What happens when you have a concussion Clifford Robbins

Each year in the United States,

players of sports
and recreational activities

receive between 2.5
and 4 million concussions.

How dangerous are all those concussions?

The answer is complicated,

and lies in how the brain responds
when something strikes it.

The brain is made of soft fatty tissue,
with a consistency something like jello.

Inside its protective membranes
and the skull’s hard casing,

this delicate organ
is usually well-shielded.

But a sudden jolt can make the brain shift

and bump against
the skull’s hard interior,

and unlike jello, the brain’s tissue
isn’t uniform.

It’s made of a vast network
of 90 billion neurons,

which relay signals through their long
axons to communicate throughout the brain

and control our bodies.

This spindly structure makes
them very fragile

so that when impacted, neurons
will stretch and even tear.

That not only disrupts their ability
to communicate

but as destroyed axons begin
to degenerate,

they also release toxins
causing the death of other neurons, too.

This combination of events causes
a concussion.

The damage can manifest
in many different ways

including blackout,

headache,

blurry vision,

balance problems,

altered mood and behavior,

problems with memory,
thinking, and sleeping,

and the onset of anxiety and depression.

Every brain is different,

which explains why people’s experiences
of concussions vary so widely.

Luckily, the majority of concussions
fully heal

and symptoms disappear
within a matter of days or weeks.

Lots of rest and a gradual return
to activity

allows the brain to heal itself.

On the subject of rest,

many people have heard that
you’re not supposed to sleep

shortly after receiving a concussion
because you might slip into a coma.

That’s a myth.

So long as doctors aren’t concerned there
may also be a more severe brain injury,

like a brain bleed,

there’s no documented problem with
going to sleep after a concussion.

Sometimes, victims of concussion can
experience something

called post-concussion syndrome, or PCS.

People with PCS may experience
constant headaches,

learning difficulties,

and behavioral symptoms that even
affect their personal relationships

for months or years after the injury.

Trying to play through a concussion,
even for only a few minutes,

or returning to sports too soon
after a concussion,

makes it more likely to develop PCS.

In some cases, a concussion
can be hard to diagnose

because the symptoms unfold slowly
over time.

That’s often true of
subconcussive impacts

which result from lower impact jolts
to the head

than those that cause concussions.

This category of injury doesn’t cause
noticable symptoms right away,

but can lead to severe degenerative
brain diseases over time

if it happens repeatedly.

Take soccer players, who are known
for repeatedly heading soccer balls.

Using a technique called
Diffusion Tensor Imaging,

we’re beginning to find out what effect
that has on the brain.

This method allows scientists to find
large axon bundles

and see how milder blows
might alter them structurally.

In 2013, researchers using
this technique discovered

that athletes who had
headed the ball most,

about 1,800 times a year,

had damaged the structural integrity
of their axon bundles.

The damage was similar to how
a rope will fail

when the individual fibers start to fray.

Those players also performed worse
on short-term memory tests,

so even though no one suffered
full-blown concussions,

these subconcussive hits added up
to measurable damage over time.

In fact, researchers know that an
overload of subconcussive hits

is linked to a degenerative brain disease
known as Chronic Traumatic Encephalopathy,

or CTE.

People with CTE suffer from changes
in their mood and behavior

that begin appearing in their 30s or 40s

followed by problems with thinking
and memory

that can, in some cases, even result
in dementia.

The culprit is a protein called tau.

Usually, tau proteins support tiny tubes
inside our axons called microtubules.

It’s thought that repeated subconcussive
hits damage the microtubules,

causing the tau proteins to dislodge
and clump together.

The clumps disrupt transport
and communication along the neuron

and drive the breakdown of connections
within the brain.

Once the tau proteins
start clumping together,

they cause more clumps to form

and continue to spread
throughout the brain,

even after head impacts have stopped.

The data show that at least
among football players,

between 50 and 80% of concussions
go unreported and untreated.

Sometimes that’s because it’s hard to tell

a concussion has occurred
in the first place.

But it’s also often due to pressure
or a desire to keep going

despite the fact that something’s wrong.

This doesn’t just undermine recovery.

It’s also dangerous.

Our brains aren’t invincible.

They still need us to shield
them from harm

and help them undo damage
once it’s been done.

在美国,每年从事

体育
和娱乐活动的运动员

有 2.5
到 400 万次脑震荡。

所有这些脑震荡有多危险?

