crocodil

👾💪💥

[Lea Alhilali, MD @teachplaygrub]

1/I always say you can tell a bad read on a spine MR if it doesn’t talk about lateral recesses.

What will I think when I see your read? Do you rate lateral recess stenosis?

Here’s a thread on lateral recess anatomy & a grading system for lateral recess stenosis

[Doc Navarrow @DocNavarrow]

✅Giant cell arteritis–related anterior ischemic optic neuropathy (GCA-AION).

💡The MRI finding is the “central bright spot sign”, representing optic nerve head enhancement. It likely reflects ischemic-inflammatory injury of the posterior ciliary circulation.

https://t.co/8xCY4l31CC

[𝑒𝑙𝑦𝑟𝑎 @elyradream]

sea view

[sikandar adwani @SikandarAdwani]

Most anticoagulation mistakes in stroke happen because we ask:

Which anticoagulant should I use?

before asking:

Does this stroke even deserve anticoagulation?”

Stroke anticoagulation is not a prescription.

It is AIR TRAFFIC CONTROL.

Every stroke subtype is a different aircraft.
And every aircraft does NOT get runway clearance.

🟢 GREEN RUNWAY
These are thrombin-rich strokes.
✔ AF-related stroke
→ DOAC usually preferred

✔ Mechanical valve
→ Warfarin only runway

✔ Rheumatic MS + AF
→ Warfarin tower

✔ LV thrombus
→ Usually 3–6 months

✔ Cerebral venous thrombosis
→ Heparin first, even if venous hemorrhagic infarct exists

✔ APS-related stroke
→ Warfarin dominates

✔ Cancer/NBTE stroke
→ LMWH often preferred

These are not aspirin diseases.

🟡 YELLOW HOLDING PATTERN
Not every AF stroke should receive immediate anticoagulation.

Before takeoff:
• How big is the infarct?
• Any hemorrhagic transformation?
• BP controlled?
• Platelets safe?
• Mass effect?
• ICU instability?
• Post-thrombectomy status?

ELAN and OPTIMAS changed the conversation:
Small stable infarct?
Earlier DOAC may be safe.

Large infarct?
Delay may save the brain.
Timing is neuroimaging plus judgment.
Not calendar mathematics.

🔴 RED NO-FLY ZONE
Do NOT empirically anticoagulate:
Lacunar stroke
Atherosclerotic stroke
Most ESUS
Routine AIS <48h
Infective endocarditis embolic stroke

NAVIGATE-ESUS and RE-SPECT ESUS reminded us:
“Cryptogenic” is not a license for DOAC.

🚨 WHEN BLEEDING HAPPENS

The first drug is not PCC.

The first drug is:
STOP.
Then:
→ CT brain
→ INR / renal function / platelets
→ Identify last dose
→ Reverse selectively
→ Reassess mechanism

Because the hardest question in stroke anticoagulation is not:
What should I start?

It is:
When should I restart?
AHA/ASA.
ELAN.
OPTIMAS.
Modern CVT guidance.
The era of one anticoagulation rule for all strokes is over.
Treat the mechanism.
Not just the MRI.
#Neurotwitter #Medtwitter #Stroke #Anticogulation

[sikandar adwani @SikandarAdwani]

Antiplatelet therapy after stroke is not:

Aspirin for everyone.
DAPT for everyone.
Or clopidogrel because the patient had a stroke on aspirin.

It is a 3-question decision.

What is the mechanism?
What is the clock?
What is the bleeding risk?

That is the whole game.

Minor non-cardioembolic stroke or high-risk TIA, early presentation, low bleeding risk?

Think short DAPT.

Aspirin plus clopidogrel.
Usually 21 days.
Then single antiplatelet.

Not 3 months by habit.
Not lifelong because the first prescription was never reviewed.

Mild to moderate stroke or high-risk TIA with selected high-risk features?

Ticagrelor plus aspirin may enter the discussion.
But it is not simply stronger clopidogrel.
It is a selected-patient decision, with bleeding and dyspnoea on the other side of the scale.

Severe symptomatic intracranial stenosis?

This is the 90-day exception.
Aspirin plus clopidogrel may be justified, but only as part of aggressive medical therapy:
statin, BP, diabetes, smoking, lifestyle.
DAPT alone is not a treatment plan.

Lacunar stroke?

Respect SPS3.
Long-term aspirin plus clopidogrel is not wisdom.
It is bleeding dressed as prevention.

ESUS?

