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The Zombie Brain: Conclusions

This post is the final installment of our collaborative venture on exploring the Zombie Brain. We hope you’ve enjoyed the ride.

Sincerely, Bradley Voytek Ph.D. & Tim Verstynen Ph.D.

Bringing it all together: The Zombie Brain

Over the last ten days we’ve laid out our vision of the Zombie Brain. To recap, we’ve shown that zombies:

1) Have an over-active aggression circuit
2) Show cerebellar dysfunction
3) Suffer from long-term memory loss due to damage to the hippocampus
4) Present with global aphasia (i.e., can’t speak, can understand language)
5) Suffer from a variant of Capgras-Delusion
6) Have impaired pain perception
7) Cannot attend to more than one thing at a time
8) Exhibit addictive responses to eating flesh
9) Have an insatiable appetite

Together, these symptoms and their neurological roots reveal a striking picture of the zombie brain.

Based on the behavioral profile of the standard zombie, we conclude that the zombie brain would have massive atrophy of the “association areas” of the brain: i.e., those areas that are responsible for the higher-order cognitive functions. Given the clear cognitive and memory deficits, we would also expect significant portions of the frontal and parietal lobes, and nearly the entire temporal lobe, to exhibit massive degeneration. As such, the hippocampuses of both hemispheres would be massively atrophied (resulting in memory deficits), along with most of the cerebellum (resulting in a loss of coordinated movements).

In contrast, we would expect that large portions of the primary cortices would remain intact. Behavioral observations lead us to conclude that vision, most of somatosensation (i.e., touch), and hearing are likely unimpaired. We also hypothesize that gustation and olfaction would also remain largely unaffected. We must further conclude that large sections of the thalamus and midbrain, brainstem, and spinal cord are all likely functioning normally or are in a hyper-active state.

Putting these elements together, we have reconstructed a plausible model for what the zombie brain would look like.

Overlay (yellow is zombie, gray is human)

It is interesting to point out, from an historical standpoint, that many of the regions we hypothesize to be damaged in the zombie brain are part of what is generally referred to as the Papez circuit. James Papez first identified this circuit in 1936. Much like our current study, Papez was trying to unify a cluster of behavioral phenomena he had observed into a neuroanatomical model of the brain. He wondered why emotion and memory are so strongly linked. Thus, he hypothesized that emotional and memory brain regions must be tightly interconnected.

To test this theory, he injected the rabies virus into the brains of cats to watch how it spread and he made note of which brain regions were destroyed as a result of these injections. He observed that the hippocampus (important for memory formation) connects to the orbitofrontal cortex (social cognition and self-control), the hypothalamus (hunger regulation, among other things), the amygdala (emotional regulation), and so on. These experiments, conducted almost three-quarters of a century ago, may shed some insight into the nature of the zombie disorder today. We’re not suggesting that some super, brain-eating rabies virus is responsible for zombies. We’re just saying that it’s not not possible.

The profile of damage we have outlined corroborates the behavioral observations we have made from zombie films. From a subjective standpoint, this pattern of cerebral atrophy represents a most heinous form of injury unparalleled in the scientific literature. It would lead to a pattern of violence and social apathy; patients thus affected would represent a grievous harm to society, with little chance of rehabilitation. The only recommendation is immediate quarantine and isolation of the subject.

However, as we learned in GI Joe “knowing is half the battle.” Based on our observations, we leave you with a few strategies to maximize survival in the event of a zombie encounter.

1) Outrun them: Climb to a high point or some other place they will have trouble reaching. Practice parkour. The slow zombie variant can’t catch up with a healthy adult human.

2) Don’t fight them: They can’t feel pain and aren’t afraid of dying, so they’ve got the edge in close combat. If you can simply out run them, why risk the bite?

3) Keep quiet and wait: The zombie memory is so terrible that if you can hide long enough, it will mill around only until something else captures its attention.

4) Distraction, distraction, distraction: Throw something behind the zombie to capture its attention. Set off a flare, use a flashbang, or whatever you need to do to distract it to get away

5) If you can’t beat ‘me, join ‘em: If you can’t out run them (or are around the fast zombie variant) take advantage of their self-other delusion and act like one of them.

