Monthly Archives: July 2016

Intuitively, the idea of “growing” sounds great.

It’s become synonymous with making something bigger, better, or more mature. We’re inundated with messages to grow our wealth, grow our networks, grow our following;it was just a matter of time before people started promoting strategies to grow our brains, too.

But before we start loading up on smart pills and brain games, we have to ask: Can we really grow our brains? And more importantly, why would we want to?

One reason may be that we feel empowered by the potential to make a lasting physical mark on our brains through our beliefs, behaviors, and experiences. By thinking that we’ve changed our neural architecture, we may feel like our effort has been more meaningful or real. (This article from the Greater Good Institute makes this argument explicitly.)

However, the “you can grow your brain” slogan hugely oversimplifies what we know about brain development and learning. Although it is based in truth, the brain actually changes in ways that are more subtle and fascinating than sheer growth.

What does the slogan “You can grow your brain” ultimately get right, and where does it miss the mark?

What it gets right: The brain is plastic 

The brain is remarkably flexible and continues to change in response to the environment throughout the lifespan.

Because networks in the brain generally become more specialized with age,¹ the brain has the greatest neuroplasticity, or ability to change, in childhood.² The brain is so flexible that people who have half of their brains removed (hemispherectomy) in childhood as treatment for severe epilepsy can, in many cases, go on to live fairly normal lives. (Check out this work on two fascinating case studies!)

One mechanism for neuroplasticity in adulthood is the birth of new neurons, called neurogenesis, in a part of the hippocampus. Though neurogenesis was once thought to be impossible past childhood, scientists now generally agree that these new neurons give brains a chance to become more fine-tuned to the environment throughout our entire lives.³ However, some research challenges the notion that there are enough new brain cells to explain changes in how adults think and behave.⁴

A well-known study demonstrating neuroplasticity in adults found that, compared to people in other occupations, on average London taxicab drivers had bigger posterior (closer to the back of the head) hippocampi.⁵ Here, volume is thought to be a proxy for the number of cells. The posterior hippocampus is associated with spatial navigation, and London taxicab drivers exercise this skill extensively, typically spending years learning the city streets before taking a challenging examination. On average, the longer people had spent as taxi drivers, the bigger their posterior hippocampi.

However, this particular study didn’t establish that more taxi driving experience causes brain growth—it was only correlational. Another plausible explanation of the findings is that people who choose to become taxi drivers and stay in the job for the long run have bigger posterior hippocampi and superior spatial navigation.

What it gets wrong: Bigger isn’t always the goal

What’s often overlooked about the London taxicab driver study is that, relative to the control group, the taxicab drivers actually had smaller anterior hippocampal volume (the part of the hippocampus closest to the front of the head).⁵ The idea that taxicab drivers sprouted a bigger overall hippocampus through practice isn’t quite right.

One fuller possible explanation of the findings is that hippocampus was re-organized with greater specialization for spatial navigation. Although this finding still demonstrates neuroplasticity, simplifying the story to “the brain grew!” paints an incomplete picture of brain development… and its goals.

In the broad scheme of things, is a bigger brain a better brain?

Bigger brains relative to body size have been correlated with more intelligent species, and among humans overall brain size is moderately correlated with IQ.⁶ However, this pattern is weak enough that you can’t necessarily tell any individual’s intelligence from their overall brain size. Albert Einstein, for instance, was known to have a pretty average-sized brain!

The answer also depends on the part of the brain in question. Life circumstances associated with early neglect such as being raised in an orphanage⁷ or having a mother with depressive symptoms⁸ are associated with larger amygdala volume. The amygdala is a part of the brain thought to be critical for processing fear, and in the orphanage study, greater amygdala volume was correlated with symptoms of anxiety and depression.⁷

Sheer growth simply isn’t a good way to describe the developing brain. The cortex thins out over the course of typical development into adulthood, and how fast it thins is correlated with intelligence.⁹ The cortex is the outermost layer of the brain, and is crucial for cognitive functions like language, memory, and consciousness. Cortical grey matter volume, which is made of the bodies of brain cells, peaks in childhood and decreases in adolescence to a stable point in the 20s.¹⁰ On the other hand, white matter increases steadily during adolescence.¹¹ White matter is named for the fatty “blankets” around neural fibers that improve the efficiency of their communication.* 

Finally, there may important reasons as to why the brain loses brain cells, drops certain neural connections, and becomes less flexible. Important messages may be more effective with fewer competing signals, and excessive neurogenesis could make the brain a noisier, less efficient system.

