jonathan: happy halloween. welcome to talks atgoogle in cambridge, mass. it's great to seesuch a big crowd. i think we all knowwhy we're here, because this office is such ahuge supporter of neuroscience. i'm sure i'm notthe only person who subscribes to alertson google scholar. tim verstynen, facultyat carnegie mellon today, this is just a smallsample of his papers.
his co-author, bradley voytekof uc san diego, similarly. these are giants in the field. they're also pioneers in thefield of zombie research. and there's not alot more to say. i know their parents areexceptionally proud of them. i know we're eagerto hear what tim has to say about developmentsin this emerging field that he is helpingto blaze a path in. so without furtherado, please join me
in welcoming theauthor of this seminal and groundbreaking book, "dozombies dream of undead sheep?: a neuroscientific view of thezombie brain, tim verstynen. tim verstynen:thank you, jonathan. and happy halloween everybody. thanks for coming. before i get intoit, i just would like point out that mycollaborator, bradley voytek, and i have kind ofteamed up on this.
and what you're goingto see is a hobby that's gone out of hand. we are both zombie geeks. and how this started wasthat in graduate school, we were both inthe same program. and on our off hours,we liked to just geek out and watch zombie movies. and being nerds,we decided, well, what would happenwith the zombie brain?
and it all wentdownhill from there. so you're about to seethe aftermath of that. but before i really get intothe nitty gritty details, just a disclaimer, i'm going to beshowing clips from some zombie movies, primarily "nightof the living dead," because it's the bestzombie movie ever. so there's goingto be a little bit of 1960-style goreand some spoilers. so just be warned.
all right. so i get askedthis question a lot by my colleaguesin neuroscience, why zombie neuroscience? why are we doing this sillyendeavour on our off hours instead of writinganother grant? well, brad and i are both bigscience outreach advocates. and one of the thingswe're interested in is trying to get generalaudiences more engaged
with basic science information. by and large, the waythe broader public gets science is filtered throughtypes of media sources that try to spin and make bigmountains out of small mole hills. and often, it gets distorted. so we need to get thegeneral public more engaged in the real corescientific literature. so we've thought aboutpossibilities of doing this.
one, we thought about usinginternet memes as our figures to illustrate our findings. so use your lol cat todisplay hebbian networks. that didn't go over so well. we pondered, accidentally,releasing sex tapes during our lectures to get abroader audience coming in. our lawyers suggestedthat we don't do that. and we thought, well, maybewe could attract more readers to our journalarticles if we just
added a kardashianto the author list. again, apparently, youneed their permission in order to put themon the author list. so this didn't work. and each one of these approacheshas the following structure. what we're doing is we'retrying to take aspects of popular culture and injectit into science to pull people into the basic science. and it's kind of hard to do.
so what we need to dois instead flip this and say, bring scienceinto popular culture. how can we start bringing yourreal scientific principles into popular culture inorder to educate the broader public on scientific issues? and so this wasour first attempt at this kind of leveragingscience information into popular culture. and so, of course, usbeings zombie nerds,
well, we're going to takea look at zombies first. they're actuallya perfect example for exploring neuroscientificideas in this broader context. so that's whyzombie neuroscience. so for the next about halfan hour or so, bear with me. we're going to besuspending our disbelief and pretending that outsidearound kendall square, the undead are walking around. in fact, on a halloweenlike today, there probably
are undead walkingaround kendall square. so welcome to "the scienceof surviving the zombie apocalypse," more importantly,the neuroscience of it. so as a scientist and as aneuroscientist, in particular, when i see a zombielike this woman here, i see an undead creature, yes. but i also see a spectrumof very particular types of behaviors thatyou see repeated again and again and againin "the walking dead."
you see things likehyper-aggression, memory deficits,attention problems. you'll see language disruption,reduced impulse control, movement disorders, and evenvisual recognition impairments. and these are seen acrossalmost every genre of the zombie movie. so as a neuroscientist,this tells us something very interesting. this gives us somepretty key insights
into what's happened tothis individual's brain as she's gone from beinga high school cheerleader into being a ravenous zombie. so using this collectiveset of behaviors that have changedinto zombie, we were able toactually reconstruct a model of what thezombie brain looks like. so let me show youour model here. so on the left right here is anormal, neurologically healthy
human individual. there's lots of tissue packedinto a really small space, so it's very wrinkly. and it's a very robust,healthy looking structure. on the right isthe zombie brain. and what you see islots of big gaps, lots of space that's unused. in fact, thislittle guy back here is completely gonein the zombie brain.
we're going to get tothat a little bit later. so this shows atrophyin the zombie brain. and this atrophy thatyou're seeing isn't random. each one of the areas that'sdecayed away in the zombie brain reflects a veryparticular symptom that we see in zombieismso the goal of "do zombies dream of undead sheep?"is to take apart the behavior of zombiesand link it back up to each one of these brainregions that's been atrophied
and destroyed in zombie brain. so that's what we'regoing to do today and just looking at afew of these symptoms. now, before we do,we're scientists. we like to take what seemslike supernatural phenomenon and make it dry and boringand clinically defined. so we're going todefine zombieism not as zombies, but asa clinical disorder. and so we're going to callit consciousness deficit
hypoactivitydisorder, cdhd, which is defined as the loss ofrational, voluntary, and conscious behaviorthat's been replaced by delusional/impulsiveaggression, stimulus-driven attention,and the inability to coordinate motor orlinguistic behaviors. there, we've strippedaway all the really weird supernatural stuff and madeit a nice, clean studyable phenomenon.