Do not guess with anticoagulation.
Start antiplatelet, investigate properly, and reclassify the mechanism when evidence appears.

AF-related stroke?

Antiplatelet therapy is not enough.
The patient needs an anticoagulation strategy when safe.

Stroke on aspirin?

First ask:
Was it really aspirin failure?

Or was it:
missed AF,
intracranial stenosis,
carotid plaque,
non-adherence,
wrong dose,
cancer-associated stroke,
or uncontrolled risk factors?

Never escalate before you re-diagnose.

The clean bedside rule:

DAPT is a bridge.
SAPT is the destination.
Anticoagulation is a different road.
Mechanism decides the map.

In stroke prevention, the most dangerous antiplatelet error is not choosing the wrong tablet.

It is forgetting to write the stop date.

#Neurotwitter #MedX #Stroke #Aspirin

[Lea Alhilali, MD @teachplaygrub]

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!

Here are the signs of NPH

🔹 Evans Index > 0.3
--Enlarged frontal horns relative to skull width → ventriculomegaly.
Remember it: “One out of three is too big for me!”

🔹 Periventricular White Matter Change
--T2/FLAIR hyperintensity from transependymal CSF flow.
Remember it: “Leaking pressure leaves a glow.”

🔹 Narrowing of the Posterior Cingulate Sulcus
--Tight high-convexity sulci from crowding at the vertex.
Remember it: “The top gets squeezed shut.”

🔹 Effaced Vertex CSF + Wide Sylvian Fissures
--Tight sulci up top but enlarged fissures laterally (DESH pattern).
Remember it: “Dry on top, wet on the sides.”

🔹 Upward Bowing of the Corpus Callosum
--Ventricular expansion pushes the corpus callosum upward.
Remember it: “If the corpus callosum is arched, the patient can’t march (wobbly)”

🔹 Temporal Horns > 6 mm
--Early temporal horn dilation from hydrocephalus.
Remember it: “Big horns before big vents.”

🔹 Focally Dilated Sulci at the Vertex
--Patchy enlarged sulci despite surrounding crowding.
Remember it: “Holes in a leaky roof = too much water on the brain!”

🔹 APV Index > 0.5
--Increased ventricular-to-parenchymal proportion suggesting hydrocephalus.
Remember it: “Glass half full is too much!”

🔹 Prominent Aqueductal Flow Void
--Increased CSF flow through the aqueduct on MRI.
Remember it: “If the aqueductal flow is super black, the ventricles are out of whack.”

Classic NPH imaging theme: enlarged ventricles + tight high convexities + disproportionate CSF redistribution.

Hopefully now you won't wobble on the diagnosis of NPH!!

[crocodil @OlennaBatir]

The spring I love 💕

[ANA Journals @ANA_journals]

What's the diagnosis? Check out the latest #NeuroImages and find out if you're correct. https://t.co/tFDiDTO0zZ @WileyBrainPsych

[Aravind Palraj @Rheumat_Aravind]

Mononeuritis multiplex is not just neuropathy.
It is a red flag.

⚠️ Painful
⚠️ Asymmetric
⚠️ Stepwise nerve involvement

Think vasculitis until proven otherwise.

This is a neurological emergency—delay can mean irreversible nerve damage.

Common culprits:
• ANCA-associated vasculitis
• Polyarteritis nodosa
• SLE
• Cryoglobulinemia
• Rheumatoid vasculitis

Key clinical clue:
➡️ Sudden wrist drop / foot drop in different limbs, at different times

What to do:
✔️ Act early
✔️ Confirm with NCS + biopsy (when needed)
✔️ Start immunosuppression promptly

Miss it → disability
Catch it → salvageable

#Rheumatology #Neurology #Vasculitis #MononeuritisMultiplex @docakx @IhabFathiSulima #MedicalEducation #ClinicalPearls #AutoimmuneDisease #EarlyDiagnosis

[Neurocritical Care Society of India @NCSIofficial]

Reversible cerebral vasoconstriction syndrome: A narrative review
https://t.co/lz4ZcdH8oV

[Whitfield Lewis, MD 🇦🇬🇺🇸 @whitfieldlewis6]

Leptin is often reduced to a satiety hormone.

But that misses the bigger picture.

Leptin is trying to defend fat balance

And in doing so, it can drive hypertension

What is leptin?

