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 3: Stroke Treatments and Prevention
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Del curso dictado por University of California, San Francisco
Introduction to Clinical Neurology
310 calificaciones
De la lección
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.
Conoce a los instructores
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
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Well, let's talk now about ischemic stroke treatments.
I want to talk about a stroke timeline.
What does it mean that Time is Brain, a term that we use frequently
clinically to encourage people to move quickly in the evaluation of patients.
And I talk about the ischemic penumbra, which is
a phenomenon related to blood flow during the ischemic stroke.
And I'll talk about two forms of
treatment, Thrombolysis and Thrombectomy.
And let's go back to this case of atrial fibrilation.
The clots that form in the heart, form over
the course of weeks and months and perhaps years.
But once their released from the atria and
go up to the brain as in this illustration.
The impact of blood flow is instantaneous on the brain.
These clots wedge into the large arteries of the brain.
And immediately reduce the blood flow to the hemisphere of the
brain, if a patient doesn't have what we call collateral flow.
Initially there's an area of infarct, we call core
infarct it starts in the first a few hours.
But that can extend over time and in this extreme
example shown here this degree of ischemia can progress over days.
Now if a person has good collateral flow which is
shown here, the clot just closes off the main vessel.
But the main vessel is back fed by other vessels in the brain.
That then causes damage to the sub-cortical regions.
Shown here as a growing infarct over the course of hours and days.
So, the death of nerve cells is time dependent.
And it's also dependent upon the degree of blood flow reduction.
The amount of blood flow reduction, then, is critical for treatment.
As shown in this illustration, when a Thrombus
includes a vessel, there's an infarct shown in white.
But around the outside of this, where collateral flow has persisted,
a person develops an area brain which is aschemic, but not infarcted.
And that volume of tissue can be quite large.
So for example, in the middle
cerebral artery stroke more than half of the area of the
brain that's at risk can be salvaged if treatments are done quickly.
It's called the ischemic penumbra because it's like the surrounding area of
an eclipse that's getting a little bit of sunlight but not maximal sunlight.
Most of our stroke therapies are directed at
saving this ischemic tissue and that is time dependent.
So in this illustration,
this is an illustration from baboon experiments done in the 1970s Where
nerve cells in the brain were looked at in various low flow states.
So the middle cerebral artery was temporarily occluded and then reopened.
And then they looked at the fate of the neurons within that part of the brain.
Turns out on that Y axis here, we have cerebral
blood flow and then on the X axis is time,
in this case in hours.
So if a blood clot lodges into a vessel into the brain and then that blood clot
dissolves, because blood vessels don't like to occluded,
they have their own endogenous enzymes that dissolve clots.
So clots that go into a brain blood
vessel with reabsorb themselves in, in, in short order.
So if blood flow is reduced to this particular part of the brain,
ablove, above this threshold called the paralysis threshold.
A patient won't develop any neurologic signs,
and they won't even know anything happened.
No tissue is damaged and the patient is non-the-wiser of the problem.
Let's say that though this time the embolysis hits a
blood vessel and blood flow's reduced just a little more.
In that case, the blood flow line crosses the
paralysis threshold and the patient develops
weakness of one side of their body.
Again, the blood vessel opens itself up after a little
bit goes above the ischemic threshold and the patient's symptoms resolve.
That's what we call a transient ischemic attack.
There's been a temporary occlusion of a blood vessel.
Then it's reperfused and the symptoms go away.
In the third example,
blood flow is reduced even more, far below the paralysis threshold.
And then before the blood vessel opens, it hits this threshold of infarction.
And in this case, nerve cells are now dying.
The middle cervical artery occlusions, one estimate is that
a million nerve cells die per minute of vascular occlusion.
So this win, time window here, is part of the
window where we can turn what would otherwise be an ischemic
stroke into a TIA, if we open up the blood vessel.
How do we do that?
Tissue plasminogen activator is one of those drugs.
This is a cloned enzyme that you have normally in your body.
It seeks out clot that is in, anywhere within
the blood vessels of the body and dissolves enzymatically.
In a clinical trial that performed
testing tissue plasminogen activator, NIH researchers randomized
over 300 patients to a trial in each arm. Those who got the drug itself, t-PA
and the other half received a bolus of placebo medication.
They looked at the outcome of patients at 90 days and
in every one of the measures of clinical outcome, patients did better.
This came at a cost though.
Because TPA opens up blood vessels that have
clot in them it may also open up
damaged blood vessels and cause bleeding into the brain.
So in this study, 3% of patients who had a
hemorrhage, had a hemorrhage and died, actually from the drug.
Overall patients did better despite these hemorrhages.
But it still raises concern to us, that
giving this drug can have a hemorrhage risk.
The longer you wait to give TPA after the onset of the stroke,
the higher the risk of bleeding. It's very time sensitive.
So we don't give this drug beyond four point five
hours after the onset of neurologic symptoms for that safety reason.
What do these hemorrhages look like?
Well, here's a patient who has an ischemic stroke,
who's then develops a hemorrhage into the brain in white.
And you can see brain herniation where the brain on the
right side here is all pushed over onto the left side.
And part of that's
because of the blood that escaped from the blood vessels.
So this hemorrhagic transformation, itself, can
be a major concern using thrombolytic drugs.
In a patient who reperfuses the brain
but doesn't bleed extensively into the brain, you
can see the brain itself is just stained
with iron products from the blood that's escaped.
So, Thrombectomy is a technique where you actually mechanically remove the
clot from the brain.
This was originally tried in the 1960s, where surgeons would go and
open the middle cerebral artery itself for example and take the clot out.
That's pretty tricky to do, and was, not helpful.