There you have it folks... scientifically validated safety tips for surviving the zombie apocalypse. Use them wisely the next time you come face-to-face with the living dead.


The Zombie Brain: Insatiable Hunger

This is the last symptom of the multi-day series on The Zombie Brain between Oscillatory Thoughts and The Cognitive Axon.

Be sure to check out our last post tomorrow in which we wrap everything up.

Symptom 9: Insatiable Hunger

What drives the zombie’s insatiable hunger for human flesh? In the last post we discussed the role of addiction in the zombie’s craving for your skin, but why are they never satisfied? Why, after having eating your entire family, will the zombie continue on to consume you as well? How can they keep eating?

Bradley Voytek & Timothy Verstynen - Shaun of the Dead Zombies

While we cannot ascertain for certain the etiology of zombie hunger, we posit two possible neural mechanisms that underlie this disorder.

First and most probable is the alteration of the hunger/satiety circuit in the zombie brain. In a previous post we outlined the nature of the zombie impulsive-reactive aggression. In that post we demonstrated that damage to the zombie orbitofrontal cortex would lead to alterations in the top-down control over subcortical nuclei such as the hypothalamus.

The hypothalamus plays an important role in maintaining control over autonomic functions such as regulating body temperature and the sleep/wake cycle, as well as modulating thirst and hunger. Dysfunction of this region due to abnormal activity--either from the loss of or damage to connecting regions, or possibly via unknown neurochemical changes--would severely affect zombie satiety and sleep.

Bradley Voytek & Timothy Verstynen - Zombie hypothalamus

For example, we are often taught that the ventromedial nucleus of the hypothalamus regulates feelings of satiety while the lateral nucleus regulates feeding (quick mnemonic: "stim the ven, get thin; stim the lat, get fat"). Thus, damage to the zombie ventromedial nucleus may result in a loss of satiety.

In other words: zombies will always be hungry. For you.

(Though, as with all things neuroscience, this may be more complicated than we are taught.)

The second possible mechanism for zombie fleshlust may be the result of a form of Klüver–Bucy syndrome.

This interesting disorder is caused by damage to both temporal lobes and is associated with an array of disorders including hyperphagia (overeating) as well as pica (eating strange objects).

Sound familiar? I would say eating flesh would constitute as eating a "strange object".

This is a very rare disorder that usually only occurs in experimental settings where researchers intentionally remove the temporal lobes of an animal. However, it is also associated with other symptoms including placidity, emotional dysregulation, and hypersexuality. See exhibit A below (from the Annals of Mad Science, circa 1930):

Bradley Voytek & Timothy Verstynen - Kluver-Bucy Syndrome Zombies

So while Klüver–Bucy would account for the eating patterns seen in zombies, few would associate placidity or sexuality with the walking dead.

In fact, hyperorality, pica, hypersexuality, and strange emotional responses sound more like symptoms of sparklevampires.

And insatiable hunger is also associated with other Awesome Beings, so these phenomena may underlie the abnormal behavioral patterns observed in other, more rare, non-zombie subjects...

Bradley Voytek & Timothy Verstynen - Galactus Zombies

ResearchBlogging.orgKing BM (2006). The rise, fall, and resurrection of the ventromedial hypothalamus in the regulation of feeding behavior and body weight. Physiology & behavior, 87 (2), 221-44 PMID: 16412483


The Zombie Brain: Stimulus-locked Attention

This is part eight(!) of our multi-day series on The Zombie Brain.

Be sure to visit The Cognitive Axon tomorrow for symptom 8!

Symptom 7: Stimulus-locked attention

If zombies are anything, they're at least highly distractible. Don't want them to see that you're looting an old corner store for supplies? Throw up a few fireworks. The walking dead will be occupied as long as the show lasts.

Of course, this type of attention can be deadly if the critters set their sights on you...

This type of stimulus-bound attention reflects another rare clinical disorder called simultanagnosia. Simultanagnosia, particularly the "dorsal form", is the inability to attend to more than one thing at time and is often seen in patients suffering from Balint's Syndrome.

Timothy Verstynen Bradley Voytek - Zombie Research Society - zombie brain parietal cortex

The only thing these patients perceive is whatever has grabbed their attention. This originates when both the left and right parietal cortex, the back and top part of your neocortex, are lesioned. If one is intact, spatial attention is still somewhat impaired, but the impenetrable stimulus-locking does not occur.

