Sunday, August 14, 2011

Pardon my brain


As social beings, we’re very good at letting others know when we’ve accidentally stopped being social. When we’ve missed something important in a conversion, we interrupt and ask: “Pardon?” “Excuse me?” “Sorry?” “What?” “Huh?” Sometimes furrowing the eyebrows a bit can suffice to communicate a sense of confusion.

We need ways to communicate when we’re lost because – let’s face it – we get lost often. We could be looking a fellow conversationalist directly in the eyes, convincing ourselves that we’re taking it all in as we listen to them clearly enunciate each syllable, when in reality every word is slipping right over our heads. “Come again?” we bid.

These lapses in attention could be driven by distracting thoughts or events in our environment, but are such diversions necessary for a conversation space-out to occur? A new study in press in NeuroImage suggests the possibility that our brains are constantly fluctuating in and out of particular states of attention. In certain brain states, we’re prepared to take in information and learn about it, whereas in other brain states, new information will likely elude us.

Study participants were scanned with functional MRI as they viewed 250 photographs of indoor and outdoor scenes, presented one at a time. The subjects were told that after the brain scan, they would be taking a test that would assess which scenes they recognize from the scan. In that test, the subjects were presented with images that either had or had not appeared during the scan, and for each image the subjects rated how confident they were that they had previously seen the indoor/outdoor scene. Out of the 250 images, the participants only correctly remembered some of them.

When the researchers analyzed the subjects’ brain activations, it was found that lower levels of activation in the parahippocampal place area (PPA, a brain region that is known to respond to visual scenes) occurring 2 seconds before presentation of an image predicted that an image would subsequently be correctly remembered in the post-scan test. However, when PPA activation was a bit higher during the 2 second period before an image was presented, the subject was likely to forget that image.

This is pretty neat. It shows that fluctuations in brain activity before we are presented with information determine whether we’ll pay attention to and remember that information. These sorts of fluctuations may also partially explain why we sometimes tune out of conversations.

But the neater part of this study was the follow-up. Based on the first experiment, the researchers called downward fluctuations in PPA activity a “good” brain state (ready to learn and remember a scene image) and upward fluctuations in PPA activity a “bad” brain state (likely not ready to process the image). The researchers used a technology known as “real-time fMRI” to monitor “good” or “bad” fluctuations in brain state as they were happening. When either a good or bad brain state occurred, a scene image was presented. As expected, when good brain states triggered an image, 2 hours later the image was more likely to be remembered than when a bad brain state had initially triggered an image.

This real-time fMRI study is particularly interesting because it demonstrates that fMRI can do more than just identify the neural correlates of human behaviours or perceptions. Rather than using stimuli to elicit brain activation, this study used brain activation to drive stimulus presentation and cause a certain behaviour (good or bad learning). Using brain activity to elicit stimuli, we can get closer to the question of a causal relationship that can otherwise only be addressed by inducing brain damage or using brain stimulation/other techniques to interrupt neural activity.

This study also might have implications for education programs that require “optimized” brain states for efficient learning to occur. And of course, there may be implications for optimizing everyday conversations. Next time you accidentally drift out of a conversation, consider adding the phrase “pardon my brain” to your repertoire of strategies for communicating that you’re not all there at the moment.

Reference:

Yoo JJ, Hinds O, Ofen N, Thompson TW, Whitfield-Gabrieli S, Triantafyllou C, & Gabrieli JD (2011). When the brain is prepared to learn: Enhancing human learning using real-time fMRI. NeuroImage PMID: 21821136

Friday, December 10, 2010

Financial incentives and the brain's reward system

Neuroeconomics is a big buzzword.



















Behavioural economics and the psychology of decision-making have rich histories, but with emerging brain imaging technology, we're now able to peer into some of the intricacies of neural processes as they occur while someone is making an important financial decision. The hope is that studies of brain activity will help guide economic theory and practice.

In a study recently published in PNAS, Japanese researchers used functional MRI to examine brain responses to a phenomenon that challenges current economic theories, known as the "undermining effect." They found that people who were most susceptible to this effect also showed greatest changes in brain responses while playing a game that involved financial incentives.

