0:01

This was another child who presented

0:04

with acute neurologic deficits.

0:07

Now, there is a broad differential diagnosis

0:09

for a child with acute neurologic deficits.

0:11

We think about a seizure disorder.

0:14

We think about complicated migraines.

0:17

We think about potential

0:18

poisoning or drug use, etc.

0:21

In this case, we looked at the DWI images.

0:24

And we saw almost immediately that there were multiple

0:27

areas of high signal intensity on the diffusion

0:30

weighted imaging that indicated that there were strokes.

0:34

And most of these strokes seemed to

0:36

be in the watershed distribution.

0:39

This is part of the white matter

0:41

watershed on the right side.

0:43

There are some areas in the

0:44

anterior cerebral distribution.

0:46

But the majority of the abnormality

0:49

was in the watershed distribution.

0:51

Here was an area that was

0:52

involving the top of the caudate.

0:54

So, as with whenever we see these abnormalities

0:58

on the DWI, we want to confirm on the A

1:01

DC map that they are indeed dark areas.

1:04

So here is the low signal intensity on the

1:07

ADC map—apparent diffusion coefficient—

1:09

decreased, corresponding to the bright

1:12

signal intensity on the DWI. And as we went

1:15

further superior,

1:16

all these areas corresponded to dark

1:18

areas representing acute infarction.

1:21

Remember, if it's bright on the ADC map,

1:23

it's more likely to be vasogenic edema.

1:27

So we have bilateral infarctions in a watershed

1:32

distribution, predominantly in a child.

1:36

So.

1:37

Did this patient have a cardiac arrest?

1:39

Did this patient have a hypoperfusion

1:42

episode, either due to dehydration?

1:45

Could it have been a patient who drowned?

1:48

Again, we would be asking the clinicians. We're on

1:50

the phone already because we have a positive DWI,

1:54

informing the clinician that the patient has a stroke.

1:57

We would go to the FLAIR scan if we wanted

2:00

to look and see whether they were bright.

2:02

So these are greater than six hours old,

2:05

because we can see them on the FLAIR scan.

2:09

And then we would look at the susceptibility

2:12

maps to look for hemorrhage in the

2:15

strokes—no dark blood products identified.

2:22

And then we would look at the MRA if it was available.

2:26

In this case, although I don't have the

2:29

MRA to show you, this is a patient

2:32

who had Moyamoya syndrome.

2:35

Moyamoya syndrome is the entity in which there

2:39

is vascular narrowing of the distal internal

2:42

carotid artery going into the M1 or A1 segments.

2:47

And when it is Moyamoya disease,

2:50

it is a bilateral process.

2:52

We have a bilateral process because of the

2:56

stenosis of the distal internal carotid artery.

2:59

It leads to.

3:01

Areas of watershed disease, watershed ischemia from

3:06

the narrowing of the distal internal carotid arteries.

3:09

The fact that this is bilateral suggests

3:12

Moyamoya disease. Moyamoya syndrome, more

3:16

likely, is a unilateral process, and it's not

3:20

that disease entity, which is a bilateral,

3:23

idiopathic, sometimes congenital genetic disease.

3:27

With Moyamoya syndrome, it can be secondary

3:30

to things like a dissection of a blood

3:33

vessel, or severe atherosclerosis of a blood

3:35

vessel, or hypoplasia of the vessel, generally

3:39

as in neurofibromatosis type 1.61 00:02:52,620 --> 00:02:56,130 We have a bilateral process because of the

2:56

stenosis of the distal internal carotid artery.

2:59

It leads to.

3:01

Areas of watershed disease, watershed ischemia from

3:06

the narrowing of the distal internal carotid arteries.

3:09

The fact that this is bilateral suggests

3:12

Moyamoya disease. Moyamoya syndrome, more

3:16

likely, is a unilateral process, and it's not

3:20

that disease entity, which is a bilateral,

3:23

idiopathic, sometimes congenital genetic disease.

3:27

With Moyamoya syndrome, it can be secondary

3:30

to things like a dissection of a blood

3:33

vessel, or severe atherosclerosis of a blood

3:35

vessel, or hypoplasia of the vessel, generally

3:39

as in neurofibromatosis type 1.