The developing brain becomes more refined

A more sophisticated way to think about brain development emphasizes refinement over growth. As my colleague Kate Mills has written previously, when it comes to brains, more connections aren’t necessarily better. It may be important that some connections are lost so that others are strengthened.

Which connections are strengthened are likely influenced by experience. Here are a few other ways that the brain changes that paint a more sophisticated picture than sheer growth—and this list is far from complete!

• Improving connections between brain regions (myelination): Laying down myelin makes connections between different neural regions more efficient, which means communication between cells can happen faster. One white matter tract (a.k.a. a group of myelinated neural fibers) called the arcuate fasciculus connects regions of the brain involved in language, and the myelin content in a part of this tract is associated with better word learning.¹² Learning to read, even as an adult, is associated with changes in the arcuate fasciculus.¹³
• Changing the structure of brain cells (dendritic spine density and arborization): Dendrites are a part of brain cells that primarily receive messages from other neurons at small protrusions called spines. Increases in the density of spines and the complexity in their organization (akin to a tree with more complex branching) have been found in adult primates after spending a month in a more complex/“enriched” environment.¹⁴In this sense, growing is important – it’s just about highly organized growthon a really tiny scale, rather than overall brain
• Changing how neurons’ genes are read (epigenetics): Epigenetics involves changes related to how DNA is read, rather than changes to the genome itself. If each cell’s DNA is a book, epigenetics is like going through and highlighting or blacking out certain lines without changing the underlying text. Though merely “surface” changes, epigenetics may explain one way that early parental neglect harms children in the long run. Glucocorticoid receptors are important proteins that, in the hippocampus, are thought to help the body regulate its stress response. In rats, poorer maternal care has been linked to more genes for this protein being set to “off,” leading to a distorted stress response.¹⁵ And there’s evidence that a similar chain of events may occur in humans who have experienced child abuse.¹⁶

The bottom line

The idea that you can grow your brain is catchy and persistent. Pop culture is filled with the smartest characters having “big brains”, sometimes literally. However, I’ve argued here that it’s not the best or even the most interesting way to describe how the brain changes with experience or development.

In most cases, when we talk about growing the brain, we actually have other goals in mind, such as becoming better learners or maintaining healthy cognitive functioning in aging. Clarifying these goals and using strategies to reach them will change the brain along the way, but growing the brain isn’t typically a goal unto itself.

On the other hand, is it harmful to think about “growing your brain” if it’s something that your or your students find motivating? In my next post, I’ll explore this by taking a critical look at how the idea that you can grow your brain has been used in pop psychology and neuroscience, such as in growth mindset.

References & Further Reading

1. Dosenbach, N. U. F., Nardos, B., Cohen, A. L., Fair, D.A., Power, D., Church, J.A, … Schlaggar, B. L. (2011). Prediction of Individual Brain Maturity Using fMRI. Science, 329(5997), 1358–1361. [Paper]
2. Center on the Developing Child at Harvard University (2016). From Best Practices to Breakthrough Impacts: A Science-Based Approach to Building a More Promising Future for Young Children and Families. [Link]
3. Opendak, M., & Gould, E. (2015). Adult neurogenesis: a substrate for experience-dependent change.Trends in Cognitive Sciences,19(3), 151–161. [Paper]
4. (2016). The Myth of Human Adult Neurogenesis? [Blog]
5. Maguire, E. A., Gadian, D. G., Johnsrude, I. S., Good, C. D., Ashburner, J., Frackowiak, R. S. J., & Frith, C. D. (2000). Navigation-related structural change in the hippocampi of taxi drivers, 97(8). [Paper]
6. McDaniel, M. A. (2005). Big-brained people are smarter: A meta-analysis of the relationship between in vivo brain volume and intelligence.Intelligence, 33(4), 337–346. [Paper]
7. Tottenham, N., Hare, T. A., Quinn, B. T., McCarry, T. W., Nurse, M., Gilhooly, T., … Casey, B. J. (2010). Prolonged institutional rearing is associated with atypically large amygdala volume and difficulties in emotion regulation.Developmental Science, 13(1), 46–61. [Paper]
8. Lupien, S. J., Parent, S., Evans, A. C., Tremblay, R. E., Zelazo, P. D., Corbo, V., … Séguin, J. R. (2011). Larger amygdala but no change in hippocampal volume in 10-year-old children exposed to maternal depressive symptomatology since birth.Proceedings of the National Academy of Sciences, 108(34), 14324–14329. [Paper]
9. Shaw, P., Greenstein, D., Lerch, J., Clasen, L., Lenroot, R., Gogtay, N., … Giedd, J. (2006). Intellectual ability and cortical development in children and adolescents.Nature, 440(7084), 676–679. [Paper]
10. Huttenlocher, P. R., & Dabholkar, A. S. (1997). Regional differences in synaptogenesis in human cerebral cortex.The Journal of Comparative Neurology,387(2), 167–178. [Paper]
11. Mills, K. L., & Tamnes, C. K. (2014). Methods and considerations for longitudinal structural brain imaging analysis across development.Developmental Cognitive Neuroscience,9, 172–190. [Paper]
12. López-Barroso, D., Catani, M., Ripollés, P., Dell’Acqua, F., Rodríguez-Fornells, A., & Diego-Balaguer, R. de. (2013). Word learning is mediated by the left arcuate fasciculus.Proceedings of the National Academy of Sciences,110(32), 13168–13173. [Paper]
13. Schotten, M. T. de, Cohen, L., Amemiya, E., Braga, L. W., & Dehaene, S. (2014). Learning to Read Improves the Structure of the Arcuate Fasciculus.Cerebral Cortex,24(4), 989–995. [Paper]
14. Kozorovitskiy, Y., Gross, C. G., Kopil, C., Battaglia, L., McBreen, M., Stranahan, A. M., & Gould, E. (2005). Experience Induces Structural and Biochemical Changes in the Adult Primate Brain.Proceedings of the National Academy of Sciences of the United States of America,102(48), 17478–17482. [Paper]
15. Weaver, I.C.G., Cervoni, N., Champagne, F. A., D’Alessio, A. C., Sharma, S., Seckl, J. R., Dymov, G., Szyf, M., Meaney, M. J. (2004). Epigenetic programming by maternal behavior.Nature Neuroscience,7(8), 847–854. [Paper]
16. McGowan, P. O., Sasaki, A., D’Alessio, A. C., Dymov, S., Labonte, B., Szyf, M., … Meaney, M. J. (2009). Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse.Nature Neuroscience,12(3), 342+. [Paper]

