An overview of the relevant aspects of the epidemiology, clinical presentation, basic disease mechanisms, diagnostic approaches and treatment options of the most common neurological diseases.
Module 2 Part 1: Introduction, Epidemiology, and Hemorrhagic Stroke
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From the course by University of California, San Francisco
Introduction to Clinical Neurology
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From the lesson
Neuroanatomy & Stroke
Welcome to Introduction to Clinical Neurology, offered by the University of California, San Francisco, on Coursera. This course provides a concise review of the most common and critical neurological diseases and conditions through a series of presentations by a variety of accomplished faculty at UCSF.
Meet the Instructors
Daniel Lowenstein, MDProfessor and Vice Chair, Department of Neurology
School of Medicine
S. Andrew Josephson, MDAssociate Professor
School of Medicine
Wade Smith, MDProfessor
School of Medicine
[BLANK_AUDIO]
Hello, I'm Doctor Wade Smith. Today we're going to talk about stroke.
A very common disease that probably many of you are familiar
with, either with a loved one or in your own practice.
Today, I'm going to talk about it to the
perspective of what is stroke and how is it treated?
I have a few relevant conflicts of interest in that.
As a professor of neurology here at UCSF, I am on
several data safety monitoring boards.
One's with the NIH and a few industry leaders [INAUDIBLE]
So, let's begin to talk about stroke. What is it and why is this a problem?
Think about what it must have been like 450 B.C., when
Hippocrates is prominent and people trust his opinion, when suddenly
a person right next to you Can't move half his body, and can't speak.
You would probably conclude at the time that something was
wrong and secondly that that person probably did something wrong.
And so the term that Hippocrates had applied to
this was apoplexy, meaning a sudden decrease in neurologic function.
And from that came the Latin word Plesso.
As to be struck down by the hand of God.
Well, this still had a theologic basis basis to it.
Until, in the 1600s, when Jacob Wepfer performed the first autopsy
on a person who died of a stroke.
This happened to be an intracerebral hemorrhage which we'll talk about And he
showed in the brain that blood had escaped into the brain's substance itself.
And that's likely what took this person's life.
So, suddenly structure and function became relevant.
And probably the next major milestone was in 1995 when the
National Institutes of Neurologic Disorders and Stroke, part of the NIH.
Investigators paid for by the federal government of the United States Took on
the first trial of T-P-A and showed
that that drug actually treated Ischemic stroke.
That time before from 1995 backwards we had no specific
treatments that reversed the brain injury that's happening in a stroke.
And as we'll talk about, time is very critical to this
and it depends upon the type of stroke that your treating.
[NOISE]
There's something you should know about me.
I'm cold.
I'm calculating. I get what I want.
If you get in my way I'll wreak havoc upon you.
I can leave you weak, limp, twisted, confused.
If you want to live to see tomorrow, you answer to me.
And you answer quickly. [SOUND] I am a stroke.
[SOUND]
>> Learn to recognize a stroke, and act quickly.
Time lost is brain lost.
>> So why did The American Heart Association put out
an informative video like this to call 9-11 during a stroke?
Was we'll talk about, the first few minutes of the
stroke can be critical for survival, so get help immediately.
So let's first take on a few definitions.
Stroke itself is a clinical phenomenon where
someone has the sudden onset and persistence beyond
24 hours of neurologic signs and symptoms
that can be explained by a vascular mechanism.
Lot of words.
What do I mean by that?
It means sudden, suddenly, somebody has a lack of neurologic function.
For example, can't move half their body or can't speak.
And you can explain it knowing the neuro-anatomy
of the middle cerebral artery.
If that's secluded on the left side, a person can have that syndrome.
So it makes logical sense that a closure of that vessel
can cause the symptoms and therefore, that's what it's due to.
So, in our anatomy lectures, we've talked
about the left hemisphere with language and
it affecting the right sided motor function,
or controlling motor function on the right side.
So it kinds of make sense.
But the only way to make a stroke diagnosis is knowing the anatomy
in the mechanism. Now whats a TIA?
A TIA is basically a clinical stroke where
you have a sudden onset of neurologic findings.
Then it goes completely away within 24 hours.
I'm going to talk about large vessel strokes
and I'm going to talk about small vessel strokes.
What's a large vessel?