Damage to this parietal network may also underlie some of the issues we previously described with the mirror neuron network, language regions, and pain sensory regions.

So, along with a good chunk of the frontal lobe, it's safe to assume that the dorsal parietal lobe is lesioned in the zombie brain as well. This could happen if the neurons themselves are destroyed, or if the axons connecting them (called "callosal fibers" because they pass through the corpus callosum) are damaged.

Timothy Verstynen Bradley Voytek - Zombie Research Society - zombie brain corpus callosum

Only careful, clinical trials can tell us the true root cause of this damage in the zombie brain. Nevertheless, by arming ourselves with the knowledge of the zombie’s simultanagnosia, we can devise further survival strategies. More on this later.


The Zombie Brain: Self/Other Delusion

This is part six of our multi-day series on The Zombie Brain.

Be sure to visit The Cognitive Axon tomorrow for symptom 6!

Symptom 5: Self/Other Delusion

So what exactly did we do to piss off the living dead? Oh sure, you probably had a grudge or two with someone who's risen from the grave, but most of the walkers coming after you have no idea who you are.

Zombies are just plain delusional; they see us as something else, something they can't make sense of. While modern neuroscience is still just beginning to understand the neural underpinnings of delusional disorders, this particular type of self/other association delusion has been linked at least two distinct circuits in the brain.

First, the inability for a zombie to recognize that they're chowing down on their bowling partner mirrors a very rare neurological disorder called the Capgras delusion.

Individuals with Capgras are convinced that the people they know well (e.g., a close friend or spouse) have been replaced by an imposter. It's like an alien came down and replaced your teammate with a lookalike that wasn't him. Think Invasion of the Body Snatchers.

Now we don't know precisely what causes the Capgras delusion, but let's suffice it to say that the zombie brain most likely has it! One hypothesis is that the brain regions that recognize faces (the fusiform face area) and the regions that assign emotional content to experience (the amygdala), which are normally communicating nicely, are somehow disrupted.

You can see Ramachandran talk about it on this TED video:

This means that people with Capgras can still recognize people as people but that they don't have any emotional ties to them. Couple that with the orbitofrontal aggression and control issues we described earlier, and you could see how this would get out of hand!

Therefore, the zombie is after you not only because they're pissed off and looking for a food source, but because they literally don't recognize you as the person they once loved.

Second, this ability to recognize "self" from "other" may also reflected in a set of frontal and parietal neurons called mirror neurons. These cells turn on when you perform an action (say picking up an ax) and when you see someone else perform the same action.

Some scientists believe that mirror neurons play an intimate role in social bonding and empathy; both behaviors that zombies clearly lack. Now, some have said that zombies completely lack mirror neurons altogether. However, that doesn't seem reasonable since zombies tend to imitate what they see (particularly things other zombies do).

Timothy Verstynen Bradley Voytek - Zombie Research Society - zombie brain mirror neurons - Shaun of the Dead

Likely, the response properties of these cells have changed. If you were to stick an electrode in a zombie's inferior frontal cortex, you’d likely observe mirror neurons that only respond when a zombie performs an action or sees another zombie performing the same action.

Both brain dysfunctions point out one key survival skill: if you want a zombie to not come after you... start acting like a zombie. They'll think you’re one of them and might even follow you into a well-devised trap. This demonstrates that, by understanding the neural basis of the zombie disorder, we can begin building protocols that will maximize our survival.


The Zombie Brain: Long-term Memory Loss

This is part four of our multi-day series on The Zombie Brain.

Be sure to visit The Cognitive Axon tomorrow for symptom 4!

Symptom 3: Long term memory loss

Why is it that it only takes you a few seconds to hide from zombies before they get distracted, forget their prey, and move on after some other helpless chap? Yet they flock in droves to places like malls and churches that they remember from their pre-zombie past?

We contend that zombies are incapable of storing long-term memories as a result of a disorder called anterograde amnesia. Anyone who's seen the movie Momento will know the symptoms well. Immediate events are available for only a few minutes at a time, at most, before their flow of conscious memories is disrupted.

