0:01

These are three different patients

0:03

who had anoxic brain injury.

0:07

On the left-hand image, what you see is predominantly

0:11

cortical involvement of the parietal and occipital

0:14

lobes, with some involvement of the caudate and

0:17

the putamen, but sparing of the globus pallidus.

0:21

On this image, again, predominantly parietal lobe,

0:25

and on the DWI, you see the dark signal intensity.

0:29

Notice that the dark signal intensity of the

0:31

ADC map is in the subcortical white matter,

0:36

with relative sparing of the gray matter.

0:39

This is another pattern of anoxic brain injury.

0:43

Finally, we have this patient who has abnormality,

0:46

which is mostly in the hippocampal formation,

0:49

the medial temporal lobe, as well as the

0:52

globus pallidus, with bright signal intensity.

0:54

This is the Ammon's horn area of the

0:58

hippocampus, which is most sensitive

1:00

to hypoxic-ischemic involvement.

1:02

Second place in the brain is the globus pallidus,

1:05

which is also sensitive to hypoxic-ischemic injury.

1:10

I will say this, that I have seen more common

1:13

involvement of the occipital lobes in patients who have

1:17

a ventilatory cause of their hypoxic-ischemic damage,

1:22

or event, rather than those who

1:26

have an ischemic involvement.

1:29

So what I'm talking about is someone who stops

1:31

breathing because of taking a certain drug,

1:35

is more likely to have occipital lobe involvement.

1:38

And those individuals who stop their heartbeat

1:41

because of a cardiac arrest or MI, it's unusual

1:45

to see this occipital posterior predilection.

1:48

That's just my observation.

1:51

Here we have the post-gadolinium enhanced scan of a

1:54

patient who has enhancement of the Ammon's horn region

1:59

of the hippocampus, as well as the globus pallidus.

2:03

When I see this type of involvement, more likely,

2:06

it's going to be a hypoxic-ischemic injury.

2:09

This is the pattern that's seen with carbon monoxide

2:11

poisoning, or it can be seen with cardiac arrest.

2:15

It's not specific for hypoxia versus

2:19

hypoperfusion ischemic injury.

2:22

Here is a patient who has an entity known

2:25

in the vernacular as "chasing the dragon."

2:29

This is opiate-induced leukoencephalopathy.

2:33

It may be secondary to snorting heroin or

2:36

cocaine, and you see a diffuse pattern of

2:39

involvement, which often affects the dentate

2:42

nucleus of the cerebellum, as well as the white

2:46

matter extending to the subcortical regions.

2:50

And this leukoencephalopathic pattern is called

2:54

"chasing the dragon," usually from heroin, most commonly.

2:58

This is a patient who shows a

3:00

relatively subtle abnormality.

3:02

If you're not used to seeing our MRI scans,

3:06

you may think, "Oh, well, this doesn't look that bad.

3:09

What's the problem?"

3:10

What I see in this case is that there is

3:13

thickening and brighter signal intensity

3:16

to the gray matter as opposed to the white matter.

3:20

It's almost as if there has been accentuation

3:23

of the gray-white matter differentiation

3:26

on this diffusion-weighted scan.

3:29

This is due to hyperammonemia, which is an entity

3:34

that's usually associated with hepatic failure.

3:37

The normal ammonia level is less than 32.

3:41

It's actually often not detectable.

3:43

This patient had over 10 times higher than normal

3:48

ammonia level due to hepatic failure that was

3:52

not detoxifying the ammonia in the blood system.

3:55

And this patient had diffuse cerebral edema.

3:58

So this is cortical diffuse gray matter

4:01

edema as a manifestation of hyperammonemia.