The Wriggling Brain

What do we mean when we talk about "the brain"?

Easy, right? It's this:

Certainly, this is the image that comes to my mind.

But this is not an image of a brain. It's an image of a dead brain.

In a living brain, all kinds of interesting things are happening. Things we literally can't begin to imagine. Because these are hard to visualize, they can't enter the mental picture.

To picture the living brain as just a yellowy lump is like picturing Wikipedia as a disc. It's accurate as far as it goes, but it misses the whole point. You could download Wikipedia onto a BluRay disc, and then you could describe that disc as "Wikipedia" and you wouldn't be wrong, but Wikipedia is much more than a silver circle.

It doesn't help much that we know that there's more to the living brain than a yellowy lump. Yes, most of us know that the living brain is somehow responsible for thought, feeling, perception, and consciousness.

But we have no idea of how it does so, we don't have any feel for this relationship. We agree with the idea that brain = mind, but that's just an abstract equation. Just as most of us know that e=mc2, but only physicists understand it.

All this leads to philosophical problems. Wittgenstein wrote:

Look at a stone and imagine it having sensations. - One says to oneself: How could one so much as get the idea of ascribing a sensation to a thing? One might as well ascribe it to a number! - And now look at a wriggling fly and at once these difficulties vanish and pain seems able to get a foothold here.

What he meant is that we only feel that we can ascribe pain (or any "internal" mental state or event) to something which is behaving "externally".

Now in most cases, that's fine. Most inanimate objects really don't have mental states. But brains do. The brain, we feel, is inanimate; it's just a yellowy lump. By itself the brain is like Wittgenstein's stone - it seems.

So, we feel, the brain itself can't really have mental states, only walking, talking, behaving people can, like wriggling flies. Except we know on an abstract level that brains do have mental states; so we tie ourselves into philosophical knots about "brains" and "persons", asking whether a person is more or less or the same as a brain, and so on.

The whole problem could be removed, I think, if instead of a yellowy lump, we could picture the living brain in all its active complexity; if we could talk about "the brain", not as an inanimate object, but as the most animate thing in the world.

In the brain there are hundreds of billions of cells, and each one is a hive of movement - not visible to the naked eye or even to a microscope, but the movement of ions and neurotransmitters and ultimately information.

I think many philosophical puzzles would lose their edge if we could somehow get a feel for all that; if we could replace the accurate, but misleading, yellowy lump picture of "the brain" with one that captures the complexity and dynamism of the thing: a city, a hive of insects, a vast machine.

Dolphins who Dream of Whales

Once in a while you come across a paper that can only be described as lovely. This is one: Do dolphins rehearse show-stimuli when at rest?

Five dolphins lived in a certain aquarium in France. Every day, they put on shows for people - jumping around, that kind of thing. One day the aquarium started playing a 20-minute clip of "intro music" for the show. This consisted of various oceanic sounds including sea birds, dolphin noises and some whale-song.

What happened next was amazing. About a month about they brought in the intro sounds, the researchers noticed some odd sounds coming from the dolphins, late at night. It turned out that the dolphins had started making whale noises.

They only did this at night, mostly between 1 am and 3 am, when they were resting, possibly even sleeping. No-one trained them to do this. The "atypical vocalizations" were much lower than the dolphin's normal whistles, and also lasted longer.

Unfortunately, it wasn't possible to tell how many of the dolphins did this.

The authors recorded the dolphin's whale impressions with an underwater microphone, and played them back to a sample of 20 biologists, who weren't told the hypothesis of the study. Many of them thought they were whale-song, especially when the clips were slowed down to half-speed, dolphin's voices being "higher" than whales'.

Why the dolphins did this is a mystery. All of them had been born in captivity, so they'd never encountered a real whale. One theory is that they were mentally rehearsing the events of the day to come. Maybe they were even dreaming about them and "talking in their sleep" - although this is unclear, because it's not known whether dolphins dream; don't exactly sleep in the same way we do.

The paper's open access and it even comes with some audio clips of the dolphins, although unless you're familiar with what they sound like normally these aren't very meaningful.

Kremers D, Jaramillo MB, Böye M, Lemasson A, & Hausberger M (2011). Do dolphins rehearse show-stimuli when at rest? Delayed matching of auditory memory. Frontiers in Psychology, 2 PMID: 22232611

What're You Lookin' At (When You Dream)?

