1/Having trouble remembering what you should look for in vascular dementia on imaging?
Almost everyone worked up for #dementia has infarcts. Which ones are important?
Here’s THE FULL #tweetorial this time on the key findings in vascular dementia
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2/Vascular cognitive impairment, or its most serious form, vascular dementia, used to be called multi-infarct dementia.
It was thought dementia directly resulted from brain volume loss from infarcts, w/the thought that 50-100cc of infarcted related volume loss caused dementia
3/But that’s now outdated. We now know vascular dementia results from diverse pathologies that all share a common vascular origin.
It’s possible to lose little volume from infarct & still result in dementia.
So if infarcts are common—which contribute to vascular dementia?
4/To understand which findings are key in vascular dementia, think of a vascular insult to the brain like a punch
Just as each punch does damage, so does each infarct
Not all punches are created equal—nor is every infarct as devastating--& both infarcts & punches are cumulative
5/So every if every punch/infarct causes injury, think of dementia as a knock out—enough damage to overwhelm the brain so that it out of the fight.
The same injuries that cause a knock out are the same ones that can cause vascular dementia. So how do you knock someone out?
6/Classic way is to just beat the daylights out of them. It’s how most fights ends—if there is enough damage, they just can’t stand.
This is multi-infarct dementia, but it’s thought of bit differently than it was in the old days
Volume makes an impact, but it’s not everything
7/It’s like a machine gun shooting at a target. You don’t need good aim, eventually something’s going to hit something important enough to take it down
The new concept of multi-infarct dementia is that it’s not volume per se, but enough volume eventually hits something important
8/We used to think that dementia was a direct relationship w/volume lost, but some infarcts are more impactful than others.
But if you have enough infarcts, you will eventually have impactful ones.
So the overall severity of infarcts does still matter.
9/Next way to take someone down? The chokehold--hypoperfusion.
Signs of hypoperfusion on imaging are infarcts in the borderzone or watershed distributions.
This is typically from a large (ICA) or medium (MCA) stenosis or occlusion.
10/But it’s not just these infarcts that cause dementia. They are just a sign of the underlying disease.
If there is hypoperfusion, there isn’t just macro hypoperfusion, but also chronic neuronal hypoperfusion at a cellular level that causes damage, dysfunction & dementia
11/But we can’t see the damage on a cellular level. We can only see the macroscopic signs on imaging—borderzone infarcts.
Remember the major vascular territories are shaped like a butterfly—infarcts at the butterfly junction are borderzone. These indicate hypoperfusion
12/Next way to take someone down? A knock out punch. A one & done.
These are strategic infarcts.
These are infarcts located in structures directly related to cognition. So damage to these structures results in dementia without any other significant volume loss.
13/Now, rather than shooting a machine gun at a target, you a like a ninja. Just one shot right to the heart to take it down.
Just one infarct in one of these important structures can cause dementia like a shot to the heart.
So which structures are these?
14/There are many structures that have been implicated in strategic infarct dementia.
But the main ones are hippocampus, internal capsule (ant & genu), thalamus (paramedian) & caudate.
I remember this w/the mnemonic:
One HIT CAUses dementia
15/Next way to take someone down? Break important connections. Breaking a leg means they ain’t getting up.
Same w/infarcts, small vessel disease or subcortical vascular encephalopathy breaks important white matter connections between parts of the brain so they can’t function
16/These small vessel infarcts disrupt connections between the frontal lobe & deep gray & parietal lobe, resulting in decreased executive function, attention & memory.
The more small vessel disease, the more impact. So always comment on the severity of small vessel disease
17/The final way to take someone down? Play dirty & make them bleed—hemorrhagic infarcts.
These are a sign of both hypertensive & amyloid small vessel disease.
Amyloid angiopathy has a very strong correlation w/dementia
18/In fact, amyloid angiopathy has such a strong correlation w/dementia that some say it should be thought of more as a neurodegenerative disorder that occasionally causes hemorrhage/stroke—neurodegeneration is its day job.
19/It causes both neurodegeneration & stroke by build up of amyloid proteins in the vessel wall & surrounding perivascular space.
In the vessel wall, it causes weakening that can lead to rupture & hemorrhage
In the perivascular space, it causes clogging & decreased clearance
20/It’s like having a bathtub you never clean
Perivascular spaces get clogged like a drain leading to clouded water (dementia).
And stagnant water is bad for the pipes so they rust & burst—just like vessels hemorrhage
So always mention microhemorrhage/signs of amyloid
21/So now you know the important signs to look for when you are reading a study for vascular dementia.
You now can make all the findings so your report is a knock out!
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1/Controversy in radiology can get tense! The Mt Fuji sign for tension pnemocephalus is under scrutiny. When should you call it?
A #tweetorial about imaging this important #neurosurgery complication
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2/Some believe that peaked, mountain like appearance of the frontal lobes is a critical sign of a life-threatening complication & should be called & reported. Others believe it is too non-specific, commonly seen when there isn’t tension & should be retired. Who’s right?
3/First, let’s clarify about what the Mt Fuji sign actually is. Most are familiar with the fact that large collections of pneumocephalus can compress the frontal lobes—making them look like the slopes of a mountain. But this isn’t actually enough to call Mt Fuji.
2/The PPF is a crossroads between the skullbase & the extracranial head and neck. There are 4 main regions that meet here. The skullbase itself posteriorly, the nasal cavity medially, the infratemporal fossa laterally, and the orbit anteriorly.
3/At its most basic, you can think of the PPF as a room with 4 doors opening to each of these regions: one posteriorly to the skullbase, one medially to the nasal cavity, one laterally to the infratemporal fossa, and one anteriorly to the orbit
2/TLICS scores a fx on (1) morphology & (2) posterior ligamentous complex injury. Let's start w/morphology. TLICS scores severity like the steps to make & eat a pizza:
@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.