The undermining effect is a well-known psychological phenomenon in which a person is less likely to voluntarily engage in a task after performing that task for some sort of extrinsic reward, such as money or good grades. An example is a potential effect of schooling -- students who are forced to read Shakespeare because they are being graded on it are probably less likely to read Shakespeare for fun afterward than someone who didn't study Shakespeare in school.

The researchers investigated the neural basis of the undermining effect by dividing study participants into two groups and scanning each person's brain twice. Both groups participated in a fun task, called the "stopwatch" task, wherein subjects viewed a stopwatch timer going from zero to five seconds, and they had to press a button within 50 milliseconds of the 5 second time point (if you don't believe this sounds fun, try it for yourself with a digital watch). One group received financial rewards (200 Japanese Yen or about $2.20) for doing this correctly, while the other group didn't receive performance-based rewards. The group receiving financial rewards showed greater activity in areas of the brain previously associated with award, the anterior striatum and midbrain, when subjects were winning money.

Then participants got out of the brain scanner and waited in a quiet room, where they had free time to play the fun game or do anything else. As predicted by the undermining effect, those who were receiving financial rewards for their earlier performance on the fun game spent less time playing the fun game than those who weren't receiving awards. Then all subjects got back into the brain scanner, and they performed the fun task again, but crucially this time nobody received any financial rewards. More free time was given after the second scan, and once again the subjects who had earlier received money for their performance spent less time playing the fun game.

The most interesting finding revealed by analysis of the brain activity was that individuals who played the fun game the least during free time also showed the greatest differences in reward-related brain activity between the two brain scans. In other words, those who felt most rewarded by financial incentives (as measured by brain activity) were the same individuals who were least likely to engage in the fun game when given free time. This suggests that the undermining effect is strongest in individuals who think of money as a reward.

If the goal of neuroeconomics is to reveal information about behaviour that cannot be attained through psychological testing alone, this study appears to have succeeded. Importantly, it shows that each brain responds differently to incentives, and reward-related brain activity can predict the undermining effect within an individual. This is particularly interesting because it shows that not all individuals should be treated as equal in economic models of decision-making and incentive-driven behaviour.

The findings also have implications for policymakers who often implement incentives in domains such as public health and schooling. As demonstrated by the undermining effect, removing extrinsic incentives to engage in an activity can have damaging effects on the desire to voluntarily engage in that activity.

As to whether the study will succeed in impacting economic theory and practice -- that's for the economists to determine.

Reference:

ResearchBlogging.orgMurayama K, Matsumoto M, Izuma K, & Matsumoto K (2010). From the Cover: Neural basis of the undermining effect of monetary reward on intrinsic motivation. Proceedings of the National Academy of Sciences of the United States of America, 107 (49), 20911-6 PMID: 21078974

Monday, November 1, 2010

Write for your brain

Remember the days when writing by hand was more common than typing?

While those days may be gone, the ability to write by hand is indisputably still useful. This is why getting writer's cramp -- an often-painful condition that inhibits one's ability to write -- can be quite an annoyance.

Luckily, there are several forms of intervention that can be effective in alleviating writer's cramp. In a new study published in NeuroImage, Oliver Granert and colleagues examined how a couple of treatments for writer's cramp affect more than just the ability to write -- they were interested in how training the hand to write changes brain structure and function.

The researchers examined 14 patients with writer's cramp who were part of a clinical trial that assessed two forms of treatment. All 14 patients had their affected hand, wrist, and lower arm immobilized with a splint for 4 weeks prior to treatment. Then for 8 weeks, half of the patients trained their cramp-hand with writing movements using a pen attached to the bottom of a finger splint, and the other half trained finger movements using therapeutic putty (I'm not sure if they used Silly Putty, but if they did, I'm upset that I wasn't eligible to be subject).

The researchers took MRI's of the subjects to assess their brain structure at four points in time: week 0 (before treatment), week 4 (after immobilization), week 8 (after 4 weeks of training), and week 12 (after 8 weeks of training). At these four points in time, a functional measure of brain activity was also taken: the area of the brain that controls movement of the writing hand (M1HAND) was stimulated with electromagnetic induction to activate hand muscles, causing movement. The minimum amount of stimulation required to cause movement in the hand was taken as a measure of 'excitability' -- an assessment of how easily the hand can be moved by brain stimulation.

