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 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 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.