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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If you don’t know the time of stroke onset, are you able to deduce it from imaging?
Here’s a thread to help you date a stroke on MRI!
2/Strokes evolve, or grow old, the same way people evolve or grow old.
The appearance of stroke on imaging mirrors the life stages of a person—you just have to change days for a stroke into years for a person
So 15 day old stroke has features of a 15 year old person, etc.
3/Initially (less than 4-6 hrs), the only finding is restriction (brightness) on diffusion imaging (DWI).
You can remember this bc in the first few months, a baby does nothing but be swaddled or restricted. So early/newly born stroke is like a baby, only restricted
1/”I LOVE spinal cord syndromes!” is a phrase that has NEVER, EVER been said by anyone.
Do you become paralyzed when you see cord signal abnormality?
Never fear—here is a thread on all the incomplete spinal cord syndromes to get you moving again!
2/Spinal cord anatomy can be complex. On imaging, we can see the ant & post nerve roots. We can also see the gray & white matter. Hidden w/in the white matter, however, are numerous efferent & afferent tracts—enough to make your head spin.
3/Lucky for you, for the incomplete cord syndromes, all you need to know is gray matter & 3 main tracts. Anterolaterally, spinothalamic tract (pain & temp). Posteriorly, dorsal columns (vibration, proprioception, & light touch), & next to it, corticospinal tracts—providing motor
1/Do you get a Broca’s aphasia trying remember the location of Broca's area?
Does trying to remember inferior frontal gyrus anatomy leave you speechless?
Don't be at a loss for words when it comes to Broca's area
Here’s a 🧵to help you remember the anatomy of this key region!
2/Anatomy of the inferior frontal gyrus (IFG) is best seen on the sagittal images, where it looks like the McDonald’s arches.
So, to find this area on MR, I open the sagittal images & scroll until I see the arches. When it comes to this method of finding the IFG, i’m lovin it.
3/Inferior frontal gyrus also looks like a sideways 3, if you prefer. This 3 is helpful bc the inferior frontal gyrus has 3 parts—called pars
1/Need help reading spine imaging? I’ve got your back!
It’s as easy as ABC!
A thread about an easy mnemonic you can use on every single spine study you see to increase your speed & make sure you never miss a thing!
2/A is for alignment
Look for: (1) Unstable injuries
(2) Malalignment that causes early degenerative change. Abnormal motion causes spinal elements to abnormally move against each other, like grinding teeth wears down teeth—this wears down the spine
3/B is for bones.
On CT, the most important thing to look for w/bones is fractures. You may see focal bony lesions, but you may not
On MR, it is the opposite—you can see marrow lesions easily but you may or may not see edema associated w/fractures if the fracture is subtle