consolidation: The physical and psychological changes that take place as the brain organizes and restructures information in order to make it a permanent part of memory.

Metabolism: The sum of all physical and chemical changes that take place within an organism and all energy transformations that occur within living cells.

Mitochondria: Small cylindrical particles inside cells that provide energy for the cell by converting sugar and oxygen into special energy molecules.

Monoamine Oxidase (MAO): The brain and liver enzyme that normally breaks down the catecholamines norepinephrine, serotonin and dopamine.

Motor Neuron: A neuron that carries information from the central nervous system to the muscle.

Myasthenia Gravis: A disease in which acetylcholine receptors on the muscle cells are destroyed, so that muscles can no longer respond to the acetylcholine signal in order to contract. Symptoms include muscular weakness and progressively more common bouts of fatigue. Its cause is unknown but is more common in females than in males and usually strikes between the ages of 20 and 50.

Myelin: Compact fatty material that surrounds and insulates axons of some neurons.

N

Nerve Growth Factor: A substance whose role is to guide neuronal growth during embryonic development, especially in the peripheral nervous system.

Neuron: Nerve cell. It is specialized for the transmission of information and characterized by long fibrous projections called axons, and shorter, branch-like projections called dendrites.

Neurotransmitter: A chemical released by neurons at a synapse for the purpose of relaying information via receptors.

Nociceptors: In animals, nerve endings that signal the sensation of pain. In humans, they are called pain receptors.

Norepinephrine: A catecholamine neurotransmitter, produced both in the brain and in the peripheral nervous system. It seems to be involved in arousal, reward and regulation of sleep and mood, and the regulation of blood pressure.

O

Organelles: Small structures within a cell that maintain the cells and do the cells' work.

P

Pain Asymbolia: People with this condition do not feel pain when, for example, stabbed in the finger with a sharp needle. Sometimes patients say they can feel the pain, but it doesn't hurt. They know they have been stabbed, but they do not experience the usual emotional reaction. The syndrome is often the result of damage to a part of the brain called the insular cortex. The stabbing sensation is received by one part of the brain. But the information is not passed on to another area, the one which normally classifies the experience as threatening and triggers - through the feeling of pain - an avoidance reaction.

Parasympathetic Nervous System: A branch of the autonomic nervous system concerned with the conservation of the body's energy and resources during relaxed states.

Parietal Lobe: One of the four subdivisions of the cerebral cortex. It plays a role in sensory processes, attention and language.

Peptides: Chains of amino acids that can function as neurotransmitters or hormones.

Periaqueductal Gray Area: A cluster of neurons lying in the thalamus and pons. It contains endorphin-producing neurons and opiate receptor sites and thus can affect the sensation of pain.

Peripheral Nervous System: A division of the nervous system consisting of all nerves not part of the brain or spinal cord.

Phantom Limbs: People who lose a limb through an accident or amputation sometimes continue to feel that it's still there. In his book, Phantoms In the Brain, Prof. Ramachandran suggests these sensations may be the result of the brain forming new connections. He describes how, when he used a cotton bud to stroke the face of the face of a young amputee, the patient felt his missing hand was being touched as well. The area of the brain that receives sensations from the hand is right next to the one dealing with the face.

Phosphorylation: A process that modifies the properties of neurons by acting on an ion channel, neurotransmitter receptor or other regulatory molecule. During phosphorylation, a phosphate molecule is placed on another molecule resulting in the activation or inactivation of the receiving molecule. It may lead to a change in the functional activity of the receiving molecule. Phosphorylation is believed to be a necessary step in allowing some neurotransmitters to act and is often the result of second messenger activity.

Pineal Gland: An endocrine organ found in the brain. In some animals, it seems to serve as a light-influenced biological clock.

Pituitary Gland: An endocrine organ closely linked with the hypothalamus. In humans, it is composed of two lobes and secretes a number of hormones that regulate the activity of other endocrine organs in the body.

Pons: A part of the hindbrain that, with other brain structures, controls respiration and regulates heart rhythms. The pons is a major route by which the forebrain sends information to and receives information from the spinal cord and peripheral nervous system.

Q

Qualia: A term for subjective sensations. In Phantoms In The Brain, Professor Ramachandran describes the riddle of qualia like this: How can the flux of ions and electrical currents in little specks of jelly the neurons in my brain generate the whole subjective world of sensations like red, warmth, cold or pain? By what magic is matter transmuted into the invisible fabric of feelings and sensations?

R

Receptor Cell: Specialized sensory cells designed to pick up and transmit sensory information.

Receptor Molecule: A specific molecule on the surface or inside of a cell with a characteristic chemical and physical structure. Many neurotransmitters and hormones exert their effects by binding to receptors on cells.

Reuptake: A process by which released neurotransmitters are absorbed for subsequent re-use.

Rod: A sensory neuron located in the periphery of the retina. It is sensitive to light of low intensity and specialized for nighttime vision.

S

Second Messengers: Recently recognized substances that trigger communications between different parts of a neuron. These chemicals are thought to play a role in the manufacture and release of neurotransmitters, intracellular movements, carbohydrate metabolism and, possibly, even processes of growth and development. Their direct effects on the genetic material of cells may lead to long-term alterations of behavior, such as memory.

Sensitization: A change in behavior or biological response by an organism that is produced by delivering a strong, generally noxious, stimulus.

Serotonin: A monoamine neurotransmitter believed to play many roles including, but not limited to, temperature regulation, sensory perception and the onset of sleep. Neurons using serotonin as a transmitter are found in the brain and in the gut. A number of antidepressant drugs are targeted to brain serotonin systems.

