0:00

The marker for subacute hematoma

0:04

is the compound of methemoglobin.

0:08

As I mentioned, Methemoglobin

0:10

has the particular chemical characteristics of

0:13

proton-electron dipole-dipole interaction,

0:17

which allows

0:18

water protons to approach the Methemoglobin molecule

0:21

in a way that leads to

0:23

T1 shortening.

0:25

T1 shortening

0:27

is represented by high signal intensity

0:30

on a T1-weighted image.

0:33

In the early

0:35

subsequent phase.

0:37

This meant hemoglobin

0:39

is within the intact red blood cell.

0:44

Therefore

0:45

you have a concentration of charge inside the cell

0:48

versus outside the cell.

0:51

This leads to

0:53

proton relaxation enhancement

0:55

1-bar magnet effect, such that water protons

0:59

see an inhomogeneous magnetic field

1:02

with a concentration of charge inside the cell

1:05

different than the concentration of charge outside the cell

1:09

leading to T2 shortening.

1:11

So you have both proton-electron dipole-dipole interaction

1:14

which leads to bright signal intensity on T1,

1:17

and you have proton relaxation enhancement

1:20

which leads to T2 shortening, which is dark

1:23

on a T2-weighted scan.

1:25

Proton-electron dipole-dipole interaction, I said,

1:28

is field-strength independent.

1:31

You have intact red blood cells and the timing for

1:34

intracellular

1:36

Methemoglobin is at about 04:57 days.

1:40

Here we have a T1-weighted scan

1:42

and here we have a T2-weighted scan.

1:45

What one sees is

1:46

bright signal intensity on the T1-weighted scan,

1:50

which is

1:52

extending from the periphery

1:54

to centrally within this hematoma.

1:58

Both the bright parts as well as the dark parts

2:02

are black

2:04

on. The T2-weighted scan

2:06

you know also that there is surrounding edema

2:10

associated with hematoma.

2:12

What exactly are we seeing?

2:14

What we are seeing is Methemoglobin

2:18

filling in the deoxyhemoglobin

2:21

from the periphery to centrally,

2:25

starts peripherally and then moves centrally

2:27

whether there is

2:30

bright signal intensity

2:31

or dark signal intensity on the T1-weighted scan.

2:35

Both of them are dark on the T2-weighted scan.

2:38

Why is that intracellular Methemoglobin?

2:42

Because the intact red blood cell

2:45

leads to

2:46

proton relaxation enhancement with concentration of

2:48

charge in and out

2:50

will lead to proton relaxation enhancement

2:53

on T2 imaging.

2:56

Similarly, deoxyhemoglobin,

2:59

which is intracellular,

3:03

leads to proton

3:04

relaxation enhancement across the

3:05

intact red blood cell membrane,

3:07

and that too

3:09

leads to dark signal intensity on tetuated imaging.

3:13

The bright is merely vasogenic edema,

3:16

not blood proxy around the hematoma.

3:19

Late subacute hematoma is characterized by

3:24

extracellular methemoglobin.

3:26

The methemoglobin molecule.

3:28

Whether it's intracellular or extracellular

3:31

has proton-electron dipole-dipole interaction

3:34

and therefore

3:35

leads to high signal intensity on T1-weighted scan.

3:39

However, what has happened at this point

3:43

is that that methemoglobin molecule

3:47

is in a setting of cellular lysis.

3:49

The cellular membrane is no longer intact

3:53

and therefore the methemoglobin is free to diffuse

3:58

from intracellular to extracellular.

4:02

Therefore, we

4:03

no longer

4:04

have separation of charge by the red blood cell

4:06

membrane, therefore we no longer have

4:10

proton relaxation enhancement

4:13

so petty. Without Puri

4:16

because there's no longer proton relaxation enhancement,

4:19

what we see is

4:20

bright signal intensity on T2-weighted scan,

4:23

so proton relaxation enhancement leads to

4:25

dark signal intensity on T2-weighted scan.

4:28

If you have cellular lysis

4:30

an absence of proton relaxation enhancement,

4:32

it will be bright

4:34

on the T2-weight scan.

4:36

This usually occurs

4:38

from about 5 days after the initial hematoma

4:41

Within about 2 weeks after. 105 00:04:45,520 --> 00:04:48,840 Remember that you no longer have an intact

4:48

red blood cell.

4:50

How's it look when emirai?

4:53

This is your T1-weight scan,

4:55

this is your T2-weight scan.

4:58

On the T1-weight scan we have a hematoma

5:01

that is bright in signal intensity.

5:04

This is due to proton-electron dipole-dipole interaction

5:08

on the T2-weight scan.

5:10

The hematoma is bright

5:12

because

5:13

there is no longer proton relaxation enhancement.

5:17

We also note that instead of surrounding edema,

5:21

there's no bright signal surrounding edema

5:23

because this is late subacute,

5:24

the edema has resolved

5:26

instead what we have

5:28

is dark signal intensity around the periphery.

5:31

This we will soon learn is hemosiderin.

5:35

Hemosiderin is dark

5:37

on T2-weight scanning

5:39

and

5:41

dark on T1-weight scanning,

5:43

so this is late.

5:46

Subacute

5:49

hematoma

5:53

with extracellular methemoglobin

5:58

demonstrating proton-electron dipole-dipole interaction

6:02

without proton relaxation enhancement.

6:07

Here is another example of saying

6:10

this is a hemorrhagic infarct

6:13

on the T1-weight scan. With this infarct

6:16

we see bright signal. Intensity methemoglobin,

6:21

but on the gradient echo scan there's no

6:26

dark signal

6:27

and therefore there is no proton relaxation enhancement.

6:31

Therefore because it's bright and bright it' must be

6:37

extracellular and hemoglobin.

6:40

If it was

6:42

intracerebral methemoglobin we would have

6:45

dark signal intensity

6:47

areas of hemorrhage in the stroke.