also, with a coolname like cdhd, maybe we can get apharmaceutical company to fund our research. all right, so fromnow on, we're going to be calling zombieism cdhd. and we're goingto try to explore the neural underpinningsof cdhd by going through a set of symptomsthat we see with the disorder. so the first symptom or thefirst behavioral characteristic
that people notice whenthey encounter the undead is their hyper-aggression. let's see an exampleof this behavior. this is karen. karen's just recentlyturned to the undead. and here she's, i believe,eating the arm of her father. and let's see what happens whenkaren runs into her mother. [video playback] -karen.
karen? karen. oh baby. baby. timothy verstynen:because you always got to get the garden shears. -ah. aaaah. [end video playback]
timothy verstynen: ok,we'll save you the blood and gore there. but i think it's prettysafe to say that karen's pretty angry withher mother, right? most normal kids who arenot angry with their parents don't grab a garden shearand start stabbing them. so this type ofaggression is interesting because it's very reflective ofa well-described type of anger known as reactive-impulsiveaggression.
this is, and thisis a quote from an actual scientific paper,"a subtype of aggression that can result in sudden,heightened, enduring, or inappropriateaggressive responses." so this is the stimulus-driventype of aggression that you'll see when you engagethe body's fight or flight responses. and it's very different than thetype of aggression you see in say something like aschool shooting, which
is a very calculated, decisive,cool type of aggression. and we know a lot aboutthe neural underpinnings of this reactive-impulsiveaggression, what we sometimes call as road rage aggression. so this type ofaggressive behavior is well-characterizedin many animal models. so we've laid out a lot ofthe neural circuits that drive this type of response. so let's take a look atthose neural circuits.
the control of aggression,normally in hopefully everyone in this room, isregulated by areas in the front of the brainin the prefrontal cortex, usually around what's knownas the orbital frontal cortex or complex. and this is a set ofhigher level brain areas that regulate a lotof different things. but one of the things theydo is they regulate control in subcorticalnetworks, networks
that are burieddeep in the brain. and in particular, onearea known as the amygdala receives extensive input fromthis orbital frontal complex. and what this does is itacts as like a cooling mechanism for amygdala function. so the orbitofrontal cortexis doing the, shh, it's ok. it's ok. and the amygdalais hypersensitive to potential threatsin the environment.
it's always lookingfor a threat. so if we wanted to couch thisin freudian terms,-- and please, i hope my department chairdoesn't hear me talking about freud in this talk-- you canthink of the amygdala as being the id and the orbitofrontalcortex is being superego. it's trying to keep thisreactive, primal, instinctive fight or flight response intact. so the amygdalacontrols aggression through a very particular setof interactions between areas
known as the hypothalamus andthalamus, which in turn send excitatory projections toan area of the brain known as the periaqueductal gray. this is buried deep,deep in the brain. and the periaqueductalgray stimulates your arousal mechanisms. so it's what gets you ramped up,and in this case, aggressive. so normally, the prefrontalcortex is saying calm down. don't react.
that guy cut you off in traffic. don't throw a brickthrough his window. but if you remove theorbitofrontal cortex from the equation, whathappens is the subcortical fight or flightresponses are unchecked. so you get an unconstrainedamygdala response, which through thisnetwork of other areas, increases sensitivityto reactive behaviors. and what you get if you wipeout those prefrontal control
mechanisms is you get aunconstrained, impulsive rage. you get more appetitediregulation, chronic stress you'll even getappetite disregulation. so these are all behaviors thatyou see in animals with damage to the orbitofrontal areas. and you also see it in zombies. so i think it's apretty good guess that that's what we'reseeing, at least in this case, with zombies.
so if we look at the humanbrain and the zombie brain side by side, theorbitofrontal areas that tend to control thosetype of reactive response rest right up here. this is the front side ofthe brain, looking at front. and this is the underviewof the brain here. if we look at thezombie brain, we see an atrophy of theseprefrontal networks. so that controlregion has gone away.
but that's not all. we don't just see extensivedamage to the zombie brain. we actually see someplasticity as well. so if we look at thosesubcortical areas, like the amygdalaand the thalamus-- so this is a slice throughthe brain right about here on the left showingthe amygdala in red. and this guy in the right, thisis a slice through the brain this way showing the thalamus.
if we look at the volume ofthese two subcortical areas, the humans are displayedin gray and zombies are displayed in orange. and we see-- actually, theseareas should be bigger. these areas are moreenlarged in the zombie, or the cdhd subtypes, thanwhat you see in humans. so they're unconstrained. they're using more resources andthey're building more neurons. so they're becomingmore sensitive.
so this explainsa little bit how you have this reactiveaggression in the zombie brain. so let's look at anothersymptom of the zombie epidemic, or the cdhd epidemic. let's look atvisual recognition. i'm going to show you two scenesof the same two individuals. the first is a scene beforethis gentleman here, johnny, has turned. and this is his sister barbara.