Short-Term Memory: A phase of memory in which a limited amount of information may be held for several seconds to minutes.

Stimulus: An environmental event capable of being detected by sensory receptors.

Stroke: The third largest cause of death in America, stroke is an impeded blood supply to the brain. It can be caused by a blood clot forming in a blood vessel, a rupture of the blood vessel wall, an obstruction of flow caused by a clot or other material, or by pressure on a blood vessel (as by a tumor). Deprived of oxygen, which is carried by blood, nerve cells in the affected area cannot function and die. Thus, the part of the body controlled by those cells, cannot function either. Stroke can result in loss of consciousness and brain function, and death.

Sympathetic Nervous System: A branch of the autonomic nervous system responsible for mobilizing the body's energy and resources during times of stress and arousal.

Synesthaesia: A condition in which a person quite literally tastes a shape or sees a colour in a sound. This is not just a way of describing experiences as a poet might use metaphors. Synaesthetes actually experience the sensations.

Synapse: A gap between two neurons that functions as the site of information transfer from one neuron to another.

T

Temporal Lobe: One of the four major subdivisions of each hemisphere of the cerebral cortex. It functions in auditory perception, speech and complex visual perceptions.

Temporal lobe epilepsy: A condition which may produce a heightened sense of self and has been linked to religious or spiritual experiences. Some people may undergo striking personality changes and may also become obsessed with abstract thoughts. One possible explanation is that repeated seizures may cause a strengthening of the connections between two areas of the brain - the temporal cortex and the amygdala. Patients have been observed to have a tendency to ascribe deep significance to everything around them (including themselves!).

Thalamus: A structure consisting of two egg-shaped masses of nerve tissue, each about the size of a walnut, deep within the brain. It is the key relay station for sensory information flowing into the brain, filtering out only information of particular importance from the mass of signals entering the brain.

U

V

Ventricles: Of the four ventricles, comparatively large spaces filled with cerebrospinal fluid, three are located in the brain and one in the brainstem. The lateral ventricles, the two largest, are symmetrically placed above the brainstem, one in each hemisphere.

W

Wernicke's Area: A brain region responsible for the comprehension of language and the production of meaningful speech.

Mind Games

Try out some of the experiments referred to by Professor Ramachandran.

Blindspot Experiments

Each eye has a blindspot. It's caused by the fact that the small area of the retina where the optic nerve is connected to the eyeball is not sensitive to light.

The following experiments prove the existence of the blindspot and demonstrate how the brain can fill in the missing information. They provide important hints about how the neural machinery of the brain works in practice.

All experiments are taken from V.S. Ramachandran's book, Phantoms In The Brain, published by Fourth Estate.

Try blindspot experiment number 1 (one of five)

Cover or shut your right eye and look at the black dot on the right with your left eye.

Move your head towards and away from the monitor.

At a critical distance the white disc on the left will disappear.

Notice that when the disc disappears you don't see a dark void or hole in its place.

The region is "filled in" with the same light blue colour as the background.

Useful Links

Below are some useful links to sites of interest.

About Professor Ramachandran

Professor Ramachandran's website

Find out more about Professor Ramachandran

Background to the lectures

The background to these lectures was a series of articles by Professor Ramachandran for the Journal of Consciousness Studies. The Journal has kindly made these articles available.

Synapses and the Self

The Artful Brain

Purple Numbers and Sharp Cheese

Other BBC sites of interest

Interactive brain (from BBCi Science)

How does the brain work? Find out where your cerebellum is and what your medulla oblongata does.

The Human Body (the brain and the spinal chord) (from BBCi Science)

A brief introduction to all aspects of the brain.

Intelligence (from BBCi Science)

An overview of issues relating to the brain and intelligence.

The Brain (from The Life of Mammals, BBCi Nature)

Another introduction to all aspects of the brain.

The Brain (from BBCi World Service)

Another introduction to all aspects of the brain.

God on the Brain (from Horizon)

Is a part of the brain closely connected with the sensations of belief?

About the Brain

The Open University - Introduction to the Brain

A comprehensive introduction to the human brain and nervous system.

The Whole Brain Atlas

A collection of images of brain scans showing all aspects of the brain.

Brain Awareness Week

Aims to elevate the public awareness of brain and nervous system research.

Brain Briefings (from the Society for Neuroscience)

A series of two-page newsletters explaining how basic neuroscience discoveries lead to clinical applications.

Brain Facts (from the Society for Neuroscience)

A 52-page primer on the brain and nervous system, published by the Society for Neuroscience.

Journal of Consciousness Studies

A peer-reviewed monthly which examines issues of the brain in plain English.

Mind-Brain.com

An internet site dealing with consciousness, transcendence, and the brain, not to mention poetry, art, and music.

Mind/ Brain Behaviour (from Harvard University)

An interfaculty initiative exploring issures of conciousness and behaviour.

The Mind/Brain Institute (from John Hopkins University)

The institute is dedicated to the study of the neural mechanisms of higher brain functions using modern neurophysiological, anatomical, and computational techniques.

Mind and Body: René Descartes to William James (from Serendip)

An overview of the debates around mind/body dualism.

Notes

Content

Vilayanur S Ramachandran
The Emerging Mind

Lecture 1: Phantoms in the Brain.

Lecture 2: Synapses and the Self

Lecture 3: The Artful Brain

Lecture 4: Purple Numbers and Sharp Cheese

Lecture 5: Neuroscience - the New Philosophy

Brain Glossary

Mind Games

Useful Links

Notes