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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1/ I always say, "Anyone can see the bright spot on diffusion images—what sets you apart is if you can tell them why it’s there!”
If you don't why a stroke happened, you can't prevent the next one!
Can YOU tell a stroke’s etiology from an MRI?
Here’s a thread to show you how!
2/First a review of the vascular territories.
I think the vascular territories look a butterfly—w/the ACA as the head/body, PCA as the butt/tail, and MCA territories spreading out like a butterfly wings.
3/Of course, it’s more complicated than that.
Medially, there are also small vessel territories—the lenticulostriates & anterior choroidal.
I think they look like little legs, coming out from between the ACA body & PCA tail.
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!
After reading this, when you see a hemorrhage, your guess on its age 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
@TheAJNR 2/Since the prehistoric days of medicine (1979!), we knew that some brain tumor patients treated w/radiation (XRT) initially declined, but then get better.
Today, we see this on imaging, where it looks worse early, but then gets better.
Now we call this pseudoprogression.
@TheAJNR 3/Why does this happen?
XRT induces a lot of inflammatory changes—from initiating the complement cascade to opening the blood brain barrier (BBB)
It’s these inflammatory changes that make the imaging look worse.