0:01

The chemistry of intraparenchymal hemorrhages as it

0:06

relates to the features on MRI scan was described

0:11

at the University of Pennsylvania in the 1980s.

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And since I am a child of the University of

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Pennsylvania Neuroradiology Fellowship, I feel it's

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my duty to talk to you about the different components

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of hemorrhage and how it is manifested on MRI

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on T1-weighted and T2-weighted scanning.

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So here we have a CT scan showing an

0:34

acute hemorrhage being bright on the CT.

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Why is it bright on CT?

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It's due to the globin content of the hemorrhage.

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And that's why, if you have low hemoglobin

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anemia, the hemorrhage is less dense than

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if you have a normal hematocrit, or for

0:51

that matter, if you have polycythemia vera

0:54

where you have a high hematocrit.

0:57

On MRI scan, T1-weighted imaging, in this case,

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time of flight, MRA, the acute hemorrhage is going

1:04

to be iso intense to dark in signal intensity.

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On T2-weighted scan, it's dark.

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On FLAIR, it's dark.

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On diffusion-weighted scanning, it's dark.

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And on susceptibility-weighted scanning, it's dark.

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All of these are effectively T2-weighted

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images that have demonstration of

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dark signal which is T2 shortening.

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This is a post-gadolinium T1-weighted scan where

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you can see it's dark or iso intense in components.

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This is a demonstration of the signal

1:37

intensity characteristics of deoxyhemoglobin,

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which is the acute hematoma blood product.

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So acute hematomas are dominated by deoxyhemoglobin,

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which is very low in signal intensity on T2-weighted

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scanning and iso intense to low on T1-weighted imaging.

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And this is due to a phenomenon known as

1:59

proton relaxation enhancement, or PRE.

2:03

Proton relaxation enhancement

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is a T2 shortening effect.

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It's field strength dependent, that is,

2:10

it's going to be more evident at high field

2:12

strength, 3 Tesla, than low field strength, 0.3 Tesla.

2:14

44 00:02:16,835 --> 00:02:18,695 And it's associated with surrounding

2:18

edema in the acute hematoma setting.

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In this situation, we have deoxyhemoglobin in

2:25

intact red blood cells that have not lysed.

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And deoxyhemoglobin is the dominant blood product

2:32

in hemorrhages within the

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first six hours to three days.

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As things evolve, deoxyhemoglobin

2:41

converts to intracellular methemoglobin.

2:43

Intracellular methemoglobin is an interesting

2:48

compound because of the methemoglobin,

2:51

it actually causes proton electron dipole-dipole

2:55

interaction, which leads to T1 shortening.

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T1 shortening on a T1-weighted scan

3:03

leads to bright signal intensity.

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So the methemoglobin causes

3:10

bright signal on T1-weighted scan.

3:12

However, because the cells are intact,

3:16

you still have proton relaxation enhancement,

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separation of charge within the cell versus

3:24

charge in the extracellular fluid nearby.

3:27

And therefore you have a T2 shortening effect

3:30

known as proton relaxation enhancement.

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This occurs at about 3 to 7 days of onset after the hematoma.

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Here is an example of the presence of methemoglobin.

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Methemoglobin is bright on T1-weighted scan,

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and it usually fills in from the periphery

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to the center in a patient's hematoma.

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So centrally, we have isointense.

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This is still deoxyhemoglobin.

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In the periphery, we see the methemoglobin

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developing as bright on T1 from proton

4:07

electron dipole-dipole interaction, a T1

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shortening phenomenon on a T1-weighted scan.

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On the T2-weighted scan, both deoxyhemoglobin

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as well as intracellular methemoglobin

4:25

cause T2 shortening by proton relaxation enhancement.

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The bright signal that you see here is

4:33

secondary to edema, vasogenic edema around

4:37

the hematoma, not blood products itself.

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I want to emphasize this.

4:42

This periphery is intracellular methemoglobin.

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The center part, which is isointense on

4:54

T1 weighted scan, is deoxyhemoglobin, both of which have

5:00

proton relaxation enhancement and T2 shortening,

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which on a T2-weighted scan

5:07

causes dark signal intensity.

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The bright signal intensity is vasogenic edema.

5:14

The bright signal on T1-weighted scan is due to proton

5:18

electron dipole-dipole interaction from methemoglobin.

5:23

That's a unique feature of the methemoglobin molecule.

5:27

Late subacute hematoma is dominated

5:30

by extracellular methemoglobin.

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What's the difference here?

5:34

Methemoglobin is still there, so we still

5:36

have bright signal on T1-weighted scan.

5:39

However, the red blood cells have now lysed.

5:44

And because the red blood cells have lysed,

5:46

we no longer have separation of charge

5:48

in the cell versus in the extracellular fluid.

