Lea Alhilali, MD Profile picture
Jun 6, 2023 25 tweets 16 min read Read on X
1/The 90s called & wants its carotid imaging back!

It’s been 30 years--why are you still just quoting NASCET?

A #tweetorial about carotid plaque imaging in collaboration w/ @SVINJournal!

Featuring this 🆓#openaccess article: ahajournals.org/doi/10.1161/SV… Image
@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! Image
@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. Image
@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 Image
@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 Image
@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 Image
@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 Image
@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 Image
@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 Image
@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. Image
@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) Image
@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 Image
@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) Image
@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 Image
@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 Image
@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! Image
@SVINJournal 17/Next is plaque irregularity.

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.

You can see this on just a routine CT angiogram. Image
@SVINJournal 18/Next is plaque ulceration.

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. Image
@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! Image
@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 Image
@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 Image
@SVINJournal 22/Next is plaque neovascularity.

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. Image
@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 Image
@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. Image
@SVINJournal 25/So go beyond NASCET!

Hopefully, now you’ll never feel vulnerable when it comes to carotid plaque imaging!

Be sure to check out the excellent review by @JimSiegler on non-stenotic carotid plaques featured in @SVINJournal!

ahajournals.org/doi/10.1161/SV… Image

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More from @teachplaygrub

Aug 19
1/Do questions about brainstem anatomy cause you to suddenly get a case of locked in syndrome?!

Do you try to localize the lesion or just wait for the MR?

Wait no more!

Here’s a thread about the brainstem Rule of Four to help you localize brainstem lesions! Image
2/The hallmark of a brainstem lesion/syndrome is:

(1) Ipsilateral cranial nerve deficit

(2) Contralateral body deficit (be it weakness, sensory loss, or ataxia) Image
3/You can remember this because often your head has certain feelings that opposite the feelings in your heart/body.

Similarly, the cranial nerve deficit can be the opposite of the body deficit

This split between head and body is key for recognizing brainstem syndromes Image
Read 12 tweets
Aug 16
1/Is your understanding of medial temporal anatomy, well, temporary?

If only there was a way to make hippocampal anatomy memorable!

Here is a thread of the basics of hippocampal anatomy that will hopefully stay in your hippocampus! Image
2/Its name “hippocampus” comes from its shape on gross anatomy.

Early anatomists thought it looked like an upside down seahorse—w/its curved tail resembling the tail of a seahorse.

Hippocampus literally means seahorse. Image
3/In cross section, it has a spiral appearance, leading to its other name, Cornu Ammonis, translated Ammon’s Horn.

Ammon was an Egyptian god w/spiraling rams horns.

The hippocampal subfields are abbreviated CA-1, CA-2, etc, w/CA standing for “Cornu Ammonis” Image
Read 17 tweets
Aug 9
1/Tired of stressing if a brain tumor is progressing?

Wish you had some insurance about calling tumor recurrence?

Here’s the cheat sheet you NEED for the best signs of tumor progression! Image
2/Just when treatment thinks it’s got tumor trapped at cliff, tumor is able to get away

Think how you would get away if you were chased to a cliff’s edge.

These are same signs of tumor progression! Image
3/Here's how both you and the tumor can escape:

1. Jump off into the water:
Tumor heads to the water—the ventricular surface

Subependmyal enhancement is very specific for tumor progression (93% sensitivity), but it isn’t commonly seen (38% sensitive). Image
Read 8 tweets
Aug 7
1/Tired of always speculating about MR spectroscopy?

If you've ever looked at an MR spectroscopy & thought: "I have no idea what I’m looking at!"--then this cheat sheet is for you!

Here's a thread on the 4 basic rules you need to understand the spectrum of basic spectroscopy! Image
2/First you need to know the peaks.

There are 3 main peaks: Choline, Creatine, NAA

Remember the order bc a spectrum looks like mountain peaks & it is cold in the mountains.

And CHOld CREATures NAp or hibernate in the mountains Image
3/First peak is Choline

It's a marker of membrane turnover

You can remember this because membranes coat or “CHOat” the cell Image
Read 11 tweets
Aug 2
1/Wish that your knowledge of autoimmune encephalitis was automatic?

Do you feel in limbo when it comes to the causes of limbic encephalitis?

Do you know the patterns of autoimmune encephalitis?

Here’s a thread with some hints to help you figure it all out! Image
2/Two pearls:
(1) Most common pattern is limbic encephalitis
(2) Small cell can cause any autoimmune pattern.

You can also remember the causes by the demographic:
🔸Young man: testicular
🔸Older: Small cell
🔸Woman with psychiatric symptoms: breast Image
3/Limbic encephalitis is the most common pattern

But it has many, many different causes

Remember--limbic involvement is shaped like a question mark!

So for limbic encephalitis, the cause remains a question bc the differential is so broad

Must question & clinically correlate! Image
Read 7 tweets
Jul 23
1/To call it or not to call it? That is the question!

Do you feel a bit wacky & wobbly when it comes to calling normal pressure hydrocephalus on imaging?

You don’t want to overcall it, but you don’t want to miss it either!

Let me help you out w/a thread about imaging in NPH! Image
2/First, you must understand the pathophysiology of “idiopathic” or iNPH.

It was first described in 1965—but, of the original six in the 1965 cohort, 4 were found to have underlying causes for hydrocephalus.

This begs the question—when do you stop looking & call it idiopathic? Image
3/Thus, some don’t believe true idiopathic NPH exists.

After all, it’s a syndrome defined essentially only by response to a treatment w/o ever a placebo-controlled trial.

However, most believe iNPH does exist--but underlying etiology is controversial. Several theories exist Image
Read 19 tweets

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