Brain Connectivity, Or Head Movement?

"It's pretty painless. Basically you just need to lie there and make sure you don't move your head".


This is what I say to all the girls... who are taking part in my fMRI studies. Head movement is a big problem in fMRI. If your head moves, your brain moves and all fMRI analysis assumes that the brain is perfectly still. Although head movement correction is now a standard part of any analysis software, it's not perfect.

It may be a particular problem in functional connectivity studies, which attempt to measure the degree to which different parts of the brain are "talking" to each other, in terms of correlated neural activity over time. These are extremely popular nowadays. It's even been claimed that this data may help us understand consciousness itself (although we've heard that before).

A new paper offers some important words of caution. It shows that head motion affects estimates of functional connectivity. The more motion, the weaker the measured connectivity in long-range networks, while shorter range connections were stronger. Also, men tended to move more than women.

The effect was small - head movement can't explain more than a small fraction of the variability in connectivity.


The authors looked at 1,000 scans from healthy volunteers. They just had to lie in the scanner at rest. They looked at functional connectivity, using standard "motion correction" methods, and correlated it with head movement (which you can measure very accurately from the MRI images themselves.) Men tended to move more than women. Could this explain why women tend to have higher functional connectivity?

Disconcertingly, head movement was associated with low long range / high short range connections, which is exactly what's been proposed to happen in autism (although in fairness, not all the evidence for this comes from fMRI).

This clearly doesn't prove that the autism studies are all dodgy, but it's an issue. People with autism, and people with almost any mental or physical disorder, on average tend to move more than healthy controls.

One caveat. Could it be that brain activity causes head movement, rather than the reverse? The authors don't consider this. Head movement must come from the brain, of course. Probably from the motor cortex. The fact that motor cortex functional connectivity was positively associated with movement does suggest a possible link.

However, this paper still ought to make anyone who's using functional connectivity worry - at least a little.

Head motion is a particularly insidious confound. It is insidious because it biases between-group studies often in the direction of the hypothesized difference....even though there is considerable variation that is not due to head motion, in any given instance, a between-group difference could be entirely due to motion.

Van Dijk, K., Sabuncu, M., & Buckner, R. (2011). The Influence of Head Motion on Intrinsic Functional Connectivity MRI NeuroImage DOI: 10.1016/j.neuroimage.2011.07.044

Brain Connectivity, Or Head Movement?

"It's pretty painless. Basically you just need to lie there and make sure you don't move your head".


This is what I say to all the girls... who are taking part in my fMRI studies. Head movement is a big problem in fMRI. If your head moves, your brain moves and all fMRI analysis assumes that the brain is perfectly still. Although head movement correction is now a standard part of any analysis software, it's not perfect.

It may be a particular problem in functional connectivity studies, which attempt to measure the degree to which different parts of the brain are "talking" to each other, in terms of correlated neural activity over time. These are extremely popular nowadays. It's even been claimed that this data may help us understand consciousness itself (although we've heard that before).

A new paper offers some important words of caution. It shows that head motion affects estimates of functional connectivity. The more motion, the weaker the measured connectivity in long-range networks, while shorter range connections were stronger. Also, men tended to move more than women.

The effect was small - head movement can't explain more than a small fraction of the variability in connectivity.


The authors looked at 1,000 scans from healthy volunteers. They just had to lie in the scanner at rest. They looked at functional connectivity, using standard "motion correction" methods, and correlated it with head movement (which you can measure very accurately from the MRI images themselves.) Men tended to move more than women. Could this explain why women tend to have higher functional connectivity?

Disconcertingly, head movement was associated with low long range / high short range connections, which is exactly what's been proposed to happen in autism (although in fairness, not all the evidence for this comes from fMRI).

This clearly doesn't prove that the autism studies are all dodgy, but it's an issue. People with autism, and people with almost any mental or physical disorder, on average tend to move more than healthy controls.

One caveat. Could it be that brain activity causes head movement, rather than the reverse? The authors don't consider this. Head movement must come from the brain, of course. Probably from the motor cortex. The fact that motor cortex functional connectivity was positively associated with movement does suggest a possible link.

However, this paper still ought to make anyone who's using functional connectivity worry - at least a little.

Head motion is a particularly insidious confound. It is insidious because it biases between-group studies often in the direction of the hypothesized difference....even though there is considerable variation that is not due to head motion, in any given instance, a between-group difference could be entirely due to motion.

Van Dijk, K., Sabuncu, M., & Buckner, R. (2011). The Influence of Head Motion on Intrinsic Functional Connectivity MRI NeuroImage DOI: 10.1016/j.neuroimage.2011.07.044

Blindsight and Consciousness In The Brain

A new paper claims to show the neural activity associated with consciously seeing something:

Awareness-related activity in prefrontal and parietal cortices in blindsight reflects more than superior visual performance.

You might think it would be easy to find the neural correlates of seeing stuff. Just pop someone in the scanner and show them a picture.

However, it's not that simple, because that wouldn't tell you which brain activations were associated with concious awareness as such, as opposed to all of the other things that happen when we see a picture, many of which may be unconscious.

The new paper makes use of a patient, "GY", who has what's known as blindsight, a mysterious phenomenon caused by damage to the primary visual cortex on one side of the brain. In GY's case this was caused by head trauma at age 8. He's now 52, and is unable to see anything on the right side of his visual field. He only sees half the world.