Why do our eyes move during sleep?

Here at Neuroskeptic we've already asked why do we sleep? and why do we dream? There are plenty of theories, but no clear answers to either of those questions.

We don't even know the function of one of the most famous sleep phenomena, rapid eye movements (REMs). It's been known for decades that during certain phases of sleep, the eyes show a pattern of rapid flickering movements, and that this REM sleep is when most (but not all) dreams occur.

But what are the eye movements?

In a new paper, French sleep researcher Isabelle Arnulf sets out the case for the "scanning hypothesis". The idea is that REMs represent the dreamer "looking at" things in the dream, just like waking eye movements - at least much of the time.

Some say that REMs are nothing to do with dreams, and it's just a coincidence that they tend to occur together. They may just be random, perhaps with the function of preventing the eyes from drying out during sleep, or maybe just a side-effect of sleeping brain activity with no function at all. A possible analogy: males usually get erections during REM sleep, even though most dreams have no sexual content.

There's lots of evidence that seems to support a deflationist view of dreams. In humans and other mammals, foetuses have lots of REMs, even though they've never seen anything. Lab animals with the visual areas of the brain removed also continue to display REMs, albeit not as many of them, and people who've been blind since birth have REMs.

Anaulf disagrees however, and discusses her work with the fascinating REM sleep behaviour disorder (RBD). RBD sufferers seemingly act out their dreams. Normally, we're paralyzed during REM by an inhibitory system which causes muscle relaxation during REM. The eyes are the exception, because they have a separate nerve pathway (which is also why some otherwise paralysed people can still communicate with their eyes). RBD can be a symptom of underlying neurological disease, such as Parkinson's, but it can also occur on its own.

Anaulf's team studied 56 patients with RBD over 1 or 2 nights (Leclair-Visonneau 2010). They found that the behaviours were correlated with the onset of rapid eye movements, although 80% of the eye movements were not accompanied by any actions. What's more, out of 19 distinct behaviours (ranging from running away from lions, to strangling someone), 60% were associated with REMs, and of these 90% were in the same direction as the actions.

This directional coherence between limb, head and eye movements during RBD suggests that, when present, REMs imitate the scanning of the dream scene. Because the REMs are similar in subjects with and without RBD, we suggest the extension of this concordance to normal REM sleep.

They suggest, however, that it may not be that the eye movements are the result of the dream content, but just correlated with it. It's not that something happens on the left in the dream, and then in response, the eyes move to the left; rather it's that whatever pattern of neuronal activity causes the dream, also causes the corresponding eye movements.

Either way it's an interesting idea, although it does rely on the assumption that RBD is a good model of normal sleep in this regard.

Arnulf I (2011). The 'scanning hypothesis' of rapid eye movements during REM sleep: a review of the evidence. Archives italiennes de biologie, 149 (4) PMID: 22205589

An Objective Measure of Consciousness...?

Could a puff of air in the eye offer a way to evaluate whether someone is conscious or not?

Yes it could, say Cambridge's Tristan Bekinschtein and colleagues in a new paper about Sea slugs, subliminal pictures, and vegetative state patients.

It's all about classical conditioning of the kind made famous by Pavlov. This is learning caused by the pairing of two stimuli, one of them somehow meaningful (usually unpleasant). So if I were to ring a little bell before, say, pepper spraying you, and I did that repeatedly, you would probably close your eyes whenever I rang that bell. Or just punch me, but you see the point.

Anyway, the key is that there are two kinds of classical conditioning. In the unhelpfully named "delay" conditioning, the warning stimulus overlaps with the painful one. Like if I started ringing my bell, then kept ringing it while I sprayed you with my other hand. In other words, there is no delay between the two stimuli... I said it was badly named.

By contrast in "trace", conditioning there is a delay - the warning stops shortly before the second stimulus. Bekinschtein et al argue that trace conditioning requires conciousness. While delay conditioning can occur without awareness of the link between the two stimuli, only conscious awareness can bridge the time gap in trace conditioning.

In trace experiments (in which rather than pepper spray, the unpleasant stimulus is just a puff of air in the eye), people who, when asked, can't explain the relationship ("sound means puff") don't learn to blink when they hear the sound. But with delay conditioning, this "unconscious" conditioning can occur. Likewise, under anaesthesia, trace conditioning is lost.