Timothy Verstynen Bradley Voytek - Zombie Research Society - zombie brain hippocampus

Once distracted, someone afflicted with anterograde amnesia will lose those memories as if they never existed at all. However, memories that were gained before the amnesia-inducing brain damage will be retained as clearly as if they had happened yesterday.

This phenomenon arises from damage to a very specific area of the brain called the hippocampus. This region sits right behind the amygdala (which we talked about earlier) and is nestled deep within the temporal lobe. For such severe amnestic symptoms, our hypothetical zombie subjects would have to lose both their left and right hippocampuses.

Timothy Verstynen Bradley Voytek - Zombie Research Society - zombie brain hippocampus

This is a rare condition that has so far really only come about for surgical reasons and doesn't really tend to happen naturally. However, there are cases in which severe vitamin deficiency can lead to memory issues and anterograde amnesia. This is due to the susceptibility of the mamillary bodies, a brain region that is heavily interconnected with the hippocampus, to vitamin deficiency degeneration.

This leads to a disorder referred to as Wernicke-Korsakoff’s syndrome, characterized by memory disruptions, which may be involved in regulation of the hippocampus. Whether a virus has destroyed the hippocampus, or zombies are simply suffering from a severe vitamin deficiency, it's safe to say that somehow they've lost their hippocampuses for good, as well as any ability to form memories of the new un-life.


The Zombie Brain: Impulsive-Reactive Aggression

This is part two of our multi-day series on The Zombie Brain.

Be sure to visit The Cognitive Axon tomorrow for symptom 2!

Symptom 1: Impulsive-reactive aggression

It’s pretty much a given that zombies are constantly pissed off and they want to eat you. The snarls, the teeth, the guttural howls as they close in on their prey... these creatures are enough of a public health danger and menace to warrant serious research funding from the National Institutes of Health!

The adrenalin-infused rage of thousands of raging beasts is unmistakable.

So what does this uncontrolled, rampant rage tell us about the zombie brain? First, the type of rage that zombies exhibit is of a very primal form known as impulsive-reactive aggression. This is more like the aggression you see when two drunks get in a fight.

It differs from the cold and calculated rage seen, for example, in a school shooting. The zombies will direct their anger at anyone and everyone simply because they're human. This type of rage has its roots in the more “primitive” (i.e., phylogenetically older) parts of the brain and reflects the engagement of the “fight-or-flight” circuitry that all mammals have. Steve Schlozman has referred to this circuit as the "crocodile brain".

Timothy Verstynen Bradley Voytek - Zombie Research Society - zombie brain orbitofrontal cortex

Normally, these every-day anger impulses are suppressed by signals that originate in the lower part of the frontal lobe: the orbitofrontal cortex. This area sends inhibitory signals to the medial amygdala, a little almond-shaped area that sits at the front of your temporal lobe. If left uncontrolled this tiny region would ramp up signals to the hypothalamus and thalamus that trigger the adrenal responses you feel when angry and frightened. But since most of us have an intact orbitofrontal cortex, the little amygdala is turned down except in rare cases.

Timothy Verstynen Bradley Voytek - Zombie Research Society - zombie brain orbitofrontal cortex

Studies of violent, pathological criminals have found that functional abnormalities of the dorsal and ventral prefrontal cortices and the amygdala may underlie some anti-social and violent behaviors. Furthermore, people with damage to the orbitofrontal cortex often have issues with social cognition, understanding and adhering to social norms and mores, as well as moral decision-making.

Some of you may have heard of the famous case of Phineas Gage who had a rod shot through his brain and went from mild-mannered middle management to uninhibited risk-taker and speaker of all things inappropriate. Well that’s because he lost his orbitofrontal cortex.

Certainly the zombie doesn’t care about social norms or morality!

Timothy Verstynen Bradley Voytek - Zombie Research Society - zombie brain orbitofrontal cortex

Given the impulsive and aggressive behavior exhibited by zombies, it’s safe to say that they
lack a properly functioning orbitofrontal cortex. So we’ve modeled the zombie brain such that the orbitofrontal cortex is more or less obliterated. As a result, the zombie amygdala, hypothalamus, and thalamus (specifically the bed nuclei of the stria terminalis) should be constantly overactive. These changes would easily produce a hair-trigger adrenal response unlike anything seen in normal humans!


