Caveat lector: This blog is where I try out new ideas. I will often be wrong, but that's the point.

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Hey. Sup?

So my last post drew a lot of new readers.

Because there are so many new people here, I'd like to play a couple of games.


The first I learned from Ed Yong:

1. Who are you?! Please leave a comment and tell me who you are and what your interest is in neuroscience (which is, I presume, why you're here). If you're a neuroscience student, tell me what you're studying!

The second is a game I first played on twitter a few months ago.

2. Ask me any neuro question and I'll try to answer it.

That one was fun, but it can take a while, since I try to support my answers with actual research. So bear with me!

For some reason my last post got passed around the internet a lot... with a strange phrase added to it in some places: "our senses would amaze us, if only we gave them our full attention, as animals do," which sounds a little... fluffy. I certainly didn't say that.

If you're expecting a blog by someone who would write something like that, I'm sorry to say you might be disappointed.

I tend to be a pretty hard skeptic. Especially so for neuroscience and my own work. Which isn't to say I don't sometimes do or say weird things. I just don't say weird things that sound like that.

Now I'd like to introduce myself a bit: I'm a neuroscience post-doc working at the University of California, Berkeley. In a few months I'm headed over to UCSF. This blog started as a way to write more openly about my own research and to share some of the analysis code I've written and projects I'm running.

For example, I run brainSCANr with my wife, Jessica Voytek, which is an experiment wherein we're quantifying connections between concepts in the neuroscience literature.
Bradley Voytek brainSCANr

I'm also kinda known as the zombie neuroscience guy because of some of my public lecturing. But don't let that fool you. It's mainly a subversive way for me goof off while also trying to be more critical about neuroscience. This is a tough field, the problems we think about are difficult, and the media plays a strange role in feeding into some weird neuroscience myths.

To share some of my favorite posts, I'd like to point out "how to be a [critical] neuroscientist", which discusses how I do my first-pass read on cognitive neuroscience research, as well as "scientific acupuncture", which looks at media reporting on neuroscience.

There's also my general take on the whole media doc phenomenon:
(Click to enlarge)

I'm also partial to neuroscience history, because there are so many amazingly weird people involved. Check out "Sir Henry Head's self experimentation" or "Brown-Séquard, spinal cord research, and sperm injections".

Finally, the vanity part. I do talk about my own research. But the biggest motivation isn't vainglory, I swear. I'm a huge believer in the idea that, if I can't explain my research in a simple manner, it's because I don't actually know what I'm talking about. It's very easy to trick myself into believing that my over-education has taught me something, only to find that when I try to explain an idea simply all I'm actually doing is parroting back phrases that don't really mean anything.

So to avoid boring all my friends at the pub all the time, I use this blog to work out ideas. Here are my research posts:

Bradley Voytek Journal of Cognitive Neuroscience Giffords Hemicraniectomy



We are all inattentive superheroes

One of the more interesting parts about being a neuroscientist is when I'm suddenly struck by how absolutely weird our brains are.

And I'm not even talking about the super trippy stuff like free-will; even the mundane things are really mind-boggling.

For example: what does it mean to experience the world around us? We "see" things because photons that manage to pass through the inside-out design of our retinal cells cause a molecular change in the photoreceptors such that 11-cis-retinal isomerizes... etc.

(Tons of way overly detailed biology cut from here...)

When we "hear" things, the sound pressure waveform hits the tympanic membrane (eardrum) and ultimately causes the basilar membrane in your cochlea to vibrate. The basilar membrane is stiffer at one end (the basal end) and less stiff at the other end (the apical end). This fact was observed by Georg von Békésy (and earned him the 1961 Nobel Prize in Physiology or Medicine).

Here's a gratuitous, yet cool, video of this frequency decomposition in action:

Okay, great, so we know a ton of the basic biology and cellular mechanisms of the signal transduction mechanisms of our sensory apparatus.

But damn if I'm still not amazed by the actual experience of sensation.

Even beyond the philosophical wonder of passively sampling our outside environment in a shared, meaningful fashion is the ridiculous sensitivity of our senses.

We're used to thinking of our senses as being pretty shite: we can't see as well as eagles, we can't hear as well as bats, and we can't smell as well as dogs.

Or so we're used to thinking.

It turns out that humans can, in fact, detect as few as 2 photons entering the retina. Two. As in, one-plus-one.

It is often said that, under ideal conditions, a young, healthy person can see a candle flame from 30 miles away. That's like being able to see a candle in Times Square from Stamford, Connecticut. Or seeing a candle in Candlestick Park from Napa Valley.