Both forms of training (writing-movements and putty-playing) were equally effective in reducing the symptoms of writer's cramp. After 4 weeks of immobilization, the grey matter of the brain area that controls movement of the hand decreased in volume, but 4 weeks after motor training the volume increased, and 8 weeks after motor training the volume increased even more. The findings from magnetic stimulation of M1HAND paralleled the changes in brain structure, in that the hand was less easily excitable after immobilization, but gradually became more easily excitable after motor training.

 This study is interesting because it essentially examined  the effects of both de-training and training on brain structure. Changes in brain structure reflected what was happening in terms of training; when the hand was immobilized, the brain area controlling hand movement shrank, but when the hand was mobilized with training, the same brain area grew. Most studies that investigate brain plasticity examine the effects of training -- alone -- on structural changes (e.g. measure brain volume; get subjects to exercise or meditate; measure brain volume again). But investigating opposite forms of training and observing opposite effects on brain structure provides more convincing evidence for a causal relationship between behaviour and anatomy.

Furthermore, the positive relationship between brain structural change and excitability of the hand provides evidence that changes in structure were activity-driven.

It was remarkable how fast the brain changed in response to both training and de-training in this study. I think of times in my life during elementary/high school, when I would write every day, but then I would basically stop writing for the whole summer. When I would come back to school in September, writing felt strange, and I didn't have the same effortless control over my pen that I left with at the end of the previous school-year. My comfort with the pen would then gradually increase as I began to write regularly again. It would be unsurprising if, in fact, these changes in writing ability were caused by my ever-changing brain, an anatomical shadow of my experiences.

Reference:
 
Granert O, Peller M, Gaser C, Groppa S, Hallett M, Knutzen A, Deuschl G, Zeuner KE, & Siebner HR (2011). Manual activity shapes structure and function in contralateral human motor hand area. NeuroImage, 54 (1), 32-41 PMID: 20708692

Thursday, October 21, 2010

The faithful Christian seizure

When I sit down to use my computer, the first thing I usually do is double-click the icon that opens up an internet browser. I do this so often, that even when I need to use the computer for purposes other than internet-browsing, I mindlessly open up the internet browser anyway. This action is an example of a learned automatism -- an unconscious behaviour that is generated as a result of trained associations in previous experiences.

Learned automatisms can last a long time, and the contexts in which they are acquired and retained can vary substantially. A couple of bizarre reports suggest that Christian individuals who learned to make the sign-of-the-cross hand gesture (also known as Signum Crucis) after having epileptic seizures may exemplify a form of long-lasting, deeply-engrained learned automatism.

In one of the reports, 4 out 530 epileptic patients at a clinic in Brazil displayed sign-of-the-cross gestures as automatic movements during seizures. None of the patients were aware of their own movements. The researchers evaluated these patients with electroencephalography (EEG) to measure electrical brain activity while seizures were experienced.





The figure above shows what the electrical brain activity of one of the four patients looked like at the time of seizure onset (first arrow), seizure duration, and sign-of-the-cross gesture onset (second arrow). The activity was measured at the right temporal lobe, the area in which all four patients regularly experienced seizures. All four patients were Christian and were raised in a religious manner, but it was not reported whether the patients learned the sign-of-the-cross gesture at a young age nor if they had a history of intentionally making these gestures at the time of seizures.

However, a second case report of an epileptic patient in Toronto demonstrates that the sign-of-the-cross gesture during seizures may be a learned automatism. The patient wasn't aware that she was making the cross gesture during her seizures, but when told that she was doing it, she explained that during childhood her mother used to teach her to cross herself at the end of her seizures. The authors of this study speculate that the patient was trained to make the cross gesture during seizures, and somehow a neural memory circuit for making the gesture gets recruited by spontaneous brain activity during her seizures.

This patient also had seizures in the right temporal lobe -- the same area as the four patients in the first study. Areas of the temporal lobe have been implicated in religious cognitive-emotional experience, although these findings are controversial. The association between epilepsy and religion has a rich history, with early Greeks referring to epilepsy as the "sacred disease."