At first glance this looks like a piece of psychological trivia, but it could have literally life-or-death consequences. If trace conditioning is a measure of concious awareness then it could be used as a way of working out whether brain-injured people in a "coma" or "vegetative state" are aware or not.

This paper is in fact a follow-up to the author's own 2009 study showing that some people in a vegetative state do show trace conditioning - and the ones who did were more likely to subsequently wake up.

One snag is that the humble sea slug, Aplysia, can undergo trace conditioning, yet it is presumably not conscious, at least not in any recognizable sense.

But Bekinschtein et al say that trace conditioning is a product of convergent evolution. Alplysia can do it and we can do it, but we use different means to the same end. Their argument is that while in Alpysia trace conditioning is known to be dependent on just a handful of individual neurons in the creature's tiny "brain", in humans it requires an intact hippocampus (containing millions of cells). People with hippocampal damage, who suffer amnesia, also can't do trace conditioning.

That's a good point but does that mean such hippocampal patients aren't conscious? That would be weird because, apart from the amnesia, they seem perfectly normal. Presumably they're just not conscious of the relationship between things separated in time...

Also, primitive pathways for conditioning might still exist in humans, able to reactivate under special conditions. They do acknowledge this with a discussion of experiments showing that trace conditioning in the absence of conscious awareness of the relationship can occur but only when the warning stimuli are "scary", like pictures of snakes. They say that with generic, neutral stimuli there is no good evidence of unconscious trace conditioning, but this seems like a fairly fine distinction.


Ultimately, it's a very nice idea but only more studies on "unconscious" patients will tell us whether it's really able to measure consciousness in a useful way.

Bekinschtein TA, Peeters M, Shalom D, and Sigman M (2011). Sea slugs, subliminal pictures, and vegetative state patients: boundaries of consciousness in classical conditioning. Frontiers in psychology, 2 PMID: 22164148

The Real "Contagion" Virus

Seen Contagion yet?

It's pretty scary. A new epidemic disease comes out of nowhere and starts killing everyone. It infects the brain - victims suffer seizures, or fall into a coma, and die. It spreads like wildfire. Humanity's only hope lies in Lawrence Fishburne and Kate Winslet.

Luckily, that's fiction. But only just.

In the movie, the killer bug is called "MEV-1", but it might as well have been called the Nipah virus, because it was closely based on a real disease of the same name. So much so that this post about Nipah contains movie spoilers.

The Nipah Virus came to the world's attention in late 1998. There was an outbreak of a severe fever accompanied in many cases by encephalitis (viral infection of the brain) in Malaysia and Singapore. 276 patients were recorded. 40% of them died.

In the initial outbreak, there was probably no person-to-person transmission of the virus. Rather, only people who came into contact with Malaysian pigs - mainly farmers and butchers - caught the disease. Over a million pigs were culled in 1999 to try and contain the outbreak, and this seemed to be effective.

But since then, there have been several other smaller Nipah outbreaks in Asia, one almost every year in fact. In some of these, person to person transmission has been detected, notably in Bangladesh and India. The fatality rate in these more recent outbreaks has also been higher (70-90%). Luckily, unlike in the movie, it doesn't seem to be very contagious - so far. Most years have seen only 10 or 12 cases. But who knows what the future holds?

The virus is distantly related to measles, but is much more severe. Symptoms can begin anywhere from 4 days to 2 months after infection, but generally within 1 to 2 weeks. More recent outbreaks seem to have a shorter incubation period. The symptoms include fever, headache, vomiting, seizures, muscular jerks, and altered consciousness (confusion, coma).

Even after the initial infection is over, a minority of patients (4-8%) later suffer a relapse encephalitis. The virus seems able to remain dormant in the body before re-emerging to infect the brain again. Survivors may suffer neurological problems such as epilepsy, movement disorders, fatigue, and others. This is especially common following relapse encephalitis.

Where did it come from? It turns out that various strains of Nipah-like viruses are common in certain bats that inhabit various Asian countries, specifically fruit bats of the Pteropus genus, aka "flying foxes". The bats don't get sick, but infected bats are highly contagious, excreting the virus in their urine.

