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Author Page for Sam McDougle

SAMUEL D. MCDOUGLE (Contributing Editor, Author of re:COGNITION) is a Ph.D. candidate in Psychology and Neuroscience at Princeton University, studying the human motor system under Dr. Jordan Taylor. Sam holds a degree in Neuroscience and Behavior from Vassar College, where he focused his studies on cognitive neuroscience and psychology while dabbling in philosophy. He previously worked as a researcher in Dr. Javier Medina’s lab at UPenn investigating the neural basis of motor learning– specifically learned reflex timing– using tools from neuropsychology, in vivo neurophysiology and computational neuroscience. Sam’s musical credits include performances with his old bands, Tumbling Bones and The Powder Kegs, at various prominent festivals and clubs in Europe and the US (including a 2007 performance reaching millions of viewers worldwide on NPR’s A Prairie Home Companion), several full-length recorded albums, and competition ribbons in bluegrass fiddle and guitar. He also occasionally writes for Vice, and also loves nachos.

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Will You Will?

[ 9 ] July 19, 2010

By Sam McDougle

The Neuroscience of Free Will

Consciousness” and “Free Will” are complicated topics.  Actually, researchers wish they were merely “complicated” topics – I would go for “staggeringly complex.”  “Philosophically and scientifically baffling” has a nice ring to it as well.

There is a two-pronged attack going on in academia in the quest to understand the feeling of “I,” involving both theorists and laboratory neuroscientists.  Theorists, like Daniel Dennett or Daniel Wegner, use a wide panoramic lens to peer into the big philosophical conundrums of consciousness and free will.  Is the physical brain the engine of the train of experience, and the feeling of “consciousness” merely steam? Or is consciousness the coal driving the brain-engine forward?  Is volitional action really caused by our conscious decisions?  Or is “deciding” simply an illusion of control superimposed on deterministic biology?

These are huge questions that will likely remain unanswered for years to come.

Neuroscientists prefer to use a microscopic lens to study consciousness and free will.  Without losing sight of the big puzzle, they work tirelessly to fit little pieces together, one by one, and their questions are usually pointed and a little more manageable:  What is the role of the posterior parietal cortex in the subjective feeling of control?  How does the pre-supplementary motor area contribute to voluntary action?

Research on these smaller questions offers much-welcomed relief from philosophy-induced headaches.


The most important aspect of free will is the impression that we consciously control our bodily actions.  The official name of this feeling is the “Sense of Agency” (SoA).  A basic example of SoA would be my current feeling that, “the words I am typing on this screen are a result of the control I have over the movement of my fingers on the keyboard.”  Furthermore, I sense that, “these are not someone else’s fingers, nor do I think that the appearance of words on the screen is a coincidental accident – there is a causal relationship between my typing and the appearance of the words.”

There are two main theories concerning the psychology of SoA — I’ll try to describe them as succinctly as possible:

  • The first theory is that we feel SoA because we constantly make predictions about our actions.  When these predictions are fulfilled, we perceive that we “willed” the consequences of our actions: If I predict that typing is going to make words appear, and it does, I feel that I caused them to appear.
  • The other main theory is that SoA is an illusion, and is experienced after the effects of our actions occur — The motor actions are biologically and subconsciously predetermined, and we only feel that we consciously willed them subsequent  to the effects: After noticing that words appear when I type, I assume I willed them to.  Because I only feel this after the words appear, my SoA did not cause the actual effect, it just “makes sense” of the whole affair.

Parsing through these heady theories is a tiring process, but if we can quantify aspects of SoA we can make the debate more concrete.

One way that neuroscientists have quantified SoA involves a phenomenon known as the “intentional binding effect.”  It goes like this:

Say you have a button in your hand that gives you a small, painless electrical shock exactly one second after you press it.  While doing this, you are looking at a timer.  At the end of the task you are asked to estimate the time lapse between pressing the button and getting shocked, and you confidently say “a half a second,” though it was actually a full second.

This is the intentional binding effect – when given a task that involves voluntary motor control over a stimulus (i.e. a shock), people’s perception of time is compressed, and they sense a more immediate consequence of their actions than the actual time lapse.  The intentional binding effect is used as a marker for SoA because it only occurs when someone has full motor control of a stimulus (i.e. they have complete “agency” over an event), it is consistent across almost all individuals, and it is quantifiable.