-to really be scared here. -johnny. -you're still afraid. -stop it now. i mean it. -they're coming toget you, barbara. -stop it. timothy verstynen:ok, so it's very obvious he knows whothis person is, right?
now, let's look at johnnyafter he's become a zombie. -no. no, get out. no. no johnny, no. no, no, timothy verstynen:so, notice he doesn't have that glint ofrecognition in his eye. he doesn't see his sister.
he just sees a human thathe can devour, right? he doesn't recognize her at all. this seems to be acommon phenomenon throughout the zombie genre. you see it many times, twohigh school sweethearts. one gets bitten andturns into a zombie. as soon as they turninto the zombie, they start to eat thecheek of their loved one because they nolonger recognize them.
they just react as if thisis just some random person that they can devour. and this type of visualrecognition problem resembles a well-describedpsychiatric disorder known as capgras delusion. capgras delusionis the false belief that the people you know wellhave been replaced by impostors and are typicallyseen of as a threat. this is the invasion of the bodysnatchers psychiatric disorder,
it's a very real disorder. so you wake up onemorning and suddenly, that's not your wifelaying next to you. that's some alien that'sinhabited your wife's body. she might look, sound,talk like my wife, but she's not really my wife. this isn't always bad. there was a casereport of a woman who was in a miserablemarriage for years.
she had a stroke,developed capgras delusion and was convinced thather husband was replaced by casanova andthat she was having illicit affairwith this casanova that was in her husband's body. and their love lifeactually improved. so it's not always bad. but capgras delusion isa psychiatric problem, which means it's characterizedat this behavioral level,
but we don't really know theneural underpinnings of it. but the phenomenonis very similar to a well-describedneurological phenomenon known as prosopagnosia. prosopagnosia is the inabilityto delink a person's identity to the visual imageof their face. so in the classic scenario,somebody with prosopagnosia, you stand them in frontof a mirror and say, who's looking back at you?
and they won't be ableto tell you who they are. they'll just say, i see a face. i see that person. they've got a beard. but i don't know who they are. or another famous exampleis an experimenter will be showing a setof faces on the screen. the experimenter's facewill come on the screen. the experimenter'sright here and the guy
asks, who are youseeing on the screen? and the patient willreply, i don't know. somebody. so this type ofdisorder has been described in the neurologicalliterature for about 100 years or so now. and it's linked todisorders or damage to a particular network of areasin the brain known as the face network.
ok so the facenetwork, particularly an area known as thefusiform face area are a well-describedset of brain areas that are sensitiveto seeing faces more than any other object. in fact, the face areawas first described at mit by nancy kanwisherabout 20 years ago. so the way the facenetwork is characterized is let's say i put you in anmri and look at the functional
activation of your brainwhen i show you pictures. so i show you a pictureof this dude here. and then i show youpictures of houses or cars. and i say, which areas aremore active to this face than to these cars? well, what youwould see is a set of regions in theback of the head on the undersideof the neocortex. so each one of these blobshere shows a separate region
that's more responsive tothis face than anything else. this is sometimes knownas the core face network. and what these are is a set ofwell-connected brain regions that basically deconstructthe visual image of the face, reassemble it, and link itcategorically to an individual. so it's a stream of information,starting in the back where the primaryvisual cortex is that just sees spatial features,and keeps moving forward to higher levelareas of the brain
until it's linked up to a face. so damage to anypart of this network can lead to prosopagnosia. and i'm going to show youan interesting example of temporarilyinduced prosopagnosia. what we're goingto see is a patient is about ready toundergo neurosurgery. he's got a tumorin the underside of his brain near thatcore face network.
and surgeons wantto resect the tumor, but they don't want tomake him prosopagnosiac. so what they did is theyimplanted stimulators on the underside of his brain. and what they'regoing to do is they're going to stimulatedifferent parts and see where does his faceperception get disrupted. and that way, they can map outwhere the face selective areas are and the neurosurgeoncan work around them.
so you're going tosee two trials here. in one trial, theexperimenter isn't going to deliver anystimulation at all. in the second trial,they're actually going to deliver stimulation. so this took place in stanford. and this patient has noneuroscience or psychology background whatsoever. so he doesn't knowwhat's going on.
-just look at myface and tell me what happens when ido this, all right? -ok. -one, two, three. -nothing. ok. i'm going to doit one more time. look at my face. one, two, three.
-you just turnedinto somebody else. -tell me about it. -your face metamorphised. your nose got saggy. it went to the left. you almost looked likesomebody i had seen before, somebody different. that was a trip. timothy verstynen: ilove that last line.
so just a brief stimulationof these face areas-- in this particular case, it wasthe fusiform form face area-- caused this disruption ofthe perception of the face. and so as the clip goes on,--i don't have time to show you the entire clip-- theexperimenter keeps turning down the voltage and keepsturning down the current. and eventually he says,your face didn't change. i just didn't know you were you. so the disconnect betweenseeing the face and the identity
of the experimenter-- he waslooking at the experimenter. he knew who this personwas-- just got disconnected. so this is a great exampleof a transiently induced prosopagnosia. the whole image of theface just got torn apart. so the face network is partof a larger visual network in the brain known as theventral visual stream. and so this is the ventralvisual stream in one of our zombieexperimental subjects.
so this is the primary visualcortex here and information that flows on theunderside of the brain, mostly along the temporal lobe. and this is theundercurrent here. it's part of theventral visual stream. so this is the fusiform facearea i talked about earlier. this is known classicallyas the "what" pathway. it's the pathwayin your brain that tries to assembleobject knowledge
and recognizeobjects in the world. so if we look at this"what" pathway in a human, if we did a slice rightthrough the brain-- this would be a saggitalslice right through here. this is the main coreof the "what" pathway on the left and right side. in the zombie brain,the "what" pathway would be extensively damaged. so they would have impaired faceknowledge, object knowledge.
and this is actuallywhere the fusiform face area sits in theright hemisphere. so we're going to saythat not only are zombies losing the prefrontalcontrol of their aggression. they've also lost theability to recognize faces in other objectswith few exceptions. another classicdeficit we see in cdhd all the time is language. zombies don't talk.