However, he is still able to respond to some kinds of visual stimuli on the right, as if he could see them. But he reports that he doesn't. Blindsight is a rare phenomenon but one that's been extensively studied, because of its obvious scientific and indeed philosophical interest.

In this study the authors used fMRI to try to work out the neural correlates of concious awareness as opposed to unconcious responses. They showed GY a set of horizontal and vertical bars. His task was to say whether the horizontal bars were on top or not.


The stimuli were shown on either the left or the right. The trick was that they set it up such that it was equally easy in either the "good" or the "blind" side of the brain. In order to do that, they had to make the contrast of the bars much less bright on the "good" side.

What happened? As expected, behavioural performace was equal whether the stimuli were on the left or the right. GY got the judgement right about 75% of the time.

However, his brain responded much more strongly to stimuli on the good side - stimuli that were consciously perceived. Activations appeared all over the cerebral cortex in the occipital, parietal and frontal lobes, as you can see in the pic at the top.

The only area more activated by the unconscious stimuli was a tiny blob in the amygdala.

So what does this show? Is it "the neural correlates of conscious awareness", that Holy Grail of neuro-philosophers?

Maybe. It's a clever experimental design, which rules out some alternative explanations. It's hard to argue that the conciously perceived stimuli were just stronger, and hence more likely to affect the brain. They were actually much fainter.

And it's hard to argue that this represents subconscious information processing, or the process of making the decision whether the horizontal bars were top or bottom, because that was also going on in the blind condition and performance was the same.

Yet my concern is that the main route by which visual information gets into the cortex from the eyes, is via V1, the part which was damaged on one side. So in a sense it's no surprise at all that the cortex was more activated in the conscious condition.

Maybe this is the whole point - maybe this study shows us that consciousness is to do with cortical processing. However, when you put it like that, it seems a bit of an anticlimax. I don't think anyone would seriously dispute that. The cortex does almost everything. The interesting debates are about where in the cortex consciousness happens, if indeed it's localized at all, and what kind of processing underlies it.

It's unlikely that all of the activated areas were directly linked to conscious awareness. But we don't know which of them were.

Persaud, N., Davidson, M., Maniscalco, B., Mobbs, D., Passingham, R., Cowey, A., & Lau, H. (2011). Awareness-related activity in prefrontal and parietal cortices in blindsight reflects more than superior visual performance NeuroImage DOI: 10.1016/j.neuroimage.2011.06.081

Blindsight and Consciousness In The Brain

A new paper claims to show the neural activity associated with consciously seeing something:

Awareness-related activity in prefrontal and parietal cortices in blindsight reflects more than superior visual performance.

You might think it would be easy to find the neural correlates of seeing stuff. Just pop someone in the scanner and show them a picture.

However, it's not that simple, because that wouldn't tell you which brain activations were associated with concious awareness as such, as opposed to all of the other things that happen when we see a picture, many of which may be unconscious.

The new paper makes use of a patient, "GY", who has what's known as blindsight, a mysterious phenomenon caused by damage to the primary visual cortex on one side of the brain. In GY's case this was caused by head trauma at age 8. He's now 52, and is unable to see anything on the right side of his visual field. He only sees half the world.

However, he is still able to respond to some kinds of visual stimuli on the right, as if he could see them. But he reports that he doesn't. Blindsight is a rare phenomenon but one that's been extensively studied, because of its obvious scientific and indeed philosophical interest.

In this study the authors used fMRI to try to work out the neural correlates of concious awareness as opposed to unconcious responses. They showed GY a set of horizontal and vertical bars. His task was to say whether the horizontal bars were on top or not.


The stimuli were shown on either the left or the right. The trick was that they set it up such that it was equally easy in either the "good" or the "blind" side of the brain. In order to do that, they had to make the contrast of the bars much less bright on the "good" side.

What happened? As expected, behavioural performace was equal whether the stimuli were on the left or the right. GY got the judgement right about 75% of the time.

However, his brain responded much more strongly to stimuli on the good side - stimuli that were consciously perceived. Activations appeared all over the cerebral cortex in the occipital, parietal and frontal lobes, as you can see in the pic at the top.

The only area more activated by the unconscious stimuli was a tiny blob in the amygdala.

So what does this show? Is it "the neural correlates of conscious awareness", that Holy Grail of neuro-philosophers?

Maybe. It's a clever experimental design, which rules out some alternative explanations. It's hard to argue that the conciously perceived stimuli were just stronger, and hence more likely to affect the brain. They were actually much fainter.

And it's hard to argue that this represents subconscious information processing, or the process of making the decision whether the horizontal bars were top or bottom, because that was also going on in the blind condition and performance was the same.

Yet my concern is that the main route by which visual information gets into the cortex from the eyes, is via V1, the part which was damaged on one side. So in a sense it's no surprise at all that the cortex was more activated in the conscious condition.

Maybe this is the whole point - maybe this study shows us that consciousness is to do with cortical processing. However, when you put it like that, it seems a bit of an anticlimax. I don't think anyone would seriously dispute that. The cortex does almost everything. The interesting debates are about where in the cortex consciousness happens, if indeed it's localized at all, and what kind of processing underlies it.

It's unlikely that all of the activated areas were directly linked to conscious awareness. But we don't know which of them were.

