Science vs. Free Will, Again

The question of whether we have "free will" has kept philosophers occupied for at least 2000 years. Wouldn't it be nice if science came along and sorted the whole thing out?
That's the reason why so many people are excited about reports like the one just published in Science, Movement Intention After Parietal Cortex Stimulation in Humans. The report itself is extremely straightforward. The authors, a team of French neurosurgeons, used electrodes to stimulate various points on the surface of the brains of seven patients. The patients were all suffering from brain tumours in various places, and they were undergoing surgery to remove them. As often happens, the authors decided to try to squeeze a little research out of the procedure as well.

The authors stimulated points in various areas of the brain, but the most interesting results came from the premotor cortex (the blue area on the picture above) and the posterior parietal cortex (red and yellow).

When certain points on the premotor cortex were stimulated, the patients moved. But they were not aware that they had done so. For example:

...during stimulation patient PM1 exhibited a large multijoint movement involving flexion of the left wrist, fingers, and elbow ... He did not spontaneously comment on this, and when asked whether he had felt a movement he responded negatively.

That's pretty interesting in itself, but even more so is what happened when the posterior parietal cortex got zapped. Stimulation here produced a desire or intention to move, although no movement actually occured:

Stimulation of all these sites produced a pure intention, that is, a felt desire to move without any overt movement being produced... Without prompting by the examiner, all three patients spontaneously used terms such as “will,” “desire,” and “wanting to,” which convey the voluntary character of the movement intention and its attribution to an internal source, that is, located within the self.

And as if that wasn't enough philosophically-provocative fun, high intensity stimulation of the same area made the patients believe that they had in fact moved, although they didn't move a muscle:

[with higher electrode currents] conscious motor intentions were replaced by a sensation that a movement had been accomplished [but] no actual movement was observed. Thus, these patients experienced awareness of an illusory movement. For example, patient PP3 reported after low-intensity stimulation of one site (5 mA, 4 s; site a in Fig. 1), “I felt a desire to lick my lips” and at a higher intensity (8 mA, 4 s), “I moved my mouth, I talked, what did I say?”

Wow. What are we to make of all this?

A while back I wrote about Wilder Penfield's idea of "double conciousness" which Christian neurosurgeon Michael Egnor described approvingly as

Penfield found that he could invoke all sorts of things- movements, sensations, memories. But in every instance (hundreds of thousands of individual stimulations- in different locations in each patient- during his career), the patients were aware that the stimulation was being done to them, but not by them. There was a part of the mind that was independent of brain stimulation and that constituted a part of subjective experience that Penfield was not able to manipulate with his surgery.

Penfield called this "double consciousness", meaning that there was a part of subjective experience that he could invoke or modify materially, and a different part that was immune to such manipulation.

So Penfield, one of the great pioneers of 20th century neuroscience, claimed that stimulation of the brain could never produce desires or intentions which were experienced as the subject's "own". The person whose brain you were stimulating always felt that whatever happened to them came from outside.

But this French report directly contradicts that. We can only speculate as to why. It could be that Penfield just never hit the right spot, but this seems extremely unlikely, as he did a lot of stimulating over the course of his career. A cynic might ask whether Penfield did observe similar phenomena and just never reported them, but if we're going to go down that road, it's equally likely that these neurosurgeons just made it all up. Fortunately, any neurosurgeon should be able to try to replicate these results with a few prods of an electrode, so it shouldn't take long before the truth becomes clearer.

If these present results hold up, they'll certainly suggest some interesting ideas about the organisation of the brain - such as that the perception of movement depends upon the neurones encoding the intention to move rather than those involved in producing the actual motor act.

It would also be interesting to find out what happens when you simulataneously stimulate the premotor spot which makes your arm move, and the posterior parietal spot which makes you want to move your arm. Would that make you want to move your arm - and do so? If so, that would suggest that something very similar to that is going on whenever we do anything. What is life, but wanting to move, and moving?

But whether that's true or not, intentions (and everything else) are still something that happens in the brain, and the brain is a material object subject to the laws of physics. Neuroscience can tell us how exactly it all fits together, but at the end of the day, it's all a bunch of cells. Free will, in other words, appears to be in trouble, whatever the details of the brain's mechanisms happen to be.

Desmurget, M., Reilly, K., Richard, N., Szathmari, A., Mottolese, C., & Sirigu, A. (2009). Movement Intention After Parietal Cortex Stimulation in Humans Science, 324 (5928), 811-813 DOI: 10.1126/science.1169896

Science vs. Free Will, Again

The question of whether we have "free will" has kept philosophers occupied for at least 2000 years. Wouldn't it be nice if science came along and sorted the whole thing out?
That's the reason why so many people are excited about reports like the one just published in Science, Movement Intention After Parietal Cortex Stimulation in Humans. The report itself is extremely straightforward. The authors, a team of French neurosurgeons, used electrodes to stimulate various points on the surface of the brains of seven patients. The patients were all suffering from brain tumours in various places, and they were undergoing surgery to remove them. As often happens, the authors decided to try to squeeze a little research out of the procedure as well.