• Immordino-Yang, M. H. (2007). A Tale of Two Cases: Lessons for Education From the Study of Two Boys Living With Half Their Brains. Mind, Brain, and Education, 1(2), 66–83. [Paper]
• Blakemore, S.J., Frith, U. (2005).The Learning Brain: Lessons for Education. Wiley-Blackwell. [Link]
• Horowitz, A. (2013). Why Brain Size Doesn’t Correlate with Intelligence. Smithsonian Magazine. [Link]

* Some information here is presented in more detail in other Learning & the Brain posts

• Mills, K.L. (2015). 3 Things Neuroscience Teaches Us About the Changing “Teenage Brain.” Learning & the Brain Blog [Link]
• Mills, K.L. (2015). The New Understanding of IQ. Learning & the Brain Blog [Link]

As an optometrist-scientist and Associate Professor of Ophthalmology at Harvard Medical School, Dr. Lotfi Merabet is passionate about investigating the complex relationship between visual impairment (including blindness) and the brain. Most recently, as director of the Laboratory for Visual Neuroplasticity, Dr. Merabet has been on the frontlines of neuroscientific research on congenital cerebral/cortical visual impairment, or CVI. CVI is a prominent condition in children born prematurely and is caused by brain damage during early development to the visual pathways and structures of the brain. Although CVI has yet to receive much attention in the media and popular press, it nonetheless affects an increasing number of children in the United States, who are often unable to obtain the care and resources they need to thrive in today’s medical, rehabilitation and education systems. I had the privilege of sitting down with Dr. Merabet to discuss his perspective on what educators should know about CVI and what they can do to improve the lives of the growing number of children living with this condition.  

For an overview on the impact of premature birth on education, see a previous Learning & the Brain article of mine here.

Hirsch: Can you tell us a little about CVI, what spurred your interest in studying this disorder and why it’s important for people to gain awareness about it?

Merabet: So right away I can give you some numbers. Cortical Visual Impairment (CVI) affects nearly 2 out of every 1000 live births and accounts for nearly 25% of visually impaired children in developed countries including the US. CVI is now the leading cause of congenital visual impairment in the developing world. So the important thing to keep in mind here is that this is developed countries, not developing countries. Prenatal care and medical technology are getting better and better, so what we’re seeing is a byproduct of this progress. So babies who were not surviving thirty, forty years ago are now surviving better, surviving longer, but now living with many sensory and motor problems: this is what these kids represent. Given this profile change in children with this kind of damage, education and rehab strategies need to evolve to account for this.

