1/ Alright, #Neurotwitter, the votes for today’s #neuroDDxThursday were overwhelmingly in favor of multiple cranial neuropathies!

Thought about one slide, but this needs a #tweetorial! So that you aren't 😬😬😬 when confronted with this:

#MedEd #FOAMed @MedTweetorials
2/
Reminder: The 12 cranial nerve nuclei are located in the brainstem, and if you have trouble remembering where they are, welcome to the club. Here’s a reminder! Will post the medulla section Monday, stay tuned.
3/
We’ll move from central to peripheral etiologies.

The brainstem is like Times Square in NYC- so much going on in a very small space.

A small insult can easily cause damage to multiple cranial nerves. amiright, #stroketwitter?
4/
Fortunately, because of the close proximity between CN and long tracts, brainstem pathology almost always causes “crossed signs” (contralateral weakness or sensory symptoms to the cranial nerve deficit). An INO or complex spontaneous eye movements = brainstem localization.
5/
So, here’s what I think of when evaluating a patient that seems to have a brainstem etiology of multiple cranial neuropathies.
6/
From the nucleus, the nerves have to get where they’re going. Which brings us to a diagram everyone remembers seeing from medical school. Things that cause compression of the brainstem can result in multiple cranial neuropathies, usually in close geographic proximity.
7/
Summary of what I consider when thinking about compressive etiologies
8/
Alright, now the nerves have left the brainstem are in the SAH and covered with the meninges. All sorts of things can go wrong now either because of damage to the meninges or nerves themselves! And this is really, I think, the exciting part!

Gonna need an LP!
9/
PS: The above slide’s list is not all inclusive, but what I think are most clinically relevant. If you want an inclusive list of pretty much everything that’s ever caused multiple cranial neuropathies check out
…me-connect.de.proxy.library.emory.edu/products/ejour…
10/
Or read this amazing single-author manifesto of nearly 1000 cases.
Multiple Cranial Nerve Palsies ja.ma/3qzxuGq via @JAMANeuro part of @JAMANetwork
11/
Not done. The nerves still have a long way to go to get to their target muscles or to get back to the brainstem from where they collected sensory information. There are lots of ganglia. It is confusing.

But there is one place that’s worth knowing about: The Cavernous Sinus!
12/
Reminder that the cavernous sinus has cranial nerves III, IV, V1, V2, and VI. When evaluating a patient with ophthalmoplegia, this is a can’t miss localization!

(Bonus foramen syndromes & geniculate ganglia, because I want you to win at trivia, right @prasad_sashank?)
13/
Now, we’re at the neuromuscular junction. These are not neuropathies, but two disorders have to be on your “can’t miss” list for a patient with facial weakness and/or ophthalmoplegia:
1️⃣ Myasthenia Gravis
2️⃣ Botulism
14/
Whew! That was a whirlwind!
In Summary: Localization is your best friend.

1️⃣ Look for long-tract signs=brainstem
2️⃣Nerves in close proximity=compression?
3️⃣Meningitis/neuropathy. Need LP!
4️⃣Cavernous sinus
5️⃣ Think mimickers!

Here’s my high yield take away! @medtweetorials
15/
What else should be included, @aaronLBerkowitz, @emoryneurology, @moiseyWoisey?

If this practical approach is helpful, keep an eye out for #acuteneurologysurvivalguide out this summer!! 🧠

Thank you @jenniferspicer4 for the great #medtweetorial tips! @emorymedicine #WHEA!

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