The Zombie Brain

The Living Dead Brain: What Forensic Neuroscience Can Tell Us about the Zombie Brain
Dr. Timothy Verstynen & Dr. Bradley Voytek
Zombie Research Society

This is a cross-post between Oscillatory Thoughts and Cognitive Axon. Stay tuned to both sites over the following days leading up to Halloween for updates on our model of the zombie brain.

What can neuroscience teach us about surviving the zombie apocalypse?

What makes a zombie a zombie or, more importantly, what makes a zombie not a human? Philosophers contend that a zombie lacks that qualia of experience that belies normal consciousness.

However this is a less than satisfying explanation for why the lumbering, flesh eating creatures are pounding outside the door of your country farmhouse.

Beyond the (currently) immeasurable idea of consciousness or the whole supernatural “living dead” theory, zombies are characterized primarily by their highly abnormal but stereotyped behaviors. This is particularly true in more modern manifestations of the zombie genre wherein zombies are portrayed not as the reanimated dead, but rather as living humans infected by biological pathogens. They are alive, but they are certainly not like us.

Neuroscience has shown that all thoughts and behaviors are associated with neural activity within the brain. Therefore, it should not be surprising that the zombie brain would look and function differently than the gray matter contained in your skull. Yet, how would one know what a zombie brain looks like?

Luckily, the rich repertoire of behavioral symptoms shown in cinema gives the astute neuroscientist or neurologist clues as to the anatomical and physiological underpinnings of zombie behavior. By taking a forensic neuroscience approach, we can piece together a hypothetical picture of the zombie brain.

Over the course of the next week, Oscillatory Thoughts and Cognitive Axon will team up to show our hypothetical model of the zombie brain. Each day we will present a new "symptom" associated with a zombie behavior and show its neural correlates in our simulated zombie brain.

This entire endeavor is partly an academic "what if" exercise for us and partly a tongue-in-cheek critique of the methods of our profession of cognitive neuroscience. We’ll be breaking up the workload and alternating days (hey... we gotta work our real jobs too) so be sure to check both places for the newest updates on zombie neuroscience.

Timothy Verstynen and Bradley Voytek - Zombie Research Society zombie brain

DISCLAIMER: We need to be very clear on one point. While we sometimes compare certain symptoms in zombies to real neurological patient populations, we are in no way implying that patients with these other disorders are in some way “part zombie”. Neurological disorders have provided critical insights into how the brain gives rise to behavior and we bring them up for the sake of illustration only. Their reference in this context is in no way meant to diminish the devastating impact that neurological diseases can have on patients and their caregivers.


Forbes "Edge Thinkers"

On Monday my interview with Forbes went live:

Neuroscientist Bradley Voytek is Bringing the Silicon Valley Ethos into Academia

This was part of their "Working The Edge" series.

Recently Forbes managing editor Bruce Upbin put out a call for "Edge Thinkers":

Forbes just launched a new section on our Tech channel to showcase intriguing people operating at the fringes of science, business, education, government, healthcare and the arts. It’s called Working The Edge. It’s a way to cover the kinds of people who innovate by merging seemingly unrelated disciplines. The kinds of people with three degrees, or else are entirely self-taught. They are the associative thinkers mixing biology and architecture, chemistry and marketing, charity and capitalism, Shakespeare and data mining, and food and physics. They’re not superheroes or brainiacs, just ordinary people who work hard and passionately at exploring a big new idea. Okay, sometimes they’re brainiacs.

Last week I got an email from Forbes writer Alex Knapp (who writes the Robot Overlords blog) saying that my name was on their list.

A few days later we did an hour-long phone interview.

We talked about zombies (of course), Uber and my "startup sabbatical", my TEDxBerkeley talk about my grandfather's Parkinsonism, brainSCANr, my PhD research, and how my wife can kick my ass at writing code.

It was a lot of fun (though it did hit some of my "what the hell am I doing?" anxiety buttons) and, I think, a good interview.

So yeah, check it out.


Why you can't individually control your toes

Man, Quora's becoming a great resource for my blog. It keeps giving me amusing ideas to write about.

Recently someone asked "Why can't I control my individual toes?".

This was a really fun answer to write, so I thought I'd share it here.