Persaud, N., Davidson, M., Maniscalco, B., Mobbs, D., Passingham, R., Cowey, A., & Lau, H. (2011). Awareness-related activity in prefrontal and parietal cortices in blindsight reflects more than superior visual performance NeuroImage DOI: 10.1016/j.neuroimage.2011.06.081

Violent Brains In The Supreme Court

Back in June, the U.S. Supreme Court ruled that a Californian law banning the sale of violent videogames to children was unconstitutional because it violated the right to free speech.

However, the ruling wasn't unanimous. Justice Stephen Breyer filed a dissenting opinion. Unfortunately, it contains a whopping misuse of neuroscience. The ruling is here. Thanks to the Law & Neuroscience Blog for noticing this.

Breyer says (on page 13 of his bit)

Cutting-edge neuroscience has shown that “virtual violence in video game playing results in those neural patterns that are considered characteristic for aggressive cognition and behavior.”

He then cites this fMRI study from 2006. It's from the same group as this one I wrote about recently.

Breyer quotes this study as part of a discussion of the evidence linking violent video game use to violence. I have nothing to say about this, but I will point out than the fact that violent crime fell heavily in America after 1990, which is when the Super Nintendo and Sega Megadrive were invented.

Anyway, does this study show that playing violent games causes aggressive brain activity? Not exactly. By which I mean "no".

They scanned 13 young men playing a shooter game. The main finding was that during "violent" moments of the game, activity in the rostral ACC and the amygdala activity falls. At least this is the interpretation the authors give.

OK, but even if this neural response is "characteristic for aggressive cognition and behavior", it only lasted a few seconds. There's no evidence at all that this causes any lasting effects on brain function, or behaviour.

The real problem though is that the whole thing is based on the theory that violence is associated with reduced amygdala (and rACC) activity.

The authors cite various studies to this effect, but they don't distinguish between reduced activity as an immediate neural response to violence, as in this study, and reduced activity in people with high exposure to violent media, in response to non-violent stimuli.

This is rather like saying that because having a haircut reduces your total hair, and because bald people have no hair, haircuts cause baldness. Short-term doesn't automatically become long-term.

Besides, the whole idea that amygdala deactivation = violence is a bit weird because they used to destroy people's amydalas to reduce violent aggression in severe mental and neurological illness:

Different surgical approaches have involved various stereotactic devices and modalities for amygdaloid nucleus destruction, such as the injection of alcohol, oil, kaolin, or wax; cryoprobe lesioning; mechanical destruction; diathermy loop; and radiofrequency lesioning...

Lovely. It even worked sometimes, apparantly. Although it killed 4% of people. You can't reduce the activity of a region much more than by destroying it, yet destroying the amygdala reduced violence, or at the very least, didn't make it worse.

The truth is that aggression isn't a single thing. Everyone knows that there are two main kinds, "in cold blood" and "in the heat of the moment". Killing someone in a spontaneous bar brawl is one thing, but carefully planning to sneak up behind them and stab them is quite another.

Just based on what we know about the rare cases of amygdala-less people, I would imagine that destroying the amygdala would reduce violence "in the heat of the moment", which is motivated by anger and fear. The kind of patients who got this surgery seem to have been that kind of violent person, not the cold calculating kind.

So, even if violent video games reduced amygdala activity long term, that would probably reduce some kinds of violence.

Weber, R., Ritterfeld, U., & Mathiak, K. (2006). Does Playing Violent Video Games Induce Aggression? Empirical Evidence of a Functional Magnetic Resonance Imaging Study Media Psychology, 8 (1), 39-60 DOI: 10.1207/S1532785XMEP0801_4

Violent Brains In The Supreme Court

Back in June, the U.S. Supreme Court ruled that a Californian law banning the sale of violent videogames to children was unconstitutional because it violated the right to free speech.

However, the ruling wasn't unanimous. Justice Stephen Breyer filed a dissenting opinion. Unfortunately, it contains a whopping misuse of neuroscience. The ruling is here. Thanks to the Law & Neuroscience Blog for noticing this.

Breyer says (on page 13 of his bit)

Cutting-edge neuroscience has shown that “virtual violence in video game playing results in those neural patterns that are considered characteristic for aggressive cognition and behavior.”

He then cites this fMRI study from 2006. It's from the same group as this one I wrote about recently.

Breyer quotes this study as part of a discussion of the evidence linking violent video game use to violence. I have nothing to say about this, but I will point out than the fact that violent crime fell heavily in America after 1990, which is when the Super Nintendo and Sega Megadrive were invented.

Anyway, does this study show that playing violent games causes aggressive brain activity? Not exactly. By which I mean "no".

They scanned 13 young men playing a shooter game. The main finding was that during "violent" moments of the game, activity in the rostral ACC and the amygdala activity falls. At least this is the interpretation the authors give.

OK, but even if this neural response is "characteristic for aggressive cognition and behavior", it only lasted a few seconds. There's no evidence at all that this causes any lasting effects on brain function, or behaviour.

The real problem though is that the whole thing is based on the theory that violence is associated with reduced amygdala (and rACC) activity.

The authors cite various studies to this effect, but they don't distinguish between reduced activity as an immediate neural response to violence, as in this study, and reduced activity in people with high exposure to violent media, in response to non-violent stimuli.