in fact, i'm going to showyou an example of the most fluent zombie we know of,if you ignore that movie "warm bodies." -brains. timothy verstynen:ok, that's tar man. tar man is the individual whosingle handedly linked brains to zombies. up until tar man, brainsand zombies weren't linked. zombies would eatany part of the body.
they would go for the liverbefore they'd go for the brain. but tar man had aparticular taste for brains. and so he was the one who wasalways going after brains. but i want you tonotice something. here, he was askingthis teenager if he could eat her brains. but he didn't say,can you come over here so that i caneat your brains or please come by because yourgray matter looks delicious.
no, he just said, brains. you got the idea, but itwas a single-word sentence. that type ofphenomenon, if we see it in clinicalneurological patients, is known as telegraphia. so the idea being that patientswho are having difficulty getting words out will resortto just the most critical parts of the sentence, the mostcritical semantic parts of the sentence, and takeaway all the other fluency.
and the name comesfrom the old telegraph for long-distance communicationa hundred and some years ago. in that case, youpaid by the character. so you had to make your notesshort, sweet, and to the point. the same is truewith these patients. they have troublegetting out words. so the whole ideajust to get out the key, most importantparts of the sentence. now telegraphia isa symptom that you
see in a larger class ofdisorders known as aphasias. and aphashias are broadterm that reflect, really, any language deficit, butthere's many sub-types. so for example,there's the inability to produce language,which is classically known as broca's aphasia,or difficulty comprehending language, which is classicallyknown as wernicke's aphashia. and each one of these two areashas different cortical sources that play a larger part in thelanguage networks of the brain.
so this is tar man in hereholding his favorite dish. so this is the humanbrain right here. we're looking in the left side. so broca's area isright up here in front. and this is the areathat if you damage it gets you broca's aphasia. it's tightly linked upto the motor cortex. and it's single handedly linkedto the language production end of things.
so it's what formsyour mouth movements and your gestural patternsto producing language. in the back, rightby the temporal lobe and the parietallobe, where they meet, you see wernicke's area,which is a region that's linked to languagecomprehension. so if you damage wernicke'sarea, you can get words out. they're just discombobulated. they're not well-structured.
you also have difficultyunderstanding people. and these two areasare connected together by a very large bundle ofwhite matter pathways known as the arcuate fasciculus. these are big superhighwaysof the brain that connect wernickeand broca's area. when you think about aslanguage, what you're doing is you're constructing theidea and semantics of what you're saying.
you're shipping allthat information out to the output area of thelanguage circuit and saying, ship out this informationto the rest of the world. so information typicallyflows from wernicke's over to broca's. and damage to anyone of these areas will impair language function. so if we look at this circuitin the human and zombie brain, this is the human on the left.
broca's would beright about up here and wernicke is rightabout back here. if you look in the zombiebrain, we see extensive atrophy in both ends of the circuit. so basically, this tells us,don't try talking to a zombie. they're not goingto understand you. and they're not reallygoing to talk back, except for maybeasking for your brains. so this couldexplain how you get
these sorts of language fluencyproblems in the cdhd disorder. the final symptom i'm going togo over for cdhd is movement. and this is what reallywhen you ask somebody to pretend to be a zombie,the first thing they do is move and walk like a zombie. so let's see a classiczombie movement here. i want you to payattention to how these creatures are walking. [music playing]
timothy verstynen: all right. so we have arms out, wide,lumbering, stiff stance. they tend to do this. so there's obviouslysomething wrong with the way their brains arecoordinating their actions. so let's take a quick lookat the general circuits in the brain thatregulate our movements. there are three, bigcollective circuits in the brain thatdrive our actions.
there's actuallymany more than this. these are just thebig sets of them. in the neocortex, you havethe cortical motor areas. so this is ourzombie subject here. this is their brain. everything shown here in grayare cortical motor areas. and this is actuallya collection of a few dozen differentareas that collectively coordinate your actions.
and they'reresponsible for things like sensory integration,movement planning, and movement execution. so they kind of plan what todo with the marionette strings of your muscles and jointsand coordinate those movements together. underneath the motor cortexand deep in the brain is an area known asthe basal ganglia. this is the secondmajor motor pathway.
so this little alienlooking creature in here, that's a subcorticalnuclei and part of the basal ganglia circuit. and what they do is they'reresponsible for gating or inhibiting actions. so really, they're thegatekeepers of the movements that you execute. so they decide whetheror not you're actually going to throw a brickthrough a window or not.
so they kind of make thatfinal output decision. and then on the backof the head here, this is shownright back here, is a little cauliflower-shapedarea of the brain known as the cerebellum. cerebellum is responsiblefor motor timing and actual temporal perceptionto coordination and error correction. so it's the qualityassessment guy
that makes sure that youractions are being conducted smoothly and withoutmajor errors. so each one of these three areascontributes in different ways to different typesof motor control. now, when most people lookat the way that zombies move, the first thingthey'll say is, oh, they look like theyhave parkinson's. in fact, "slate" just had awrite up of one of our chapters from the book yesterday.
and their first title, beforewe got them to change it, was, "do zombies have parkinson's?" and parkinson's is a disorderof the basal ganglia. so patients with parkinson'slose a major pathway in this system. and it results in avery particular type of movement disorders. but let me show you whatparkinson's patients look like when they havefull-blown movement disorders.
