Here, we’ll take a look
at Pick’s disease.
Pick’s disease really is a name
that’s falling out of favor.
The one that you
definitely want to know,
and the one that makes much more clinical
sense is frontotemporal dementia, FTD.
Rare, compared to Alzheimer’s disease.
Rare, but yet know everything
about F – Frontal lobe,
T – Temporal.
So, you tell me,
if you have problems with the frontal
lobe, how are you going to behave?
Like, Dr. Raj, crazy, insane,
mood, behavior, instability.
What about temporal?
We’ll see that in a second.
Think about temporal.
There you go. Good.
And that’s what you’re going to predict.
Clinically, often have a combination
of frontal and temporal.
Frontal lobe includes personality
changes, mood behavior or disorders,
Does this sound like me?
Temporal lobe, we have disturbances
predominantly of the language.
Frontotemporal dementia, rare.
Let me quickly go through this with you.
So grossly, what are you
going to find here?
Well, I told you this is a
differential of Alzheimer’s disease.
There is going to be --
as opposed to global atrophy that
we saw with Alzheimer’s disease,
with the frontotemporal dementia, you’re
going to find asymmetrical atrophy.
What does that mean?
It means that you’re not going to
have the same type of global atrophy.
You might find deepening of the sulci
in some places but not in others
And often, it will spare
the posterior two-thirds
of the superior temporal
gyrus, and that’s important.
So, there’re sparing here.
Severe atrophy results in gyri.
Well, what happens?
The gyri is going to thin,
and then you have a knife-like appearance
that you’re going to find because it
looks like you’re cutting right through,
cutting right through.
severe neuronal loss as you can imagine,
especially in the outer
three layers of the cortex.
And you have these things
called Pick cells,
and this I would know.
These are neuronal swellings that you
find with frontotemporal dementia.
Remember, rare when compared
to Alzheimer’s disease.
So, if you’re suspecting frontotemporal
dementia, make sure that you’re darn sure
that this is what it is because they’re
going to give you specific information.
They have to.
So, there’s no really such
thing as your plaques,
things of that nature,
but you will find tau,
so be careful there.
The Pick bodies,
well, it's cytoplasmic,
round to oval,
filamentous inclusions, which
are very weakly eosinophilic.
What color is eosinophilic?
But stain strongly with silver stain.
Now, be careful with that.
Last time we saw silver stain was
actually of the beta-amyloid plaque.
Composed of neurofilaments,
vesiculated type of
and paired helical filaments that are similar
to those found in Alzheimer’s disease
referring to the tau.
So be careful there, please.
You really, really want to pay attention
to that asymmetrical type of atrophy
that you find with
In Alzheimer’s, it’s
more or less global.
Here is a picture once again
of a tau positive structure.
This could be found with
So, whenever you hear about tau,
top on your differential should be,
obviously, Alzheimer’s disease,
rarely could be
Next, we move on to
In other words, these are
Let me stop there for one second.
What does cortical dementia mean to you?
Cortical meaning higher, higher type
of cognitive functioning, right?
We talk about language and
perception of language
and being able to do
those kinds of things.
Subcortical, you start getting closer
to what can make your life easier.
Basal ganglia, Parkinson’s disease.
What do you know about Parkinson's?
You lose the dopamine.
palsy, we’ll talk about.
Corticobasal type of degeneration,
and Wilson’s disease are movement
disorders that we’ll take a look at.
Our focus will be on basal
ganglia, for the most part.
Let’s first begin our discussion
by looking at Lewy body dementia.
And Lewy body dementia,
second most common cause of
dementia after Alzheimer’s disease.
So, it is a big deal.
Marked by progressive
I’m going to show you something here
that is a clinical pearl for sure,
that you want to pay attention
to with Lewy body dementia.
Memory and attention impaired.
Fluctuating course of good days.
This is what you’re paying attention to.
Your clinical pearl that you
want to know for sure here
with Lewy body dementia would
be visual hallucinations.
Can you do that for me?
Makes your life so much
easier, doesn’t it?
Ha-Lewy-cinations and delusions prominent
and early feature, early feature.
That’s a big deal,
and may present
So, what are we looking
at in these pictures?
Is it Lewy body?
Specifically, they are in the middle.
Do you see that structure?
That looks rather eosinophilic and pink.
Perfectly, perfectly circular.
That is something called
a synuclein, synuclein.
I’ll talk to you about
that in a second.
It’s important that you pay
attention to synuclein.