This is rather like saying that because having a haircut reduces your total hair, and because bald people have no hair, haircuts cause baldness. Short-term doesn't automatically become long-term.

Besides, the whole idea that amygdala deactivation = violence is a bit weird because they used to destroy people's amydalas to reduce violent aggression in severe mental and neurological illness:

Different surgical approaches have involved various stereotactic devices and modalities for amygdaloid nucleus destruction, such as the injection of alcohol, oil, kaolin, or wax; cryoprobe lesioning; mechanical destruction; diathermy loop; and radiofrequency lesioning...

Lovely. It even worked sometimes, apparantly. Although it killed 4% of people. You can't reduce the activity of a region much more than by destroying it, yet destroying the amygdala reduced violence, or at the very least, didn't make it worse.

The truth is that aggression isn't a single thing. Everyone knows that there are two main kinds, "in cold blood" and "in the heat of the moment". Killing someone in a spontaneous bar brawl is one thing, but carefully planning to sneak up behind them and stab them is quite another.

Just based on what we know about the rare cases of amygdala-less people, I would imagine that destroying the amygdala would reduce violence "in the heat of the moment", which is motivated by anger and fear. The kind of patients who got this surgery seem to have been that kind of violent person, not the cold calculating kind.

So, even if violent video games reduced amygdala activity long term, that would probably reduce some kinds of violence.

Weber, R., Ritterfeld, U., & Mathiak, K. (2006). Does Playing Violent Video Games Induce Aggression? Empirical Evidence of a Functional Magnetic Resonance Imaging Study Media Psychology, 8 (1), 39-60 DOI: 10.1207/S1532785XMEP0801_4

The Brain Is Not Made of DNA

A new paper claims to have found A novel functional brain imaging endophenotype of autism.
They used fMRI to show that the brains of teenagers with autism showed no activation differences to looking at smiling happy faces, or afraid faces, compared to unemotional ones. In teens without autism, there was strong activation in many emotional and face-related brain regions. The unaffected brothers and sisters of the autistic people showed intermediate effects.

This is a fine study. The finding that siblings of people with autism have weakened neural responses to emotional faces is quite important as it suggests that this finding correlates (to some degree) with your position on the autism "spectrum".

The abstract of the paper actually downplays this, and says "The response in unaffected siblings did not differ significantly from the response in autism". However, there was a significant linear trend of group, and looking at the graphs, it's clear the siblings were In The Middle, like Malcolm.


There's plenty more nice things you could do with these results, which is an unusally large and rich dataset (120 people - 40 in each group). You could see, for example, whether siblings tend to be similar in terms of neural response. You could see whether the siblings who are most alike in brain response, are closest in symptoms. Or just look a the structural data on brain size and shape to see if there are characteristic differences between siblings that make one of the autistic and the other not.

There are a few problems. Most of the analyses are subject to the non-independence problem, because they defined their regions of interest based on the areas that showed a significant happy vs neutral face effect in the control group. So it's no surprise that when they generated graphs from these areas, the control group showed the strongest effect. However, they also do whole-brain analyses which avoid this problem and I don't think it undermines the main results.

So it's a decent study. But is this a "biomarker", or "endophenotype", as the title of the paper has it?

These are both hot topics in neuroscience at the moment. As the authors put it (emphasis mine):

An endophenotype is a heritable feature associated with a condition, present in affected individuals regardless of whether their condition is manifested, which co-segregates with the condition in families and which is present in unaffected family members at a higher rate than in the general population.

In such family members, endophenotypes represent instances in which genes associated with a particular condition exert measurable effects in individuals in whom they are insufficient to cause the condition itself...

The promise of characterizing endophenotypes lies in their hypothesized intermediate position between genotype and phenotype... the etiology of the endophenotype is likely to be correspondingly simpler: it can be said to be ‘closer to the level of gene action’.

The idea, in other words, is that if we can find a difference in the brains of people with autism, and their unaffected relatives who (presumably) share some of the same genes, we might have found a mechanism by which the genes ultimately cause the symptoms.

It might be easier, then, to find the genes for brain-not-lighting-up-to-happy-faces, than it will be to find genes for autism. Then once we've found those, we can use them to better understand autism.

My concern is that, while in theory endophenotypes seem "closer to the genetics" because they're "biological" rather than "behavioural", this is just a philosophical illusion based on the idea that the mind is not the brain.

We actually have no idea whether brain-not-lighting-up-to-happy-faces is closer to genetics than autistic behaviour. I'd say that our default assumption should be that everything is exactly the same "distance" from DNA, that is to say, everything is the product of complex interactions between genes and environment.

Some things are under the more or less exclusive control of a small number of genes, and these are called "genetic", but it's important not to assume that just because something's "in the brain", it's probably "more genetic" in this sense. The brain is a product of the environment as well.

If you scanned my brain while playing an audio recording of Urda love poetry, not much would happen. I don't know Urdu. In someone who did speak Urdu, all kinds of language and emotional areas would light up. That doesn't mean Urdu-brain-response is genetic. It's exactly as genetic as speaking-Urdu, which isn't genetic.

