Zombie Brain: Conclusions

This post is the final installment of our collaborative venture (between Oscillatory Thoughts and Cognitive Axon) exploring the Zombie Brain.  We hope you’ve enjoyed this little 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 causing them to move slowly.

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 neocortex: 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. Also, 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. Relatedly, 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. This is shown in yellow below and presented over a normal human brain for comparison.
 

Overlay (yellow is zombie, gray is human)

It is interesting to point out, from a 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. His hypothesis was 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 them, join them: 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.

Zombie Brain: Flesh Addiction

This is yet another installment of multi-day series on The Zombie Brain. Be sure to visit Oscillatory Thoughts tomorrow for another post in this series!

Symptom 8: Flesh addiction

“Braainss... BRAAAINS!” Zombies call out for them like a man calls out for water after a week in the desert. Yet no matter how much they eat, they can never be satisfied. It’s as if the craving to consume brains and/or human flesh is the sole thought running through a zombie’s “mind”. Zombies will even risk loss of “life” and limb to satisfy these urges.

These symptoms mirror those seen in dysfunction of the “reward circuits” in the brain. It’s as if the living dead are addicted to flesh and flesh consumption is a compulsion. 

The sense of reward, or the “high”, that you experience originates first from dopamine cells that rest in an area of the brain collectively known as the ventral striatal reward pathway. This includes a larger network of areas in the neocortex, midbrain and brainstem.

Adopted from Wise (2002)

In many ways this circuit starts and ends in the brainstem with the release of dopamine. Note that these are a different set of dopamine neurons than those involved in the aggression circuit we discussed earlier.  Activating these “reward cells” with stimulation (e.g., drugs, food, sex, etc., in humans, or direct electric stimulation in animals) causes them to transmit dopamine to other regions in the cortex and subcortex such as the striatum. This reinforces the drive for future reward seeking behaviors. 

These signals converge to a set of cells in the nucleus accumbens, which is essential for determining the motivational significance of the reward stimulus, causing the person to think, “Mmmmm that was fun; I’ll do that again.” 

In cases of extreme drug abuse, simply showing pictures of drugs to an addict will engage this reward circuit. The same is true for people addicted to eating: showing them pictures of food can reengage the same reward regions as eating.

In zombies, this dopamine reward circuit is likely in overdrive. Paired with a loss of the feeding “off-switch” in the brain, this could lead to the insatiable appetite that zombies have. Of course, in humans fatty diets cause more hunger and the brain is a highly fatty substance, so unfortunately, the more the zombie eats... the more it wants… But we'll discuss that a bit later.

We expect that if you put a zombie in an MRI machine and showed it pictures of human flesh, you would detect activation in many regions of this ventral reward circuit. In fact, these would be the same activation patterns we'd expect to see in the brain of a (living) drug addict when presented with pictures of their drug of choice.

What fMRI would look like in the zombie brain.

But why isn’t a zombie satisfied even after it has consumed an entire human on its own? Well that's a whole other blog post. Let's just say the zombie brain doesn't know or doesn't care when it's full.


So today's lesson shows us that zombies are depraved flesh addicts who will stop at nothing to get their next fix (i.e., you).

Symptom 7: Stimulus-locked attention

Head over to Oscillatory Thoughts for today's Zombie Brain factoid: Stimulus-locked Attention.

Zombie Brain: Pain Perception

This is part six of our multi-day series on The Zombie Brain. Be sure to visit Oscillatory Thoughts tomorrow for symptom 7!

Symptom 6: Pain Perception

Cut off an arm, yet they keep coming. Shoot them in the chest, they keep coming. Light them on fire, they keep coming. How does the zombie continue to chase us despite wounds that would cause debilitating pain in a normal person?

It's quite simple really. They’re not aware of the damage done to them.  More specifically, they may not be feeling the damage being done.

That toaster's going to leave a mark!

Scientifically we call the sensation of painful stimuli nociception.*  The physiological systems that regulate our experience of pain are incredibly complex.  So I'm going to give you the short and simple version. 


Receptors in the skin pick up mechanical, thermal or chemical changes relay this information to neurons in the spine.  This information goes up the spine through a few different different routes and gets relayed to several cortical regions.  The combined recruitment of these neocortical regions then gives rise that "Ouch! F#$% that hurt!" response.  

The pain pathways (from Basbaum et al. 2009)

A majority of these pain signals are processed in a forward part of the parietal cortex, known as the somatosensory cortex.  These area sits right behind the region of the brain that consciously controls movements.  Now the somatosensory cortex actually regulates our experience of all physical sensations (touch, vibrations, etc.) and processes most of the conscious signals that we are aware of feeling.  However, this area is actually made up of  two distinct areas : the primary and secondary somatosensory cortices. Each regulates the processing of different types of sensory information.