New research by Moore et al in the latest Proceedings of the Royal Society sheds some light on the neurological foundations of SoA.  Using a technique called “theta-burst stimulation” the researchers were able to temporally “turn-off” specific areas of their human subjects’ brains with bursts of electricity.  This was done while they performed the button-pressing shock task described above.  Because volitional motor movements are at the heart of SoA, they tested two motor areas – the sensorimotor cortex and the pre-supplementary motor area.  While the sensorimotor cortex is responsible for “processing signals directly related to action execution and sensory feedback,” the pre-supplementary motor area is involved in “the preparation and initiation of voluntary actions (Moore et al, 2010).”

The authors found that when they turned-off the sensorimotor cortex there was no effect on intentional binding.  That is, the subjects still reported a squished perception of time between pressing the button and feeling the shock.  However, when the pre-supplementary motor area was shut down, the subjects no longer perceived a compressed time interval – The pre-supplementary motor area seems to have an effect on SoA while the primary sensorimotor cortex does not.


While this all might seem like run-of-the-mill cognitive neuroscience, the authors put on their theorist caps to show the significance of this result:

Theoretically, SoA could arise from either of two distinct processes. On the one hand, SoA may involve a prediction—based on the neural commands for action—that the sensory effect will occur. On the other hand, the brain might infer, or postdict, from the conjunction of action and effect, that the action caused the effect, as in illusions of conscious will (Moore et al, 2010, emphasis added).”

Their results point toward the former – the predication-based theory – because the role of the pre-supplementary motor area is the preparation of motor actions, not the sensory feedback that occurs afterward.


In essence, this research scores points for a non-illusory free will. Maybe we have a “sense of agency” because we predict the effects of our actions before we act, and this sense is validated when the predictions are correct.

If you were scared of being a deterministic robot, this work offers some hope.

At the present, my pre-supplementary motor area is preparing me for a walk to the coffee-maker…am I consciously willing my legs to move me through the corridor, or is my mechanic subconscious just pushing me along?

Mouse OCD linked to Immune System

[ 12 ] July 15, 2010

A recent study published in Cell magazine has shown that mice who exhibit “excessive grooming behavior,”  which is analogous to Obsessive-Compulsive Disorder in humans (OCD), can be cured by a bone marrow transplant.  The disorder was linked to deficient immune microglia cells, the street-cleaners of the body (they clear-up cluttery microbes and broken down cellular byproducts).  Healthy-mouse bone marrow was transferred to the OCD mice and within four months they returned to normal grooming patterns.  The gene responsible for healthy microglia – Hox8 – is a vital developmental gene, and it’s connections to observable behavioral patterns, like OCD, are intriguing and will certainly inspire further research.

Audio from the Authors:  Pathological Grooming in Mutant Mice


The Substrate of Courage

[ 1 ] July 4, 2010

Some intriguing new research published in the most recent issue of Neuron seeks to elucidate the neural substrates of courage.  The researchers used a experimental paradigm by testing subjects with snake phobias and allowing them to press a button that moves a snake (a non-poisonous one of course) closer and further from their body while they lied in an fMRI machine. Moving the snake closer was consider an act of “courage.”

Activity in the subgenual anterior cingulate cortex (sgACC) was found to be correlated with courageous behaviors, and was even shown to diminish activity in the fear-sensitive amygdala.

I hope the snake-fearing subjects in this study were compensated nicely!

View the video abstract here:

The Country of the Face-Blind

[ 10 ] June 6, 2010

Contributor Sam McDougle Reports on Friday evening’s “Strangers in the Mirror” event at the 2010 World Science Festival in New York City.

Prosopagnosia, or “Face Blindness,” can be a devastating affliction.

Imagine: after suffering a stroke, the faces of your loved ones are no longer the unmistakable visages they once were, but are now unrecognizable collages of noses, lips, eyes, and ears.  You can’t tell your loved ones from strangers, and mirrors are less reflections of yourself than they are opportunities for embarrassing run-ins with a similar looking person who has a spot-on impression of you.