The authors stimulated points in various areas of the brain, but the most interesting results came from the premotor cortex (the blue area on the picture above) and the posterior parietal cortex (red and yellow).

When certain points on the premotor cortex were stimulated, the patients moved. But they were not aware that they had done so. For example:

...during stimulation patient PM1 exhibited a large multijoint movement involving flexion of the left wrist, fingers, and elbow ... He did not spontaneously comment on this, and when asked whether he had felt a movement he responded negatively.

That's pretty interesting in itself, but even more so is what happened when the posterior parietal cortex got zapped. Stimulation here produced a desire or intention to move, although no movement actually occured:

Stimulation of all these sites produced a pure intention, that is, a felt desire to move without any overt movement being produced... Without prompting by the examiner, all three patients spontaneously used terms such as “will,” “desire,” and “wanting to,” which convey the voluntary character of the movement intention and its attribution to an internal source, that is, located within the self.

And as if that wasn't enough philosophically-provocative fun, high intensity stimulation of the same area made the patients believe that they had in fact moved, although they didn't move a muscle:

[with higher electrode currents] conscious motor intentions were replaced by a sensation that a movement had been accomplished [but] no actual movement was observed. Thus, these patients experienced awareness of an illusory movement. For example, patient PP3 reported after low-intensity stimulation of one site (5 mA, 4 s; site a in Fig. 1), “I felt a desire to lick my lips” and at a higher intensity (8 mA, 4 s), “I moved my mouth, I talked, what did I say?”

Wow. What are we to make of all this?

A while back I wrote about Wilder Penfield's idea of "double conciousness" which Christian neurosurgeon Michael Egnor described approvingly as

Penfield found that he could invoke all sorts of things- movements, sensations, memories. But in every instance (hundreds of thousands of individual stimulations- in different locations in each patient- during his career), the patients were aware that the stimulation was being done to them, but not by them. There was a part of the mind that was independent of brain stimulation and that constituted a part of subjective experience that Penfield was not able to manipulate with his surgery.

Penfield called this "double consciousness", meaning that there was a part of subjective experience that he could invoke or modify materially, and a different part that was immune to such manipulation.

So Penfield, one of the great pioneers of 20th century neuroscience, claimed that stimulation of the brain could never produce desires or intentions which were experienced as the subject's "own". The person whose brain you were stimulating always felt that whatever happened to them came from outside.

But this French report directly contradicts that. We can only speculate as to why. It could be that Penfield just never hit the right spot, but this seems extremely unlikely, as he did a lot of stimulating over the course of his career. A cynic might ask whether Penfield did observe similar phenomena and just never reported them, but if we're going to go down that road, it's equally likely that these neurosurgeons just made it all up. Fortunately, any neurosurgeon should be able to try to replicate these results with a few prods of an electrode, so it shouldn't take long before the truth becomes clearer.

If these present results hold up, they'll certainly suggest some interesting ideas about the organisation of the brain - such as that the perception of movement depends upon the neurones encoding the intention to move rather than those involved in producing the actual motor act.

It would also be interesting to find out what happens when you simulataneously stimulate the premotor spot which makes your arm move, and the posterior parietal spot which makes you want to move your arm. Would that make you want to move your arm - and do so? If so, that would suggest that something very similar to that is going on whenever we do anything. What is life, but wanting to move, and moving?

But whether that's true or not, intentions (and everything else) are still something that happens in the brain, and the brain is a material object subject to the laws of physics. Neuroscience can tell us how exactly it all fits together, but at the end of the day, it's all a bunch of cells. Free will, in other words, appears to be in trouble, whatever the details of the brain's mechanisms happen to be.

