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Signal Intensity of IPH on MRI by Age

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The chemistry of intraparenchymal hemorrhages as it

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relates to the features on MRI scan was described

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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

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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

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that matter, if you have polycythemia vera

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where you have a high hematocrit.

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

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time of flight, MRA, the acute hemorrhage is going

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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

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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

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proton relaxation enhancement, or PRE.

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Proton relaxation enhancement

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is a T2 shortening effect.

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It's field strength dependent, that is,

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it's going to be more evident at high field

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

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

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edema in the acute hematoma setting.

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In this situation, we have deoxyhemoglobin in

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intact red blood cells that have not lysed.

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And deoxyhemoglobin is the dominant blood product

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in hemorrhages within the

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first six hours to three days.

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As things evolve, deoxyhemoglobin

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converts to intracellular methemoglobin.

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Intracellular methemoglobin is an interesting

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compound because of the methemoglobin,

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it actually causes proton electron dipole-dipole

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interaction, which leads to T1 shortening.

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T1 shortening on a T1-weighted scan

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leads to bright signal intensity.

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So the methemoglobin causes

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bright signal on T1-weighted scan.

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However, because the cells are intact,

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you still have proton relaxation enhancement,

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separation of charge within the cell versus

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charge in the extracellular fluid nearby.

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And therefore you have a T2 shortening effect

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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

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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

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cause T2 shortening by proton relaxation enhancement.

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The bright signal that you see here is

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secondary to edema, vasogenic edema around

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the hematoma, not blood products itself.

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I want to emphasize this.

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This periphery is intracellular methemoglobin.

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The center part, which is isointense on

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T1 weighted scan, is deoxyhemoglobin, both of which have

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proton relaxation enhancement and T2 shortening,

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which on a T2-weighted scan

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causes dark signal intensity.

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The bright signal intensity is vasogenic edema.

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

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electron dipole-dipole interaction from methemoglobin.

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That's a unique feature of the methemoglobin molecule.

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Late subacute hematoma is dominated

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by extracellular methemoglobin.

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What's the difference here?

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Methemoglobin is still there, so we still

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have bright signal on T1-weighted scan.

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However, the red blood cells have now lysed.

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And because the red blood cells have lysed,

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we no longer have separation of charge

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in the cell versus in the extracellular fluid.

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It's freely diffusible extracellular methemoglobin.

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So we no longer have proton relaxation

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enhancement and dark signal on T2.

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You notice the difference is now we

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have high signal on T2-weighted imaging.

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And this usually occurs at five

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days to about two weeks of duration

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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.

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However, this hematoma is not dark centrally.

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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

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due to extracellular methemoglobin

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because cellular lysis has occurred.

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

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What about that?

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

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This is not vasogenic edema.

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That dark signal is due to hemosiderin, and that is

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the final blood product, the chronic blood product

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

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

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It's an old hemorrhage.

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And the old hemorrhage product, the cleanup product,

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

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So, bright on T1, because of proton electron

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dipole-dipole interaction from the methemoglobin.

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Bright on T2, because of water content and

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the absence of proton relaxation enhancement.

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With a periphery of dark signal, which is hemosiderin.

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Here we have proton electron dipole-dipole

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interaction without proton relaxation enhancement.

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This is a T1-weighted scan.

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We see on the T1-weighted scan that there is

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bright signal intensity in this hemorrhagic stroke.

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This is the bright signal intensity

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of blood products, methemoglobin,

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proton electron dipole-dipole interaction.

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This is a gradient echo scan.

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You notice that there's nothing dark here.

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

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Therefore, there is no proton relaxation

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enhancement, which is a T2 shortening

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phenomenon, that would cause decreased signal.

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This bright signal of hemorrhage is

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still bright on the gradient echo scan

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because it's extracellular methemoglobin.

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Were it intracellular methemoglobin, because you have

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separation of charge in the cell versus outside the

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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.

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As I mentioned, hemosiderin is the final and the

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chronic blood product that we see in hematomas.

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These are all descriptions of

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intraparenchymal hematomas.

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It's low on T2-weighted scan because it

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does have proton relaxation enhancement.

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Why is that?

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You have macrophages that are eating up the

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iron of the blood product and therefore the

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charges within the macrophages or the charges

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in ferritin and that leads to T2 shortening.

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You have a focal bar magnet effect of separation

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of charge in the cell versus outside the cell.

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And that leads to T2 shortening

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and proton relaxation enhancement.

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Hemosiderin may last forever.

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

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a cleanup product in the intraparenchymal

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hemorrhage, but it may stain the brain forever.

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Here, for example, is a hemosiderin slit.

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T1-weighted scan, dark in signal intensity.

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This is our T1-weighted scan, dark CSF.

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Here's the hemosiderin slit.

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You notice that there's no mass effect.

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If you look at the distance between the

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third ventricle and the Sylvian fissure and

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compare it to this distance, this is larger

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than that because there's been volume loss.

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This on the T2-weighted scan is darkened signal

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intensity and this is that hemosiderin slit.

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This patient previously had a big

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hemorrhage in the putamen on the right side.

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But after the cleanup products by the macrophages,

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

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associated with volume loss on

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this side compared to that side.

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

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What you're seeing here as bright signal intensity is

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just the subarachnoid space, which is somewhat dilated,

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associated with the volume loss from the old hematoma.

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

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proton relaxation enhancement, a T2 shortening effect.

Report

Faculty

David M Yousem, MD, MBA

Professor of Radiology, Vice Chairman and Associate Dean

Johns Hopkins University

Tags

Trauma

Neuroradiology

MRI

Emergency

Brain

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