These are vessels like the middle cerebral artery or the posterior cerebral artery.
Arteries that were reviewed
in the anatomy lecture that are large conducting vessels to
the brain, that if occluded, produce very large stroke sydromes.
These are about a millimeter or two in size.
The small is maybe half a millimeter.
Small vessels, on the other hand, are actually quite small.
They're probably, the majority of them are about the thickness of a human hair.
Now, if they're in a particularly important place, like within
a lenticular stride, off the meta cerebral or basal artery, or other regions in
the brain, they irrigate parts of the
brain that are very important for function.
So they can produce very large clinical symptomatology But in
general, large vessel strokes are much worse than small vessel strokes.
So who gets strokes and what are the risk factors for them?
Well I'm sure, I'm sure that you're aware that stroke is a very serious disease.
In fact, it's the #1 cause of death in many countries, including China.
In the United States, it's dropped to 4th
place recently, primarily because of good prevention efforts.
But still. There's 750,000 reported strokes per year.
Might leave somewhere around
three million people disabled at any one time.
About 150,000 a year die from stroke in the United States alone.
And depending upon the type of stroke that you have,
some, some forms of stroke are more fatal than others.
Interestingly, [COUGH] the stroke incidences following among the affluent.
And, I think that's because the message of prevention is getting to those people
who have means.
But, unfortunately, among the poor and
lower socioeconomic groups, stroke is actually rising.
And we think some of that has to do with diet.
We think some of it has lack of getting preventative medical care.
And it highlights that stroke is highly preventable as a disease.
So what are the risk factors that might lead a person to get a stroke?
Well I'm going to break em into 2
categories, non modifiable, meaning you can't really fix it.
And modifiable categories.
Now, the non-modifiable, so far no one's figured out how to slow aging.
As you get older in age, your, your risk of stroke goes up.
There's a complex interplay between gender, or sex, in that men typically
get more strokes but women are more likely to die from them.
And, that's a complex interplay between vascular disease.
Lower socioeconomic status and race, both correlate with stroke incidence.
And, we believe that's related, primarily, to lack of prevention.
And, then, diabetes, which is primarily a disease of small
blood vessels throughout the body is a frequent cause of stroke.
It's preventable only in that, if you prevent
ever getting diabetes, you don't have that risk factor.
But once you have diabetes, it's very hard for us to reverse the impact
it has on blood vessels.
Now, among the modifiable factors, where you can actually do something now if you
have this risk factor, to reduce your risk of stroke in the future, include.
High blood pressure being the most significant relative risk.
If you smoke cigarettes, you double your risk of stroke.
If you have certain heart diseases, like atrial fibrillation, which we'll
talk about, there can be a 6-fold elevation in stroke risk.
If you've had a prior TIA, which we'll talk about.
That's the harbinger of a stroke to come.
That actually, if we intervene rapidly in TIA
patients, we can prevent a stroke to follow.
Carotid disease.
Disease of the internal carotid artery bifurcation, due to
atherosclerosis, can lead to embolic occlusions of brain vessels.
Causing stroke, and if you fix that carotid disease before
it causes stroke or typically following TIA, you can
prevent a stroke to happen. High serum lipids, hy,
hypercholesterolemia, does raise stroke risk, but look at the difference between
how much stroke risk is increased by Hypertension as compared
with hyperlipidemia so a stroke is primarily
a disease of hypertension and therefore quite preventable.
Alcohol has a minor risk factor.
Too much alcohol appears to increase your risk of interceral hemorrhage and no
alcohol at all has been correlated with an increased risk of Ischemic stroke.
We're not quite sure if there's a cause
and an effect there but patients that do not
drink alcohol at all have a slightly higher
risk of stroke compared to those who drink mildly.
So lets talk about how a
clinical neurologist and physician classifies strokes.
This dichotomy that's shown here.
Remember stroke itself is a clinical diagnosis.
So as a sudden onset of neurologic deficits that last for 24 hours.
It's due to one of two things.
It's either due to a hemorrhage into the
brain, which we'll talk about in detail or ischemia.
Remember, ischemia is lack of blood flow and as a consequence, nerve cells
die quite rapidly. So, specifically, hemorrhagic stroke due
to hemorrhage is defined, as we'll talk about, by location in the brain it occurs.