Similarly, it appears that the limits to our threshold of hearing may actually be Brownian motion. That means that we can almost hear the random movements of atoms.

We can also smell as few as 30 molecules of certain substances.

I mean, we're talking serious Daredevil-level detection here!

(Frank Miller. Daredevil(c) Marvel Comics via Drawing Files)

These facts suggest that we all have some level of what we'd normally think of as "super human" sensory abilities already.

But what the hell? If I can supposedly see a candle from 30 miles away, why do I still crack my frakkin' shin on the coffee table when it's only slightly dark in my living room?

Well, for one thing, attention plays a very important role. For example, consider the very famous visual attention experiment below:

How can we see TWO PHOTONS, but miss THAT!?

The easy hypothesis? Attention.

You see, in the experiments testing the physical limits of the human sensory systems, the subjects involved are dedicating a lot of attention to the one sense being tested, almost certainly at the exclusion of the other senses.

I think we all have a pretty intuitive grasp of this. And sometimes our intuitive corrections are pretty damn funny. If you watch people's behavior carefully you'll notice some strange behaviors that we do.

Have you ever been driving around, trying to find a particular address, and then turn down the radio as you get close to where you think your destination is? Why would you turn down the radio when what you're doing is looking for an address? Seems pretty silly.

Do you close your eyes when you're trying to do calculations in your head? Why?

I think the answer to these questions is because we're trying to reduce sources of noise to maximize the amount of attention we can pay to the task at hand. The sounds from the radio capture your attention, making it hard to visually search for the address numbers on the house you're trying to find. Visual distractions in our surroundings may prevent us from maximally focusing our attention internally when trying to do hard math problems in our heads.

It strikes me that the experiments on the physical limits of our perception are probably also related to the adage that if you lose one sense, your remaining senses get heightened. This is a pretty common saying, but is it really true that if I became blind that I'd suddenly gain super-human hearing?

In a series of Nature studies published in the 1990s, it was shown that blind subjects reading via Braille actually use their visual cortex when reading by touch. This was demonstrated not only using brain imaging (PET, in this case), but also more causally via disruption of the visual cortex via TMS, a technique that can safely and reversibly disrupt the ability of a small region of the brain to process stimuli.

(See my basic primer on brain imaging techniques for a little more detail.)

When TMS was used to disrupt the visual cortex of blind subjects, their ability to read Braille characters dropped!

Anecdotally, the impressive sensory adaptations by blind people can be seen in two particularly striking subjects.

The first is a blind boy who was able to navigate so well via echolocating his own clicking sounds that he could ride a skateboard.

The second example is of another blind young man who was able to play video games by sound alone. The guy could track the sounds in a game and use them to play through to completion.

(That second story, by the way, would make for an amazing addition to the Serious Games Summit...)

In my own research I've tried to identify which regions of the brain are critical for attention and working memory, to understand how cognitive functions reorganize after brain damage, and to provide a physiological basis for how sensory and cognitive systems could interact.

In my future research I will further examine how sensory and cognitive systems interact and interrelate in more detail.

For now, sometimes the only thing I can do is sit back and marvel at how amazing it is that this three pounds of fat and water in my head does anything at all.
(No matter how much beer I throw at it!)

Bialek, W. (1987). Physical Limits to Sensation and Perception Annual Review of Biophysics and Biophysical Chemistry, 16 (1), 455-478 DOI: 10.1146/annurev.bb.16.060187.002323
Sadato N, Pascual-Leone A, Grafman J, Ibañez V, Deiber MP, Dold G, & Hallett M (1996). Activation of the primary visual cortex by Braille reading in blind subjects. Nature, 380 (6574), 526-8 PMID: 8606771
Cohen LG, Celnik P, Pascual-Leone A, Corwell B, Falz L, Dambrosia J, Honda M, Sadato N, Gerloff C, Catalá MD, & Hallett M (1997). Functional relevance of cross-modal plasticity in blind humans. Nature, 389 (6647), 180-3 PMID: 9296495


Rectal ballon inflation

In my previous neuroscience life I worked as a radioactive urine cleaner at UCLA.

The lab I worked in did some really cool research on the long-term neurological and behavioral effects of methamphetamine abuse. One of the researchers I worked with in that lab, Dr. Berman, was a great guy who had a pretty esoteric research specialty.

A few years ago he published an interesting, unique paper in The Journal of Neuroscience titled "Reduced brainstem inhibition during anticipated pelvic visceral pain correlates with enhanced brain response to the visceral stimulus in women with irritable bowel syndrome".

