Lea Alhilali, MD Profile picture
Aug 19 12 tweets 5 min read Read on X
1/Do questions about brainstem anatomy cause you to suddenly get a case of locked in syndrome?!

Do you try to localize the lesion or just wait for the MR?

Wait no more!

Here’s a thread about the brainstem Rule of Four to help you localize brainstem lesions! Image
2/The hallmark of a brainstem lesion/syndrome is:

(1) Ipsilateral cranial nerve deficit

(2) Contralateral body deficit (be it weakness, sensory loss, or ataxia) Image
3/You can remember this because often your head has certain feelings that opposite the feelings in your heart/body.

Similarly, the cranial nerve deficit can be the opposite of the body deficit

This split between head and body is key for recognizing brainstem syndromes Image
4/There is a medial & lateral organization to the brainstem blood supply.

Medially, there are paramedian vessels & laterally long circumferential branches

As a result of this design, you tend to get medial & lateral brainstem syndromes depending on where the occlusion is! Image
5/There are 4 rules of 4 to help us to localize brainstem lesions.

Rule 1: Four structures that are Medial that begin w/M

This helps us tell if the lesion is medial

It's medial if there's contralateral motor weakness or loss of light touch, vibration & proprioception Image
6/Rule 2: Fours structures on the Side that begin w/S

Involvement of these structures tells us that it is a lateral lesion

Results in contralateral loss of pain & temperature sensation Image
7/Motor is anterior.

Motor involvement tells you if the lesion is anterior or posterior.

So now we can localize not only medial & lateral, but anterior & posterior! Image
8/Rule 3: Motor/medial cranial nerves divide into 12

This helps us know which CNs are medial & which are lateral

If the cranial nerve can divide into 12, then it's a motor nerve and it's medial. This means a medial lesion! Image
9/Rule 4: Four CN in the pons w/4 above the pons & 4 below

Helps to localize superior/inferior in the brainstem by which CN is involved

CNs are like mile markers along a highway--they let you know how far along you are Image
10/There are 4 CNs in each section (medulla, pons, & above the pons).

Counting up from 12, we see 9-12 are in the medulla, 5-8 in the pons, and 1-4 above the pons.

So depending on what CN is involved, we know if the lesions is in the pons, below the pons or above the pons! Image
11/So for every brainstem lesion, you can now do 3 things:

1. Find where it is along the length of the brainstem using CN involvement
2. See if it’s ant or post based on whether motor is involved
3. Determine if it’s med or lat based on type of sensory deficit & CN involvement Image
12/Now you can localize brainstem lesions in all 3 planes based on their clinical presentation!

Localization is actually quite complex, but the Rule of Four is a great foundation!

Hopefully now when confronted w/a brainstem syndrome, you will no longer be locked in! Image

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More from @teachplaygrub

Aug 16
1/Is your understanding of medial temporal anatomy, well, temporary?

If only there was a way to make hippocampal anatomy memorable!

Here is a thread of the basics of hippocampal anatomy that will hopefully stay in your hippocampus! Image
2/Its name “hippocampus” comes from its shape on gross anatomy.

Early anatomists thought it looked like an upside down seahorse—w/its curved tail resembling the tail of a seahorse.

Hippocampus literally means seahorse. Image
3/In cross section, it has a spiral appearance, leading to its other name, Cornu Ammonis, translated Ammon’s Horn.

Ammon was an Egyptian god w/spiraling rams horns.

The hippocampal subfields are abbreviated CA-1, CA-2, etc, w/CA standing for “Cornu Ammonis” Image
Read 17 tweets
Aug 9
1/Tired of stressing if a brain tumor is progressing?

Wish you had some insurance about calling tumor recurrence?

Here’s the cheat sheet you NEED for the best signs of tumor progression! Image
2/Just when treatment thinks it’s got tumor trapped at cliff, tumor is able to get away

Think how you would get away if you were chased to a cliff’s edge.

These are same signs of tumor progression! Image
3/Here's how both you and the tumor can escape:

1. Jump off into the water:
Tumor heads to the water—the ventricular surface

Subependmyal enhancement is very specific for tumor progression (93% sensitivity), but it isn’t commonly seen (38% sensitive). Image
Read 8 tweets
Aug 7
1/Tired of always speculating about MR spectroscopy?

If you've ever looked at an MR spectroscopy & thought: "I have no idea what I’m looking at!"--then this cheat sheet is for you!

Here's a thread on the 4 basic rules you need to understand the spectrum of basic spectroscopy! Image
2/First you need to know the peaks.

There are 3 main peaks: Choline, Creatine, NAA

Remember the order bc a spectrum looks like mountain peaks & it is cold in the mountains.

And CHOld CREATures NAp or hibernate in the mountains Image
3/First peak is Choline

It's a marker of membrane turnover

You can remember this because membranes coat or “CHOat” the cell Image
Read 11 tweets
Aug 2
1/Wish that your knowledge of autoimmune encephalitis was automatic?

Do you feel in limbo when it comes to the causes of limbic encephalitis?

Do you know the patterns of autoimmune encephalitis?

Here’s a thread with some hints to help you figure it all out! Image
2/Two pearls:
(1) Most common pattern is limbic encephalitis
(2) Small cell can cause any autoimmune pattern.

You can also remember the causes by the demographic:
🔸Young man: testicular
🔸Older: Small cell
🔸Woman with psychiatric symptoms: breast Image
3/Limbic encephalitis is the most common pattern

But it has many, many different causes

Remember--limbic involvement is shaped like a question mark!

So for limbic encephalitis, the cause remains a question bc the differential is so broad

Must question & clinically correlate! Image
Read 7 tweets
Jul 23
1/To call it or not to call it? That is the question!

Do you feel a bit wacky & wobbly when it comes to calling normal pressure hydrocephalus on imaging?

You don’t want to overcall it, but you don’t want to miss it either!

Let me help you out w/a thread about imaging in NPH! Image
2/First, you must understand the pathophysiology of “idiopathic” or iNPH.

It was first described in 1965—but, of the original six in the 1965 cohort, 4 were found to have underlying causes for hydrocephalus.

This begs the question—when do you stop looking & call it idiopathic? Image
3/Thus, some don’t believe true idiopathic NPH exists.

After all, it’s a syndrome defined essentially only by response to a treatment w/o ever a placebo-controlled trial.

However, most believe iNPH does exist--but underlying etiology is controversial. Several theories exist Image
Read 19 tweets
Jun 27
1/Blast from the past!

Sometimes to be next gen, you gotta to go old school!

Cutting edge pituitary imaging must be MRI, right?

Or can we go back to the future w/CT?

Here’s the latest in pituitary imaging in this month’s @theAJNR SCANtastic!

ajnr.org/content/45/6/7…
Image
2/Pituitary imaging is actually very difficult.

First challenge is the small size of the gland & even smaller adenomas, requiring high resolution.

And the difference between adenomas & the gland is subtle—both enhance, but adenomas enhance SLIGHTLY less Image
3/The difference in enhancement is transient & ends quickly

So pituitary imaging must be done dynamically to catch this small window of difference

So we have to do very high resolution imaging very quickly—the worst of both worlds! Image
Read 12 tweets

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