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!
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.