so typically, they'llhave slouched posture. they're losing postural control. their hands arecloser to their sides. and the way they walk areshort, shuffling steps. this is a very characteristicparkinson's walk. that's not what we see inthe cdhd disorder at all. we see wide legs,stiff, arms out. there's a balance problems andthese kind a lumbering walks. that kind of movement actuallyresembles a different motor
disorder known asspinocerebellar ataxia. so individuals with sca,or spinocerebellar ataxia, suffer from aninability to produce smooth, coordinated actions. and it results in these kindof lumbering movements, balance problems, tremors, slurredspeech, visual eye movement problems, so a host ofdifferent movement problems. and they all resolvearound the fact that patients with thisdisorder are suffering
from a degeneration ofthe cerebellum itself. so the cerebellumatrophies away and it causes these movement disorders. in fact, if you want toknow just very little bit what it's like to sufferfrom this disorder, think about the lasttime you were drunk. you had balance problems,your slurred speech, your stumbled walk. those are allcerebellar symptoms,
because the alcohol's explicitlyinfluencing and affecting the cerebellum. so that's what these individualssuffer on a daily basis, without the euphoria of alcohol. so those kind of movementsare very, very characteristic of cerebellar damage. now, the cerebellum is probablymy favorite area of the brain. it's kind of underappreciated in the neuroscientific community.
it contains half of theneurons in the brain. so even though theneocortex is bigger, the cerebellum containshalf of the neurons. and it had a sordid history. there were a ton of reallyoff the wall theories about what the cerebellum did. early on, it wasthought to just regulate the fluids of the body. there was once a theory that itwas the battery of the brain.
so it was just doingvoltaic battery generation in order to produceelectrical impulses. but, perhaps, my favoriteearly theory of the cerebellum came from the phrenologists. the phrenologists werethe early neuroscientists who tried to map outlumps on the head with certain personalitycharacteristics. and the phrenologiststhought that the cerebellum was the root of the libido.
they thought thatall your sexual drive came from the cerebellum. and they were scientists. i like to knockthe phrenologists, but they practicedthe scientific method. and they figuredthis out because they would go to frenchprisons and then feel bumps on the heads ofdifferent criminals. and they just noticedthat criminals
with chronic, habitualmasturbation problems had larger bumps overthe back of their head by where the cerebellum was. so they thought, ah, they'vegot large cerebellum. so that's what's drivingthese sexual impulses. and to their credit,they'd actually tried an experimentalmanipulation to see if they couldprove this theory. so in one individual,this poor female inmate,
they strapped an ice cubeto the back of her head, strapped it in, tied itin, a giant block of ice, and noticed that this inmatestop touching yourself when the ice cube was strappedto the back of her head. so voila, they provedthat the cerebellum is responsible for the libido. so if you're like me,you could probably see many differentreasons why people would stop touching themselveswith a giant block of ice
to the back of their head. and anotherindividual who shared this theory was this gentlemanhere, pierre fluorens. pierre fluorens was aclassic neuroanatomist and neurophysiologist. he was really a pioneerof early neurology. and he thought thiswas ridiculous. so i'm going to read youa quote from an article about his discovery of howthe cerebellum is actually
linked to motor control. "fluorens dismissed asunfounded the claims for the sexual functionin the cerebellum. he removed the cerebellumof a mature rooster. the animal was still deeplyinterested in the hens, but motor dysfunctionmade it difficult for him to express hisfeelings towards them." i love that littledelicate ending there. so basically, therooster was still randy,
but he couldn't reallycoordinate his actions to make his affections known. so this was actuallythe first explicit case showing that the cerebellumwas linked to motor control. it didn't happenuntil the mid 1800s. so since then, we'vedone a lot of work characterizing howthe cerebellum is now, cerebellum sits rightback here in the humans. and over here inthe zombie brain,
you see that thecerebellum is pretty much completely atrophied. so these kinds ofmovement disorders that you see in zombies reflectssevere cerebellar dysfunction. any zombie moviefan in the audience is going to be alittle bit frustrated at this pointbecause so far, i've only been talking about one veryparticular subtype of the cdhd disorder, known as theslow zombie subtype.
these are theclassic early forms of the disease as we saw it. but more recently,another subtype has emerged, particularlystarting around 2002, 2004. and that's the fastzombie be subtype. these guys don't lumber. they don't havediscoordinated actions. they can climb. if you've watched the movie"world war z," they can swarm.
and these are vicious,vicious predators out there. so we wanted tosay, ok, well, what is the difference betweenthis guy and this guy? so brad and i flewout to england, grabbed ourselves aset of fast zombies, brought them back to the laband looked at their brains. and if you compare thebrains of the slow zombie to the fast zombie, you seesome very interesting things. first off, you seethat the fast zombie
has an attached cerebellum. so they still have this motorcoordination ability intact. they also have no atrophy inthe superior parietal portions of the brain. these are the brainportions up here, which means they have actuallybetter spatial attention as well. so there's not asextensive brain damage in the fast zombies as whatyou see in the slow zombie
variant of the cdhd disorder. so what drives this difference? why do we suddenly seethis different subtype in the disease? well, again, we didextensive research. we watched a tonof movies and then had to rewatch themwhen we were sober. the one thing wenoticed time and time again was that in thenew, fast zombie subtype,
the time between infectionand resurrection of zombie became quite short. so we developed whatwe call now the time to resurrection hypothesis. so according to thishypothesis, the time between sudden death due toinfection and resurrection, if it's short, as you see in thefast zombie, the amount of time that the brain is starvedof oxygen and glucose is relatively short.
