Diagnosing a zombie Brain and body Part one Tim Verstynen Bradley Voytek

Translator: tom carter
Reviewer: Bedirhan Cinar

(Zombie sounds) Doctor 1: So, how did it get to be this way?

Doctor 2: Well, it’s my professional opinion that the large gaping bite mark on its shoulder might have something to do with it.

D1: Thanks. I mean, what causes its behavioral abnormalities?

D2: Well, we know all behaviors are rooted in the brain,

so I’d expect that something’s gone terribly wrong probably in there.

D1: Thanks again, Doctor Obvious.

Let me be more specific.

What changes in the brain would have to occur in order to cause this kind of behavior?

D2: Hmm. Well, let’s see.

The first thing I notice is how it moves.

Stiff legged, with long, lumbering steps, very slow and awkward.

Almost like what you’d see in Parkinson’s disease.

Maybe something’s wrong with his basal ganglia?

Those are a collection of deep brain regions that regulate movement,

through a neurochemical called dopamine.

Although most people think of dopamine as the “happy” chemical of the brain,

the dopamine-containing neurons in the basal ganglia die off in Parkinson’s disease,

that’s what causes it.

Makes it more and more difficult to initiate actions.

D1: What?

Look again at how it moves. Stiff legs, long stance,

These aren’t Parkinsonian movements, Parkinson’s patients take short, shuffling steps,

and the posture’s all wrong.

This looks to me like what happens when the cerebellum is damaged.

The cerebellum’s a little cauliflower-shaped area in the back of your head, but don’t let its size fool you.

That little guy contains almost half of the neurons in the entire brain.

Patients who suffer degeneration from this region,

something called spino-cerebellar ataxia,

show a lack of coordination that results in stiff legs, wide stance, and a lumbering walk.

My money’s on the cerebellum.

D2: Touché. OK. So we’ve nailed its motor problems.

Now what about that whole groaning, lack of talking thing?

D1: Hmm. You know, it sounds kind of like expressive aphasia, or Broca’s aphasia,

which makes producing words difficult.

This is caused by damage to the inferior frontal gyrus,

or possibly the anterior insula,

both regions behind your temple on the left side of your head.

D2: I think you’re only half right. Zombies definitely can’t communicate, that’s for sure.

But they don’t seem to do a good job of understanding things either.

Watch this. Hey, Walker! Your father smelt of elderberries!

(Laughs) See? No reaction.

Either it’s not a Monty Python fan, or it can’t understand me.

I’d say this is like spot-on fluent Wernicke’s aphasia,

damage to an area at the junction of two of the brain’s lobes, temporal and parietal,

typically on the left side of the brain, is the culprit.

This area is physically connected to Broca’s area, that you mentioned,

by a massive bundle of neurofibers called the arcuate fasciculus.

I hypothesize that this massive bundle of connections is completely wiped out in a zombie.

It would be like taking out the superhighway between two cities.

One city that manufactures a product,

and the other that ships it out to the rest of the world.

Without that highway, the product distribution just shuts down.

D1: So, basically it’s a moot point to reason with a zombie,

since they can’t understand you, let alone talk back.

D2: (Laughs) I mean, you could try, man, but I’m going to stay on this side of the glass.

译者:tom carter
审稿人:Bedirhan Cinar

(僵尸声音) 医生 1:那么,它是怎么变成这样的呢?

医生2:嗯,我的专业意见是,它肩膀上的大张咬痕可能与它有关。

D1:谢谢。 我的意思是,是什么导致了它的行为异常?

D2:嗯,我们知道所有行为都植根于大脑,

所以我预计那里可能出现了严重错误。

D1:再次感谢Obvious博士。

让我更具体一点。

为了引起这种行为,大脑必须发生哪些变化?

D2:嗯。 好吧,走着瞧。

我注意到的第一件事是它是如何移动的。

腿僵硬,脚步又长又笨重,非常缓慢而笨拙。

几乎就像你在帕金森病中看到的一样。

也许他的基底神经节有问题?

这些是通过称为多巴胺的神经化学物质调节运动的深部大脑区域的集合

虽然大多数人认为多巴胺是大脑的“快乐”化学物质,

但基底神经节中含有多巴胺的神经元在帕金森病中死亡,

这就是它的原因。

使开始行动变得越来越困难。

D1:什么?

再看看它是如何移动的。 僵硬的腿,长的姿势,

这些不是帕金森的动作,帕金森的病人走的短,拖着脚步

,姿势都是错误的。

在我看来,这就像小脑受损时会发生什么。

小脑是你脑后的一个小花椰菜状区域,但不要让它的大小欺骗了你。

那个小家伙包含了整个大脑中几乎一半的神经元。

患有该区域退化的患者,

称为脊髓小脑共济失调,

表现出缺乏协调,导致腿部僵硬、站姿宽阔和行走笨拙。

我的钱在小脑上。

D2:触摸。 行。 所以我们已经解决了它的电机问题。

现在整个呻吟,缺乏说话的东西呢?

D1:嗯。 你知道,这听起来有点像表达性失语症,或者说布罗卡的失语症,

这使得造词变得困难。

这是由于额

下回或前岛叶受损所致,

这两个区域位于头部左侧的太阳穴后面。

D2:我认为你只说对了一半。 僵尸绝对不能交流,这是肯定的。

但他们似乎也没有很好地理解事物。

看这个。 嘿,沃克! 你父亲闻到了接骨木的味道!

(笑)看到了吗? 没有反应。

要么它不是 Monty Python 的粉丝,要么它无法理解我。

我想说这就像流利的韦尼克失语症一样,

对大脑两个叶(颞叶和顶叶)交界处的区域的损伤,

通常在大脑的左侧,是罪魁祸首。

这个区域与你提到的布罗卡区物理连接,

通过大量称为弓状束的神经纤维束。

我假设这个庞大的连接捆绑在僵尸中完全消失了。

这就像拆除两个城市之间的高速公路。

一个生产产品的城市,另一个将产品

运往世界其他地方的城市。

没有那条高速公路,产品分销就会关闭。

D1:所以,基本上和僵尸讲道理是没有意义的,

因为他们无法理解你,更不用说顶嘴了。

D2:(笑)我的意思是,你可以试试,伙计,但我会留在玻璃的这一边。