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Today, we're going to talk a

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little bit about subacute stroke.

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The timing is variable depending

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on who you read, but it's about 24

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hours to several weeks to a month.

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What happens after you have the initial

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restricted diffusion and not much flair

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abnormality, you get increased edema and

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breakdown of the blood-brain barrier and mass

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effect, which is maximal at 48 to 72 hours.

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So in non-contrast CT, you'll

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be seeing increased hypodensity.

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On MR, you'll see increased flair hyperintensity

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and swelling and effacement of sulci.

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The edema goes up and then starts to decrease.

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In approximately two weeks, you can get what's

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called fogging and non-contrast CT and T2

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weighted images, but you can't see the stroke

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because there are macrophages coming in and some

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of the edema is going away and it looks normal.

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So, that's called fogging.

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At one to two weeks, the

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ADC goes back to normal.

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It's called pseudonormalization

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and then it increases after that.

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DWI remains high because The strokes

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still bright on T two, you might

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get some cortical laminar necrosis.

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You can get hemorrhagic transformation

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mostly in the first 48 to 72

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hours, and that's defined by ECAs.

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So you have hemorrhagic infarction one,

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which is just petechiae along the margins.

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HI two is confluent Pete

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within the infarcted area.

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PH1 is parenchymal hematoma one,

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which is a hematoma less than 30

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percent of the infarcted volume.

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PH2 is hematoma greater than 30 percent

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of the infarcted volume with mass effect.

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PH1 doesn't have significant mass effect.

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And then you can get gyriform

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enhancement that starts at one week and

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may last for up to one to two months.

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So basically increased swelling,

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increased flair hyperintensity.

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transformation, and gyriform enhancement.

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So in this segment we'll talk about how to

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differentiate subacute arterial infarction from

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subacute arterial infarction mimics, such as

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high-grade glial tumor and venous infarction.

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So let's talk about the clinical scenario.

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Usually seizure, you see that commonly

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with tumor and venous sinus thrombosis,

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but it's uncommon for arterial stroke.

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How about enhancement?

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Gyriform enhancement is much more common

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with stroke, usually occurring five

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days and later, and venous infarction.

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High-grade tumor has usually much more

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irregular enhancement, and low-grade

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tumor usually doesn't have enhancement.

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Susceptibility with arterial and venous

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infarction, you might have petechial

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hemorrhage or parenchymal hematomas.

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With a complete hemosiderin rim,

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venous sinus thrombosis, you might have

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a thrombus vein or sinus, and tumor will

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have much more irregular susceptibility

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consistent with hemorrhage or vessels.

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Location, acute ischemic stroke

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should be in a vascular territory.

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It doesn't usually involve the corpus

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callosum, and it's usually more peripheral.

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Venous sinus thrombosis is

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a non-arterial territory.

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It doesn't usually involve the corpus

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callosum, it is peripheral, and tumor is

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usually in a non-arterial distribution and

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frequently does involve the corpus callosum,

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unlike arterial and venous stroke, and

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it tends to be more central than venous

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stroke and acute arterial infarction.

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These are images of a 50-year

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old with dizziness, ataxia, and

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who had a subacute pica stroke.

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When he came in, we didn't

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know what the diagnosis was.

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You can see it.

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There's flare hyperintensity in the

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right cerebellum, T2 hyperintensity,

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and there's gyriform enhancement.

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So once I see gyriform enhancement,

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I'm going to be thinking either

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arterial stroke or venous stroke.

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So the next thing I'm going to ask

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is, is this an avascular distribution?

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gadolinium-enhanced coronal image.

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Again, beautiful gyriform enhancement, but

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you can see it's in the PICA territory.

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So we correctly made the diagnosis

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of PICA stroke, although this

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did get biopsied, unfortunately.

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So this is a case where a patient

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presented with left-sided weakness.

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And he'd had it for weeks and we took a

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look at the study and you can see on the

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diffusion there's some restricted diffusion.

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It kind of looks like it's in the MCA territory,

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posterior insula, temporal lobe, however it's

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going into the corpus callosum which is unusual.

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You can see the same thing, it's T2

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hyperintense and it kind of looks

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like there's gyriform enhancement.

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So the MCA territory except for the corpus

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callosum, the gyriform enhancement except for

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the corpus callosum made us I think that this

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was initially an unusual subacute stroke,

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but it kept getting worse and worse, and

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this proved to be a glioblastoma multiforme.

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So the lesson here is, it's a difficult

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case, but the involvement of the

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corpus callosum should have raised

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red flags that it was a glioblastoma.