(CDC website woman indicating bowel discomfort)

Irritable bowel syndrome is an interesting condition which, according to wikipedia and its sources (I know... lazy me), has no clear organic cause, but definitely has a physical effect on sufferers. As Berman et al. say:

Symptom-related anxiety is a key predictor of IBS diagnostic status and mediates the relationship between psychological distress and symptom severity. Brain mechanisms underlying this relationship are unknown but may involve altered preparation for expected pain.

Their idea was simple, and the experiment--while weird--was well done and fairly straightforward. They set out with three hypotheses to test via fMRI; namely that patients with IBS would have:

(1) failure to inhibit arousal and limbic brain circuits during expectation, which would correlate with (2) affective stimulus ratings and (3) brain responses to the aversive stimulus.

What was so weird about this study was the way they induced expectation of pain:

The current study sought to characterize abnormalities in preparatory brain response before aversive pelvic visceral distention in irritable bowel syndrome (IBS) patients and their possible relationship to the consequences of distention.

(Emphasis mine.)

According to their visceral distention procedure:

Distention of the rectum was accomplished using a computer-driven pump (barostat) programmed to deliver phasic pressure steps (38 ml/s) separated by interinflation intervals at the resting pressure... All studies were performed after an 8 h fast and application of 2 Fleet enemas. Affective and perceptual responses to controlled rectal distention were assessed before the MRI protocol.

Basically they took a bunch of IBS patients and control subjects and inflated a balloon in their buttholes until it kinda hurt.

That must have been an interesting IRB meeting.

But you can't say that it's not an effective technique. How do you make people anxious about their bowels hurting? Well, you let them know you're about to make their bowels hurt by blowing up a balloon in their anus. QED.

So, what'd they find?

During anticipation of visceral pain, healthy subjects, but not IBS patients, downregulate homeostatic afferent processing network activity... Anticipatory downregulation is inhibited by negative emotions (stress, anxiety, anger), and these are higher in IBS patients.

The image above shows their major IBS patient finding.

Covariation of negative affect with anticipatory BOLD response. Higher BOLD signal during the cue period (less deactivation) was directly correlated with negative affect (p < 0.01; shown in red) in [the locus coeruleus] (location of crosshairs) and left amygdala (for anger and stress)...

There's a nice behavioral effect here, too, wherein:

Negative emotions support a competing strategy of tonic [locus coeruleus] arousal to disinhibit behavioral response, consistent with IBS patients having greater DBS and dACC activation during actual distention and false positive detection of interoceptive information (INS activity) during sham distention.

It's actually a really cool finding in a well-controlled study. It's just... kinda out there methodologically.

I'm not sure that I'd have volunteered as a control for that experiment.

Berman SM, Naliboff BD, Suyenobu B, Labus JS, Stains J, Ohning G, Kilpatrick L, Bueller JA, Ruby K, Jarcho J, & Mayer EA (2008). Reduced brainstem inhibition during anticipated pelvic visceral pain correlates with enhanced brain response to the visceral stimulus in women with irritable bowel syndrome. The Journal of neuroscience : the official journal of the Society for Neuroscience, 28 (2), 349-59 PMID: 18184777


On scientific outreach

Neuroscience outreach has been an important part of my graduate career. I've talked about all of this stuff here before. This post isn't about me.

This post is, in a very small way, my attempt to thank the UC Berkeley Cognitive Science Student Association (CSSA).

Over the years I've done a lot of (often repetitive) talks for them, starting with the Feel Dead Brains lectures I inherited from a fellow neuroscience grad student, Aubrey Gilbert.

Every time I've done these talks the CSSA students have been super thankful and just outright awesome.

Although some researchers think that public lectures and outreach are pointless (or worse), I've found that public talks are a great way to meet some extremely smart, cool people.

And the CSSA has those in spades.

I've never met a more motivated group of undergraduate scientists. (Hell, I've rarely met career scientists as motivated as the CSSA members.) They're certainly a lot more engaged and organized than I was as an undergrad. They've run a conference for three years now, organized entirely by themselves, and attracted speakers such as John Searle, Patricia Churchland, Mike Merzenich, and George Lakoff.

It's great to see people so in love with the science, and I find that interacting with people at these kinds of public lectures helps reinvigorate my own interest. I hope that the CSSA students stay in touch through their own careers as they go on to become independent researchers.

Check out the video they made in preparation for this year's conference:

Thanks, CSSA.