There is also a second pain pathway that regulates our rapid unconscious experiences of pain.  Most of this engages the inappropriately named "fight-or-flight" circuit via the amygdala.  Signals are relayed to a few separate areas such as the cingulate (that processes conflict) and the insula (that, well appears to do everything).  It is thought that these areas regulate the emotional salience of pain.  

Now let's think about this... when was the last time you saw a zombie get emotional about anything let alone a little thing like having a limb chopped off?  This suggests that this second pain pathway is disrupted in the zombie brain.

It’s also clear that zombies can still move and they have an idea of basic sensations (they know where their own bodies are, and they do react reflexively to stimuli), but they don’t appear to have conscious awareness of pain and other sensations. This gives us good reason to believe that the nerves that sense pain, pressure, and so on in the body are intact, because zombies do still react to stimuli. We also know that the spinal cord that transmits those sensations up to the brain (and movement signals down from it) must also be intact. Furthermore, before touch senses get to the brain, they stop in the brainstem where they can be mediated and controlled before entering “conscious” perception.

Thus, we believe that there are a couple of vectors for the zombie’s immunity to pain.

First, their secondary somatosensory regions in the parietal cortices are impaired. This would minimize experiencing some types of painful sensations, but not all.  Note that the primary somatosensory cortex (regulating fine touch, sense of limbs, etc.) is still intact.

More importantly, neocortical regions like the insula and cingulate should also be obliterated in the zombie brain.  This would eliminate any emotional reactions to the residual painful stimuli processed in the somatosensory cortex.

Thus zombies may actually feel pain and really just not give a crap about it.  Just like Chuck Norris.

There you have it folks.  A numb, cold-hearted creature incapable of feeling pain (please save the lawyer jokes for another forum).

* Contrary to popular belief, we don't have just 5 senses.  We probably have closer to 20, and most of them involve different types of physical senses.  There's a sense for feeling your limbs in space (proprioception).  There's a sense of fine touch and vibrations called epicritic touch.  There's the feeling of heat, sharp pain, etc.  

Zombie Brain: Language Deficits

This is part four of our multi-day series on The Zombie Brain. Be sure to visit Oscillatory Thoughts tomorrow for symptom 5!

Symptom 4: Language deficits

Let's face it, zombies aren’t known for their oratory skills. Usually you’ll hear nothing but a collective set of moans as they’re pounding at the barricaded doors. Keep in mind that the most fluent phrase we ever hear Tarman say in Return of the Living Dead is "Braaaaaains!"

Tarman goes on a short lived speaking tour

At best you’ll get a disjointed burst of individual words. For example, a somewhat intelligent zombie might utter into the walkie-talkie of a recently consumed police officer, “send... more... cops...” in order to get a new delivery of fresh meat (as observed in Return of the Living Dead). But that would be considered the Shakespeare of zombies.

This type of speaking is called telegraphia, characterized by the fact that the words are present, but the execution is jammed. Neurologically, this relates to a specific disorder known as expressive aphasia or, as it is classically known, Broca’s aphasia.  

Now in the normal living human, this language production ability is mediated by an area of the brain that rests just behind your temple. More often than not, just behind your left temple.

Broca's area is named after Paul Broca, who described the language deficits of Patient "Tan." Tan was reportedly was unable to say anything but the word "tan" after this region of the frontal cortex was damaged. (Historical side note: Tan could actually say many other things however, they were all just vulgar profanities. Apparently French neurological societies frowned upon the idea of naming him Patient "Foutre!").

Okay, back to zombies!  Zombies don't just have a problem producing language, they also don't seem to be able to comprehend it either. They never respond to verbal commands and rarely seem to stop read road signs (hence they are chronically lost). This inability to comprehend language reflects another type of classical deficit called receptive aphasia, known by it's more common name Wernicke’s aphasia. You guessed it... that's because the guy who discovered it was Carl Wernicke.

Wernicke's aphasia comes from damage to a different region of the brain. This sits farther back in your head, at the junction of the temporal and parietal lobes (basically behind and slightly above your ear).

What does this tell us about the zombie brain? Well it would appear that the frontal language production areas and the temporal/parietal language comprehension areas are both atrophied in the zombie cortex. Since these regions communicate with one another via a large bundle of white matter called the arcuate fasiculus, its safe to say that this “arcuate circuit” is obliterated in the zombie brain, as well as the frontal and parietal language regions. 

