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.