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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@TheAJNR 2/In the lumbar spine, it is all about the degree of canal narrowing & room for nerve roots.
In the cervical spine, we have another factor to think about—the cord.
Cord integrity is key. No matter the degree of stenosis, if the cord isn’t happy, the patient won’t be either
@TheAJNR 3/Cord flattening, even w/o canal stenosis, can cause myelopathy.
No one is quite sure why.
Some say it’s b/c mass effect on static imaging may be much worse dynamically, some say repetitive microtrauma, & some say micro-ischemia from compression of perforators
1/Do radiologists sound like they are speaking a different language when they talk about MRI?
T1 shortening what? T2 prolongation who?
Here’s a translation w/an introductory thread to MRI.
2/Let’s start w/T1—it is #1 after all! T1 is for anatomy
Since it’s anatomic, brain structures will reflect the same color as real life
So gray matter is gray on T1 & white matter is white on T1
So if you see an image where gray is gray & white is white—you know it’s a T1
3/T1 is also for contrast
Contrast material helps us to see masses
Contrast can’t get into normal brain & spine bc of the blood brain barrier—but masses don’t have a blood brain barrier, so when you give contrast, masses will take it up & light up, making them easier to see.
1/Asking “How old are you?” can be dicey—both in real life & on MRI! Do you know how to tell the age of blood on MRI?
Here’s a thread on how to date blood on MRI so that the next time you see a hemorrhage, your guess on when it happened will always be in the right vein!
2/If you ask someone how to date blood on MRI, they’ll spit out a crazy mnemonic about babies that tells you what signal blood should be on T1 & T2 imaging by age.
But mnemonics are crutch—they help you memorize, but not understand. If you understand, you don’t need to memorize
3/If you look at the mnemonic, you will notice one thing—the T1 signal is all you need to tell if blood is acute, subacute or chronic.
T2 signal will tell if it is early or late in each of those time periods—but that type of detail isn’t needed in real life
Here's a little help on how to do it yourself w/a thread on how to read a head CT!
2/In bread & butter neuroimaging—CT is the bread—maybe a little bland, not super exciting—but necessary & you can get a lot of nutrition out of it
MRI is like the butter—everyone loves it, it makes everything better, & it packs a lot of calories. Today, we start w/the bread!
3/The most important thing to look for on a head CT is blood.
Blood is Bright on a head CT—both start w/B.
Blood is bright bc for all it’s Nobel prizes, all CT is is a density measurement—and blood is denser (thicker) than water & denser things are brighter on CT
MMA fights get a lot of attention, but MMA (middle meningeal art) & dural blood supply doesn’t get the attention it deserves.
A thread on dural vascular anatomy!
2/Everyone knows about the blood supply to the brain.
Circle of Willis anatomy is king and loved by everyone, while the vascular anatomy of the blood supply to the dura is the poor, wicked step child of vascular anatomy that is often forgotten
3/But dural vascular anatomy & supply are important, especially now that MMA embolizations are commonly for chronic recurrent subdurals.
It also important for understanding dural arteriovenous fistulas as well.