Damage to the frontal (Broca’s) region leads to expressive (Broca’s) aphasia, and damage to the parietal (Wernicke’s) region leads to receptive (Wernicke’s) aphasia. Thus, all language and communication skills would be severely disrupted in the zombie brain.


Bottom line: Don't try talking to a zombie. It's not worth your time.

Symptom 3: Long Term Memory Loss

Be sure to head over to Oscillatory Thoughts for our third symptom of the Zombie Brain: Long Term Memory Loss

Zombie Brain: Lumbering Walk

This is part three of our multi-day series on The Zombie Brain. Be sure to visit Oscillatory Thoughts tomorrow for symptom 3!

Symptom 2: Lumbering walk

As soon as zombies rise from the dead, they begin walking. Well not walking... more like lumbering. Each step is slow and arduous. Their stance is wide and steady. This presents us with a very important clue about their brains.

Now a lot has been said about the origins of the zombie “walk.” Given the pervasiveness of the disease, some have argued that zombie movements are like those seen in Parkinson’s disease. Parkinson’s is a devastating neurodegenerative disorder caused by the loss of dopamine neurons in the brain that project to a group of regions collectively known as the basal ganglia. It is partly characterized by a slow decrease in the coordination and ability to move (not spastic, jerking movement as is stereotyped... that’s a side effect from the medications).

However, consider this, persons afflicted with this disease will shuffle when they walk, adopting short sliding movements, and a hunched posture. Shaking and tremors are also present while patients are not moving. This does not sound like the zombie movements we see on the silver screen. Zombies can move quickly when striking and show no signs of a hunched posture or tremor. Therefore, we believe that it’s time to do away with the basal ganglia theory of zombie locomotion!

Example of a Parkinsonian Gait (skip to 0:30 mark)

The lumbering zombie walk more resembles the movements characterized by damage to an area of the brain called the cerebellum.* The cerebellum is a little cauliflower shaped region at the back and base of your brain.

It is involved in many functions (e.g., learning, language, memory, sensations), however it is classically described as a motor coordination region. Indeed, this “little brain” has about half of the neurons in your entire brain!

Example of Cerebellar Ataxia Gait

Patients with degeneration of the cerebellum exhibit a syndrome referred to as spinocerebellar ataxia, which is characterized by uncoordinated movements of many kinds, including a wide-stance and lumbering walk.

Although patients with cerebellar ataxia exhibit many coordination problems, the symptoms are alleviated somewhat with the assistance of vision. This may be another important clue about the zombie brain.

Thus, we contend that zombies suffer from a severe spinocerebellar ataxia.  Well, the “slow zombies” do, at least.

What about fast zombies? Given the terrifyingly coordinated movements that “fast zombies” exhibit (think 28 Days Later or the recent remake of Dawn of the Dead) their cerebellums are likely intact. Thus we can also begin to develop neurological classifications of different subtypes of the zombie disorder that may give important clues to the etiology of the zombie epidemic.

* Truth be told, when we had the opportunity to ask George Romero why he made his ghouls walk they way they did in the Living Dead Movies, he responded “They’re suppose to be dead. They’re stiff. That’s how you’d walk.” Not quite the answer that appeals to our neuroscience instincts, but a good alternative hypotheses to test in the next zombie apocalypse.  Check out part of the interview below.

Symptom 1: Impulsive-Reactive Aggression

Be sure to head over to Oscillatory Thoughts for our first symptom of 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.

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.

When good science is used badly

In a recent New York Times op-ed piece, branding guru and self-described scientist Martin Lindstrom gives a perfect example of why scientific tools should only be used by professional scientists and not self-trained hacks.  In his article titled "You love your iPhone. Literally." Mr. Lindstrom made the case that we are not addicted to our smart phones, but that we have established a relationship with our technology that is on par with the process of "love."

Mr. Lindstrom would have you believe that he's not just giving his professional opinion as a marketing consultant, but that he has scientific data to validate this claim.  However let's take a close look at these spurious claims.

First, Mr. Lindstrom describes an imaging experiment that he undertook to see if marketed brand names engage the same brain circuits as religious symbols.

"A few years back, I conducted an experiment to examine the similarities between some the world’s strongest brands and the world’s greatest religions. Using functional magnetic resonance imaging (fMRI) tests, my team looked at subjects’ brain activity as they viewed consumer images involving brands like Apple and Harley-Davidson and religious images like rosary beads and a photo of the pope. We found that the brain activity was uncannily similar when viewing both types of imagery."

