Lea Alhilali, MD Profile picture
Feb 22, 2023 16 tweets 8 min read Read on X
1/Having trouble remembering how to differentiate dementias on imaging?

Here’s a #tweetorial to show you how to remember the imaging findings in dementia & never forget!

#medtwitter #meded #neurorad #radres #dementia #alzheimers #neurotwitter #neurology #FOAMed #FOAMrad #PET
2/The most common functional imaging used in dementia is FDG PET. And the most common dementia is Alzheimer’s disease (AD).

On PET, AD demonstrates a typical Nike swoosh pattern—with decreased metabolism in the parietal & temporal regions
3/The swoosh rapidly tapers anteriorly—& so does hypometabolism in AD in the temporal lobe. It usually spares the anterior temporal poles.

So in AD look for a rapidly tapering Nike swoosh, w/hypometabolism in the parietal/temporal regions—sparing the anterior temporal pole
4/Medially, in AD, there’s involvement of the precuneus & posterior cingulate. In fact, the earliest AD findings may be in the precuneus

So medially, instead of a Nike swoosh, you see an Adidas logo—w/a wedge in the region of the precuneus widening anteriorly to the cingulate
5/So in AD, look for the sneaker signs:

—Adidas logo medially in the region of the precuneus

—Nike swoosh along the parietal & temporal regions, sparing the anterior temporal pole.

So if you see sneaker logos—it’s AD. Just call it!
6/Dementia w/Lewy Bodies (DLB) also has temporoparietal hypometabolism—but it also involves the occipital cortex—a very specific finding for DLB. DLB also extends to the ant. temporal cortex.

Together, these regions of hypometabolism look more like an L. And Lewy starts w/an L
7/Next is frontotemporal dementia. As one might expect, it has hypometabolism in…wait for it…the frontal & temporal regions. This is one for Captain Obvious. However, it is a little more complicated than that.
8/Medially, frontotemporal dementia involves the anterior cingulate gyrus. I remember this bc the involvement of the anterior cingulate gyrus makes a hook—so it looks like a lowercase letter f—and frontotemporal starts with f
9/There are also variants of frontotemporal dementia that will not show the classic frontal & temporal involvement.

First, is the frontal variant. This only involves the frontal lobe. It presents w/disinhibition as one would expect to see with frontal lobe involvement
10/Temporal variant involves temporal lobe only. Language processing is here (Wernicke’s anyone?). So this presents w/language difficulties (semantic dementia)

So you DON’T have to have BOTH frontal & temporal involvement to have frontotemporal dementia bc there are variants
11/Corticobasilar degeneration involves the sensorimotor cortex & basal ganglia.

I remember this bc CORTICObasilar goes along the CORTICOspinal tract—so it has hypometabolism at the home of the corticospinal tract, the sensorimotor cortex
12/You also see basal ganglia & thalamus hypometabolism in corticobasilar degeneration. This makes sense bc corticobasilar contains “BASilar” referring to the BASal ganglia

So the 2 regions of hypometabolism in corticobasilar degeneration are in the name—cortex & basal ganglia
13/A rare dementia is posterior cerebral atrophy (PCA). As its name implies, hypometabolism is POSTERIOR—occipital cortex & post temporal lobe

I like to call it posterior CAPE atrophy bc the distribution looks a cape—w/arms (ant temporal lobes) sticking out from under the cape
14/You might say PCA looks like Lewy Body dementia—but PCA doesn’t usuallly involve the ant temporal lobes

So the ant temp lobe involvement that gave Lewy body its L shape is cut short—making the PCA distribution look more like a c than an L

Remember C is PCA & L is Lewy body
15/Finally, vascular dementia has a variable distribution, depending on the regions infarcted (V is both for Vascular & Variable)

These patients may have wedged shaped regions of hypometabolism corresponding to cortical infarcts—remember this bc a wedge is just an inverted V.
16/So now you know the patterns of hypometabolism on PET for the major dementias

This list isn’t all inclusive & there can be variations or even mixed dementias

But hopefully this gives you a starting point you won’t soon forget!

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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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