Is it Lewy body dementia?
And we have another structure that
we’ll take a look at as well,
and this is quite indicative.
Can you see that
That’s all for Lewy
Cortical Lewy body must be present
to diagnose definitively.
So, what is Lewy body?
That’s what I’m showing you
on the picture on your left.
Lewy body is composed of,
that is what that circular eosinophilic
structure that you’re referring to.
That is synuclein.
Be able to identify it, please.
And overall, that circular eosinophilic
structure that you’re finding in
this bigger structure is the Lewy body.
Plaques and tangles are frequently present,
identical to those seen
in Alzheimer’s disease.
Please be really careful.
What you will not find, obviously, in
Alzheimer’s disease will be Lewy body.
This is the second most
common cause of dementia.
What are you paying
attention too clinically?
What is that that we
are seeing circular?
What is the body?
The Lewy body.
Is this Parkinson?
Vascular dementia, also known
as multi-infarct dementia.
What does that mean?
Number of blood vessels that
are undergoing compromise.
And the number of blood vessels
that undergo compromise
will then cause decreased
Risk factors are those for any
type of vascular disease.
Maybe seen with large artery stroke
or severe subcortical disease,
this is known as Binswanger’s.
Abrupt onset or more
commonly, clinical pearl,
step-wise progression is
the key to diagnosis.
But here, we have blood vessels
that are being affected.
So maybe atherosclerosis resulting
in stroke, hypertension.
If you go down into the subcortical
region penetrating deep arteries,
then you’re worried about things
like Charcot-Bouchard aneurysm
and lacunar infarcts.
Focal deficit on neurologic
exam suggests the diagnosis.
Vascular dementia, a.k.a.,
and step-wise progression are the key
points on this particular slide.
We’ll move on to normal
Slow down here for one second.
There are couple of things that I want
to make sure that we’re clear about.
Hydrocephalus has been a topic that
we’ve covered in great detail.
We have talked about communicating
hydrocephalus, which means what?
You’re thinking about the flow or
the path of cerebrospinal fluid.
You’re moving from lateral ventricle,
third ventricle, fourth ventricle,
bathing the spinal cord up
through the subarachnoid
and then going into the
arachnoid granulation, right?
would be post-meningitis,
when you have scarring or fibrosis
of the arachnoid granulation.
Maybe tuberculous meningitis in which
you will then be blocking off the
Luschka and Magendie.
If it’s obstructive or your
a list of differentials or large and wide
in which we have Arnold-Chiari
or you have Dandy Walker.
You could have medulloblastoma.
We’ll talk about a bunch of
this causing obstructive.
But in those cases, what happens?
You have increase in
Now, we talk about Alzheimer’s disease
in which we then have global atrophy
of the cortex resulting in a
compensatory ventricular enlargement
or we call it compensatory
I didn’t even make that up, I kid you not.
It’s called ventriculomegaly.
How beautiful is that name?
Yes, I’m a dork, but the point is
that’s hydrocephalus ex-vacuo.
In that case, we have intracranial
pressure that is normal,
and here, we have normal
How is this possible?
First, please be able to
identify your patient.
Please know the triad.
No doubt, please know the triad.
Gait difficulty, incontinence, and
this dementia is actually reversible.
So, why is it normal pressure?
Well, the concept is over a
long period of time, chronicity,
maybe there is adaptation that
is taking place in the brain.
And with that adaptation, maybe the
pressure now in the intracranium
has actually become normal.
Lumbar puncture may reveal
elevated opening pressure.
Now, you want to be really,
really careful with this, right?
Because if your intracranial
pressure is elevated,
you’ll never do a
You’re going to kill your patient.
But here, if you know for a fact
that there is no signs or symptoms
of increased intracranial pressure,
well, just keep this in mind.
Prolonged CSF monitoring may reveal
abnormal, what’s known as B waves.
Imaging will reveal enlarged ventricles.
It looks like it’s hydrocephalus.
And your treatment is with shunting.
Okay, so even though
you call this normal
there could be increased accumulation
of fluid, so shunting is necessary.
And excellent success,
and this is important
because you’re able to then drain the
fluid from your ventricles and such,
you actually would be able to reverse
the dementia, the gait difficulty.
That is quite rare.
apart from the reversible type of
dementias we’ve talked about such as
B12 deficiency, hypothyroidism,
Wernicke-Korsakoff and so on and so forth,
there is every possibility that
this could also be reversed
in normal pressure hydrocephalus
with simple shunt placement.