0:00

Dr. Laser, as you know,

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this is a patient I've been

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following for 20 years.

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I've been observing her cognitive decline,

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which has been very slowly progressive

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over time and recently accelerated.

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Here's a scan from five years previous at age 85.

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Here's a scan from when she was 90.

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Look at the difference in the temporal horns.

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They're getting bigger five years later.

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Look at the size of the hippocampus.

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It's much thinner on the right and left

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than it was before, so there's volume loss.

0:28

That is the number one biomarker for

0:30

primary neurodegenerative disease,

0:32

specifically Alzheimer's.

0:33

And I wanted to take this opportunity

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to make two major points.

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One,

0:38

when you're going to make the diagnosis

0:40

of Alzheimer's disease,

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when we've discussed this before,

0:43

most attendings,

0:44

experienced attendings,

0:46

don't like to put that on a piece of paper.

0:47

Because you've now labeled the patient,

0:49

you make it very difficult for them to drive,

0:51

to get insurance and other areas.

0:54

So, I prefer using the term,

0:56

unless I know the patient is overtly demented.

0:59

I'll say

1:00

Mild Cognitive Impairment Syndrome.

1:02

And the clinician knows exactly what I mean.

1:05

In other words,

1:06

the patient has some degree of cognitive

1:08

impairment by imaging,

1:09

and we're not prepared to say whether it's full

1:11

blown ALZ or not.

1:13

That's completely up to them.

1:14

Now, if we know they have full blown ALZ,

1:16

that's a whole different story.

1:18

So I do try and tiptoe around the

1:20

ALZ diagnosis where possible.

1:23

The second thing I wanted to do is take this

1:25

opportunity to discuss pathology in ALZ.

1:29

So, the pathology is degeneration of the hippocampus,

1:32

in association with other areas

1:34

involving the cerebral cortex,

1:36

mostly parietal and temporal, less than frontal.

1:39

But the frontal will be involved

1:41

in the middle to end game.

1:42

And sometimes,

1:44

isolated parietal involvement will be affected.

1:46

That's called Benson Syndrome.

1:48

And sometimes

1:49

just the left speech hemisphere is affected,

1:51

and that is called semantic aphasia with dementia.

1:54

The patients get neurofibrillary tangles

1:58

and amyloid plaques,

1:59

which are well known.

2:00

And the timing of these plaques is characteristic.

2:03

The beta amyloid precedes the deposition of

2:06

tau protein and neurofibrillary tangles.

2:10

And you can detect the presence of amyloid using FDG

2:15

Fluorodopa.

2:16

Sorry, using Fluorodopa PET.

2:18

Now, classically on fluoridopet,

2:20

and this is pretty interesting,

2:21

you can't appreciate it on MRI,

2:23

but eloquent areas are frequently spared.

2:27

Another area that you should look very carefully

2:29

at is the posterior cingulum,

2:31

which is going to be right here.

2:33

And then, look at the parietal occipital fissure.

2:35

Right in this spot.

2:37

Look how big her parietal occipital fissure is.

2:40

That is very typical

2:42

of ALZ.

2:43

Also, look at her cingulate sulcus.

2:45

Also really big as it approaches the

2:48

marginal sulcus area right here.

2:51

That's another typical finding that

2:53

you see in Alzheimer's disease.

2:54

So, she's got transition from MCI to

2:58

ALZ with a lot of the findings.

3:00

Hippocampal loss,

3:01

the number one marker.

3:03

Generalized temporal parietal atrophy.

3:05

Atrophy of the parietal occipital sulcus.

3:08

Atrophy of the cingulate sulcus,

3:10

extending up to the margin and the

3:13

typical clinical findings,

3:14

which began as subtle cognitive decline and now

3:17

avert cognitive decline

3:19

with short-term memory loss and anomia.

3:21

Let's move on, shall we?

3:23

Pomeranz and Laser out.