However, although these cases provide an interesting insight to consciousness, it is unlikely that there is something special or miraculous about the sign-of-the-cross gesture during seizures. If the movement is due to a learned automatism, or some other mechanism, other gestures can likely be trained to be associated with seizures too. Maybe even single-clicking to close internet browsers.

References:

Lin K, Marx C, Caboclo LO, Centeno RS, Sakamoto AC, & Yacubian EM (2009). Sign of the Cross (Signum Crucis): observation of an uncommon ictal manifestation of mesial temporal lobe epilepsy. Epilepsy & behavior : E&B, 14 (2), 400-3 PMID: 19059360

Wennberg R, McAndrews MP, Zumsteg D, & Velazquez JL (2009). The sign of the cross as a learned ictal automatism? Epilepsy & behavior : E&B, 15 (3), 394-8 PMID: 19393765

Monday, September 13, 2010

The wandering male versus female brain

There has certainly been a good amount of recent controversy over the science of sex differences and the brain. Pop-science books such as The Male Brain and The Female Brain that emphasize (and probably exaggerate) sex differences have drawn major criticism. A couple of new books expose flaws in the stereotypical 'men think about sex every 5 seconds because they are programmed to' theory and related ideologies.
The above figure summarizes the well-accepted theory of male versus female brain function. A new groundbreaking study of brain activity in males and females at rest has brought the theory into question.

It turns out that, when males and females are scanned by fMRI while told to close their eyes and not think about anything in particular, their brain activations are virtually the same.

Researchers examined the brain activity of 26 females and 23 males who rested in a scanner and daydreamed. Three different well-characterized neural networks were analyzed for differences between males and females: the executive control network, the salience network, and the default mode network. The first two networks include several brain regions that have been associated with cognitive task performance in many previous studies. When subjects are at rest, these cognitive networks are deactivated but the resulting signal provides insight to their intrinsic behaviour. The researchers chose to look at these 2 cognitive networks because of mixed findings from previous work that indicated possible differences between associated male and female cognitive performance and brain activity. However, when the signals among different regions within these networks were compared (in a functional connectivity analysis), no differences between males and females were found.

The third network that was analyzed (default mode network) is a network that is activated when subjects are at rest. Although the function of the default mode network is controversial, activity in the brain regions of the network are thought to be associated with daydreaming, thinking about the past and future, and gauging others' perspectives. Or if you accept the classic theory of males versus female brain function, this is the network that represents thoughts of sex and lame excuses for men, and thoughts of shopping and musical sitcoms for women. The problem is: no differences between males and females in functional connectivity of the default mode network were found either.

It should be noted that the findings did not match the hypothesis of the researchers, who thought that differences between the sexes would be found because that would support the findings of previous reports. However, this study had more subjects than most previous studies on male versus female brain differences, so the statistical power is higher. Furthermore, this is the first study to directly investigate male-female differences in resting brains, so the findings do not necessarily contradict other studies that involved concentration or attention.

The researchers go as far as to suggest that resting state fMRI studies do not need to be controlled for sex because males and females have the same brain activity anyway.

Now that this blog post is done I feel my beer lobe lighting up and telling me to grab a cold one. Wait a second... is that possible? 

ResearchBlogging.orgWeissman-Fogel I, Moayedi M, Taylor KS, Pope G, & Davis KD (2010). Cognitive and default-mode resting state networks: Do male and female brains "rest" differently? Human brain mapping PMID: 20725910

Wednesday, September 8, 2010

Neuroscience, Psychology and Inception

If you're a neuroscience nerd and you saw the movie Inception, you probably couldn't help but think of some kind of neuro-theory to explain the plot or themes of the film. It seems that this is the case, anyhow, in the neuroscience blogosphere where there is no shortage of articles on Inception from a neuroscience perspective. Here is a list of good articles:

Malcolm MacIver at the blog Science Not Fiction provides a more in-depth look at current research on the neuroscience of sleep with reference to Inception.

The Stanford Neuroblog gives even more detail on the neuroscience of sleep and Inception (and promises to come out with part 2 of this discussion).

Christof Koch reviews Inception in Nature, explaining that "Inception is a visionary science-fiction film that does for dreaming what The Matrix did for virtual reality in 1999."

