A Harvard Psychiatrist Explains Zombie Neurobiology

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By Mark Strauss

In Night of the Living Dead, zombies are brought back from the dead by a "mysterious force" that allows their brains to continue functioning. But how exactly does a zombie brain function? Finally, a Harvard psychiatrist has the answers.

Through education Dr. Steven C. Schlozman is an assistant professor of psychiatry at Harvard Medical School and a lecturer at the Harvard School of Education. He is also an avid sci-fi and horror fan - and, apparently, the world's leading authority on the neurobiology of the living dead. He has even drafted a fake medical journal article on the zombie plague, which he calls Ataxic Neurodegenerative Satiety Deficiency Syndrome, or ANSD (the article has five authors: one living, three "deceased" and one "humanoid infected").

Schlozman's foray into necro-diagnostics began when he volunteered to give a talk for the "Science on Screen" lecture series at the Coolidge Corner Theatre in Brookline, MA. He conducted extensive research by talking with George Romero and immersing himself in genre literature and memorabilia - which is why the alternate title for his lecture is "A Way Cool Tax Deduction for a Bunch of Cool Books, Action Figures and a Movie."

So yes, Schlozman's lecture is actually quite funny, and liberally sprinkled with other pop culture references including Buffy the Vampire Slayer and Firefly. But the underlying science is serious. His lecture is a tour of the human brain, using the living dead as a narrative theme.

According to Dr. Steven C. Schlozman, this is your brain on zombies:

The Frontal Lobe

This part of the brain is involved with "executive functioning" - enabling us to think carefully and solve problems in an abstract way. Clearly, there's not much going on there if you have the misfortune of being afflicted with living deadness. But we do know that zombies can see us and sense us. Schlozman concludes that zombies possess just enough frontal lobe activity to "listen" to the thalamus, through which sensory input is processed.

But the frontal lobe function most relevant to understanding zombie behavior is the control of "impulsivity"-the general term for when you do something and, if you had two more seconds, you might not have done it. For instance, if in a fit of rage you have the sudden urge to punch your boss in the face, the frontal lobe intervenes and allows you to consider why that might be a bad idea.

The Amygdala and Anterior Cingulate Cortex

Absent a properly functioning frontal lobe, a zombie is driven entirely by base emotions - such as rage - that are housed in the primitive parts of our brain, notably the amygdala. There's precedence for this in nature. A crocodile brain, for instance, is mostly driven by the amygdala. Researchers have confirmed this by introducing lesions into the amygdala of animal specimens: the result is a drop in the attack and retreat response that correlates significantly with the amount of damage that's done to that region of the brain. A crocodile without an amygdala isn't really a crocodile. As such, Schlozman argues, "you can't really be mad at zombies, because that's like being mad at a crocodile," adding that it's the delicate balance between frontal lobe and amygdala "that makes us human."

That balance is maintained by the anterior cingulate cortex, which modulates and dampens the excitability of the amygdala as it talks to the frontal lobe. So, when the amygdala gets all stirred up by fear, anger or lust, the anterior cingulate cortex steps on it a little bit, giving the frontal lobe time to think everything through before it sends signals toward the motor cortex and we act upon those impulses.

A zombie would have a dysfunctional anterior cingulate cortex, rendering it unable to modulate feelings of anger. The result? Hyper-aggression.

The Cerebellum and the Basal Ganglia

Science may once and for all settle the heated debate over whether "the infected" in 28 Days Later could be classified as zombies.

Schlozman says "no," observing that "the infected" possess "some sort of higher cortical function going on that allows them to hunt humans." Moreover, the fake zombies in 28 Days Later exhibit fluidity of motion. They can run, jump, climb and quickly change direction-activities that the true Romero zombies are incapable of performing.

Clearly, zombies suffer from cerebellar and basal ganglia dysfunction (duh!). Those are the parts of the brain that make fluidity of motion possible. The basal ganglia helps us with coordinated movement. The cerebellum helps us with balance. In fact, if you visit the website of the National Institutes of Health and read about cerebellar degeneration (such as ataxia), the symptoms match the familiar gait of the living dead: "a wide-legged, unsteady, lurching walk, usually accompanied by a back and forth tremor in the trunk of the body…"

Mirror Neurons

This is recent, cutting-edge research in the field of neuroscience. Schlozman describes mirror neuron theory as a "neurobiological model for empathy, which suggests, in a very hopeful way, that we might be wired to connect with one another." Regions of the brain are recruited in response to social interactions in which we watch and thus experience the experiences of the "other."

As a press release issued by the European Science Foundation explains it: in

Just as the same mirror neurons fire when observing and doing certain tasks, so other mirror neurons may be triggered both when experiencing a particular emotion and when observing someone else with that emotion.

But, Schlozman asks, what if the things we're fighting have brains that are incapable of connecting? In response, we disconnect from each other. Schlozman quotes a veteran of the Battle of Yonkers in the book World War Z: "Shock and Awe! But what if the enemy can't be shocked and awed? Not just won't, but biologically can't?"

At the Battle of Yonkers, the humans hit the zombie horde with everything they've got. But the zombies keep coming. They don't look scared. They don't look excited. They don't look enraged. And that actually freaks out the humans more than anything else, prompting the humans to turn on each other.

Schlozman suggests that mirror neurons also help explain the popularity of the zombie genre among the living. While watching these movies, "we like the permission to look at these things that look human - but aren't human - and have utter and complete permission to blow their heads off." In other words, we get off on the thrill of guiltless violence. We enjoy a brief vacation from empathy, and take our crocodile brains out for a spin.

By way of example, I came across an interview with actor Mike Christopher Berhosky, who played the iconic Hare Krishna zombie in the 1978 movie, Dawn of the Dead. Berhosky describes the audience reaction to the film's screening:

I got bashed in the head and everyone CHEERED. Took the wind right outta' my sails. Everyone hated the Hare Krishna devotees for their incessant pestering and swarming them at the airports and such….Killing off my character had the effect of releasing a lot of pent up frustration….bashing in the Hare Krishna zombie's head was much more than getting rid of another pesky zombie…it was VENGEANCE.

But the fun lasts only up to a point. As the movies progress, Schlozman says, we start to feel uncomfortable with the loss of our humanity-that we are "so willing to forsake those mirror neurons."

The Ventromedial Hypothalamus

In the movies, zombies are always hungry, no matter how many supporting actors they consume. The most likely explanation is that zombies don't have a properly functioning ventromedial hypothalamus: the region of the brain that lets you know whether you've eaten enough. The result is hyperphagia. Zombies will eat and eat and eat, but never feel satiated.

That raises a slightly awkward question: If zombies are constantly eating, then how come they never poop?

Schlozman doesn't know for sure, but he has at least one promising theory: Maybe the living dead are constipated.

Now we know why zombies are always moaning.

Mark Strauss is a senior editor at Smithsonian magazine.