Typically, in the past, children who went to schools for the blind had problems with their eyes and typically everything else was fine. What we’re finding now more and more is that children who go to these schools have multiple disabilities as well as hearing, speech or sensory motor issues; but at the same time there is the issue of children who have problems with their vision not because of specific disease with their eyes but rather due to damage to their brain. As you might imagine, these individuals are very different in profile than individuals who have problems with their eyes. What spurred my interest in this disorder was not only the large number of these individuals, but also the observation that the strategies used to teach these children who are normally blind because of damage to their eyes (e.g. teaching them how to read braille or how to use a cane) were not effective or very difficult to learn in the kids who have CVI.

I think that this is an important aspect not only from a society standpoint but also from the educational standpoint as well, because two children who may have similar levels of profound visual impairment may be completely different given the site of damage to their visual processing areas of the brain. 

Hirsch: What are the main issues experienced by kids living with CVI?

Merabet: Visual impairments in CVI can be very broad However, you can break this down on multiple levels. The first level is what’s referred to as “visual acuity” which is a measure of how well you can see small detail. On a second level, what we typically see in these children is referred to as “visual field restriction”, typically in the loser visual field area. This means that these kids will typically fall over or trip over things and this is a result of damage to pathways to the visual brain. The third thing that we see really can’t be explained by problems with the eyes alone and this has to do with visual processing in the brain. So for example, they will talk about not being able to find their favorite toy in a box of toys or find their friends or family members in a crowded room. When there’s a lot of action, they tend to get overwhelmed and have a very hard time following that action. They can get very distracted and also may have a hard time staying focused.

This speaks to the ability of how the brain is able to process and put together complex visual information. So depending on where the damage happens in the brain, this will lead to the various perceptual deficits. This is what makes this condition so challenging; not only for the child, but also for the families, and ultimately the educators who see undiagnosed kids in the classroom.

Hirsch: What do you think are the main issues for the families of these kids?

Merabet: One major problem is that families just don’t know how to find a doctor or provider who recognizes this condition. Again, because this damage is typically associated within the brain and not the eyes, very often they go see their family eye doctor who will look at the eyes and not notice anything out of the ordinary or fits with the child’s visual problems. As a result, these doctors might start assuming that these visual problems stem from psychiatric issues or developmental delays without taking into consideration that there’s actually something specifically wrong with their visual system. So this is a big cause of frustration from the family’s standpoint.

To make matters worse, a child with CVI and who has a visual acuity of say 20/60 (in other words, very blurry vision but still able to recognize large objects) may not qualify for benefits under the strict guidelines that define blindness, but yet clearly the same child has visual problems and could benefit from services.

So the fact that we live in a world that defines blindness based on acuity makes this very challenging because there are clearly individuals who need help but may not qualify based on visual acuity criteria. The last thing I would say is because this is a relatively new diagnosis; there aren’t any standardized strategies out there to help these kids. As a result, many families are left searching for answers on their own (e.g. online). Based on what they read, they try to forge their own strategies and plans and that makes it also very challenging because there’s no real clear consensus or dialogue regarding what needs to be done.

We need to change the way that we define visual impairment so that kids with these types of conditions can get access to the help they need.

Hirsch: Is it important for educators who don’t work with disabled kids to know about CVI? Given the high prevalence of CVI, teachers might play an important role because many kids might not get adequate recognition until they start in the classroom.

Merabet: That’s exactly right, I think educators need to be alert to this condition. For instance, if a child isn’t doing well in school, it makes sense to understand whether there is a visual or perceptual problem (not be quick to jump on necessarily behavioral or psychosocial issues), but this is not often the case. You could think of situations like dyslexia in the past or other developmental/learning issues that needed to be identified so that the child could get put on the education path best for them.

The issue with CVI is very much the same. To complicate matters, just because the child goes to see the family eye doctor and doesn’t see anything wrong with the eyes, doesn’t mean necessarily that there isn’t something wrong with the way the child sees the world.

So I stress upon this in terms of educators because very often they could be the first advocate for these kids. They spend a lot of time in class and they see when the child is having difficulties in specific situations versus others. As a result, they are in a very prime situation to not only recognize this and detect this but also be their advocate.

Hirsch: What do you think that people in the field of education can do to facilitate the implementation of these more scientific findings into schools?

Merabet: I would say the first and foremost there has to be awareness on behalf of teachers that this could very well be a child in their class. At the same time, they should not be quick to jump to conclusions about a child’s difficulties, which might be related to something completely unrelated to the actual inherent visual problem.