Friday evening’s World Science Festival event “Strangers in the Mirror” was a poignant , compelling, and surprisingly (though respectfully) humorous glance into the lives of the face-blind.  The event was moderated by Robert Krulwich (Radiolab, Nightline, Frontline) and the guests were neurologist and author Oliver Sacks and the artist Chuck Close.  Both men are notable thinkers in their respective fields, prolific in their bodies of work, talented orators and educators, and severe prosopagnosics.


Sacks began the narrative of his disease with a story:  He and a physicist made plans to meet at a restaurant for some scientific musing.  On his arrival, the hostess sent Sacks to the table where the physicist was sitting, and they began their conversation.  Unbeknownst to Dr. Sacks, his dinner guest also suffered from severe face blindness.

This improbable fact was not discovered by either man until the physicist, after a course or two, went to the bathroom. He emerged to find that neither he nor Sacks remembered each other’s faces.  An amusing man hunt ensued as the physicist looked for the right table and Sacks wondered where his guest was, like two blind-daters searching for each other at a crowded restaurant.

Sacks first acknowledged his deficit when he was twelve.  He recounted “saying hi to people I didn’t even know,” in a kind of lottery strategy so that he may eventually say hi to a friend and put on that he recognized them.

While Sacks noted sometimes remembering the faces of his loved ones after years of exposure (an important consolation that some prosopagnosics lack), at times he is subject to forgetting even the most recognizable faces – he playfully remarked about “apologizing for almost running into an older bearded man,” who happened to be his reflection.  Krulwich then asked if he recognized his neighbors and Sacks swiftly quipped, “I recognize their dogs.”


Chuck Close has a similar story.  He also felt he was “born with” the deficit and believed it to be his main push towards painting portraits.  He knew he was disabled (though there was likely no word for face blindness at the time of Close’s youth), and thoughtfully mentioned that disabilities often implore one to “find other venues for their intellect.”  Without explaining what “other” really meant, his implication was clear – face blindness certainly blocked some “traditional” professional paths, professions that involve working closely with people and managing day-to-day social interactions.  Close chose the life of the artist.

Close’s inimitable portraits are known for their juxtaposition of the part and whole of the image – each portrait is made up of small square paintings that, on their own, resemble abstract shapes.  However, when the viewer pulls back from the painting the whole face is revealed.

Chuck Close, self portrait

Chuck Close, "Self Portrait"

Curiously, Close mentioned having less trouble recognizing celebrity faces than faces in his daily life.  He found it easy to recognize faces when they were static, “flattened out” images (portraits!), but struggled in 3-dimnesions, saying, “move your head one half inch and it’s a face I’ve never seen before.”


The neurophysiology of face blindness is certainly not completely understood, but there are some hints.  The fusiform gyrus is the area of the cortex involved specifically with facial recognition, and surely plays a role in face blindness.  Acute damage to the area (stroke, cancer, injury) is thought to be related to trauma-induced face blindness.  However, Sacks and Close both have congenital face blindness, and they both report other deficits, including problems with remembering places and navigating.  I caught up with Dr. Sacks after the event and asked him if this points to a more systematic (rather than acute) problem in the congenital vs. acquired prosopagnosic brain.  He said that probably is the case, and referred to his own illness as less of a specific face-recognition deficit than as a more categorical issue – the face as a whole is not a category-worthy object to him because he only sees it in parts (eyes, mouth, nose), and this makes it less likely to lodge in his memory.  It seems that congenital prosopagnosics have trouble seeing the forest instead of the trees.

At the end of the meeting, Krulwich, Sacks, and Close discussed the prevalence of face blindness in the world, and it seems clear that many more people have it than we think and much more can be done to help them.  Sacks painted a picture of hundreds of thousands living in “private embarrassment,” while Close lightheartedly joked about the vast number of prosopagnosics that are likely incarcerated.  Eventually those who suffer from face blindness will know they don’t suffer alone, and perhaps seek therapies that can mitigate the social and personal fallout of the disease.  It only takes the successes of two men like Dr. Sacks and Chuck Close to see that there are always “other venues,” for the disabled among us.  I await a prosopagnosic-written comedy screenplay about a man who incessantly apologizes to a stranger in the mirror.

The Crack Rocky Road

[ 5 ] May 30, 2010

by Sam McDougle

Can One Be “Addicted” to Food?

Addiction is hard to define.

Does it merely refer to any uninhibited behavior that is habitually repeated?  This definition feels too loose – I wouldn’t say I was addicted to tying my shoes or going to the bathroom.