Leptin is an adipokine released by fat cells

More fat → more leptin
Less fat → less leptin
Its job:

• tell the brain you’ve had enough
• tell the body to burn stored fat

How does it burn fat?
Leptin activates the sympathetic nervous system

→ norepinephrine release
→ β-adrenergic stimulation on fat cells
→ activation of hormone-sensitive lipase
→ breakdown of triglycerides into free fatty acids

Leptin is not just saying “stop eating”

It’s saying:
→ “use what you’ve stored”
But biology doesn’t work in isolation
There is signal crosstalk

Think about insulin.

Its goal is to lower glucose

But when chronically elevated, it spills over:

• fat storage
• sodium retention
• increased uric acid
• growth signaling → acanthosis nigricans, skin tags

All in an attempt to control glucose

Leptin behaves the same way

Its goal is to reduce fat mass

But in metabolic disease:

• leptin levels are high
• the hypothalamus becomes resistant to satiety signaling
Yet—
The pathways driving the sympathetic nervous system remain active
So now you have:

Leptin trying harder to:
• suppress appetite
• burn fat

But instead creating:

• chronic sympathetic activation
• increased heart rate
• vasoconstriction
• renal sodium retention

→ elevated blood pressure

This is centrally driven hypertension
The leptin-resistant hypothalamus ignores satiety
but keeps the sympathetic nervous system turned on

Bottom line

Leptin is not malfunctioning

It is overcompensating

Trying to fix fat balance in a resistant system
But that signal spills over
→ into sympathetic overdrive
→ into hypertension

Control leptin
Control insulin
Restore signaling

And you don’t just affect weight
You affect blood pressure

Drop your thoughts below 👇👇
See my previous blood pressure post below 👇👇

[Lea Alhilali, MD @teachplaygrub]

1/Do scans for dizziness make your head spin?

Need to know what to look for?

Just hear me out!

This month’s @theAJNR SCANtastic will show what to look for:

https://t.co/oLdQvuIDR6

[Lea Alhilali, MD @teachplaygrub]

Does the work up for dizziness make your head spin?

Wondering what you should look when a patient presents w/dizziness?

This month’s @theAJNR SCANtastic has what you need to hear!

https://t.co/glUq8OwQdB

For every patient w/dizziness, remember the mnemonic VESTIBULAR to remind you what to look for:

V is for vestibular schwannoma, vestibular neuritis
E for endolymphatic hydrops (Meniere’s)
S for stroke
T for TIA
I for internal otitis (labyrinthitis)
B for BBPV
U for under hydration
L for loops of vessels (vascular loops)
A for arrhythmia
R for recurrent migraine (vestibular migraine)

In this month’s @the AJNR, de Pont et al. looked at delayed post contrast imaging for Meniere’s. They found that when the filling defect for the endolymph herniates into the semicircular canal, Meniere’s disease is usually more severe & chronic

I think it looks like a bird pooping!

So now you know this finding for Meniere’s disease on delayed post contrast MRI! Hopefully now an MRI for dizziness won’t put you off balance!

Follow @theAJNR & check it out for yourself!

https://t.co/glUq8OwQdB

[Doc Navarrow @DocNavarrow]

🤵‍♀️A 41-year-old woman develops progressive dysphagia, diplopia, and limb weakness. Days later she deteriorates with seizures and decreased consciousness. Brain MRI is performed during ICU admission.

🥼What is the most likely diagnosis?

[crocodil @OlennaBatir]

Diffuse Reversible Leukoencephalopathy in Intracranial Aspergillus Infection https://t.co/m9QsI5DEXt

[crocodil @OlennaBatir]

Very useful thread 🌺

[Isaac Lamb, MD @IsaacLamb01]

New guidelines for acute migraine treatment in the emergency department just dropped! Top line: we need to be offering a lot more peripheral nerve blocks. Let’s dive in!

#neurology #emergencymed #EM #FOAMed #medicine #MedX #EBM #migraine #neuroX #medschool #headache #AAN #AHS

[Doc Navarrow @DocNavarrow]

🙆‍♀️A 42-year-old woman with septic shock and coma undergoes brain MRI after status epilepticus.

🧠Supratentorial cortical abnormalities are present, but the cerebellum shows contralateral involvement despite no primary lesion.

Which phenomenon explains this crossed pattern?

[crocodil @OlennaBatir]

Very interesting case

[Doc Navarrow @DocNavarrow]

😓66-year-old man with sudden left arm weakness and dysarthria. MRI: acute infarct in the left capsule-thalamic region. CTA: left PCA (P2) occlusion.

🙀But the deficit is ipsilateral.

😎Left–right confusion? Exam error? A glitch in the Matrix… or is there another explanation?