Archive for January, 2014

Cool infographic on neuroplasticity

Friday, January 31st, 2014

Here’s a neat infographic from, with tons of interesting factoids about the brain, and about the effects of traumatic brain injury.


The most studied man in the history of neuroscience

Wednesday, January 29th, 2014

This is pretty cool. A team has recently done a detailed study of the brain of patient H. M., and performed analyses on what is undoubtedly the most famous brain in the world. The study was published yesterday in the journal Nature Communications, here.

H. M. was the only name by which brain science and psychology students around the world knew Henry G. Molaison, who became the most-cited and most interesting case study in the history of neuroscience. As the authors review in their article, Henry had severe epilepsy from age 10 onward, which led eventually to his undergoing surgery at age 27 at the hands of neurosurgeon William Beecher Scoville. In cases of severe epilepsy that can’t be controlled with medication, surgery to remove the parts of the brain that initiate the seizures is not uncommon. Scoville drilled two holes in Henry’s forehead, and through them he cut off and removed fairly large segments from the middle part of each of Henry’s temporal lobes. The parts of Henry’s brain that were removed are shown in the following photograph, taken from underneath, looking up at the bottom of his brain:

You can see (or maybe you can’t! So take my word for it) that he lost the tip and much of the medial (middle-most) portion of each of his temporal lobes. There’s also a little injury on the bottom of his left frontal lobe, probably incurred when the surgeon pried up the frontal lobes so he could get in underneath them with his instruments.

Now, the reason H. M. became famous was what happened after the surgery. It became quickly apparent that, after his operation, Henry lived in a perpetual present. He was unable to store new memories of things that had happened, or of any sort of factual information. That means someone could walk into his room and introduce herself, walk out, and return a few minutes later, and Henry would have no knowledge of ever having seen her before. Henry had no knowedge that his personal story had continued beyond the day of his surgery in 1953, because he remembered nothing of what had happened since then. His memory for everything up to the day of his surgery remained completely intact, and his IQ remained above-average, meaning that all his reasoning, perceptual and language abilities were completely unaffected. He performed normally on nearly every neuropsychological test, but he was unable to remember anything for longer than he could actively rehearse it in his mind. Fascinatingly, Henry was also able to acquire new motor or perceptual skills (skill knowledge is called procedural knowledge), but was unable to account for where he had come by them (declarative knowledge). In addition to that, the post-surgery Henry seemed emotionally flat, unrepsonsive, and lacking in initiative compared to his pre-surgery self.

Henry died in 2008, 55 years after his surgery. The authors of the Nature study were able to examine his brain in close detail, and they sliced it into thin layers so that it could be available for researchers to study. What the authors determined was that Henry had lost his temporal poles, his amygdalae on both sides, and the front half of each of his two hippocampi (that’s plural for hippocampus, which is Greek for “sea-horse”). That part is interesting, because it had been previously assumed that his hippocampi had been completely destroyed, and the entire field up to this day has been focused on the hippocampus as the critical structure for the formation of new memories. Nevertheless, a lot of the connections on the way in and out of the remaining portions of the hippocampus were severed, so they may have been unable to do their job properly.

The study may raise some questions about whether the hippocampus is as exclusively responsible for the formation of new memories as had previously been thought. But what fascinates me about H. M.’s story is that it is a limiting case for human narrative and human identity. We all identify ourselves by our story: where we came from, what has happened to us, whom we’ve known and loved. But Henry’s story stopped abruptly when he was 27, while his biological life continued for an incredible 50 more years. What would it have been like to be Henry? To wake up every day and have no knowledge that the day before had even happened? To see people come and go from your presence, each one a complete stranger, although they may insist they’ve known you for years? Maybe to have flickers of response to people or situations, based on past experiences, register deep in your gut, but not to recognise them as such, or to have any idea where they’d come from? Is a person’s story still his story if he himself doesn’t even know it? Do we go deeper than our own consciousness of ourselves, of our experiences?