An ischemic stroke I like to classify as large vessel versus small vessel.
You see that there's a couple other categories
in here, which I'm not going to dwell on
in this lecture.
There are many different forms of
intracerebral hemorrhage, which account for a
minority of all hemorrhages and similarly of ischemic stroke, but I'm going to point
out the main Ones that you see here, because these are the ones
that we know most about treatment, and we know the most about prevention.
So, let's first turn to hemorrhagic stroke.
Hemorrhagic stroke can be divided into the departments in which it
occurs One is in the parenchymal of the brain, intracerebral hemorrhage.
Or, it can go into the subarachnoid space.
And, these have very different risk factors
and they have very different treatments for them.
So let's first talk about intracerebral hemorrhage.
here's a typical story of an individual who might have that.
A 57 year old man who has untreated high blood pressure, he's not, hasn't gone to
doctors, doesn't get his blood pressure checked, and
probably has had elevated blood pressure for many years.
He develops progressive onset, not sudden onset, but
progressive onset of left sided weakness with headache.
So he begins
first with the face being a little bit weak, and
because the face is face he's slurring his words a
little bit, and then over the course of about 20
to 30 minutes his left arm starts to get weak.
And then by the time it gets to the hospital his face, arm, and leg are weak.
So progression in onset.
Not sudden, maximum deficits.
When you examine him he's pretty lethargic.
He would be called stuporous or [UNKNOWN] from
the altered mental status lecture which you'll review.
His neck is stick probably because of iritation of the meningial
surface of the brain and he's gazing off to the right.
He can't see to the left.
Left [UNKNOWN] and he has the left field cut.
Excuse me, he has the left [UNKNOWN]. What do we see on his scan?
Well on CT
imaging, blood appears as bright, so all of this in the brain actually is new
intracerebral blood that has escaped from a
blood vessel in the brain into the parenchyma.
You also see some blood in the ventricular system, which is also an important sign.
What does this look like on pathology?
Well, from a different patient, this is an acute
intracerebral hemorrhage into the basal ganglia.
And you can see this blood, which is in a clotted fashion inside the brain
substance itself, and what it's surrounded by is a whole bunch of areas of iron
staining We know that iron is toxic to the brain, but the primary problem of
this patient's death is the mass effect,
the actual sudden expansion of hematoma into the
brain that moves brain structures aside and can cause death from that.
For patients who survive, the blood gets absorbed, much like
a bruise in your skin or muscle would get absorbed.
And what it leaves behind is a little cleft
in the brain, as in this prior basel langlea hemorrhage.
Once the mass is gone, patients can experience
a tremendous amount of recovery in motor function.
So, for [UNKNOWN]
hemorrhages the concern is up front.
If the hemorrhage is large, there's a higher
risk of brain injury from that hemorrhage and a
high risk of death, but once a patient recovers
the amount of recovery can actually be quite substantial.
Well, why did the, why do these patients experience hemorrhage?
Surprisingly, given the size of that hemorrhage, you would think
it's because a large blood vessel in the brain had ruptured.
But, in fact, it turns out that the blood vessels
that rupture in these times of hemorrhages are typically quite small.
So, here's an artist rendering Of a small vessel
in the brain that's only 50 microns in diameter.
So, .05 millimeters,
very tiny vessel.
And chronic hypertension, we think, sort of
takes these vessels which should be good and
straight, off of vessels and turns them into
these cork screw altered very bizarre looking vessels.
As if they're kind of extruded from the large vessels that they come off of.
This, we fee, we feel deranges the surface of
the vessel and makes it incompetent, so that over time,
there is a certain statistical risk, that the vessel
will rupture, and when they rupture, they start bleeding directly
into the brain parenchyma Which likely shears other small
vessels like this and then begets this very large hemorrhage.
So that's why this patient's symptoms began progressively when he first started
out with a minor [UNKNOWN] and then it went on to completion.
So that's classic of hypertensive
hemorrhages or hemorrhages into the brain from long standing hypertension.
Now a different type of hemorrhage, again we talked about [UNKNOWN] hemorrhage.
Now let's talk about [UNKNOWN] hemorrhage.
This is also a typical story of a 42
year old woman who has high blood pressure and smokes.
Let's try not to be too.
Risk factors for for subarachnoid hemorrhage.
And, she developed sudden onset severe headache then, coma.