so what happens whenthe brain is starved of oxygen and glucose isit starts to die away. it induces itself into thishypoxic state and tissue loss occurs. so if that'srelatively short, you don't get as extensiveof tissue loss. but if as in theolder variant, like we saw in "night ofthe living dead," it would take hours,days, weeks or months
in order to resurrect. and that's going to lead tomuch more extensive damage, because the brain isstarved of those resources for much longer. the cerebellum andearly visual areas are particularlysensitive to hypoxia. so this would predictthat we should see a negative correlationbetween the walking speed of an undead individualand the time at which it
took them to resurrect. so this could explain why weget the two different subtypes of the cdhd disorder. so what might cause cdhd? well, there's lots ofpotential pathogens that could cause this disorder. viruses are knownto attack the brain. what you're seeinghere is an individual who had a neural infectionwith the herpes simplex virus.
so everything yousee here in white is calcified neural tissue. this is the samevirus that gives you cold sores in your mouth,except every once in awhile, instead of travelingout a cranial nerve, it travels up to the brain. and it can causeextensive damage up in particularly theprefrontal cortex. but most viral damageswe know to the brain
are very nonspecificand just very global. they wouldn't lead toa very specific pattern of a global behavioral deficit. so we don't think virusesare what's causing the zombie brain, much to the frustrationof the producers of "28 days later." bacteria is another potentialsource of the infection. this is an image ofan individual who had meningitis, which isa bacterial infection.
and you see that meningitisate away, basically, the lower quarter of thisindividual's brain. it's a massiveinfectious disease. and the damage that it doesis, again, very nonspecific. so while virusesand bacteria are known to influencethe brain, they don't lead to these coordinated,specific regional changes in brain tissue. another potentialcandidate is prions.
so prions are littleforms of protein that can unfold the cellularstructure of basically all cell types, but particularly neurons. and so this is a brainimage of an individual with creutzfeldt-jakob'sdisease. everything in white, again,is areas of calcified tissue that have been damaged. and again, prionsare nonspecific. now, i apologize if youdon't sleep tonight.
but another potentialcandidate is brain worms. yes, brain worms are real. this is a syndrome knownas neurocysticercosis. these arrows are pointingto these little sacks here. can you guess what'sin the little sacks? yes, a little tape worm thatburies itself in the brain and siphons off nutrientsfrom your blood supply. and this happens from eatingfecally contaminated foods. and we actuallythink it's probably
epidemic in thirdworld countries. but normally, these brainworms don't do any harm. they just take up alittle bit of space. they siphon off alittle bit of resources. but they don't causebig behavioral problems until you have, asi tell you now-- one patient had threedozen worms in his head. he started showingbehavioral symptoms, but that was becausehis head basically
turned into swiss cheese. so we can imagine the case wheremaybe a subtype of these worms is forming a chemicalinteraction with the brain and leading to these slow,specific behavioral changes. another hypothesis that wasput out in the literature is if anybody seen themovie "the signal," is that tv and radiotransmissions can emit a particular em frequencythat causes the neuron activity patterns to changefundamentally.
and we know that youcan actually kill cells by letting them just fire a lot. so you could see coordinatedbrain damage, which we sometimes callexcitotoxicity, induced by particularstimulus inputs. again, this is the premisefor the movie "the signal." and at first i thought thiswas silly until i saw this. [music rick astley,"never gonna give you up"] timothy verstynen: soi don't know about you,
but that makes mewant to kill somebody. so i'm going to gowith the rick astley theory of the cdhd disorder. all right, so fari've shown you how you can look at this sillypop culture supernatural entity, this little zombiehere, characterize it in a very rigorous wayin a scientific manner where we can link up specificbehavioral traits to the brain, and use real scienceto kind of explain
a relatively silly, supernaturalorganism like the zombie. so this reallyshows the potential of trying to pushthis scientific idea into popular culturein order to educate real scientific principlesin the general public. so in a way, whatwe're trying to do is keep building this bridgebetween popular culture and science and get theseto interplay more in order to facilitate greaterscientific education.
so if you want to know more,you can obviously read our book, "do zombies dreamof undead sheep?" we also have a set ofanimated videos released through the ted-ed foundation. they are great supportersof science outreach. i love the ted-ed foundation. so we have twovideos up about how to diagnose the zombiebrain and some fallacies in using neuroimaging to explainbrain-behavior relationships.
we also have a set of colleaguescollective in the zombie research society. and this is a bunchof academics who use zombies to teachtheir particular field. actually, two members ofthe zombie research society are here in bostonand cambridge. dan drezner teaches thepolitics and political science of zombies. and he's over at tufts.
and steve schlozman is at mgh. and he's a psychiatrist. and he does thesepsychiatry of zombies. and he actually published anovel on the zombie disorder as a psychiatric condition,which is really fun. and so if you'renot just interested in neurosciencebut other fields, check out the people who areassociated with the zombie research society becausethey do great work like this.