Spencer, M., Holt, R., Chura, L., Suckling, J., Calder, A., Bullmore, E., & Baron-Cohen, S. (2011). A novel functional brain imaging endophenotype of autism: the neural response to facial expression of emotion Translational Psychiatry, 1 (7) DOI: 10.1038/tp.2011.18

The Brain Is Not Made of DNA

A new paper claims to have found A novel functional brain imaging endophenotype of autism.
They used fMRI to show that the brains of teenagers with autism showed no activation differences to looking at smiling happy faces, or afraid faces, compared to unemotional ones. In teens without autism, there was strong activation in many emotional and face-related brain regions. The unaffected brothers and sisters of the autistic people showed intermediate effects.

This is a fine study. The finding that siblings of people with autism have weakened neural responses to emotional faces is quite important as it suggests that this finding correlates (to some degree) with your position on the autism "spectrum".

The abstract of the paper actually downplays this, and says "The response in unaffected siblings did not differ significantly from the response in autism". However, there was a significant linear trend of group, and looking at the graphs, it's clear the siblings were In The Middle, like Malcolm.


There's plenty more nice things you could do with these results, which is an unusally large and rich dataset (120 people - 40 in each group). You could see, for example, whether siblings tend to be similar in terms of neural response. You could see whether the siblings who are most alike in brain response, are closest in symptoms. Or just look a the structural data on brain size and shape to see if there are characteristic differences between siblings that make one of the autistic and the other not.

There are a few problems. Most of the analyses are subject to the non-independence problem, because they defined their regions of interest based on the areas that showed a significant happy vs neutral face effect in the control group. So it's no surprise that when they generated graphs from these areas, the control group showed the strongest effect. However, they also do whole-brain analyses which avoid this problem and I don't think it undermines the main results.

So it's a decent study. But is this a "biomarker", or "endophenotype", as the title of the paper has it?

These are both hot topics in neuroscience at the moment. As the authors put it (emphasis mine):

An endophenotype is a heritable feature associated with a condition, present in affected individuals regardless of whether their condition is manifested, which co-segregates with the condition in families and which is present in unaffected family members at a higher rate than in the general population.

In such family members, endophenotypes represent instances in which genes associated with a particular condition exert measurable effects in individuals in whom they are insufficient to cause the condition itself...

The promise of characterizing endophenotypes lies in their hypothesized intermediate position between genotype and phenotype... the etiology of the endophenotype is likely to be correspondingly simpler: it can be said to be ‘closer to the level of gene action’.

The idea, in other words, is that if we can find a difference in the brains of people with autism, and their unaffected relatives who (presumably) share some of the same genes, we might have found a mechanism by which the genes ultimately cause the symptoms.

It might be easier, then, to find the genes for brain-not-lighting-up-to-happy-faces, than it will be to find genes for autism. Then once we've found those, we can use them to better understand autism.

My concern is that, while in theory endophenotypes seem "closer to the genetics" because they're "biological" rather than "behavioural", this is just a philosophical illusion based on the idea that the mind is not the brain.

We actually have no idea whether brain-not-lighting-up-to-happy-faces is closer to genetics than autistic behaviour. I'd say that our default assumption should be that everything is exactly the same "distance" from DNA, that is to say, everything is the product of complex interactions between genes and environment.

Some things are under the more or less exclusive control of a small number of genes, and these are called "genetic", but it's important not to assume that just because something's "in the brain", it's probably "more genetic" in this sense. The brain is a product of the environment as well.

If you scanned my brain while playing an audio recording of Urda love poetry, not much would happen. I don't know Urdu. In someone who did speak Urdu, all kinds of language and emotional areas would light up. That doesn't mean Urdu-brain-response is genetic. It's exactly as genetic as speaking-Urdu, which isn't genetic.

Spencer, M., Holt, R., Chura, L., Suckling, J., Calder, A., Bullmore, E., & Baron-Cohen, S. (2011). A novel functional brain imaging endophenotype of autism: the neural response to facial expression of emotion Translational Psychiatry, 1 (7) DOI: 10.1038/tp.2011.18

The NeuROFLscience of Jokes

A new paper in the Journal of Neuroscience investigates the neural basis of humour: Why Clowns Taste Funny.

The authors note that some things are funny because of ambiguous words. For example:

Q: Why don’t cannibals eat clowns?
A: Because they taste funny!

Previous studies, apparently, have shown that these kinds of jokes lead to activation in the lIFG (left inferior frontal gyrus), although it's also involved in processing ambiguity that's not funny, and indeed, language in general.

In this study they gave people fMRI and played them audio clips of sentences that were either funny or not, and that either contained ambiguity or not. Examples of non-funny ambiguity included crackers like this:

Q: What happened to the post?
A: As usual, it was given to the best-qualified applicant.

They found that, relative to straightforward ones, ambiguous sentences led to increased activation in two areas, the lIFG and also the left ITG. That fits with previous work.

By contrast, funny stimuli, whether ambiguous or not, sent the brain into overdrive, with humour causing activation all over a wide range of hilarious areas such as the amygdala, ventral striatum, hypothalamus, temporal lobes and more.

Many of these areas are known to be involved in emotion and pleasure, although some are fairly random such as visual area BA19.

There were strong associations between BOLD signal change and funniness in the midbrain, the left ventral striatum, and the left anterior and posterior IFG.

The problem is, like so many neuroimaging studies, it's not clear what this adds to our understanding of the topic. All this really shows is that linguistic ambiguity activates language areas, and enjoyable stimuli activate pleasure areas (amongst many others); it doesn't tell us why some things are funny.

