0:00

So our last case case number 13 is a

0:03

70 year old with memory loss and balanced difficulties.

0:06

So they had an MRI of the brain with neural Quant

0:09

in 2012. You look here that

0:12

the DWI and that is negative. The GRE is

0:15

also negative. No evidence of bleed.

0:19

But when you look at the t2 weighted sequence, you see ventricular magely

0:22

of the third and lateral ventricles sort of

0:25

out of proportion in size to the high midline Soul

0:28

side. Now, I don't use the lateral soulcine because

0:31

when you have Baseline atrophy, which

0:34

this patient does those lateral Souls I

0:37

run large what I really primarily look at is the high midline

0:40

society and the ventricles are just a little bit.

0:43

Too big for the appearance of the high midline sulcide.

0:46

You can see this often best in

0:49

the coronal plane. So let's take a look here on the coronal plane. See

0:52

how big the ventricles are compared to

0:55

the high midline soulside. So it's quite subtle in

0:58

this case, but I read this case as a

1:01

suspected normal pressure hydrocephalus, in

1:04

addition. The patient has very mild, you know

1:07

microvascular ischemic disease as we mentioned there

1:10

is baselines scrubali atrophy. There's also some

1:13

sort of mild to moderate surveilleract fee as well.

1:16

So the patient then came back they were lost to follow up for three

1:19

years and came back for an MRI in 2015. If

1:22

we look at the DWI images

1:25

here. We see a very subtle focus of

1:28

DWI hyperintensity and the right basal ganglia.

1:31

This is here in the right caught a nucleus. It

1:34

extends into the interest of the right detainment.

1:38

Here's the GRE sequence.

1:40

There is very minimal susceptibility artifact around

1:43

this. This is what it looks like on the flare sequence.

1:46

So it's hyperintense on Flair but not yet in

1:49

cephalomalacia there. So this has the appearance

1:52

of a Subacute to early chronic

1:55

infarct in the right basil ganglia, which was not present on

1:58

the prior study. So it's probably between one

2:01

and three weeks of age since we still have some DWI hyperintensity. This

2:04

was normalized on ADC. However,

2:07

and there's likely Trace surrounding Hemisphere and

2:10

staining there.

2:12

And incidentally here. I'm going

2:15

to pull up the t2 weighted sequence.

2:18

The patient does have acute right maxillary sinusitis.

2:21

You see the air fluid level here in the right.

2:24

Maxillary sinus there has been

2:27

some progression in the mild to moderate microvascular

2:30

ischemic disease again, we see some mild to

2:33

moderate cerebellar actually which was stable and we also

2:36

still see that little left parietal craniotomy and

2:39

underlying zone of cortical encephalomalacia

2:42

involving the precentral gyrus of

2:45

the left frontal lobe and post Central gyrus of the left parietal

2:48

lobe likely due to Prior surgery

2:51

there.

2:53

If we look at the lateral ventricles, the lateral ventricles have

2:56

progressed in size. There's now more narrowing

2:59

of the high convexity. Sulcus. I'm

3:02

going to show you here a comparison. Let's drop

3:05

the coronal view here and the coronal

3:08

from the prior study in 2012.

3:12

And you can see here that if

3:15

we try to match the levels there is more

3:18

narrowing of the Soul side. Then what

3:21

we saw here in the midline area. Then on the prior study. Another

3:24

thing that you can do is you can measure the Colossal angle.

3:27

This is how you would measure the closer angle

3:30

here. You should do this at the level of the posterior commissure. I'll

3:33

show you where the posterior commissure

3:36

is.

3:38

If you look here at the superior click this here's the pineal gland

3:41

right in between there that band of tissue. That's the posterior commissioner.

3:44

And that's kind of where you want to measure the coastal angle normal

3:47

would be a hundred a hundred and twenty n pH

3:50

patients will often be lower than that often sort

3:53

of 60 to 80 type range, but there is variability

3:56

because obviously there's a spectrum of when you start to

3:59

progress with NPH but we know this also are

4:02

more narrow here. So now we are convinced that this is an NPH

4:06

Case so the patient then went on to have an

4:09

ftg brainpet CT in 2015. This

4:12

is the brainpetsy team 2015 and

4:15

it showed hypo metabolism in

4:18

the bilateral mesial temporal lobes. Although it was not statistically significant

4:21

when I ran it through the neuronalysis software

4:24

on the right side, but it was statistically significant

4:27

on the left side.

4:30

The patient then went on to have an amyloid pet study

4:33

in 2016.