Neurodevelopmental impact of poverty

Monday, January 20th, 2014

Just read an interesting study, published last month in the journal PLOS One. The study’s authors are Jamie Hanson, Nicole Hair, Dinggang Shen, John Gilmore, Barbara Wolfe, and Seth Pollak. You can read it online here. They measured the rates of brain growth, and the total amount of brain growth, in children between infancy and age four. To do this they used Magnetic Resonance Imaging (MRI), a technique that is able to image the brain with a high degree of resolution, and to distinguish grey matter (where most of the connections are, the brain’s cortex) from white matter (fibre tracts connecting grey matter regions to other areas).

What the authors found was that children from lower-income households (below the income representing twice the poverty-line amount) had less grey matter in the frontal and parietal lobes than children with middle and high income. Moreover, the rate of growth in these areas was slower in poorer children. The interpretation the authors gave was that poverty leads to impaired brain development. This is certainly consistent with animal studies showing that animals who are well fed and raised in a nurturing and stimulating environment have different brains from those raised in a more sparse environment, or one lacking in nurture. All the children in the study started out in infancy with brains that were the same size, which suggests that it really was their exposure to poverty that caused the differences in brain development to emerge over time. The authors also found that children with less grey matter in the frontal cortex were more likely to have disruptive behavior problems such as hyperactivity, impulsivity, or explosive anger.

It’s suggestive, anyway; these studies always have difficulty demonstrating that one variable really caused the other one, as opposed to merely being correlated with it.  To really nail down the effect would require having some children start out in poor socioeconomic conditions, then have a change in fortune, such as being supported with income supplements or adopted out into a more well-off family. But, like I said, there’s plausibility to it in light of the animal literature.

If turned out to be true that poverty negatively impacts brain development, then there would be a lot of social implications. Being raised poor would be not only a social disadvantage, it would also be a neurodevelopmental disadvantage, reducing the likelihood that raised-poor children would succeed in school and increasing their chances of getting into trouble later in life, all of which would sow the seeds for more economic problems in the next generation. Children’s parents need good jobs and basic human dignity, so they can provide a good environment for their little ones. And let’s not have any talk of “child poverty”, a meaningless phrase if ever there was one. Children are poor because their parents are poor, and we do them no favours by artificially carving the natural unit of the family up into little bits and creating fictitious entities out of the individual members.

Fascinatin’ rhythm: fundamental to brain function

Saturday, January 4th, 2014

I just read a fascinating paper by György Buzsáki, Nikos Logothetis, and Wolf Singer, published a couple of months ago in the journal Neuron. In it the authors present evidence that across many different mammalian species, from mice to humans to blue whales, patterns of oscillating (rhythmic) activity in the brain remain remarkably constant — despite huge changes in the size and complexity of the different species’ brains. Take a look a this figure from their paper:

From Buzsaki, Logothetis, and Singer (2013). Scaling brain size, keeping timing: Evolutionary preservation of brain rhythms. Neuron, 80, pp. 751-764

Notice how remarkably similar the waveforms look from one species to the next. The second part of the figure shows just how little the frequency (how many cycles per second) of the various EEG waves changes as one moves from mice, through lower mammals and primates, to the much larger brains of humans — this is depicted by the more or less flat lines on the figure.

Now, maintaining these timing characteristics was no simple matter as brains got bigger: because neurons move information at a finite (and really not very fast) rate, that means making distances in brains bigger was bound to screw up their timing. For example, the authors point out that for a mouse to get its two hemispheres to oscillate together in the gamma frequency (about 40 cycles per second) requires the information to move between five and ten millimetres, which means that the information would have to move at about five metres per second. For a human brain to do the same thing, the information would have to travel 70 to 140 millimetres, which means that in order to arrive at the same time (necessary for preserving the 40-Hz rhythm) it would have to travel 14 times faster. Thus, as brains grew during evolution, they had to develop some fancy ways of getting information over long distances without sacrificing any speed. (If you’re curious, they’re believed to have done so by increasing the width of fibres and modifying the fatty sheath around the fibres, called myelin, among other modifications.)

The authors suggest — and I think they’re right — that this makes a strong case for the principle that oscillatory timing is fundamental to the operation of brains, so much so that evolutionary development went to great lengths to preserve this timing, more or less unchanged, across hugely diverse species and aeons of time.

The way brain activity oscillates is going to turn out to be critical to understanding how brains work, and potentially to understanding why they don’t work well in cases of neurological or psychiatric illness.