Let’s talk about embolism
and its pathophysiology.
We just had this conversation.
Let’s say that you have
a patient who’s elderly
and is suffering from or had a
history of myocardial infarction.
And now the patient starts having
a heart rate that’s racing.
Upon physical examination, the heart rate
is approximately 200 beats per minute.
You take a look at the electrocardiogram,
you find that the P waves are pretty
much non-existent or wavy in nature.
At this point, you’re
suspecting atrial fibrillation.
And for sure, you’re worried about
thrombotic formation in the heart.
The next step of management, please?
Prophylaxis with anticoagulant.
Such as warfarin.
Because warfarin has shown,
on current day practice,
to be the most effective anticoagulant
drug to prevent cerebrovascular accident.
Now, granted a cerebrovascular
accident could be only ten percent
of the time when you
embolize from the heart.
The other places that you would embolize
would be maybe the renal artery,
maybe the superior mesenteric artery,
and those are much more
common, much more common.
when it comes to warfarin,
it’s important that you pay
attention to atrial fibrillation
and its prevention of CVA.
Valvular heart disease, same
thing, thrombi formation.
You’re always run into the risk
of embolic type of focal stroke.
Wall motion abnormality.
What does that mean to you?
Patient has suffered, let’s
say, myocardial infarction
or if patient has been
drinking for a while
and this alcohol is then
causing damage to the heart.
And all of these, at some point in time,
you’d recognize that the
patient is getting fatigued.
And upon echocardiogram,
you then calculate that the
ejection fraction is less than 55%.
What’s going on?
Well, now you’ll also notice that the
wall motion is not present in the heart.
So if there’s no wall –
Or if there’s, let’s say, decreased wall
motion taking place with the heart,
where is your blood?
And once again, a perfect environment
for thrombi/embolic type of event.
Septal aneurysm with
patent foramen ovale.
Patient has a DVT,
may result in a paradoxical emboli.
PFO, patent foramen ovale.
In the carotid artery, maybe
beginning in the carotid
artery, a common occurrence.
It could embolize into the head. Not good.
Or there could be even dissection
taking place of the carotid,
therefore resulting in embolization,
resulting in focal ischemic stroke.
Are things becoming clear for
you now at this juncture?
Are you seeing as to what are the
differences between focal and global?
And at this point, under focal, our
specific pathophysiology is emboli.
Another type of ischemic stroke, but this
time we’ll have a thrombus formation.
So we’re not embolizing to
the brain, is that clear?
So it’s a thrombus formation
taking place where?
Oh, maybe in the middle
Picture that for me, please.
Middle cerebral artery.
Because I’m going to spend a
little bit of time with that.
You have spent time with
this in neuroanatomy.
And also please understand that MCA
is going to supply the parietal lobe.
The parietal lobe.
In other words, the lateral portion
of the parietal lobe, right?
In the homunculus,
the parietal lobe on the lateral aspect
is going to supply what part of the body?
What about this? Remember this?
See that ugly face that I just made?
That face, plant it on the lateral
aspect of the parietal lobe, please.
Because that’s what it’s affecting,
the upper, upper portion of
the head and neck and such.
Middle cerebral artery.
Now, depending as to which side is
dominant or non-dominant for example,
if you know your patient is left-handed,
and then the right side
of the brain is dominant.
If your patient is right-handed,
then please note that it’s
the left side of the brain.
And depending as to what side
of the brain is dominant,
if there’s a middle cerebral artery type
of issue, maybe a thrombus formation,
then you’re going to have a
different type of symptoms
that you’ve talked about before such
as hemineglect and so on and so forth.
Majority are due to atherosclerosis.
Remember, we’re not embolizing
up here into the brain.
We’re forming a thrombus most
commonly due to atherosclerosis.
Risk factors are the common ones
that we know so well, unfortunately.
Metabolic syndrome X including
hypertension, diabetes, hyperlipidemia.
Other etiologies will include once
again, those hypercoagulable states
or maybe even drug abuse.
We’ve seen that amphetamine,
Drugs are a big, big
part of our society.
And oftentimes, you find these
patients who are suffering from
thrombotic type of focal ischemic stroke
and on sickle cell disease as well.
Sickle cell disease, remember here,
that sickling that will be
taking place of your RBCs,
anywhere up and down the body.
Anywhere, including up in the brain.
carotid bifurcation for
origin of the middle cerebral artery
or perhaps even the basilar artery
or common sites where atherosclerosis
would be settling in
or thrombus formation would be settling in
resulting in decreased
blood supply to the brain.
Other causes of focal
Here, we have arteritis.
Earlier, I mentioned a
few conditions to you.
They included Henoch-Schönlein purpura
or now called IgA vasculopathy.
I told you about temporal arteritis, a.k.a.
giant cell arteritis,
or something like
The point is when you have an artery
that’s undergoing inflammation,
there might be decreased blood
supply, resulting in a stroke,
primary or secondary.
Etiologies, primary CNS
angiitis, maybe even syphilis.
In worst case scenario, remember your
blood vessels could be affected.
Some of these infections
may result in a type of
arteritis or inflammation
that’s taking place.
Others as I have mentioned earlier,
temporal arteritis, PAN, polyarteritis
nodosa, or connective tissue diseases.
Any of these could result in
inflammation of your blood vessel,
resulting in focal
Your patient has suffered a stroke.
And this time, the patient
is unable to properly
use different parts of
the brain to speak.
But it’s actually the fact that the
learning in the brain has been affected.
For example, you could
have a Broca’s aphasia.
You’ve learned about
that in neuroanatomy.
That’s your motor aphasia, which
means you can understand,
but the problem is you’re not able
to properly carry out language.
Or you could do Wernicke aphasia depending
on that part of the brain, 22 and such.
And so therefore, here
you’re not able to properly
as sensory aphasia,
but my goodness you’re just rambling
off whatever type of garbage.
Meaning to say that,
you know what?
"I think that so and so is
going to become president."
We’re not going to name who,
but then, oh my goodness,
at the same time, "Did you know about
how well I went to potty this morning?"
Do you understand? It’s a lot of garbage
that’s just coming out of your mouth.
And that would be a type
of maybe a sensory.
Alexia would be inability to
properly perceive written words.
Agraphia. Graphia, think of it as trying to
write down a graph but you’re not able to.
So you’re not able to properly write words,
but it’s not related to
weakness or sensory deficit.
That must be understood.
Now dysarthria, it will be
slurred or stuttering speech
due to motor weakness
But once again, the language
centers would be intact.
If it’s apraxia, inability to
carry out learned motor tasks.
And you just learned how to do, let’s say,
you’ve learned how to do a Rubik's Cube.
But the problem is you’re not able to
properly it out with the motor aspect.
We have ataxia
and this literally would
mean that the fact
that you have a widened
gait type of a stance.
And here once again, not due to weakness.
Usually, it’s the cerebellum
that will be affected.
and here it’s an inability
to properly swallow.
All could be parts of