When on May 16, the CDC, a normally staid agency whose mission includes issuing recommendations for disaster preparedness, released its advice to help Americans prepare for a zombie apocalypse, many critics lauded it as pure genius. But it was not the first time that the public's fascination with the “undead” was used as a ploy to steer attention to a typically mind-numbing subject. On Jan. 19, Bradley Voytek, PhD, presented his work with Timothy Verstynen, PhD, on the Living Dead Brain at San Francisco Nerd Night, describing it as “50 percent nerd fun and 50 percent a way to make fun of cognitive neuroscience.”
THE SIMULATED FULL z...Image Tools
The two neuroscientists became friends in graduate school where they realized that they both shared a fascination with the zombie movie genre. In their day jobs, Dr. Verstynen, a post-doctoral research associate at the University of Pittsburgh in the Learning Research and Development Center and the Center for the Neural Basis of Cognition, maps cognitive and motor networks in the human brain; Dr. Voytek, a post-doctoral fellow at the University of California-San Francisco, focuses on the role of neuroplasticity in cognition and stroke recovery.
DR. BRADLEY VOYTEK (...Image Tools
Neurology Today spoke to the two self-proclaimed geeks to try to find out how their brains tick. (Readers, be forewarned — this discussion about zombie brains requires some stretch of the imagination!)
WHAT WAS YOUR FIRST EXPOSURE TO ZOMBIE ENTERTAINMENT?
TIMOTHY VERSTYNEN (TV): I think I was 10 or 11 years old when I first watched “Return of the Living Dead” on late night TV at a friend's house. My friend and I didn't watch the whole movie but we were nevertheless so terrified that we didn't sleep the rest of the night. I didn't really see the classics — “Night of the Living Dead,” “Dawn of the Dead,” etc. — until I was in high school or even grad school. But I always remember thinking “how could it happen?” Later, when I was in grad school, I watched movies like “28 Days Later” with Brad; they had a slightly more biologically plausible approach — that is, the zombies weren't really dead, but just out of control and pissed off humans; they arose from a pathogen rather than supernatural source, for example. It was then that we started thinking about how you'd have to change the brain in order to turn a person from a logical/semi-rational human being into a blood thirsty, stimulus-driven zombie. It turned out to be much easier than we expected.
BRADLEY VOYTEK (BV): Growing up I was always a fan of the '80s slasher flicks like “A Nightmare on Elm Street.” I was also really into comics and sci-fi. It wasn't until a little later — after I started studying psychology and neuroscience in college — that I started to appreciate the zombie “genre.” Max Brooks' recent novel World War Z was exceptionally well-written and a great read. The Walking Dead comic book series and TV show are also excellent. As far as movies go, however, I'm also a huge fan of the first zombie film, George Romero's “Night of the Living Dead.” But in terms of complexity and depth I think “28 Days Later” is a phenomenal film. That said, I'm really into the modern zombie comedies, especially “Shaun of the Dead.”
WHOSE IDEA WAS IT TO PURSUE THIS PROJECT?
TV: The seed of the project was festering in our heads for a while. But last year, after Matt Mogk of the Zombie Research Society (ZRS) saw a video of a talk Brad gave about neuroscience and neuroanatomy, he asked if he'd like to give a talk on the zombie brain.
BV: Now we're both on the ZRS advisory board with film director George A. Romero, and I'll be on a couple of panels at Comic-Con this year with writers such as Max Brooks. It's all quite surreal, as I've attended Comic-Con just about every year since I was 14 or 15. As a scientist, I never thought I'd find myself in a place where I'd be speaking there! It's awesome.
WHAT WAS YOUR OBJECTIVE?
TV: Our first and foremost goal was to use this as a science outreach project. So the only fictional component of the talk was to be the target organism. Otherwise, everything else had to be couched in real neuroscience. Brad was actually the one who came up with the Capgras delusion connection and the link to the Papez circuit. My graduate advisor had always said how people with cerebellar ataxia had a “zombie walk” and used that to differentiate from the shuffle you see in people with Parkinson's. So that was the next logical link-up to known diseases. We just kept going with that kind of “forensic neuroscience” logic and after a while, we identified several “symptoms” that we could link to known circuits. Once we had a working model of what a brain should look like, I used some MRI image analysis tools to modify a template MRI brain that we use in research to resemble that atrophy you should see in the zombie brain.
IS YOUR FASCINATION RESTRICTED TO ZOMBIES OR DO YOU LIKE SCIENCE FICTION, IN GENERAL?
TV: I'm a pretty much a half-time nerd. I love most science fiction because it allows you to think outside the box and view the world from an alternative perspective. I'd say I'm less of a “Trekkie” kind of nerd and more of a Carl Sagan or cyber-punk/steam-punk dork.
YOU COINED THE TERM CDHD, OR CONSCIOUSNESS DEFICIT HYPOACTIVITY DISORDER — I REALLY LIKE THAT. WAS EITHER ONE OF YOU EVER DIAGNOSED WITH ADHD? I'M JUST GUESSING, SINCE NOT MANY PHD CANDIDATES HAVE EXTRA TIME ON THEIR HANDS!
TV: Yeah. Brad and I both agreed that part of this project would be a satire of the field. I think we settled on CDHD explicitly as a poke on the ubiquitous diagnosis framework used regularly in neuroscience. I've definitely never been diagnosed with ADHD, but I've been told that I don't sleep enough, so I think that's where I got the time.
