@SVINJournal 2/Everyone knows the NASCET criteria: If the patient is symptomatic & the greatest stenosis from the plaque is >70% of the diameter of normal distal lumen, patient will likely benefit from carotid endarterectomy. But that doesn’t mean the remaining patients are just fine!
@SVINJournal 3/Yes, carotid plaques resulting in high grade stenosis are high risk.
But assuming that stenosis is the only mechanism by which a carotid plaque is high risk is like assuming that the only way to kill someone is by strangulation.
@SVINJournal 4/Carotid disease not only harms by strangulation (stenosis), but also by serving as a source of emboli.
A gun isn’t less dangerous bc it shoots from a distance—similarly, a plaque without stenosis is still dangerous if it causes emboli, even if the harm is from a distance
@SVINJournal 5/In fact, non-stenotic carotid plaque likely plays a key role in embolic stroke of undetermined source or ESUS.
Source may be unknown bc a full work up never found an embolic source or a full work up wasn’t completed to find a source.
We will deal w/the former
@SVINJournal 6/If the ESUS involved a unilateral infarct in the anterior circulation, as many as 2 in 5 of these infarcts may be the result of emboli from non-stenotic carotid plaque
@SVINJournal 7/This is especially true in ESUS in young patients, where other cryptogenic causes such as intermittent AFIB are rarer.
In older patients, these vulnerable plaques more commonly reach a point of stenosis, and may cause harm by both emboli and restricted flow
@SVINJournal 8/So how can we tell which plaques are high risk for emboli stroke and which are stable? Well, we need to need to leave NASCET behind and look at the plaque itself for clues
@SVINJournal 9/For this, we need noninvasive imaging. Catheter angiography only looks at the lumen. We need to image the plaque itself to look for features that are associated with high risk of emboli.
CT can help look at plaque size & morphology, while MR can look at plaque composition
@SVINJournal 10/The way you can remember which imaging features indicate a high-risk plaque is by remembering what foods are high risk for you to eat. If it’s bad for your bod, it’s bad for your brain.
@SVINJournal 11/First feature is plaque size, regardless of stenosis.
Only caring about a plaque if there’s stenosis is like saying you’re only fat if your pants don’t fit.
You can be fat even if you wear big sweats that fit—big plaques can be high risk even if they fit (no stenosis)
@SVINJournal 12/Plaques tend to remodel outward first, so they initially don’t narrow the lumen. Only later in the course do they cause stenosis.
It's just like you wear big sweat pants to hide your dad bod, until finally you get so big those don’t fit either
@SVINJournal 13/Plaques grow outward until fibrofatty changes restrict them, then their growth tends to press inward on the lumen.
It's just like how your dad bod pot belly grows out until your belt restricts it, then further growth tends to make your pants very tight (stenosis)
@SVINJournal 14/So you can remember that plaque size is a high-risk feature bc big meals are a high-risk factor for a dad bod. No matter what the meal is composed of, eating too much puts you at risk.
Same w/plaques. No matter the composition, large absolute plaque size is a risk factor
@SVINJournal 15/Next is intraplaque hemorrhage. You can remember that blood in the plaque is a high risk feature bc eating rare, bloody steaks puts you at high risk for the dad bod. You don’t want to eat this = high risk feature
@SVINJournal 16/On imaging, intraplaque hemorrhage is bright on precontrast T1 images, just like how brain hematomas are bright on precontrast T1.
MR angiograms have some T1 weighting, so plaque hemorrhage is a feature you can see on routine MRA—it will be bright outside the lumen!
Just like how you wouldn't want to eat something that someone had pressed their finger into—if the plaque looks like it has lots of fingerprint indentations, it's high risk.
This is a step up from irregularity. Now someone hasn’t just stuck their finger in your food—they have taken a bite out of it! You certainly don’t want to eat that!
You can see these bites out of the plaque on routine CT angiograms.
@SVINJournal 19/Next is a lipid rich necrotic core.
You can remember that lipid/fat in the plaque is a high risk features b/c eating rich, fatty foods puts you at high risk for the dad bod.
Remember, if you don’t want to eat it—you don’t want it in your carotid plaque either!
@SVINJournal 20/To see the lipid core, we need black blood MRI.
Black blood MR nulls the signal in the vessels so they’re black (hence the name “black blood”). This helps us to see the plaque surface & enhancement, which would otherwise be covered up by the signal from the vessel
@SVINJournal 21/Black blood MR is often the same sequence used on an MR dissection protocol—you just add contrast to see regions of inflammation & vascularity
On black blood MR, the lipid rich necrotic core looks just how necrotic things look in the brain—low signal, w/non-enhancing core
Just like how you wouldn’t want to eat food where new moldy things were growing into it—you don’t want a plaque that has new blood vessels growing into it.
You can see neovascularity as adventitial enhancement on black blood MRI.
@SVINJournal 23/Finally is loss of the normal fibrous cap.
Think of the fibrous cap covering like ziplock bag, keeping everything clean & fresh. If there’s a tear in the bag, well, that food is kind of sketchy now. Similarly, you don’t want a plaque w/a tear in its protective covering
@SVINJournal 24/Normally, the fibrous cap enhances on black blood MRI bc it has vascular fibrous tissue.
Thinning or loss of this normal enhancing margin between the lumen and the plaque indicates a high risk plaque.
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!