so thank you guys. [applause] timothy verstynen: so questions. yeah. audience: i had a question aboutpopular zombie movies and tv shows, where you see them astruly scientifically inaccurate either in general or inspecific important scenes. timothy verstynen: ah. actually, i would say 99% ofthe zombies i've seen in tvs
and movies are so unrealisticas to make them impossible. there are a few exceptions. there's a video game,"the last of us," in which a evolution ofthe cordyceps fungus, which actually induceszombieism in ants. really, it does. it somehow mutates andcauses the same thing to happen in humans. so you see thesezombies running around
with giant fungiattached to their heads. and that is one thati thought was actually a fairly realistic one, becausethey're also not undead. you can easily kill them. and then the mostrealistic representation of zombies that i would sayhad the biological plausibility were the zombies in the "28days later" and "28 weeks later" movies. and for those youwho haven't see them,
the premise of the movie isthat scientists in oxford are trying to understand rage. and they develop a virusknown as the rage virus, which plays with the aggressioncircuits in the brain. and it gets loose inthe general public. and what happens ispeople just being become really justravenously aggressive. they're not undead. in fact, the premiseis that 28 days later
means that they're notthinking about eating. so they're going to starveto death in 28 days. and so you can ideally waitout the zombie apocalypse just by letting themstarve to death. so i thought thatprobably "28 days later" was the most biologicallypossible one. but even then, the behavioralpatterns and the transmission rates were nowherenear plausible. the scene that frustratedme the most was
at the end of "the walkingdead's" first season when they were in the cdc andthere was this biologically plausible explanation ofthe neuroscience of zombies was so bad that it made me cry. audience: so speakingof realistic zombies, there's this notionof the voodoo zombies and being controlled by drugson plantations and stuff. i'm just curious howthat plays into-- timothy verstynen:yeah, so that's
actually another littleside tangent to mine. because the zombieismthat you see in haitian voodoo culture is quiteinteresting in that it has a proposedneuropharmacological explanation. so there's a classicbook by wade davis, who was an ethnobotanist,who went down to haiti and made two particularpharmacological links to haitian zombies.
and one wastetrodotoxin, which was the poison usedto simulate death. and tetrodotoxin works byblocking the sodium channels that allow neurons to fire inthe peripheral nervous system. so your musclesbecome paralyzed. and it actually won't killyou unless your diaphragm stops working. so basically, it kills youbecause the diaphragm muscle but if you get a lowenough dose, what'll happen
is that your diaphragm willkeep moving so slowly that you can't really detect it. but in all intents andpurposes, you look dead. so that's the simulated death. and then the controlaspects, he proposed that the bokors, who are thebad or evil voodoo priests, would dose the individual afterthe tetrodotoxin had worn off when they dug themout of their grave that they were buriedalive in, would douse them
with datura, which hasthree major psychoactive ingredients, [? hyoscapines ?],scopolamine, and atropine, i think. each one of those willinduce a psychotic state. and so the idea is that youcan make this person who is now convinced this he's dead,because he saw himself dead. he was well aware of everythingthat's happening to him, felt buried. and then he gets raised.
and then there's apsychoactive chemical that keeps him compliant. that was the wade davis theory. it's controversial. it hasn't been replicated yet. and people are saying thatthere's probably other aspects to it that link more topsychological belief. but yeah, the haitian voodoozombie links to neurobiology are quite interesting that way.
audience: i had two questions. so one was, whatcauses zombieism? and so in some formsof movies, it's kind of like a venomousthing, that if you're bitten, you're infected-- timothy verstynen: right. audience: you get it. in other more recent ones,it's everyone's infected. when you die, you're a zombie.
audience: they're reallydifferent outcomes. audience: so i don'tknow if you had any thoughts aboutthat difference. timothy verstynen: yeah. the we're all infectedand we're just going to reanimate when whenever we-- audience: romero-- timothy verstynen:--transition from one state. romero was-- so we actuallygot to interview george romero.
and we were asking him about it. he said, the way hemade up, particularly in his first three movies,he didn't care about it. he was trying to use thezombies as a metaphor. so in the first one,he kept it vague. there was the satellite fromouter space that had come back. and it was somehowlinked to that. but it could havebeen space radiation. and he was sayinghe explicitly didn't
care about what caused it. he just wanted them to be there. in fact, he put the nailin our coffin of our theory about zombie movement. but i'll tell youabout that later. so i think what happenedwas because the early zombie cultures didn't reallycare about the mechanism, there was lots ofdifferent explanations. from a biologicalstandpoint, it doesn't
seem like thatwould be the case. so i like the idea of theinfection theory of zombieism. audience: so like a latent-- the real phenomenon that i thinkfascinates me the most in this is toxoplasmosis. so toxoplasmosis is asingle cell organism. it's what lives in cat poop. and it's why pregnant womenshouldn't be around cat poop. it's because it inducesflu-like symptoms
if you get the infection. and it'd be dangerous tofetuses and young children. but normally, if you'rean adult and you get it, you just get a flu. it seems to go away. but really what happens isit's a single organism that reproduces sexually inthe gut of a feline. so that's where it getsits most genetic diversity. when it's outside the feline,it can only reproduce asexually.
so it clones itself. so what this organism doesis even after the infection, it stays latent in your system. and in the mammalsthat it infects, so the rodents,humans, it actually starts modifying theneuropharmacology of the individual's brain. and what you see is you seecharacteristic behavioral differences in people who havehad toxoplasmosis assistant
and survived versusthose who don't. and the mostclassic case of this was an experimentalstudy where they took a rat-- and ratsnormally hate cats. they're instinctivelyafraid of cats-- gave it a toxoplasmosis intervention. and across time, ifyou had a glass wall between the rat and the cat,normally the rat's over here. but as the infectionrate occurs,
the rat actuallystarts to not only not be afraid, but wantto be near the cat. so there's increasedrisk taking behavior that happens as aresult of the infection. and actually, that same kindof behavior, not towards cats obviously, but morerisk taking behavior is seen in individualhuman individuals who've had the infection. so somehow, thesingle cell organism
is hijacking thecomplex circuits that induce our ability to beafraid of certain things and it increased risk taking. so that coupled with thepopularization of the infection theory of zombies is themore interesting link there. and if you're going to ask meabout biologically plausible, with the caveat that it'sstill way, way far away, that is more the route that youwould see something like this. audience: ok.