Secondly, I would say it is important to work closely with the family and whatever providers they’re working with when it comes to implementing strategies they find works for that child. Every case is unique but it might be something like the lighting in the room, or the size of letters on a blackboard, or more generally the speed and modality by which information is presented to them in the classroom. Some children, for example, are much better learners via multiple sensory inputs, such as a combination of tactile, visual and auditory input. Obviously, this is still a big challenge right now but I think that’s ultimately how this can be done. It all starts off with recognizing that this could be the situation and understanding i) who the child is, ii) what they’re going through and iii) how to adopt curriculum and strategies that are best for their needs.

Hirsch: What would you advise the teacher to do if s/he is faced with a child suspected of having CVI?

Merabet: Like I mentioned previously every child is different, however there are things that you can consider to facilitate learning and well-being. For example, in addition to room lighting, clutter in the visual environment is also extremely important: there might be ways to simplify the visual environment so that it’s not distracting for the child allowing them to follow along more easily. A second thing that’s very important is patience, because we know mental and cognitive processing can be slower for these children. This is not to say that this is always the case but sometimes the visual confusion and “crowding” (a phenomenon in which objects easily recognized in isolation are rendered unrecognizable in clutter) means that it takes more time for the same cognitive processes to happen.

How to reconcile these accommodations with the pace of a normal curriculum continues to be a challenge, but I think it starts off with the awareness and with knowing what types of workarounds are available. Knowing what applies to that child and finally coming up with a game plan whereby the teacher finds a way to integrate the child with the rest of a class as much as possible.

Hirsch: What do you think the implications are for education policy from a systems perspective? What role can science play?

Merabet: I think first and foremost it starts off with a thorough characterization of the visual deficits that these children have, from the ground up. In other words, is it largely an acuity or visual field issue, or is it mostly perceptual? And so on. Having an understanding of what those deficits are is really the most important of doing this in a comprehensive fashion. As an eye doctor myself, I can tell you that what we do during a standard eye exam will not always reveal these deficits. So first and foremost it involves the family going to an eye care professional who can spend the time and evaluate those aspects thoroughly. It also entails working closely with an educator who has a specialty in learning disabilities who understands how things in the developmental trajectory might be different and can go through the proper educational evaluation of that individual.

So from the very start, it starts with proper recognition, proper diagnosis, and proper characterization of deficits. I think science can help in that regard by standardizing and developing appropriate batteries of tests that can be quantified and that are robust and at the same time can be transferred to other settings as well, so we can get a handle on how these deficits manifest throughout the country. The second piece is trying to correlate brain damage with visual deficits and hopefully turning that into some sort of prognostic value.

The last role we all have to play, whether we’re educators, neuroscientists, or doctors is to become advocates for these individuals, because ultimately we’re the ones who work with them in multiple settings. In other words, along with their families, educators and scientists must work together to advocate for these kids in terms of what they need. For example, how do we change legislation so that receiving benefits is not limited to visual acuity levels? This is the type of question we need to be asking so that kids who need help get the help that they need and deserve.

Hirsch: Let’s say an educator is reading this interview. What advice would you give them to get involved and be more proactive and helping kids with these kinds of disabilities?

Merabet: Well, it always starts with awareness and I would also say an important thing is dispelling myths. One thing that is important to realize is that kids with CVI don’t “look” blind; they don’t look like your typical blind child in terms of their mannerisms, their gestures and other things like that. This brings us back to the situation like dyslexia whereby the disability may not be immediately obvious off the bat. In terms of visual impairment, what’s important to realize is that that visual impairment means many things, many profiles and many possibilities. For instance, this condition doesn’t just occur independently but can occur co-morbidly with other disorders such as Autistic Spectrum Disorder (ASD), Cerebral Palsy (CP) or Epilepsy. Anything that affects brain development will ultimately affect the development of that child.

Finally, we need to distinguish what we know from what we don’t know, particularly when it comes to dispelling myths about disabilities. We have this idea that people with disabilities can’t “do” things and that has to change from a cultural standpoint. In the end, the brain changes, the brain learns, the brain develops and the brain rewires. So, what can we do to promote that? What can we do to put the child on a path to maximize that developmental potential as much as possible? I think it behooves us to want to try to understand that and try to figure that out.

Since we are talking about something that happens early in life, there’s still a lifetime ahead of these children. My argument is that if we understand what the deficits are, and we work with the families, the doctors and educators, we can design appropriate strategies so that these children can thrive and ultimately become the people that they can, and want, to be.

Further information:

• The Laboratory for Visual Neuroplasticity website: http://scholar.harvard.edu/merabetlab
• CVI Neuroplasticity Research Group Facebook Page: https://www.facebook.com/CVI.Neuroplasticity