Her headache is as if, if you ask her, is it a headache that
started slowly or suddenly, she'll say sudden.
And, then you ask her, does it feel as if
somebody hit you in the head with a blunt object.
Like, that fast, the pain came on. She'll say, absolutely!
So, it goes from one, one second maximum head pain and stays maximum for a while.
This, we'll talk about in the headache lecture.
Her exam also shows neck stiffness.
If you look in her retina with your ophthalmoscope, you'll see
That she has blood actually in what we call the subhyloid membrane.
She's comatose.
Eyes closed, unresponsive.
And her brain stem exam, all of her cranial nerves work fine.
What do we see on a non contrast heat CT? Again, blood is bright.
And you can see throughout the brain, all of these areas of blood that have escaped
into the brain.
Into the brain substance in the subarachnoid space,
so as opposed to our prior hemorrhage, this
is not into the brain substance itself, it's
in the surrounding structures, it's in the subarachnoid space.
That implies that she probably has an aneurism of the brain that's a weakening
of a large blood vessel that has broken, and blood has escaped into the brain.
What a Aneur,
what a, what are Aneurysms and how do they form?
This is a typical Aneurysm by artist rendition.
Now notice here that we're talking about a five millimeter sized blood vessel.
For, for example the Basilar artery in the back of your brain.
At bifurcation points that these vessels, there can
be a weakening and the growth of these aneurysms.
And you'll notice that actually, the blood vessel wall typically
has a nice a stiffness to it.
A little muscle layer that is used to
constrict and change the size of the vessel.
In the aneurysm itself.
All's you're really left with is the intima, the inner
lining and maybe a little bit of this fibrous outer lining.
And the muscle layer and other layers seem, tended to degenerate.
That makes it weak and then in episodes either high blood pressure,
surges or for reasons we're not quite sure.
The aneurysm can rupture.
And they tend to occur at these branch points.
So in the Circle of Willis, within
the anterior communicating artery, very common location,
in the top of the carotid in the posterior communicating artery origin is common.
As well as the Basilar apex.
Each of these aneurism locations determine what's the best
way to treat them, and there's a couple different
ways to treat them. So what does this look like grossly?
As we talked about, the blood escapes into the subarachnoid
space, so when this gross specimen in autopsy from a patient
who died quiet recently of a subarachnoid hemorrhage One can actually
see the aneurysm right here off of the circle of Willis.
But more importantly, there's blood that's escaped throughout a sub-arachnoid space,
staining the brain.
That blood in that space is either due to trauma or an aneurysm, as I said.
And in this case, it's due to a ruptured aneurysm.
Well how do you treat this?
There's two methods.
If you don't fix the aneurysm by fixing I mean close it off.
The patient's at high risk of re rupture of the aneurysm
and that's one reason why we consider this a neurological emergency.
[INAUDIBLE] every minute that goes by the aneurysm is at risk
for re-rupturing and we know that about half of those are fatal.
About 25% of aneurysm rupture is fatal up front in the
first place so among those who actually make it to the hospital.
And don't have a re-rupture, then we can do our best to get them through
that process, but key to that is securing the aneurysm so it doesn't break again.
In this artist's rendition, there's two methods.
One method is the, the traditional surgical method where a
aneurysm clip is placed across the neck of the aneurysm.
This is much like an alligator clip, and
it's very carefully placed over the neck of the
aneurysm, and that causes immediate closure of it
and eliminates the risk of rupture in most cases.
An alternative way is take catheter going to
the femoral artery in the groin Past the catheters
up through the aorta.
Up into the capacitance arteries running to the
brain say the carotid or the [INAUDIBLE] artery.
Place a catheter into the aneurism neck itself, and then
extrude, what we would call coils, which are basic, basically platinum.
metal.
That's extruded into the sac of the anurism, filling it.
Then you allow the anurism to thrombose,
by platelettes aggregating with it, causing no flow
into the annurism, and eventually over the course of
weeks, the anurism neck walls itself off much like paving a pot hole in a free way.
And that reduces the risk of rerupture these two techniques are available in most
advanced medical centers and we know that
taking a patient and treating them in medical
centers that treat aneurysmal subracnoid hemorrhage frequently.
Lowers mortality and improves outcome.
[BLANK_AUDIO]
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