4:36

So this is the amyloid pet and this is diffusely positive.

4:39

So we have a diffuse finding of the animal a

4:42

tracer throughout the cortex.

4:44

So this is a positive study and you notice here in

4:47

2016. Finally. The patient was shunted the

4:50

patient then came back to have an MRI of

4:53

the brain with quantitative analysis in 2016.

4:57

And we see here on this study that the ventricles are

5:00

now improving in size the

5:03

midline sulci are now larger in

5:06

size. So after shunting

5:09

The patient's ventricles are getting smaller noted. Well,

5:12

I wanted to note that whenever a patient shunted friend

5:15

pH the ventrals typically never go back to normal in size, but

5:18

they do definitely get smaller in size when compared to the pre-shunt

5:21

images and here's again that inferc that

5:24

we saw on the prior study.

5:27

So this is again a 78 year old with memory loss and balanced difficulties. This

5:30

was the initial MRI in 2012 where

5:33

I had said that I thought

5:36

that this was probably an early NPH case given the

5:39

ventricular medley out of proportion size.

5:42

To the high midline sulci there were lost to

5:45

follow for three years. They came back in 2015 and you

5:48

can see here the difference in the high midline. So I'll say more

5:51

narrow than what they were in 2012 this confirms

5:54

a diagnosis of NPH and they

5:57

were finally shunted in 2016. And now

6:00

at sort of a similar level here, we see that the soul Side

6:03

High midline souls are larger.

6:05

In size So the patient's ventricles are

6:08

now smaller post shunt.

6:10

Some other findings that we saw was this Subacute

6:13

or early chronic infarct in the right basal ganglia

6:16

here.

6:17

That emerged in 2015 and then

6:20

the patient did have quantitative of volumetric Imaging and

6:23

both 2012 and 2016. Now

6:26

both of these showed some reduction in

6:29

the hippocampal volume and then as expected the

6:32

ventricles are statistically significantly in large

6:35

for age because this is an NPH case.

6:38

So they're up here in the pink zones.

6:41

Now, this is the Michael brain

6:44

report here and what we

6:47

see is the whole brain volume has actually

6:50

gone down from 2012 to 2016

6:53

despite the fact that the

6:56

size of the lateral ventricles.

6:59

Has actually gotten smaller and the

7:02

lateral ventricles have gotten smaller in size because the patient's

7:05

been shunted but the whole brain volume has really dropped

7:08

since the study four years ago. In fact,

7:11

the whole brain volume is decreased by 68 milliliters in four

7:14

years that's gone from 39 percentile down to

7:17

13 percentile. So when you're worried about

7:20

in an mph case, it can almost sort of

7:23

present as a false top positive type appearance on

7:26

quantitative Imaging for hippocampal volume

7:29

loss because as those Imperial ventricles in

7:32

large because of the hydrocephalus, they

7:35

can put pressure on the hippocampi and they

7:38

can appear to show hippocampal atrophy, but

7:41

that may be actually unrelated to whether there

7:44

is true hippocampal atrophy or not in this

7:47

particular patient. There is true hippocampal attribute, but it's hard to

7:50

tell when you have in NPH and the hydrocephalus is

7:53

pressing on the hippocampi. So I encourage you always to

7:56

keep an eye on the whole brain volume and that

7:59

will really help.

7:59

You to tell whether there is Progressive atrophy. The

8:02

other thing that's great about quantitative volumetrics in

8:05

NPH cases is it's a really

8:08

great way to objectively measure the lateral ventricles our

8:11

eyes often tend to keep calling things stable stable.

8:14

When we look at MRIs over time when they're actually

8:17

really maybe change in the ventricular size and the

8:20

neurosurgeon really needs to know which way the ventricles are going and getting

8:23

bigger or getting smaller. So the quantitative analysis gives

8:26

you the actual volume of the ventricles. So that's a

8:29

very helpful thing. This is the fdg brainpit

8:32

CT in 2015 here. Here's the

8:35

PET CT.

8:36

Fusion images and here is the pet MRI Fusion

8:39

images. There was hypo metabolism the bilateral

8:42

temporal lobe so statistically significant only on

8:45

the left side here when I ran it through the mineral analysis

8:48

software the patient then went on to have the amyloid pet

8:51

in 2016. You can see

8:54

the shunt here in place and there is diffuse binding of

8:57

the amyloid Tracer throughout the cortex. Here's the PET CT.

9:00

Here's the pit Mr. Fusion. So this

9:03

patient has two diagnoses both NPH and Alzheimer's

9:06

disease.