Desmurget, M., Reilly, K., Richard, N., Szathmari, A., Mottolese, C., & Sirigu, A. (2009). Movement Intention After Parietal Cortex Stimulation in Humans Science, 324 (5928), 811-813 DOI: 10.1126/science.1169896

Annotated Links #2

In the NY Times, Daphne Merkin writes about her life with recurrent and "treatment-resistant" depression. A Journey Through Darkness is eloquent and honest, but it offers no convincing explanations as to the origin of her bouts of melancholy. Sometimes she is depressed and then eventually the state passes. In Merkin's account, and in my personal experience, being depressed is a brute fact. It is experienced, not understood. To call it a "journey" or anything else which implies some kind of narrative is misleading. And when a depression passes, it goes with a whimper not a bang:

It was about 4:30, the time of day that, by mid-August, brings with it a whiff of summer’s end. I looked up into the startlingly blue sky; one of the dogs was sitting at my side, her warm body against my leg, drying me off after the swim I had recently taken. I could begin to see the curve of fall up ahead. There would be new books to read, new films to see and new restaurants to try. I envisioned myself writing again, and it didn’t seem like a totally preposterous idea. I had things I wanted to say. Everything felt fragile and freshly come upon, but for now, at least, my depression had stepped back, giving me room to move forward. I had forgotten what it was like to be without it, and for a moment I floundered, wondering how I would recognize myself. I knew for certain it would return, sneaking up on me when I wasn’t looking, but meanwhile there were bound to be glimpses of light if only I stayed around and held fast to the long perspective. It was a chance that seemed worth taking.

The Royal Swedish Academy of Sciences issues a welcome statement condemning "lie-detector" peddlers Nemesysco for their attempt to gag two Swedish scientists. (See also Ministry of Truth for an extensive take-down of Nemesysco and all who use their products). Although, given that this happened several months ago, they certainly took their time about it...

Incidents of this kind are a threat to research freedom and, by extension, to the free dissemination of information in society. Threats to sue must not be used to restrict scientific discussion.

Finally, I know I said I don't believe in music reviews, but Neko Case is brilliant.

Annotated Links #2

In the NY Times, Daphne Merkin writes about her life with recurrent and "treatment-resistant" depression. A Journey Through Darkness is eloquent and honest, but it offers no convincing explanations as to the origin of her bouts of melancholy. Sometimes she is depressed and then eventually the state passes. In Merkin's account, and in my personal experience, being depressed is a brute fact. It is experienced, not understood. To call it a "journey" or anything else which implies some kind of narrative is misleading. And when a depression passes, it goes with a whimper not a bang:

It was about 4:30, the time of day that, by mid-August, brings with it a whiff of summer’s end. I looked up into the startlingly blue sky; one of the dogs was sitting at my side, her warm body against my leg, drying me off after the swim I had recently taken. I could begin to see the curve of fall up ahead. There would be new books to read, new films to see and new restaurants to try. I envisioned myself writing again, and it didn’t seem like a totally preposterous idea. I had things I wanted to say. Everything felt fragile and freshly come upon, but for now, at least, my depression had stepped back, giving me room to move forward. I had forgotten what it was like to be without it, and for a moment I floundered, wondering how I would recognize myself. I knew for certain it would return, sneaking up on me when I wasn’t looking, but meanwhile there were bound to be glimpses of light if only I stayed around and held fast to the long perspective. It was a chance that seemed worth taking.

The Royal Swedish Academy of Sciences issues a welcome statement condemning "lie-detector" peddlers Nemesysco for their attempt to gag two Swedish scientists. (See also Ministry of Truth for an extensive take-down of Nemesysco and all who use their products). Although, given that this happened several months ago, they certainly took their time about it...

Incidents of this kind are a threat to research freedom and, by extension, to the free dissemination of information in society. Threats to sue must not be used to restrict scientific discussion.

Finally, I know I said I don't believe in music reviews, but Neko Case is brilliant.

Lithium and Antidepressants in Tap Water

Lithium, as everyone knows, is a song by Nirvana. (It's also a different, and worse, song by Evanescence). It's also a chemical element. And it's a drug, used in psychiatry to treat bipolar disorder and, sometimes, severe depression.

One thing which lithium seems to do rather well - or at least better than other drugs - is make people less likely to commit suicide. At least, that's what most authorities say, so let's assume it's true.

Now a Japanese team report that the amount of lithium in tap water are negatively correlated with suicide rates - Lithium levels in drinking water and risk of suicide. (Someone has helpfully put this up on Scribd for people without academic access).

They analyzed the water supplies in the 18 subdivisions of Oita prefecture in southern Japan, and compared the lithium levels in the water with the average suicide rate (normalized for age and gender). Here's what happened -
Now, on paper that's a pretty solid correlation. But how believable is it? The maximum lithium level in the water was found to be 59 micrograms per liter. By contrast, if someone were taking lithium for bipolar disorder, they would on average be taking about 1 gram of lithium carbonate (Li2CO3) per day, which works out at about 100 mg of lithium (and 900 mg of inert carbonate).

Assuming that people drink about two liters of tap water per day (almost certainly they drink less), that's about 120 micrograms per day. That's 0.12 mg. So about a thousand-fold less than you'd take if you were bipolar.