答案很复杂

,在于大脑在受到
撞击时的反应。

大脑由柔软的脂肪组织组成,
其稠度类似于果冻。

在它的保护膜
和头骨的硬壳内,

这个精致的器官
通常被很好地保护着。

但是突然的震动会使大脑移动


撞到头骨坚硬的内部,

而且与果冻不同,大脑的组织
并不均匀。

它由
900 亿个神经元组成的庞大网络组成,这些神经元

通过长
轴突传递信号,在整个大脑中进行交流

并控制我们的身体。

这种细长的结构使
它们非常脆弱,

因此当受到撞击时,神经元
会伸展甚至撕裂。

这不仅破坏了它们
的交流能力,

而且随着被破坏的轴突
开始退化,

它们也会释放毒素,
导致其他神经元死亡。

这种事件的组合会导致
脑震荡。

损害可以
通过许多不同的方式表现出来,

包括停电、

头痛、

视力模糊、

平衡问题、

情绪和行为改变

、记忆、
思维和睡眠问题,

以及焦虑和抑郁的发作。

每个大脑都是不同的,

这就解释了为什么人们
对脑震荡的体验差异如此之大。

幸运的是,大多数脑震荡
完全愈合

,症状
在几天或几周内消失。

大量的休息和逐渐
恢复活动

可以让大脑自我修复。

关于休息,

很多人都听说

脑震荡后不能马上睡觉,
因为可能会陷入昏迷。

那是一个神话。

只要医生不担心
可能还会有更严重的脑损伤,

比如脑出血,脑震荡后睡觉

没有任何记录的问题

有时,脑震荡的受害者可能会
经历一种

叫做脑震荡后综合症或 PCS 的事情。

患有 PCS 的人可能会经历
持续的头痛、

学习困难

和行为症状,这些症状甚至

在受伤后数月或数年内影响他们的人际关系。

尝试通过脑震荡进行比赛,
即使只有几分钟,

或者
在脑震荡后过早恢复运动,

都更有可能患上 PCS。

在某些情况下,脑震荡
可能难以诊断,

因为症状会
随着时间的推移缓慢展开。 亚震荡冲击

通常是这样的,
这种

冲击是
由于对头部的冲击

比引起脑震荡的冲击低。

这类损伤不会立即引起
明显的症状,

但如果反复发生,随着时间的推移会导致严重的退行性
脑病

以足球运动员为例,他们
以反复带球而闻名。

使用一种称为
扩散张量成像的技术,

我们开始找出
它对大脑的影响。

这种方法使科学家能够找到
大的轴突束,

并了解较轻的打击
如何在结构上改变它们。

2013 年,使用
这项技术的研究人员发现

,每年
头球次数最多(

约 1800 次)的运动员

已经破坏
了轴突束的结构完整性。

这种损坏类似于

当单根纤维开始磨损时绳索将如何失效。

这些球员
在短期记忆测试中的表现也更差,

所以即使没有人遭受
全面的脑震荡,随着时间的推移,

这些次脑震荡的伤害加起来
是可衡量的。

事实上,研究人员知道,

脑震荡的超负荷与
称为慢性创伤性脑病

或 CTE 的退行性脑病有关。

患有 CTE 的人会

在 30 多岁或 40 多岁时开始出现情绪和行为的变化,

随后出现思维

记忆问题,在某些情况下甚至会
导致痴呆。

罪魁祸首是一种叫做tau的蛋白质。

通常,tau 蛋白支持
我们轴突内称为微管的微小管。

人们认为,重复的亚震荡
撞击会损坏微管,

导致 tau 蛋白脱落
并聚集在一起。

这些团块破坏了
沿神经元的运输和交流,

并导致大脑内连接的破坏

一旦 tau 蛋白
开始聚集在一起,

它们就会形成更多的团块

并继续在
整个大脑中扩散,

即使在头部撞击停止后也是如此。

数据显示,至少
在足球运动员中,

有 50% 到 80% 的脑震荡
没有报告和治疗。

有时那是因为很难说

一开始就发生了脑震荡

但这也常常是由于压力

尽管出现问题但仍想继续前进的愿望。

这不仅会破坏复苏。

这也很危险。

我们的大脑不是无敌的。

他们仍然需要我们保护
他们免受伤害,并在造成伤害后

帮助他们消除
伤害。