But now we can do it with catheters.
So we can go from the groin up into the
brain with devices that actually ensnare the clot and remove it.
One of the examples is shown here, where the clot going into the
middle cerebral artery. Where blood flow is shut off downstream.
Then a catheter is placed up into the
vessel inside the brain, piercing through the clot with
a small micro wire and then placing a device which is a, which is a, a stent.
It's actually a device that dilates open blood vessels that is retrievable.
Once that stent is put into place and you can see the operator
unsheathe the stent itself, and the stent will expand into the clot.
The clot is sort of rubbery.
Once it, it, expands into the clot itself it actually opens up a
channel, a flow, so the brain is immediately restored with some blood flow.
And that we think is helpful to the brain during this process.
So once flow is restored, now the trick is to get the clot out of there.
And because the stent has been embedded
into the clot matrix itself, you can arrest flow in the vessel with
a proximal balloon, and then pull the clot out of the brain itself.
These techniques have been under, undergoing
clinical trials and is a very active
area of investigation to see whether it truly helps patients restore blood flow.
We know we can open vessels pretty safely with these devices.
But we don't know yet whether or
not they actually make patients better off having the treatment than not at all.
Another example is a patient with a
left middle, left middle cerebral artery stroke.
In this AP angiogram, here's the internal carotid artery, the
anterior cerebral running up to the left side of the brain.
And then the left middle cerebral artery has this cut off,
right here because there's a clo, a clot in that vessel.
The device is placed into the patients vessels, from the groin, pulled back and
removed from the body.
Here we can see the vessels now has restored profusion to it.
These devices actually have the clot itself
embedded within the device itself which would
now looked at histologically and can determine
what some of these clots are made of.
Another example of this is of a young man who had a stroke of the basilar artery.
So in this graphic here on
the the left, remember the basilar artery itself
is going to be supplying most of the brain stem.
In this particular case, this occlusion is right where
my arrow is, in the left half of the illustration.
This caused the patient to be very sleepy, somnolent
and developed a hemiparesis because of the motor involvement.
A device was placed very rapidly into his vessels and
the clot was moved from his brain.
And he had complete restoration of blood
flow and fortunately made a complete recovery.
So these types of treatments are encouraging.
And there are ways for us to convert a stroke like this, which
we think is about 50% fatal to a person who can recover fully.
Well, how do we prevent stroke in the first place?
We certainly talked about its causes.
And how we can treat it in the when a patient comes into the hospital acutely.
But how can we prevent this from happening in the first place?
Stroke prevention is heavily based on first detecting
whether or not a patient has atrial fibrillation.
This can be done simply by an electrocardiogram
to record the heart's rhythm.
Some cases we're detecting this in patients who wear
heart monitors as an outpatient for up to 30 days.
To see whether or not their heart goes in
and out atrial fibrillation, that's called intermittent atrial fibrillation.
We now with very good medical evidence, so if you give patients blood thinners,
true anticoagulants which there are many now it reduces the risk of stroke to come.
Aspirin works a little bit but true anticoagulants work much better.
If the stroke was due to Carotid Stenosis
where there's disease of the carotid artery themselves.
Cleaning out that plaque with a procedure called Endarterectomy.
Where you surgically incise the skin, get to the artery, open the artery up,
and shell out the atheroma that's in it and then sew the artery back up.
Or placing a metal
stent across it, that reduces the risk of stroke to come.
Following that, we give patients, drugs like aspirin.
As well as statins or other agents to lower cholesterol.
In all of these people, we all
else besides the carotid stenosis and atrial fibrillation.
There's a good data that that antithrombotic drugs like aspirin,
clopidogrel and others that are coming through the pipeline.
Reduce the risk of second stroke by as much as 20, 25%.
If you have atrial fibrillation, we don't use aspirin or clopidogrel.
We use true anti-coagulants, like warfarin and factor 10A inhibitors and
others, that are present in the, that are now available to patients.
But for everybody else, there needs to be an antithrombotic drug,
added on, even if you've had carotid stenosis.
Another factor is to lower blood pressure.
We want blood pressure to be under 130 over 85, if not lower.
We know that all the diseases we've talked
about in this lecture are primarily related to hypertension.
And there's very good data that lowering blood pressure and keeping it
low long term prevents second stroke and it also prevents first stroke.
So,
screening a blood pressure and treatment of
high blood pressure is key in stroke prevention.
Statins have been shown to reduce the
risk of stroke, certainly risk of second stroke.
We target the LDL less than 100, and in some patients, less than 75.
That can be done with diet, exercise, and statins together.
But the goal is to get the LDL cholesterol down.
If the patient smokes, we plead with them to
not and give them tools to stop cigarette smoking.
It's very clear that you, when you stop smoking you
reduce the risk of arterial disease and second stroke, as well.
And lastly, exercise is of incredible value.
It helps your HDL LDL ratio, it lowers blood pressure,
it keeps a lower body mass index, it prevents diabetes.
It's one of the most
important things a patient can do on a daily basis to reduce stroke risk.
So, that's been a summary of stroke, we talked
about stroke as a disease that is clinically diagnosed.
It's a disease that has two important
distinctions, a hemorrhagic stroke and an ischemic stroke.
We talked about the treatment of ischemic stroke
with thrombolytic drugs and potentially thrombectomy type of devices.
And most importantly, we talked about prevention.
Prevention in, in stroke is one of the most important factors
that we can convey to our patients and to society at large.
It's estimated that if we treated high blood pressure
throughout the world, we could cut stroke in half.
And for a disease that is the number one killers,
in several countries, that's something which we should put a lot
of effort towards. I thank you for your attention.
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