Neuroskeptic describes how it is possible to induce inception, or the planting of an idea into one's mind, with a little modern neuroscience.

Jonah Lehrer at the Frontal Cortex explains that Inception is about movie-making and movie-watching by describing similarities in the brain during sleep versus movie-watching.

Over at Mind Hacks, a compelling case is made that Inception borrows more from Jungian psychology than it does from contemporary neuroscience.

And of course, I posted my interpretation of Inception here after I saw the movie a couple of months ago.

Thursday, July 29, 2010

Endocannabinoids and the runner's high

Throughout most of human history, our hunter-gatherer ancestors had to engage in physical activity to obtain food. But nowadays we can drive to the supermarket, briefly walk through its aisles, check-out, then drive back home. This may seem like a luxury, but evolution hasn’t prepared us for such a drastic shift in behaviour.

A possible explanation for the “runner’s high,” a feeling of intense euphoria associated with going on a long run, is that our brains are stuck thinking that lots of exercise should be accompanied by a reward. Perhaps our ancestors who were able to achieve the runner’s high while hunting for food ran more often than those who could not achieve the high. These ‘high-achievers’ (no pun intended) would gather more food as a result of their enhanced motivation, and would be more fit to pass on their genes to the next generation.

Anecdotal reports of the runner’s high often come from endurance runners. However, there has been little scientific study of the runner’s high, so it is difficult to speculate about its role or mechanism. The traditional, widely-publicized explanation for the runner’s high is an “endorphin rush” that inhibits pain during vigorous exercise. However, other chemicals that potentially contribute to the high are epinephrine, serotonin, dopamine and endocannabinoids.

In a study recently published in Experimental Neurology, investigators deleted the gene for the cannabinoid receptor CB1 in mice, and examined how this change to the endocannabinoid system affects voluntary running. The mice with CB1 deletions exhibited 30-40% less running activity than mice that did not get deletions. The knockout mice also had reduced hippocampal neurogenesis, or neuron birth that is known to be induced by exercise, but they were able to increase neurogenesis at a regular rate when they exercised.

These findings indicate that the endocannabinoid system is somehow involved in the regulation of voluntary running activity. In particular, a reduction in CB1 levels could lead to less binding of endocannabinoids to receptors in brain circuits that drive motivation to exercise. It appears that the endocannabinoid system does not play a major role in controlling neurogenesis caused by exercise.

It is easy to point to endocannabinoids as a candidate mediator of the runner’s high, since endocannabinoids are the body’s natural tetrahydrocannabinol (THC), the psychoactive ingredient of marijuana. The study described here doesn’t directly speak much to this proposed parallel, but if the motivation to exercise is considered to be related to the runner’s high, then endocannabinoids may be a driving factor to achieve the runner’s high.

Physical activity has been associated with obtaining rewards throughout evolution. Today we might be left with a certain high associated with the prospect of obtaining a reward – a motivational high mediated by endocannabinoids. This ‘pre-runner’s high’ is an anticipation of the runner’s high, so the two experiences cannot necessarily be thought of as separate. That is – of course – assuming that the runner’s high happened often enough in history that our brains continue to develop to anticipate it. But even if the runner’s high was not common throughout our past, the peaceful feeling that almost everyone experiences after an exhausting run or bike ride should be adequate motivation to start moving.

Endocannabinoids have previously been shown to increase in blood levels after exercise, so there is still a possibility that endocannabinoids mediate the runner’s high. It is most likely, however, that many chemicals converge on brain circuits that underlie the experience. Given the newly discovered role of endocannabinoids in motivation for exercise, it would be unsurprising if endocannabinoids played an important part in directly inducing the runner’s high.

So kids out there: don’t smoke weed if you wish to activate your CB1 receptors. Run.

References:

Dubreucq S, Koehl M, Abrous DN, Marsicano G, & Chaouloff F (2010). CB1 receptor deficiency decreases wheel-running activity: consequences on emotional behaviours and hippocampal neurogenesis. Experimental neurology, 224 (1), 106-13 PMID: 20138171

Fuss J, & Gass P (2010). Endocannabinoids and voluntary activity in mice: runner's high and long-term consequences in emotional behaviors. Experimental neurology, 224 (1), 103-5 PMID: 20353785