The virus seems to have made the leap into humans not once but several times, from different kinds of bats. Each outbreak could represent a new crossover event. Often there was an intermediate animal host, such as the domestic pigs in Malaysia .

Nipah is a classic zoonotic disease - it jumps from animals to humans. Zoonoses are scary for two reasons. They're new to humans, so humans haven't had a chance to develop immunity. And they may be especially deadly, because they haven't evolved not to be deadly to us.

Viruses and bacteria don't actually want to kill you. They want you alive, so that you can keeping breathing, walking, having sex, and otherwise spreading them. So pathogens tend to evolve to be less lethal to their primary hosts. Unfortunately, that's only good news if you are the primary host, and in the case of zoonoses, we're not. Bats don't get sick, but we do.

Lo, M., & Rota, P. (2008). The emergence of Nipah virus, a highly pathogenic paramyxovirus Journal of Clinical Virology, 43 (4), 396-400 DOI: 10.1016/j.jcv.2008.08.007

Is Sleep Brain Defragmentation?

After a period of heavy use, hard disks tend to get 'fragmented'. Data gets written all over random parts of the disk, and it gets inefficient to keep track of it all.





That's why you need to run a defragmentation program occasionally. Ideally, you do this overnight, while you're asleep, so it doesn't stop you from using the computer.



A new paper from some Stanford neuroscientists argues that the function of sleep is to reorganize neural connections - a bit like a disk defrag for the brain - although it's also a bit like compressing files to make more room, and a bit like a system reset: Synaptic plasticity in sleep: learning, homeostasis and disease



The basic idea is simple. While you're awake, you're having experiences, and your brain is forming memories. Memory formation involves a process called long-term potentiation (LTP) which is essentially the strengthening of synaptic connections between nerve cells.



Yet if LTP is strengthening synapses, and we're learning all our lives, wouldn't the synapses eventually hit a limit? Couldn't they max out, so that they could never get any stronger?



Worse, the synapses that strengthen during memory are primarily glutamate synapses - and these are dangerous. Glutamate is a common neurotransmitter, and it's even a flavouring, but it's also a toxin.



Too much glutamate damages the very cells that receive the messages. Rather like how sound is useful for communication, but stand next to a pneumatic drill for an hour, and you'll go deaf.



So, if our brains were constantly forming stronger glutamate synapses, we might eventually run into serious problems. This is why we sleep, according to the new paper. Indeed, sleep deprivation is harmful to health, and this theory would explain why.





The authors argue that during deep, dreamless slow-wave sleep (SWS), the brain is essentially removing the "extra" synaptic strength formed during the previous day. But it does so in a way that preserves the memories. A bit like how defragmentation reorganizes the hard disk to increase efficiency, without losing data.



One possible mechanism is 'synaptic scaling'. When some of the inputs onto a given cell become stronger, all of the synapses on that cell could weaken. This would preserve the relative strength of the different inputs while keeping the total inputs constant. It's known that synaptic scaling happens in the brain, although it's not clear whether it has anything to do with sleep.



There are other theories of the restorative function of sleep, but this one seems pretty plausible. It stands in contrast to the idea that sleep is purely a form of inactivity designed to save energy, rather than being important in itself.



What this paper doesn't explain, and doesn't try to, is dreaming, REM sleep, which is very different to slow-wave sleep. REM is not required for life, so long as you get SWS, and some animals don't have REM, but they all have SWS, although in some animals, only one side of the brain has it at a time.



So it makes sense, but what's the evidence? There's quite a bit - but, it all comes from very simple animals, like flies and fish.



The pictures above show that, in various parts of the brain of the fruit fly, measures of synaptic strength are increased in flies that have been awake for some time, compared to recently rested ones. In general, synapses increase during the wake cycle and then return to baseline during sleep.



There's similar evidence from fish. But the authors admit that no-one has yet shown that the same is true of any mammals - let alone humans.



I'd say that this is important, because the fly brain is literally a million times smaller than ours. Synaptic overgrowth could be a more serious problem for a fly because they just have fewer neurons to play with. Sleep may have evolved to prune extra connections in primitive brains, and then shifted to playing a very different role in ours.



Wang G, Grone B, Colas D, Appelbaum L, & Mourrain P (2011). Synaptic plasticity in sleep: learning, homeostasis and disease. Trends in Neurosciences PMID: 21840068