Does addiction refer to a habitually repeated behavior that is carried out despite its negative consequences?  Again, I would argue that biting my nails or cracking my knuckles is not, technically, an addiction (the colloquial hyperbole in stating that one is “addicted” to biting their nails, or another such potentially unhealthy habit, seems to prove the point).  These behaviors seem to lie under the bigger umbrella of “habits.”

So are addictions just particularly nasty habits?


“Physically addictive” is a popular buzz phrase in the modern jargon.  Marijuana legalization activists use the term to highlight the drug’s innocuousness, and nicotine is often cited for its extreme “physically-addictive” properties.  The phrase implies a biological definition of addiction – addiction is a chemical occurrence in the brain.

But isn’t all behavior a chemical occurrence in the brain?  What differentiates my compulsive intake of coffee and my compulsive knuckle-cracking?  Both behaviors are products of chemical transfers in my brain and body, both result in some kind of reward, and I perform both behaviors too often for my own good.  Why am I “addicted” to coffee, but simply have the “bad habit” of knuckle-cracking?

Let’s ditch these questions for a minute, and look at a behavior that is widely agreed to be a “proper” addiction – repetitive cocaine use.  Cocaine causes euphoria by blocking dopamine reuptake in cells, flooding your brain with an excess of pleasurable neurochemicals.  In the short-term, this causes excessive partying, in the long term, it rewires your brain’s response to the reward of the drug and incites further (and heavier) use.  The common signs of full blown addiction are increased tolerance, amplified motivation to use, bingeing, and withdrawal.

Additionally, one of the common signatures of addiction is continuing the addictive behavior in light of palpable negative consequences.  This is clear with cocaine addicts, who continue to heavily use the drug even with their heart failing, body withering, and bank account dwindling.

Alcohol, nicotine, and heroin are also truly “addictive” substances, and have similar addictive characteristics.

But what about junk food?  Recent research suggests that the brain reacts similarly to both the intake of high-calorie foods and the use of addictive substances (i.e. cocaine).  Our society may not be snorting pixie sticks or main-lining Pepsi, but the analogies are staggering.


It’s no question that the intake of dense, fatty foods causes increased motivation to use – just give someone a bowl of potato chips and see if they can eat only one.  Bingeing is another obvious correlate, with entire pints of ice cream as the most common victims. Withdrawal behaviors, that is, depression and anxiety, were observed when experimental rat subjects were deprived of sugar after a prolonged binge.  In a recent paper in Nature Neuroscience, increased tolerance was observed in rats who were exposed to a high-fat diet, and rats exposed to high-fat foods (bacon and cheesecake, as supposed to their normal gruel) showed changes in their brain’s dopamine system that were comparable with cocaine-addicted rats.

The rats were getting high on cheesecake.

This same paper also showed that rats who were habituated to eating high-fat foods would continue eating them even if they were electrically shocked afterwards.

On the comparison to drug addiction, the authors write:

Given all of this, how far shall we go in drawing parallels between drug addiction and food addiction? Unlike drugs, food is essential for survival, but frequent consumption of bacon, sausage and cheesecake is not. The availability of such foods in most developed societies has increased so quickly that, similar to addictive drugs, they may stimulate brain reward systems more powerfully than we have evolved to handle, signaling a false fitness benefit and thereby reinforcing unhealthy patterns of consumption. In that respect, a parallel is defensible (Epstein & Shaham, 2010).

Food addiction can be connected to our ever ballooning waist lines as well.  Food addiction can not be cited as the only cause of obesity, though it probably plays a role – while there are cases where obesity is a result of genes or the limited availability of leaner foods, addiction to junk food can surely lead to serious weight gain, especially in the obese, drive-thru West.


Mill once said something about “personal experience” bringing truths home.  To me, no personal experience better supports the “junk food addiction theory” than childhood candy obsessions.  And, in my first post after a month, I’ll leave you with a YouTube video instead of a haughty painting.


[ 5 ] April 25, 2010

by Sam McDougle

A young physics graduate student is sitting at a table of undergrads.  He is telling a joke about mathematicians.

He begins confidently. “How can you tell when a mathematician is an extrovert?

A wide-eyed sophomore quickly asks “I dunno…how?”