So more research is needed, and future neuro-humour studies will need a new set of neuro-jokes in order to maximize the laughs. Here's a few I came up with:

Q: Why did the chicken cross the road?
A :Because of activation in the motor cortex, causing muscle contractions in his legs.

Q: What neuroimaging methodology is most useful for studying the brains of cats and dogs?
A: PET scanning.

Knock knock.
Who's there?
John.
I doubt that. The 'self' is an illusion. The concept of 'John' as an individual is incompatible with modern neuroscience.

Bekinschtein TA, Davis MH, Rodd JM, & Owen AM (2011). Why Clowns Taste Funny: The Relationship between Humor and Semantic Ambiguity. The Journal of neuroscience : the official journal of the Society for Neuroscience, 31 (26), 9665-71 PMID: 21715632

The NeuROFLscience of Jokes

A new paper in the Journal of Neuroscience investigates the neural basis of humour: Why Clowns Taste Funny.

The authors note that some things are funny because of ambiguous words. For example:

Q: Why don’t cannibals eat clowns?
A: Because they taste funny!

Previous studies, apparently, have shown that these kinds of jokes lead to activation in the lIFG (left inferior frontal gyrus), although it's also involved in processing ambiguity that's not funny, and indeed, language in general.

In this study they gave people fMRI and played them audio clips of sentences that were either funny or not, and that either contained ambiguity or not. Examples of non-funny ambiguity included crackers like this:

Q: What happened to the post?
A: As usual, it was given to the best-qualified applicant.

They found that, relative to straightforward ones, ambiguous sentences led to increased activation in two areas, the lIFG and also the left ITG. That fits with previous work.

By contrast, funny stimuli, whether ambiguous or not, sent the brain into overdrive, with humour causing activation all over a wide range of hilarious areas such as the amygdala, ventral striatum, hypothalamus, temporal lobes and more.

Many of these areas are known to be involved in emotion and pleasure, although some are fairly random such as visual area BA19.

There were strong associations between BOLD signal change and funniness in the midbrain, the left ventral striatum, and the left anterior and posterior IFG.

The problem is, like so many neuroimaging studies, it's not clear what this adds to our understanding of the topic. All this really shows is that linguistic ambiguity activates language areas, and enjoyable stimuli activate pleasure areas (amongst many others); it doesn't tell us why some things are funny.

So more research is needed, and future neuro-humour studies will need a new set of neuro-jokes in order to maximize the laughs. Here's a few I came up with:

Q: Why did the chicken cross the road?
A :Because of activation in the motor cortex, causing muscle contractions in his legs.

Q: What neuroimaging methodology is most useful for studying the brains of cats and dogs?
A: PET scanning.

Knock knock.
Who's there?
John.
I doubt that. The 'self' is an illusion. The concept of 'John' as an individual is incompatible with modern neuroscience.

Bekinschtein TA, Davis MH, Rodd JM, & Owen AM (2011). Why Clowns Taste Funny: The Relationship between Humor and Semantic Ambiguity. The Journal of neuroscience : the official journal of the Society for Neuroscience, 31 (26), 9665-71 PMID: 21715632

Consciousness? FFS...

An interesting paper on the neurobiology of conscious awareness: Unconscious High-Level Information Processing.


The authors propose that consciousness may be associated, not with activation in any given area of the brain, but with recurrent information processing between areas, a kind of neural ping-pong.

When presented with sensory information, say the sight of an object, signals travel up through the brain from "primary" sensory areas to "higher" areas associated with more complicated processing. They call this the Fast Feedforward Sweep, or "FFS". Maybe not the best acronym.

Anyway, depending on the nature of the stimulus, this can lead to activation in almost any part of the brain. However, they say that it's not enough to generate consciousness; only if the later areas feedback to the earlier areas, and start a recurrent processing loop, does this happen.

This stands in contrast to the popular view, which seems to fit with common sense, that primary areas are unconscious and that consciousness is directly associated with activity in the higher areas, in particular, the prefrontal cortex (PFC).

The authors refer to fMRI and EEG studies showing that even "high level" processes, such as selective attention to stimuli, and inhibition of an action, can be triggered by subconscious cues, and that this is associated with activation in the prefrontal cortex - unconscious activation.

The details of these studies are fairly arcane but the point is that the prefrontal cortex is generally agreed to be the most developed, "highest level" part of the brain. If anywhere in the brain was going to be the seat of the soul, it's the PFC.


This shouldn't come as a surprise, though. While it's tempting to look for a part of the brain which "does" conscious experience - the "me module" - Daniel Dennet pointed out a while ago that this temptation is motivated by a fundamental confusion.

Likewise, while it seems common sense that conciousness is the "highest mental function" and therefore must be located in the highest brain area, this is a presumption: consciousness is a mystery, and we don't know if it's a high level function or not, or whether that question even makes sense.

Nor should the fact that consciousness isn't an inevitable consequence of high-level cognition come as a shock: in fact, that would be impossible. As Ryle pointed out in The Concept of Mind, this would create an infinite regression. Any conscious experience has to come from somewhere.

Right now I'm concious of choosing certain words rather than others in typing this post, in a conscious attempt to make it read better. But I'm not aware of all of the rules and experiences that guide my choices. I just feel that some words work. This feeling seems to come out of nowhere, or rather, out of the words themselves.

