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Smart Reads: Bradley Voytek’s ‘Do Zombies Dream of Undead Sheep?’


When neuroscientists Bradley Voytek and Timothy Verstynen got together for regular beer and horror film sessions, they naturally started wondering what was going wrong in the brains of zombies shuffling across the screen. Now, they’ve buckled down and delivered an exhaustive report on the science of zombie symptoms in their new book, Do Zombies Dream of Undead Sheep?: A Neuroscientific View of the Zombie Brain. We recently got a chance to chat with Voytek about the neuroscience of the undead:

(Note: This interview has been lightly edited for clarity and length.)

World Science Festival: So what is the most plausible way for “zombieism” to be transmitted?

Bradley Voytek: I like to joke that I know nothing about the human body once you get below the brain. So if you’re asking me about immunology and epidemiology and genetics and infection, I have no idea. The canonical method is usually some blood-borne or bodily fluid-borne virus or infection of some sort.

If we’re going to go for plausibility, there’s certain things in the animal kingdom like the Cordyceps fungus, which infects ants, and causes their behavior to change—the ant will climb up onto a leaf and bite down and hold on so they don’t get blown off, and then the fungus essentially causes them to explode, spraying spores everywhere. The higher up they are, the farther the spores spread, that’s the idea.

WSF: Do we know what the fungus is doing in the ant brain?

BV: No, it’s still a major area of ongoing research. Evolution is crazy, man!

WSF: How did you guys approach writing this book?

BV: We’re taking a forensic neuroscience approach, like back in the pre-imaging days, before you had fancy brain scanners and all that. Back in the gladiatorial days of ancient Rome, the famous physician Galen was treating the gladiators, and he noticed that certain kinds of brain or spinal injuries led to specific kinds of behaviors or deficits. After the person died, he’d look at their brain and find some kind of traumatic lesion or injury to a particular brain area that caused them to, say, lose the ability to speak.

We kind of reversed that process. Given what we know about neuroscience, after observing zombie behavior, what would we say the zombie brain would have to look like to cause it to lose the ability to speak, and walk in shuffling movements and not be conscious of its surroundings? We broke the behavior down into symptoms, basically.

WSF: Can you give an example of a zombie symptom and a possible cause?

BV: Taking the classic 1960s zombie, why do they walk so slowly? Well, motor control—how our brain translates neurons firing into body movements—is incredibly complicated. You have a cauliflower-shaped structure in the back of your head called the cerebellum, which is only about 15 percent of brain volume, but has about half of the neurons in your brain. We think this area is doing really fast calculations to correct for movement errors.

You can be missing your cerebellum and be doing pretty okay, but you’ll have these moving deficits: you tend to walk with this wide gait, you have relatively poor balance, it’s hard for you to react quickly to things. So, based on the evidence, we can say that something in the zombie’s cerebellum has gone awry. Either it’s missing, or the signals its sending to the rest of the brain are not quite right. And we can keep doing this for every zombie symptom.

WSF: What consequences are there when a zombifying agent brings a dead brain back to life?

BV: Neurons start to die off within minutes when there’s a lack of oxygen—especially neurons in the hippocampus, this seahorse-shaped area a couple inches in from your temple, which is pretty important for forming memories. So if, as in The Walking Dead, the zombie infection takes hold after someone dies and reanimates them, if there’s that couple minutes of delay before restarting, there’s going to be some brain areas dying off.

In the book, we call this the “time to resurrection” hypothesis. If you look at “fast zombies,” like in the movie 28 Days Later, the infection there takes just seconds to transform somebody from a normal person into this rage-fueled monster. We argue that because you’re only dead for a few seconds, there hasn’t been much damage to the physical substrate of the brain, so you’re still coordinated. But in Night of the Living Dead, the undead may have been dead for weeks or months, so they would have decayed quite a bit.

WSF: Does neuroscience offer hope for zombies? Can they be cured?

BV: There’s this movie, Fido, where humans take the remaining zombies and put this little remote control collar on them that keeps their behavior in check—and they start using zombies as manual laborers, housekeepers, things like that. That’s not too far-fetched. I can actually use a device called a transcranial magnetic stimulator—a non-invasive tool we use to investigate brain function—to stimulate different parts of your motor cortex, the neurons on the outer part of your brain that send signals to your muscles, and make different parts of your body twitch. So it’s not super-far fetched that we could create a remote-controlled zombie.

Curing them, though, goes into infection, epidemiology, and all that. But if it’s an organic cause, potentially there would be a cure.

WSF: It seems the book is a good way for people to absorb principles of neuroscience that maybe they wouldn’t have gotten from a textbook!

BV: Yes! We hope that people who don’t normally care about this will end up accidentally learning something about the brain. If I walk into a lecture hall and start talking about excitation and inhibition ratios, the eyes glaze over after that first Powerpoint slide. But if I go in and start talking about, OK, why is it that the zombie infection causes the undead to crave human flesh, suddenly peoples’ eyes light up, and high school kids are paying attention and asking these really pointed questions.

Below, check out an excerpt from the book where Voytek and Verstynen investigate the sleep habits of zombies (or lack thereof):

There are three major symptoms that we see in modern zombies that make us think that these deep brain systems regulating sleep are dysfunctional. First, zombies never really appear to sleep. They can wander around day and night looking for prey, without rest. This extreme form of insomnia suggests that the reticular activating system is chronically engaged and may never shut off. This is similar to what you see in animals with lesions (localized tissue damage to the sleep-promoting VLPO neurons).

Second, while they are awake enough to move around and act, zombies appear to lack definite forms of awareness that are the hallmark of being completely awake. Instead they appear to move with stupor and slowness that we all experience in those liminal moments between being asleep and being awake. Thus, there appears to still be some engagement of the sleep-promoting neurons in the deep brain. This at first seems counterintuitive, given the first symptom of insomnia… but remember, the switch between awake (“on”) and asleep (“off”) normally happens in fast cascades. If the cascades don’t happen in such a fast “flip-flop” fashion then you get sleep disorders like somnambulism.

Third, zombies appear to have horribly deficient spatial and experiential memories such as are encoded by the hippocampus. They get lost fairly easily, even in indoor malls where they’ve been stuck for weeks. We know that the creation of this form of memory is a sleep-dependent process. This further supports the hypothesis that zombies do not have well-formed sleep cycles.

Excerpted from Do Zombies Dream of Undead Sheep? A Neuroscientific View of the Zombie Brain by Timothy Verstynen & Bradley Voytek © 2014 by Princeton University Press. Reprinted by permission.




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