BV: I've certainly never been diagnosed with ADHD, but I do have a bit of a tendency to go after the new shiny thing when I get a new project idea. I know a lot of researchers don't have a lot of free time, but I find that a few hours of focused work each day goes a very long way. I've got a special interest in neuroscience history, and have written pieces for Scientific American's guest blog. I find that these kinds of science-related but non-research activities help me think on my feet and keep me amused and fascinated by science in general. CDHD is a bit of a stab at modern psychiatry, psychology, and neuroscience. We researchers have a propensity for oversimplification and convoluted naming schemes, so we decided to follow suit.
I'M GOING TO SUSPEND DISBELIEF FROM THIS POINT FORWARD, BUT FOR THE SAKE OF SCIENCE: CAN YOU DESCRIBE THE CAUTIONS YOU TOOK TO SCAN THE ZOMBIE BRAIN AND WHY THEY WERE NECESSARY?
TV: Hah! We actually have portions in the talk where we joke about the difficulties of scanning zombies or doing electroencephalography on them. Originally, Brad had thought that we could just decapitate the zombie in order to minimize motion in the magnet. However, at that point we were talking about “doing” fMRI and we thought, “Hmmm… no blood flow means no BOLD signal.” Also, those darn cranial nerves would still allow for head motion. So we scrapped that idea and decided that the best approach was to use tetrodotoxin to induce whole body paralysis. Suddenly head motion — and potential zombie bites — aren't a problem anymore. It also gave us an opportunity to talk about sodium channels to the audience.
BV: Incidentally, tetrodotoxin is what Wade Davis [the ethno-botanist who wrote The Serpent and the Rainbow, which inspired a film of the same name] first hypothesized caused “zombism.”
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WHAT WERE YOUR FINDINGS ON CDHD?
BV: We worked out what brain regions would have to be affected to cause those behavioral symptoms. This was a lot of fun, and harkened back to a question that Prof. Jeffrey Winer would give his neuroanatomy students on their final, on occasion, which basically said: “You're sitting in your chair at home, watching TV when you hear the doorbell ring. You get up, open the door, and say hello. Describe the neuroanatomical substrates for these behaviors.” It's brutal, but a great mental exercise.
TV: We found that the zombies suffer from a global impairment of several systems. First, they suffer from impulsive-reactive aggression disorder linked to a loss of the orbitofrontal control signals to the amygdala. Thus, they have a hyper-amygdala disorder; Steven C. Schlozman, MD, at Harvard Medical School wrote a novel about this, The Zombie Autopsies. This is clearly present in the “28 Days Later” [movie] zombies. We also found they suffer from ataxic movements due to a loss of the cerebellum. Additionally, they have bilateral hippocampal damage, which explains the lack of long-term memory consolidation. Obviously, the whole arcuate language circuit is destroyed in the zombies, which explains their aphasias. In some cases, Broca's circuit may be intact enough to allow limited communication abilities, such as moaning, but assuredly, the posterior language areas are all destroyed leading them to lack verbal comprehension. Their reduced pain response is due to damage to the secondary somatosensory cortex, although this may also be mediated by damage to ascending spinal pathways. They also have attentional locking problems, such as Balint's syndrome, due to bilateral degeneration of the posterior parietal cortices, which also affects their coordination abilities. This is exemplified in the opening scene in “Land of the Dead” where the zombies are constantly distracted by fireworks. Dysfunction of the ventral striatal reward pathways leads to addictive behaviors, particularly a “flesh addiction.” Finally, as the name states, they suffer from a completely lack of meta-consciousness thanks to an ablation of the claustrum.
BV: I pointed out to Tim that many of the brain regions we were implicating were part of the Papez circuit, which was great because the way that James Papez showed that his hypothesized “emotion” circuit was actually neuroanatomically connected was by injecting a cat's brain with the rabies virus —did I mention I'm a neuroscience history buff? This was perfect, because “modified rabies virus” is one of the more popular theories about what could actually “cause” zombism.
YOU ALSO MENTIONED CAPGRAS DELUSION. IS THERE A PARTICULAR FILM THAT CAPTURES THIS WELL?
TV: Well, of course, there's the classic “Invasion of the Body Snatchers” in which everyone is replaced by pod-people. There's also a really bad 90s movie called “The Faculty” in which all the teachers at a school are being replaced by aliens. I've always imagined these movies show what it might be like to experience Capgras delusion (assuming the aliens weren't real). Since we don't know the underlying neural architecture of this delusion, we linked it up to a dysfunctional mirror neuron system — that one was just for fun! Basically, the zombies don't show mirror neuron responses from humans, only other zombies.
ZOMBIES ARE SO YESTERDAY. ANY THOUGHTS ABOUT WHAT A VAMPIRE BRAIN LOOKS LIKE?
BV: You're putting us on the spot with this! Off-the-cuff, supernatural aspects such as turning into a bat aside, what are the basic behavioral traits of (modern) vampires? They drink blood, they ve got heightened senses, and theyvre emotionally roffo but highly charismatic and hypnotic. So the first thing that jumps to mind is Klüver-Bucy syndrome, which is caused by bilateral damage to the medial temporal lobes. This leads to symptoms including hyperorality, hypersexuality/indiscriminant mating, emotional placidity, overeating, and pica (eating strange objects). Right off the bat (pun intended), we've got one disorder that hits of lot of the vampire behaviors.
TV: Zombies will always be around. Matt Mogk (of the ZRC) likes to point out that zombies wax and wane in popularity with the state of the economy. As economic conditions improve, zombies become less popular. When recessions come in, zombies return. That said, I've always thought of doing a neurobiological analysis of superheroes. But, I think I'll have to wait on that until after I get tenure somewhere.