It isn't, of course, it's a product of calculations taking place in my brain, but I've no idea what they are. I wouldn't want to be, either: I'm too busy typing.

van Gaal S, & Lamme VA (2011). Unconscious High-Level Information Processing: Implication for Neurobiological Theories of Consciousness. The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry PMID: 21628675

Consciousness? FFS...

An interesting paper on the neurobiology of conscious awareness: Unconscious High-Level Information Processing.


The authors propose that consciousness may be associated, not with activation in any given area of the brain, but with recurrent information processing between areas, a kind of neural ping-pong.

When presented with sensory information, say the sight of an object, signals travel up through the brain from "primary" sensory areas to "higher" areas associated with more complicated processing. They call this the Fast Feedforward Sweep, or "FFS". Maybe not the best acronym.

Anyway, depending on the nature of the stimulus, this can lead to activation in almost any part of the brain. However, they say that it's not enough to generate consciousness; only if the later areas feedback to the earlier areas, and start a recurrent processing loop, does this happen.

This stands in contrast to the popular view, which seems to fit with common sense, that primary areas are unconscious and that consciousness is directly associated with activity in the higher areas, in particular, the prefrontal cortex (PFC).

The authors refer to fMRI and EEG studies showing that even "high level" processes, such as selective attention to stimuli, and inhibition of an action, can be triggered by subconscious cues, and that this is associated with activation in the prefrontal cortex - unconscious activation.

The details of these studies are fairly arcane but the point is that the prefrontal cortex is generally agreed to be the most developed, "highest level" part of the brain. If anywhere in the brain was going to be the seat of the soul, it's the PFC.


This shouldn't come as a surprise, though. While it's tempting to look for a part of the brain which "does" conscious experience - the "me module" - Daniel Dennet pointed out a while ago that this temptation is motivated by a fundamental confusion.

Likewise, while it seems common sense that conciousness is the "highest mental function" and therefore must be located in the highest brain area, this is a presumption: consciousness is a mystery, and we don't know if it's a high level function or not, or whether that question even makes sense.

Nor should the fact that consciousness isn't an inevitable consequence of high-level cognition come as a shock: in fact, that would be impossible. As Ryle pointed out in The Concept of Mind, this would create an infinite regression. Any conscious experience has to come from somewhere.

Right now I'm concious of choosing certain words rather than others in typing this post, in a conscious attempt to make it read better. But I'm not aware of all of the rules and experiences that guide my choices. I just feel that some words work. This feeling seems to come out of nowhere, or rather, out of the words themselves.

It isn't, of course, it's a product of calculations taking place in my brain, but I've no idea what they are. I wouldn't want to be, either: I'm too busy typing.

van Gaal S, & Lamme VA (2011). Unconscious High-Level Information Processing: Implication for Neurobiological Theories of Consciousness. The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry PMID: 21628675

The Unhelpful Brain

A reader pointed me to this study from a few months back which used fMRI to look at the effects of "Coaching With Compassion".

Unfortunately, the authors say at the outset that their paper is "Not to be quoted or reproduced without the expressed permission of one of the authors prior to publication" so I'm not going to... oh, hang on. Have I just broken the rules by quoting that? I hope not. But fair enough.

The paper describes an fMRI study of brain responses to being shown a variety of statements. The participants were students and the statements were about the university experience. They were either positive, negative, or neutral.

The authors found that the human brain responds differently to different kinds of stuff.

That's it. Well that ought to be it. The paper discusses things like Coaching With Compassion, The Ideal Self, and Intentional Change Theory, which are awesome no doubt, but they're not what this study is about.

Here's why. Before getting scanned, the students got two sessions of academic and career coaching. One session was focussed on hopes and goals for the future, dreams, and what they wanted to achieve in their studies. Yes you can! The other session, with a different coach, was all about challenges, fears, and disappointments. Maybe you can't.

The positive and the negative statements in the fMRI bit were based on these coaching interviews. The coach who did the nice bit said the nice statements (via recorded video clips) and vice versa. The positive and negative coaches were randomly assigned to each participant to avoid coach effects, and so on, which is good, the fMRI methodology was fine, and the data analysis looks good.

Who'd have thought it? Different parts of the brain were activated by positive, negative and neutral statements, and these were roughly what you'd expect from previous studies.

The reason this says nothing about coaching is that while participants got coaching beforehand, they all got the same coaching. These statements would have been positive or negative anyway - coaching or no. We don't know what, if any, effect coaching had.

Had half of them been randomized to get coached, and the other half assigned to a "placebo" coaching, say chatting about sports or the weather, then it would tell you something about coaching.

But that wouldn't mean it told you anything interesting about it, and this is the deeper problem with studies like this, of which this is only a good example.

Suppose that you found that positive, Compassionate Coaching made the brain respond more strongly to positive statements, or changed brain activity during decision-making, or whatever. That would be a result, and it might be really strong and statistically very significant, but for the life of me I can't see why you'd care, if you were interested in coaching.

Of course coaching affects the brain, and not just as a side effect: if it works, it'll work via changing the brain, in some way. But everything that changes behaviour changes the brain. That's what the brain does. How it does so is a detail of interest only to neuroscientists.

If you're a coach, or want to get coaching, or want to know whether coaching is effective, then you should look at coaching. The brain will be there, in the background, activating and deactivating happily, but it's not going to help you.