Could such a tiny amount of lithium do anything? Well, maybe. It's not impossible that it would have some small effect on suicide rates, but it seems very unlikely that it would account for the difference between a rate of 120 and a rate of 80 which is what the graph seems to imply. The effect is just too large to be credible, if you ask me.

Although that said, another paper just out found that tiny amounts of antidepressants (the amounts that you find in rivers because so many people take them and some of them are stay in urine) could affect the behaviour of baby fish. And presumably also baby humans. Unfortunately I can't access this study, so I don't know whether that's nonsense or not, but it's food for thought.

Ohgami, H., Terao, T., Shiotsuki, I., Ishii, N., & Iwata, N. (2009). Lithium levels in drinking water and risk of suicide The British Journal of Psychiatry, 194 (5), 464-465 DOI: 10.1192/bjp.bp.108.055798

Lithium and Antidepressants in Tap Water

Lithium, as everyone knows, is a song by Nirvana. (It's also a different, and worse, song by Evanescence). It's also a chemical element. And it's a drug, used in psychiatry to treat bipolar disorder and, sometimes, severe depression.

One thing which lithium seems to do rather well - or at least better than other drugs - is make people less likely to commit suicide. At least, that's what most authorities say, so let's assume it's true.

Now a Japanese team report that the amount of lithium in tap water are negatively correlated with suicide rates - Lithium levels in drinking water and risk of suicide. (Someone has helpfully put this up on Scribd for people without academic access).

They analyzed the water supplies in the 18 subdivisions of Oita prefecture in southern Japan, and compared the lithium levels in the water with the average suicide rate (normalized for age and gender). Here's what happened -
Now, on paper that's a pretty solid correlation. But how believable is it? The maximum lithium level in the water was found to be 59 micrograms per liter. By contrast, if someone were taking lithium for bipolar disorder, they would on average be taking about 1 gram of lithium carbonate (Li2CO3) per day, which works out at about 100 mg of lithium (and 900 mg of inert carbonate).

Assuming that people drink about two liters of tap water per day (almost certainly they drink less), that's about 120 micrograms per day. That's 0.12 mg. So about a thousand-fold less than you'd take if you were bipolar.

Could such a tiny amount of lithium do anything? Well, maybe. It's not impossible that it would have some small effect on suicide rates, but it seems very unlikely that it would account for the difference between a rate of 120 and a rate of 80 which is what the graph seems to imply. The effect is just too large to be credible, if you ask me.

Although that said, another paper just out found that tiny amounts of antidepressants (the amounts that you find in rivers because so many people take them and some of them are stay in urine) could affect the behaviour of baby fish. And presumably also baby humans. Unfortunately I can't access this study, so I don't know whether that's nonsense or not, but it's food for thought.

Ohgami, H., Terao, T., Shiotsuki, I., Ishii, N., & Iwata, N. (2009). Lithium levels in drinking water and risk of suicide The British Journal of Psychiatry, 194 (5), 464-465 DOI: 10.1192/bjp.bp.108.055798

Neuroskeptic Voted Person of The Year

...well, not quite. At least not yet. But I have been linked to by Time Magazine.

The Time article discusses a paper that I also blogged about recently, Can Phase III Trial Results of Antidepressant Medications Be Generalized to Clinical Practice? A STAR*D Report

In a nutshell, this paper found that out of a large sample of depressed people who are fairly representative of the general population of patients presenting with depression in America, only 22% would have been accepted into a typical antidepressant trial. They were on average richer, better educated, more likely to have a job, and less likely to be black or Hispanic. In other words, typical antidepressant trials only recruit a narrow cross-section of society, tending to exclude the poor and disadvantaged and those with multiple mental health problems.

The study also found that this 22% tended to report a better response to an antidepressant, citalopram, than the rest. But as I said at the time...

Does this mean that rich white people really get more benefit from citalopram? Or do they just tend to report more benefit? Or do they experience larger placebo effects? It's impossible to say.

One of the problems with the this trial was that there was no placebo group. So the fact that the select 22% reported better response doesn't mean that they actually experienced a more powerful drug effect. It's entirely possible (and I would say, likely) that they could be just the kind of people who like to play along, comply with expectations and report greater benefits, for example. Whereas in fact they might have done equally well without any drugs, whereas the people who reported a smaller benefit might have done even worse with no treatment. We just don't know.

So when Time says that

a major new study suggests that both critics and proponents might be right about SSRIs: the drugs can work, but they appear to work best for only a subset of depressed patients — those with a limited range of psychological problems. People whose depression is compounded with, say, substance abuse or a personality disorder may not get much help from SSRIs —

That's one possibility, but not the only one.