0:00

I'm here with neuroradiology stud,

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Dr. Ben Laser,

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and we're looking at a crazy case.

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This is an 80-year-old with severe memory loss,

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balance disturbance, dizziness, numbness,

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speech disturbance, hearing loss.

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Everything's here.

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Dogs and cats living together.

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Ten days of darkness in the plague.

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We've got an axial T2, a sagittal FLAIR,

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and an axial BSI SWI, or SWAN.

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Now, this patient has known Parkinson's disease

0:26

and has severe memory loss and these other symptoms.

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So, how do we tease out?

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This is our third major point

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from the prior vignette.

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We probably have three things going on here.

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How do we tease them out?

0:37

And those three things are probably some vascular disease.

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In fact, vascular disease,

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some primary neurodegenerative disease,

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because there's a heck of a lot of atrophy,

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including the cerebellum and the parietal

0:48

occipital fissure and the calcarine fissure or sulcus.

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And the third thing is,

0:53

we know he's got Alzheimer's disease.

0:55

So, where would you like to look first?

0:57

So the first thing we could look at would be,

0:59

in terms of Parkinson's disease,

1:01

let's look at the midbrain and look at the

1:02

pars compacta, identify the red nucleus,

1:05

identify the substantia nigra,

1:07

and evaluate if the pars compacta stripe is intact.

1:11

Yeah.

1:12

And here is the area that you're talking about.

1:14

And there should be something that looks like this.

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For those of you newcomers,

1:18

you should be seeing something

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that looks like this,

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and then you should be seeing the

1:22

red nucleus underneath it.

1:24

And there should be an area of tissue that is not

1:27

siderotic or black-laden. So this would be.

1:30

If. I'll color it in for you,

1:31

just so it makes sense.

1:32

So this would be black, and that would be black.

1:36

And then you have some intervening tissue in between.

1:39

And we certainly don't have that.

1:41

The red nucleus, it looks like it's bled to

1:45

and through the substantial...

1:46

through the pars compacta,

1:48

through the substantia nigra,

1:49

obliterating the pars compacta.

1:50

Yeah, they look like one structure, pars compacta,

1:53

which should be a stripe,

1:54

a gray stripe is obliterated.

1:56

And the amount of iron that should kind

1:58

of fade away along the lateral side,

2:01

like the tail of a bird,

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is gone.

2:05

So, the patient does have findings consistent

2:08

with Parkinson's disease.

2:10

And clinically, they did as well.

2:12

We could explain the dizziness also with that

2:16

and the cerebellar atrophy that's present,

2:19

as well as the balance disturbance.

2:20

I think the numbness we could probably write off

2:22

to the extensive white matter abnormality

2:25

that suggests that there's underlying

2:27

hypertension or arteriosclerosis.

2:29

Might call it Binswanger phenomenon.

2:32

And if we look at the sagittal,

2:35

what else supports a primary

2:36

neurodegenerative disorder?

2:38

So the next thing that I would

2:39

look at would be the volume,

2:40

the volume of the cerebrum and the pons

2:43

in the midbrain.

2:43

So in this case,

2:44

you can see there's marked

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volume lost posteriorly,

2:47

essentially involving the occipital lobes.

2:50

And there is an isolated form of Alzheimer's

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disease that affects the occipital lobe.

2:55

It's called Benson's disease.

2:57

It's histologically identical to classic Alzheimer's,

2:59

and then it spreads.

3:01

It may present with visual symptoms.

3:03

This could be a variation of that, by the way,

3:06

the parietal occipital sulcus, variatrophic,

3:08

Calcarine, variatrophic.

3:10

Gliosis around there.

3:11

Pons preserved,

3:12

even though there's gliosis.

3:14

So we know there's small vessel disease in the pons.

3:17

So, a lot going on here.

3:18

A primary neurodegenerative disorder

3:20

affecting the whole brain.

3:21

How about the hippocampus?

3:23

The hippocampi are markedly abnormal and small.

3:25

Yeah, especially anteriorly.

3:27

Look how atrophic they are.

3:29

And so we have limited coronal imaging,

3:31

but when we pull down our limited coronal image,

3:33

look how small the entorhinal cortex is.

3:36

Choroidal fissure, big.

3:37

Temporal horn, big.

3:39

So, we would consider Alzheimer's or one of its

3:42

variants to be comorbid with the Parkinson's

3:45

disease and the vascular disease.

3:46

Now, you might say three diseases. Really.

3:48

Well, we know that 15% of all dementias are both a

3:52

primary neurodegenerative disorder

3:54

and vascular disease,

3:55

and 5% to 7% have three major

3:59

causes of dementia.

4:00

So, this patient maybe fall into that category

4:03

where we have Parkinson's disease producing some

4:06

symptoms, a primary neurodegenerative,

4:08

ALZ-like illness,

4:10

producing some of those symptoms,

4:12

and certainly small vessel arteriopathy and

4:15

venopathy from Binswanger syndrome

4:17

contributing to that disease,

4:18

with extensive periventricular

4:20

white matter abnormalities.

4:22

One thing that does go against the diagnosis

4:24

of ALZ is the cingulate sulcus.

4:26

Really? Isn't that atrophic?

4:28

So we could be dealing with another primary

4:30

neurodegenerative disorder.

4:32

And you pointed out before

4:34

that the pituitary gland is small.

4:37

There's complete empty sella.

4:38

So it would be wise to check maybe, what, a TSH?

4:41

Thyroid levels.

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Cortisol levels,

4:43

to make sure that he doesn't have a superimposed

4:46

metabolic problem lopped on all these others.

4:49

What about NPH?

4:50

How do you feel about that as a diagnosis here?

4:52

Because the ventricles are big.

4:53

The ventricles are big.

4:55

However, there is,

4:56

as you already pointed out,

4:58

extensive white matter disease.

4:59

So predominantly,

5:00

this also could be due to ex-vacuo dilitation.

5:04

Yeah,

5:04

and I like to see the sulci more effaced in NPH.

5:07

I also like to see crazy bounding pulsations

5:10

against the stiff ventricular wall,

5:12

so you get really weird swirling right here.

5:14

Pulsation artifact.

5:15

Yeah, pulsation artifact.

5:16

We don't have that for NPH.

5:18

And then we go down to the fourth ventricle

5:19

and the aqueduct.

5:20

Really, they're not big,

5:21

so that goes, you know,

5:23

that would be dilated NPH.

5:24

So, I don't think NPH is a consideration here.

5:27

Even though the patient's ventricles are big.

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So, let's check out on this one.

5:32

We've got Parkinson's disease,

5:34

with evidence thereof on the susceptibility

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weighted image.

5:37

We've got a primary neurodegenerative

5:39

disorder that is ALZ-like,

5:41

and we have extensive small vessel arteriopathy,

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and/or venopathy,

5:46

so-called subcortical arterial

5:48

sclerotic encephalopathy,

5:49

or Binswanger's phenomena.

5:50

Pomeranz and Laser are out.