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It's freely diffusible extracellular methemoglobin.

5:56

So we no longer have proton relaxation

5:59

enhancement and dark signal on T2.

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You notice the difference is now we

6:03

have high signal on T2-weighted imaging.

6:07

And this usually occurs at five

6:08

days to about two weeks of duration

6:11

after the initial hematoma.

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Here is an example of extracellular methemoglobin.

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Bright signal on this T1-weighted scan.

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Why?

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Because of proton electron dipole-dipole interaction.

6:27

However, this hematoma is not dark centrally.

6:33

It's bright centrally.

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This is the difference.

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This is a T2-weighted scan.

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So we no longer have proton relaxation enhancement.

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Bright on T1 and bright on T2

6:46

due to extracellular methemoglobin

6:49

because cellular lysis has occurred.

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Now, you may ask, well, what about this dark signal?

6:55

What about that?

6:56

Well, you notice that that dark signal is not bright.

7:00

This is not vasogenic edema.

7:02

That dark signal is due to hemosiderin, and that is

7:05

the final blood product, the chronic blood product

7:08

that we see in hematomas. In the absence of edema,

7:15

we know that it's not an acute hemorrhage any longer.

7:17

It's an old hemorrhage.

7:19

And the old hemorrhage product, the cleanup product,

7:23

is hemosiderin, which is dark on a T2-weighted scan.

7:27

So, bright on T1, because of proton electron

7:30

dipole-dipole interaction from the methemoglobin.

7:34

Bright on T2, because of water content and

7:39

the absence of proton relaxation enhancement.

7:43

With a periphery of dark signal, which is hemosiderin.

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Here we have proton electron dipole-dipole

7:51

interaction without proton relaxation enhancement.

7:56

This is a T1-weighted scan.

7:58

We see on the T1-weighted scan that there is

8:00

bright signal intensity in this hemorrhagic stroke.

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This is the bright signal intensity

8:07

of blood products, methemoglobin,

8:11

proton electron dipole-dipole interaction.

8:14

This is a gradient echo scan.

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You notice that there's nothing dark here.

8:18

It's a T2-weighted scan with nothing dark.

8:21

Therefore, there is no proton relaxation

8:23

enhancement, which is a T2 shortening

8:25

phenomenon, that would cause decreased signal.

8:30

This bright signal of hemorrhage is

8:32

still bright on the gradient echo scan

8:37

because it's extracellular methemoglobin.

8:40

Were it intracellular methemoglobin, because you have

8:45

separation of charge in the cell versus outside the

8:47

cell, you would see proton relaxation enhancement.

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But this is extracellular methemoglobin.

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Bright on T2-weighted imaging.

8:59

As I mentioned, hemosiderin is the final and the

9:02

chronic blood product that we see in hematomas.

9:05

These are all descriptions of

9:07

intraparenchymal hematomas.

9:08

It's low on T2-weighted scan because it

9:11

does have proton relaxation enhancement.

9:14

Why is that?

9:15

You have macrophages that are eating up the

9:18

iron of the blood product and therefore the

9:21

charges within the macrophages or the charges

9:24

in ferritin and that leads to T2 shortening.

9:28

You have a focal bar magnet effect of separation

9:31

of charge in the cell versus outside the cell.

9:34

And that leads to T2 shortening

9:36

and proton relaxation enhancement.

9:39

Hemosiderin may last forever.

9:41

It starts, we say, about one to two weeks as

9:46

a cleanup product in the intraparenchymal

9:48

hemorrhage, but it may stain the brain forever.

9:52

Here, for example, is a hemosiderin slit.

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T1-weighted scan, dark in signal intensity.

10:00

This is our T1-weighted scan, dark CSF.

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Here's the hemosiderin slit.

10:05

You notice that there's no mass effect.

10:07

If you look at the distance between the

10:10

third ventricle and the Sylvian fissure and

10:13

compare it to this distance, this is larger

10:16

than that because there's been volume loss.

10:20

This on the T2-weighted scan is darkened signal

10:22

intensity and this is that hemosiderin slit.

10:26

This patient previously had a big

10:29

hemorrhage in the putamen on the right side.

10:32

But after the cleanup products by the macrophages,

10:36

the only thing that's left is a little hemosiderin slit

10:39

associated with volume loss on

10:41

this side compared to that side.

10:44

There is no edema, because this is weeks to months old.

10:49

What you're seeing here as bright signal intensity is

10:51

just the subarachnoid space, which is somewhat dilated,

10:54

associated with the volume loss from the old hematoma.

10:58

This is hemosiderin, dark on T1, dark on T2, due to

11:04

proton relaxation enhancement, a T2 shortening effect.