1/
Why is cranial nerve 6 uniquely affected by⬆️ intracranial pressure? Why is it special? A common question after the CN6 tweetorial.
Here is a maybe #tweetorial, but maybe a🧵about why CN6 is alone affected by ⬆️ pressure. #FOAMed#medtwitter#Medstudenttwitter#neurotwitter
2/ Think of the intracranial CSF space like a balloon, distended by CSF instead of air. Cranial nerves begin inside the balloon, and then they exit as they begin their extradural portion
3/ Most cranial nerves move immediately away from the CSF space after they exit—usually going out through their respective foramina. However, CN6 uniquely runs along the outside of the “balloon” in Dorello canal
4/ Increased intracranial pressure is like expanding the balloon. Most cranial nerves are not affected by the expanded balloon because they move away from the surface of the balloon right after they exit
5/ However, because of the unique course of CN6 along the surface of the “balloon” in Dorello canal, the increased intracranial pressure or expanding “balloon” pushes against the extradural portion of CN6
6/ Unfortunately, CN6 has nowhere to go to escape this increased pressure, as on the other side of it is the clivus. So in the increased pressure pushes it against the clivus in Dorello canal
7/ This makes a “CN6 sandwich”! CN6 gets sandwiched between clivus & dura. It's this compression that uniquely gives you an isolated CN6 palsy w/⬆️pressure!
So when you see an isolated CN6 palsy in intracranial hypertension, think of balloons & sandwiches & you’ll remember why!
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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 a thread on the key findings in vascular dementia
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3/But that’s now outdated.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?
1/Have MULTIPLE questions about the new criteria for MULTIPLE sclerosis?
ECTRIMS 2024 just came out w/proposed new changes to the McDonald criteria for multiple sclerosis.
The changes are complex, but here is a thread w/the basics that you NEED to know!
2/The 2017 criteria were complex as well, but the basic theme was that they required dissemination in both time & space.
So you needed lesions in multiple locations and of multiple different ages.
3/Proposed new criteria bring a paradigm shift from relying on a combination of dissemination in both space in time, to relying on other factors that can replace dissemination in time
It also proposes that new imaging features specific to MS can be used in diagnosis as well
How back pain radiates can tell you where the lesion is—if you know where to look!
Do YOU know where to look?
Here’s how to remember the lumbar radicular pain distributions!
2/Why is it important to know the radicular pain distributions?
Most times patients have many POSSIBLE sources of pain--and when you are looking at an MRI, it's your job to decide which finding is the most LIKELY source of pain
These pain distributions can help you do that!
3/Let’s start with L1. L1 radiates to the groin.
I remember that b/c the number 1 is, well, um…phallic.