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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Brain MRI anatomy is best understood in terms of both form & function.
Here’s a short thread to help you to remember important functional brain anatomy--so you truly can clinically correlate!
2/Let’s start at the top. At the vertex is the superior frontal gyrus. This is easy to remember, bc it’s at the top—and being at the top is superior. It’s like the superior king at the top of the vertex.
3/It is also easy to recognize on imaging. It looks like a big thumb pointing straight up out of the brain. I always look for that thumbs up when I am looking for the superior frontal gyrus (SFG)
@TheAJNR 2/Everyone knows about the spot sign for intracranial hemorrhage
It’s when arterial contrast is seen within a hematoma on CTA, indicating active
extravasation of contrast into the hematoma.
But what if you want to know before the CTA?
@TheAJNR 3/Turns out there are non-contrast head CT signs that a hematoma may expand that perform similarly to the spot sign—and together can be very accurate.
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.