this is more than therat simply becoming acclimated to having a cat onthe other side of the wall. so you don't seeit all in rats that have never exposed to the virus. they stay far away. audience: the other questioni had, pretty quickly. so you talked about the amygdalaand rage and anger aggression. so i've heard of kluver-bucysyndrome, which is basically uncontrolled appetite.
audience: you didn't talkmuch about why the appetite side, rage can be all sortsof aggressive behavior. so kluver-bucy syndrome isa rare neurological disorder that happens-- itcan only occur when you get both amygdala damaged. and they exhibithyperorality, hypersexuality. and it's a very oddcharacteristic feature. so you caught ahole in our theory. because according to our theory,zombies should be hyperoral,
hypersexual. they should alsobe hyperfearful, because the amygdala actuallycontrols fight and flight. so what it's doing isif you leave it intact, zombies should be just aseasily spooked as pissed off. so you did catch thehole in the theory. audience: [inaudible]different way. right. any more questions?
go ahead. audience: so with thiscdc blog post a while ago about what to do in theevent of a zombie outbreak, do you have anycritiques of that? did they do a good job? timothy verstynen: i loved that. i thought they did a great job. because really,what they were doing is epidemic preparednessand emergency preparedness,
but just couched in zombies. it got people's attention. it got people excitedabout doing it. instead of justdoing, ok, we're going to pretend that there'sa sars virus out, people habituateto these things. but if you do it tongue incheek, people got engaged. i think it got a lot morepeople interested in thinking about preparedness forepidemics and emergencies
than if they had just doneanything else, except for maybe now, they could probablydo it with ebola. but otherwise, yeah, ithought it was a great idea. and i like seeing agenciesdo that tongue in cheekness to engage in awarenessand attention. did you still haveyour question? audience: yeah, just real quick. first of all, thankyou, super helpful. i added more cardio into my lifeafter i watched "zombieland."
so now, i feel more prepared. the second was, do you and yourfriends at the zombie research society plan on doing researchinto other parts of the zombie body, so beyond the brain? so we did a reddit ama. and one of the questionswas about the gut system. and the next avenueof zombie science is zombie internal medicine. because how do zombiesget their nutrients
when you've got your entrailsdragging on the ground? i think that's afascinating question. so i think that gettingpeople interested in talking about digestive systemsand poop is normally not that interesting. but you couch it in zombies,it can be interesting. same with cardiacsystems and blood systems from a biological angle. i think there's lotson the biological side
that you could exploreon the zombie body, because their physiology. how do you explain howyou could have somebody that's got thick,goop, viscous blood but somehow stillmanages to be animated? so yeah, that would be a funavenue on the biological side. and of course, onthe social side, you can use zombiesto explain anything, different hierarchicalsocieties.
zombie cognitive phenomenonwould be really interesting. so i don't reallythink there's anything you can't do with zombies justbecause they keep changing. they're not likevampires and werewolves, which have a verystatic structure. zombies keep changing with time. so you can alwaysfind an example of a zombie doing somethingthat you want to study. but yeah, i'm waiting forthe zombie internal medicine.
audience: so one connectionthat you didn't touch on is between rabies and zombieism. i've heard peopletalk about that. any comments on whether rabieswould be or a form of rabies-- timothy verstynen: so alonger version of the talk, we actually go over this. because when we go over thememory systems and the impulse control systems, thoseare all linked up to a system known asthe papez circuit.
that's a classicneurological circuit that was discoveredin the 1930s. and it was discoveredusing the rabies virus. and so what this guyjames papez would do is he was trying to findthe link between emotion and intention. how is it that we can't rememberwhat we did at the store yesterday, buteverybody remembers where they were at 9/11?
how do we have theseemotional bonding of memories? and so he mapped outthis theoretical circuit and then would map it out incats by injecting the rabies virus and watching thevirus propagate from one area to the next, lookfor the connections. and he actually made catsthat were memory problems. they were hyperaggressive. so we do a tongue incheek thing saying that james papez madethe first zombie cats.
but the rabies virus is a veryspecific type of infection. and it's very general. so what it does is itattacks a particular cell, jumps across what's knownas the synapse, which is the gap between cells,and keeps propagating down to the next cell. and it just wanders. it just followsfrom place to place. so if you get an infectionin one part of the brain,
it's-- where it goesis determined by who it's connected with. and it'll keep travelinguntil it basically kills the organism. now, normally youget some symptoms like the cognitive disorders. you'll get delusions anddementia with rabies infection. you get hydrophobia. so individuals infectedwith the rabies virus
will be afraid of water. they won't drink. they'll become dehydrated. and some of those areexplained by the virus doesn't survive well whenthere's lots of brain swelling. so it automaticallydehydrates you to keep that brainswelling down. things like thathave been put forth as explanations forthose kind of behaviors.
but a lot of themjust happen to be-- people show those when thevirus has spread so far throughout the brain asto basically wipe away most of the neocortex. and so it's nonspecific in thesense of where it's attacking. but we really startto see the symptoms once it's just so widespreadas to be catastrophic. so yeah, the rabiesvirus has been linked to zombies moretimes than anything else.
so the book "world war z,"the first name for the virus was african rabies,because they first talked about in south africa. and there's been a lot ofmovies that talk tongue in cheek about arabies-like infection. that's just because more ofthe hyperaggressive, impulsive but we don't really seehow that's occurring yet until you get to thiscatastrophic stage. audience: you also see thatwith the association of bites.
timothy verstynen:. yeah audience: rabiesget's transmitted-- oh that's true. that's true. yeah, so it's a goodinfectious disease that way, to use as a metaphor. any other questions? thank you guys very much.
thanks for inviting me out. happy halloween.
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