1/Time is brain! So you don’t have time to struggle w/that stroke alert head CT.
Here’s a #tweetorial to help you with the CT findings in acute stroke.
2/CT in acute stroke has 2 main purposes—(1) exclude intracranial hemorrhage (a contraindication to thrombolysis) & (2) exclude other pathologies mimicking acute stroke. However, that doesn’t mean you can’t see other findings that can help you diagnosis a stroke.
3/Infarct appearance depends on timing. In first 12 hrs, the most common imaging finding is…a normal head CT. However, in some, you see a hyperdense artery or basal ganglia obscuration. Later in the acute period, you see loss of gray white differentiation & sulcal effacement
4/Hyperdense artery sign occurs when you see the thrombus in the artery. The thrombus appears hyperdense bc clot is denser than normal flowing blood—& CT is just a measure of density. So an artery filled w/clot will be denser than arteries filled with flowing blood.
5/Bc the hyperdensity you are seeing is clot, there will not be flowing blood in this region on CTA. So the hyperdense artery will be the inverse of the CTA--where there is hyperdensity on non-contrast CT, there will be no density/contrast on CTA—like a negative of a photograph
6/The other sign in the first 12 hours is the blurred basal ganglia/lentiform nucleus. Usually this region is a triangle of low density white matter (ant limb internal capsule, post limb internal capsule, external capsule) surrounding the high density lentiform nucleus
7/In an acute infarct, this triangle becomes blurred, as the lentiform nucleus becomes more edematous, it becomes similar in density to white matter. So instead of clean line between white and gray matter, they look like they are smear together.
8/The lentiform nucleus is commonly infarcted bc it receives blood from the lenticulostriate arteries that come off of the M1, so unless there is an occlusion more distal in the MCA, the blood supply to the lentiform nucleus is cut off and it infarcts early.
9/Why do regions become low density when they infarct? This is bc when O2 & ATP run our, Na/K pump stops working & bc of the osmotic gradient, Na & H20 rush into the cell. More water in the cell = lower density. For every 1% increase in H20 there is a 2.5 HU decrease in density
10/This brings us to our next sign—hypodense regions of brain outside the basal ganglia. If the brain is low density, that means it has run out of ATP and swelled, which means the damage is irreversible. Low density = dead brain = poor prognostic sign.
11/Another region that infarcts early is the insula. This is bc the insula is actually an internal watershed in the MCA territory. It is the watershed between the lenticulostriates and the M2 sylvian branches, so it will infarct relatively early with low blood supply
12/Later you will get sulcal effacement. Normally, the brain should have lots of sulci that look like ice cracks/crevasses along its surface. As more water accumulates in the dead cells, more swelling occurs, and these crevasses become effaced by the swollen brain.
13/So now you know the 5 main signs of acute infarct on CT—remember, if you see these five, soon that brain won’t be alive!
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3/At its most basic, you can think of the PPF as a room with 4 doors opening to each of these regions: one posteriorly to the skullbase, one medially to the nasal cavity, one laterally to the infratemporal fossa, and one anteriorly to the orbit
1/My hardest thread yet! Are you up for the challenge?
How stroke perfusion imaging works!
Ever wonder why it’s Tmax & not Tmin?
Do you not question & let RAPID read the perfusion for you? Not anymore!
2/Perfusion imaging is based on one principle: When you inject CT or MR intravenous contrast, the contrast flows w/blood & so contrast can be a surrogate marker for blood.
This is key, b/c we can track contrast—it changes CT density or MR signal so we can see where it goes.
3/So if we can track how contrast gets to the tissue (by changes in CT density or MR signal), then we can approximate how BLOOD is getting to the tissue.
And how much blood is getting to the tissue is what perfusion imaging is all about.
1/”That’s a ninja turtle looking at me!” I exclaimed. My fellow rolled his eyes at me, “Why do I feel I’m going to see this a thread on this soon…”
He was right! A thread about one of my favorite imaging findings & pathology behind it
2/Now the ninja turtle isn’t an actual sign—yet!
But I am hoping to make it go viral as one. To understand what this ninja turtle is, you have to know the anatomy.
I have always thought the medulla looks like a 3 leaf clover in this region.
The most medial bump of the clover is the medullary pyramid (motor fibers).
Next to it is the inferior olivary nucleus (ION), & finally, the last largest leaf is the inferior cerebellar peduncle.
Now you can see that the ninja turtle eyes correspond to the ION.
3/But why are IONs large & bright in our ninja turtle?
This is hypertrophic olivary degeneration.
It is how ION degenerates when input to it is disrupted. Input to ION comes from a circuit called the triangle of Guillain & Mollaret—which sounds like a fine French wine label!