Smiling, he replies, “He looks at your shoes when talking to you!”

The undergrads chuckle.  Some genuinely laugh, others pretend to get it.  The grad student relishes in his successful attempt at humor – the students are putty in his hands.  Suddenly, his gratification is interrupted when a prolifically published professor joins the table and, with a penetrating squint asks what joke he missed.

The grad student, who greatly admires his superior’s accomplished reputation (though barely knows him) becomes stressed, blushes and fumbles over the joke.  The professor giggles in an act of mercy, nods at the enthralled undergrads, and hastily moves on.

We can all relate to situations like these – when poise quickly turns to angst at the mere presence of a superior.

Humans, like many other primates, live in a social hierarchy.  This hierarchy exists in all areas of our lives: our families, schools, neighborhoods, and workplaces (academia struck me as a noteworthy example, thus, the above vignette).  We continually jockey between positions of dominance and subordination, and our emotions, thoughts, and behaviors seem to be at the mercy of this balancing act.  So it’s no surprise that new research reveals a vast neurological divergence when we’re confronted with, respectively, “superior” and “inferior” individuals.

Consider this article by Caroline Zink et al, published in the most recent issue of Neuron.  The researchers used a simple competitive task (i.e. clicking a blue circle as soon as it changed color) to establish an experimental, skill-based hierarchy (clicking faster = better) among participating subjects (Zink et al, 2010).

The subjects were pitted against two competitors, and all three were ranked relative to each other.  Each task consisted of three phases: viewing a photo of one of the other players, playing the game, and viewing the outcomes. FMRI readings were taken to measure brain activity during the tasks.  (note – while this experimental “social” situation may seem unnaturally plain, it succeeds in focusing in on the very common scenario of an inferior-middle-superior hierarchy).

Their results characterized greater activation in several important brain regions at the sight of a superior individual compared with an inferior one:

“Brain activity when viewing a more superior player compared with viewing a more inferior player was significantly greater in occipital/parietal cortex, ventral striatum, and parahippocampal cortex, implicating these brain areas in the neural encoding of hierarchical rank.”

These structures (specifically, the occipital/parietal cortex and ventral striatum) have been correlated with greater attentional processing.  The medial prefrontal cortex, an area cited for its role in social cognition (especially an individual’s status relative to others) exhibited heightened activity when the player was confronted with a superior, as did vital emotional processing areas (i.e. the amygdala).  In other words, peers representing an “inferior” role in a given social hierarchy represent an “inferior” role in the brain as well.

The author’s made another intriguing finding by conducting a control experiment where the “rank” of each player stayed static regardless of their performance in the game. It turned out that the prospect of rank mobility (analogous to “social mobility?”) had a strong effect on the heightened brain activity linked to confronting a superior.  The potential to “overtake” a superior player (or be overtaken yourself) made the brain work harder in the areas mentioned above.

These results paint a familiar picture:  When faced with a superior, our emotions are heightened, our attention sharpened, and our social position closely analyzed.  This effect is amplified in situations where your own status is subject to change.  Think of the last time you met a superstar in your field or an artist you greatly admire.  Did their status not stir your emotions? Did you find yourself paying close attention to your words while carefully tracking their reactions?  Did you, on leaving the encounter, dwell on the possible social advantages or disadvantages gleaned from the confrontation?  If your answer to these questions is unequivocally no, I would guess you are either being untruthful or have a rare, and somewhat enviable, phenotype rendering you apathetic to status.


Zink’s model certainly carries over to our primate cousins. Baboons closely watch their superiors and often ignore their inferiors. They also exhibit increased stress when their hierarchies are in flux (especially individuals in superior positions).  Chimps are very sensitive to hierarchical structure as well.

Even though we often want to avoid these feelings and conceal any interest in social status (“I don’t care what people think about me!”), I believe we’re stuck with our status fascination.  This data seems to say we’re built for it.

It would be remiss to not mention human variability in these behaviors. There are certainly individual differences when it comes to one’s feelings about status – we label some individuals as persistent “social climbers,” and other’s as “shoegazers” (*subcategories: those who gaze at their own shoes and those who gaze at yours).  Differences aside, our fixation on status is clearly reflected in the brain – we may not all be mathematicians, but, like it or not, we are all statusticians.

Portrait of Philip II, King of Spain
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