Before explaining this, I want you to try a quick experiment for me: hold your hand in front of you, fingers straight and pointing upward. Now, flex your index finger and just your index finger. Did your middle finger flex, too? Maybe your ring finger even twitched a little? Try flexing just your ring finger. Unless you're a piano or string instrument player, it's unlikely that you were very successful at doing so.

The reason why that happens is closely related to why you can't control your individual toes. Stick with me.

This sexy beast is the motor homunculus:

He's built to reflect the relative area in the motor cortex that is devoted to controlling specific muscle groups. Notice how overrepresented the hands, lips, and eyes are and how underrepresented the arms, legs, and feet are?

Here's the motor cortex in the brain:

Basically, the more motor cortical area devoted to a region, the greater and finer the voluntary control over those muscles groups that we have.

Originally this map was created by Canadian neurosurgeon Wilder Penfield in 1937. Penfield pioneered brain surgery on awake patients. He would use a small electrical stimulator to map out different parts of the brain, which is still done by neurosurgeons to this day. The logic was simple: stimulate a part of the motor cortex and watch which parts of the body twitched. This gives a mapping between brain and body, and what he found was a clear topography in the motor cortex.

Journalist and science writer Mo Costandi wrote an amazing history of Penfield that's well worth reading, by the way.

As I said in my answer to:

Are all the wrinkles on a brain's cortex the same across people?

...neurosurgeons will perform electrical stimulation mapping of awake people if they have to remove any brain tissue near what they call "eloquent cortex"... [because] [t]he only way even an experienced surgeon can be sure that specific brain area in a specific person is motor, or speech, or sensory, is via this mapping technique... This is because, although gross neuroanatomical features are generally conserved across people, there can be a huge range of variation.

Penfield used a highly invasive means to map out the motor homunculus. But it turns out we have some pretty cool modern technology with which we study the motor cortex non-invasively: Transcranial Magnetic Stimulation (TMS).

TMS induces an electrical current using a rapidly changing magnetic field.

Pictures speak volumes:

As do videos. Watch the TMS disrupt conscious motor control:

The stimulation of the motor cortex by the TMS sends a "fake" signal to the hands, causing muscular contractions. (MEP is "motor evoked potential": the electrical signal recorded from the hand muscles.)

By combining TMS with individual MRIs, we can get relatively fine mapping between TMS and the brain.

In 1995 a group of neuroscientists published a paper called, "Modulation of muscle responses evoked by transcranial magnetic stimulation during the acquisition of new fine motor skills" in the Journal of Neurophysiology.

In this paper, they showed that they could map the amount of motor cortical territory devoted to specific fingers.

The authors had their subjects train on a piano and mapped motor cortex finger representation before and after training. Here's what they found:

Over the course of 5 days, as subjects learned the one-handed, five-finger exercise through daily 2-h manual practice sessions, the cortical motor areas targeting the long finger flexor and extensor muscles enlarged, and their activation threshold decreased.

Thus, they demonstrated that even adults show cortical plasticity after some simple muscle training. That is, piano practice caused the amount of brain devoted to voluntary muscular control grow.

So although you may not currently be able to flex your ring finger or control your individual toes, there's no reason that you can't learn how!

Amputees, for example, can learn to be quite dexterous with their toes.

Here's a man writing perfectly well:

And a woman demonstrating how she bathes:

So to (finally!) answer your question: you can't control your toes because you haven't practiced, and therefore the "toe" area of your motor cortex is too small to allow fine control.

Exercise your brain's plasticity and practice writing with your toes! Get back to me after a few weeks of practice and let me know how it went.

For science!

(Note, some of the above images probably came from my friend and zombie collaborator Timothy Verstynen many moons ago during our PhDs.)

ResearchBlogging.orgPascual-Leone A, Nguyet D, Cohen LG, Brasil-Neto JP, Cammarota A, & Hallett M (1995). Modulation of muscle responses evoked by transcranial magnetic stimulation during the acquisition of new fine motor skills. Journal of Neurophysiology, 74 (3), 1037-45 PMID: 7500130
Penfield, W., & Boldrey, E. (1937). Somatic motor and sensory representation in the cerebral cortex of man as studied by electrical stimulation Brain, 60 (4), 389-443 DOI: 10.1093/brain/60.4.389