These kinds of studies happen, I think, because there's an inherent allure to seeing "the neural basis of" thoughts and feelings. It seems paradoxical and disturbing: you can't see thoughts! They're made of pixie dust and magic!

In the same way, quantum physics is universally agreed to be "weird". But it's always there, everywhere in the universe, and always has been. We're the weird ones, with our strange conviction that the most everyday thing in the world is really bizarre. God must find quantum physics incredibly boring.

Brains are not quite as commonplace as quarks, but they are at work whenever anyone, or most animals for that matter, does anything. Of course: how else would behaviour happen? We find this odd and fascinating. As a neuroscientist I'm no exception, the allure never "wears off". But that's just us.

Even people trying to be neuro-skeptical often fall into this trap. Here's Steven Rose in book review:

The weird locution – “it was not me; it was my brain that made me do it” – is increasingly used by neuroscientists who are sure that human thought and action are reducible to brain processes, and by legal defence teams pleading diminished responsibility for their clients. The trouble is that this way of speaking – and thinking, if such a term remains permissible – leaves unresolved who is the “me” that the brain drives.”

Well, human thought and action are reducible to brain processes. To deny this or (as is more common) imply that it's unhelpful, but not explain why, gets us nowhere.

The point is that all behaviour is brain activity, and that's why saying "It's brain activity" tells us nothing about any given behaviour. It’s an empty truism, like saying that a fire was started by something hot. Well, duh.

The Unhelpful Brain

A reader pointed me to this study from a few months back which used fMRI to look at the effects of "Coaching With Compassion".

Unfortunately, the authors say at the outset that their paper is "Not to be quoted or reproduced without the expressed permission of one of the authors prior to publication" so I'm not going to... oh, hang on. Have I just broken the rules by quoting that? I hope not. But fair enough.

The paper describes an fMRI study of brain responses to being shown a variety of statements. The participants were students and the statements were about the university experience. They were either positive, negative, or neutral.

The authors found that the human brain responds differently to different kinds of stuff.

That's it. Well that ought to be it. The paper discusses things like Coaching With Compassion, The Ideal Self, and Intentional Change Theory, which are awesome no doubt, but they're not what this study is about.

Here's why. Before getting scanned, the students got two sessions of academic and career coaching. One session was focussed on hopes and goals for the future, dreams, and what they wanted to achieve in their studies. Yes you can! The other session, with a different coach, was all about challenges, fears, and disappointments. Maybe you can't.

The positive and the negative statements in the fMRI bit were based on these coaching interviews. The coach who did the nice bit said the nice statements (via recorded video clips) and vice versa. The positive and negative coaches were randomly assigned to each participant to avoid coach effects, and so on, which is good, the fMRI methodology was fine, and the data analysis looks good.

Who'd have thought it? Different parts of the brain were activated by positive, negative and neutral statements, and these were roughly what you'd expect from previous studies.

The reason this says nothing about coaching is that while participants got coaching beforehand, they all got the same coaching. These statements would have been positive or negative anyway - coaching or no. We don't know what, if any, effect coaching had.

Had half of them been randomized to get coached, and the other half assigned to a "placebo" coaching, say chatting about sports or the weather, then it would tell you something about coaching.

But that wouldn't mean it told you anything interesting about it, and this is the deeper problem with studies like this, of which this is only a good example.

Suppose that you found that positive, Compassionate Coaching made the brain respond more strongly to positive statements, or changed brain activity during decision-making, or whatever. That would be a result, and it might be really strong and statistically very significant, but for the life of me I can't see why you'd care, if you were interested in coaching.

Of course coaching affects the brain, and not just as a side effect: if it works, it'll work via changing the brain, in some way. But everything that changes behaviour changes the brain. That's what the brain does. How it does so is a detail of interest only to neuroscientists.

If you're a coach, or want to get coaching, or want to know whether coaching is effective, then you should look at coaching. The brain will be there, in the background, activating and deactivating happily, but it's not going to help you.

These kinds of studies happen, I think, because there's an inherent allure to seeing "the neural basis of" thoughts and feelings. It seems paradoxical and disturbing: you can't see thoughts! They're made of pixie dust and magic!

In the same way, quantum physics is universally agreed to be "weird". But it's always there, everywhere in the universe, and always has been. We're the weird ones, with our strange conviction that the most everyday thing in the world is really bizarre. God must find quantum physics incredibly boring.

Brains are not quite as commonplace as quarks, but they are at work whenever anyone, or most animals for that matter, does anything. Of course: how else would behaviour happen? We find this odd and fascinating. As a neuroscientist I'm no exception, the allure never "wears off". But that's just us.

Even people trying to be neuro-skeptical often fall into this trap. Here's Steven Rose in book review:

The weird locution – “it was not me; it was my brain that made me do it” – is increasingly used by neuroscientists who are sure that human thought and action are reducible to brain processes, and by legal defence teams pleading diminished responsibility for their clients. The trouble is that this way of speaking – and thinking, if such a term remains permissible – leaves unresolved who is the “me” that the brain drives.”

Well, human thought and action are reducible to brain processes. To deny this or (as is more common) imply that it's unhelpful, but not explain why, gets us nowhere.

The point is that all behaviour is brain activity, and that's why saying "It's brain activity" tells us nothing about any given behaviour. It’s an empty truism, like saying that a fire was started by something hot. Well, duh.