To someone who doesn't live in the world of brain images all day (like I do), this sounds pretty promising right?  You might think, "Huh? My brain is activated the same way when I see the Apple logo as when I see the Madonna of Brugges."  But that is nowhere close to what these results reflect.  Now I haven't seen the details of his study, so I can't lay claim to the soundness of his methodologies.  However, I can point out two major inconsistencies in his interpretations.

First, seeing "uncannily similar" brain areas engaged when seeing objects and religious symbols is not that surprising. It's not surprising that visual symbols are encoded in the same brain networks.  They're visual stimuli with interpretive meaning.  But that doesn't mean that you value them the same way.  A symbol may just be a symbol as far as the brain is concerned.

Second, Mr. Lindstrom is committing one of the most basic of scientific fallacies.  Not detecting a difference between two conditions isn't the same thing as there not being a difference.  It is called "arguing the null hypothesis".  In science we can't say anything definitive about differences that we don't see, only difference that we do.  Just because monkeys and children pick their noses at the same rate does not mean that they're the same creature.  But this is essentially Mr. Lindstrom's conclusion.

Okay, so he's a bad fMRI researcher.  Big deal... there are a lot of them these days.  Let's look at some of Mr. Lindstrom's other data.

"...I gathered a group of 20 babies between the ages of 14 and 20 months. I handed each one a BlackBerry. No sooner had the babies grasped the phones than they swiped their little fingers across the screens as if they were iPhones, seemingly expecting the screens to come to life."

This again is wrong in so many ways.  As anyone who has ever interacted with children can tell you, they aren't the most coordinated of folks.  In fact the brain systems that regulate our movements aren't fully developed until you're almost a teenager.  Did Mr. Lindstrom give phones to children from countries where iPhones aren't as common for a control group?  Presumably not, but that would be one way to see whether this behavior is just random grasping from people without fully formed cerebellums.

Perhaps most importantly, children imitate adults.  They adopt the behaviors of the people around them as a way of learning the world.  That's a key part of development (as evidenced by these two kids who obviously don't know how to speak, but sure know how to act like it). Just because children are imitating their parents doesn't mean that they value them in the same way as Mr. Lindstrom appears to be suggesting.

Finally, and perhaps most egregiously, Mr. Lindstrom reports on yet another brain imaging study.  In this case he presented either a visual movie of a ringing phone or the sound of a ringing phone.  

"In each instance, the results showed activation in both the audio and visual cortices of the subjects’ brains. In other words, when they were exposed to the video, our subjects’ brains didn’t just see the vibrating iPhone, they “heard” it, too; and when they were exposed to the audio, they also “saw” it. This powerful cross-sensory phenomenon is known as synesthesia."

Had Mr. Lindstrom bothered to go to Wikipedia, he would know that this effect is not synesthesia.  Synesthesia is an inherent, hard-wired "cross connection" in the brain.  It's not learned.

What Mr. Lindstrom is in fact reporting is the very simple result of Hebbian learning: "neurons that fire together wire together."  Seeing visual areas light up with certain auditory (or tactile) stimulation is a fairly commonplace finding in the brain imaging literature.  We often both see the phone light up (or vibrate) and hear it ringing at the same time.  Eventually an association is formed within the brain.  Mr. Lindstrom would probably see the same thing if he showed his subjects a picture of a baby crying, a doorbell, etc.

Finally, there's this last bit of "evidence" (quotes are mine).

"But most striking of all was the flurry of activation in the insular cortex of the brain, which is associated with feelings of love and compassion. The subjects’ brains responded to the sound of their phones as they would respond to the presence or proximity of a girlfriend, boyfriend or family member."

There are a host of other areas that are also associated with "love and compassion" in the brain.  There's not one single area that encodes these concepts.  As far as I know, there is no definitive conclusion about where the concept of "love" is encoded in the brain.

So this becomes a guilt by association conclusion: brain area A is active when experiencing X and Y, therefore X is the same as Y (or worse, X causes Y). If Mr. Lindstrom had seen the same area of the brain engaged when he presented an image of a fire-truck and an image of a t tomato, it doesn't mean that your brain thinks of the truck as being made of tomatos (nor that tomatoes are baby fire-trucks).  Sadly, this is a fallacy that many established neuroscientists also make.  But that's a topic of another post.

As a professional neuroscientist, my reaction to the findings Mr. Lindstrom presents in his op-ed is "So what?" Nothing he reports provides a shred of evidence that we "love" our iPhones, at least neuroscientifically speaking. Nor does he show that the experience of using your smart phone is the same as falling in love or having a religious experience.  All Mr. Lindstrom demonstrated was what can happen when the tools of sciences are placed in the wrong hands.

Perhaps all neuroimaging articles should come with the disclaimer: "Performed by trained professionals, do not try this at home."