Portable MRI

 Portable MRI
Hyperfine – Swoop®
-FDA cleared (2020)
-Field strength: 0.064 Tesla (ultra‑low‑field)
-Indication: Brain imaging (all ages) at point of care (ICU, ED, wards, clinics)
-1st and currently most widely adopted FDA‑cleared portable MRI
-AI‑enhanced reconstruction (Optive AI™ software, FDA‑cleared)
neuro42 
-FDA cleared
-Field strength: Low‑field (no public Tesla rating)

MRI Market

MRI Market
Core Sequences
-Regardless of the machine, these classics keep the same meaning:
>T1 – anatomy, fat, hemorrhage age
>T2 – edema, pathology
>FLAIR – suppresses CSF, highlights periventricular lesions
>DWI / ADC – acute ischemia detection

Hemorrhage or Ca?

GRE (T2*)
-The traditional workhorse
-Picks up blood and calcium as dark “blooming” foci

SWI (Susceptibility‑Weighted Imaging)
-A more sensitive evolution of GRE
-Detects microbleeds, venous structures, and subtle susceptibility changes

Left or Right-handed systems

Left-handed→ Siemens, Canon
Calcium = dark
Blood = bright

Right-handed→ GE, Philips
Calcium = bright
Blood = dark

*If you ever forget, look for an internal reference area of known calcification

Cranial Nerves

(1) Spin Echo–based 3D
DRIVE / FRFSE / RESTORE
-Clean, stable anatomy
-Great near bone or metal
-Ideal for IACs, CN VII/VIII irritation, and anatomy-focused questions

(2) Gradient Echo–based 3D
b‑FFE / FIESTA / CISS
-Razor-sharp nerve detail
-Best for vascular loops (e.g., trigeminal neuralgia)
-Prone to banding artifacts near the skull base

*Choose based on artifact sensitivity and clinical question

Why Some Scans are Faster (but Look Worse)
-In MRI, speed comes at a price:
>Gradient sequences (2–4 min): Fast, beautiful detail, but artifact-sensitive
>Spin-echo sequences (4–8 min): Slower, but more reliable with fewer “false lesions”

Post-Contrast 3D T1
-Same concept, but ≠ name
>MPRAGE (Siemens)
>BRAVO (GE)
>3D TFE (Philips)

Summary
*Gradient echo is an umbrella term for many sequences
*GRE is an specific sequence of gradient echo

EEG - Critical care terminology

ACNS Standardized Critical Care EEG Terminology
1) Start with the Background
To assess the degree of encephalopathy

-Symmetry
>Is it symmetric? Mildly asymmetric? Markedly asymmetric?
>You determine this by comparing amplitude and frequency between hemispheres
-PDR
>Present or absent, and what frequency
-Background frequency
>Delta / Theta / Alpha, or “> Alpha”
-Reactivity
>Does the EEG change with stimulation?
-Voltage
>Normal (>20 μV), low (10–20 μV), or suppressed (<10 μV)
-Continuity
>Continuous; nearly continuous, discontinuous, burst‑suppression, suppressed
2) Label RPPs
Every RPP pattern uses a 2‑term structure:

Main Term 1: Location

G = generalized
L = lateralized
BI = bilateral independent
UI = unilateral independent
Mf = multifocal

Main Term 2: Pattern type

PD = periodic discharges
RDA = rhythmic delta activity
SW = spike‑wave

Example
L-PDs = lateralized periodic discharges
G‑RDA = generalized rhythmic delta activity
3) Add plus (+) modifiers present
These modifiers show increased epileptogenic potential

+F = superimposed fast activity
+R = superimposed rhythmic activity
+S = superimposed sharp waves
EDB = extreme delta brush

Example:
L‑PDs +F = higher risk for seizures than plain L‑PDs
G‑RDA +S
4) Add modifier features
-Frequency (0.5–4 Hz)
-Sharpness (spike, sharp, blunt)
-Amplitude
-Triphasic morphology (yes/no)
-Evolution (evolving, fluctuating, static)

Example:
L‑PDs +F at 1.5 Hz, medium amplitude, sharply contoured, fluctuating
G‑RDA +S at 2 Hz, sharply contoured delta with superimposed sharp waves, fluctuating
5) Classify
a) Is it a szs? (ESz or ECSz)
b) If it lasts longer → status (ESE or ECSE)
c) If it’s short but suspicious → BIRDs
d) If it’s not a seizure but not normal → IIC


Arnold-chiari malformations

Arnold-chiari malformations
Hans Chiari (1851-1916) was an Austrian pathologist

Definition
>5 mm tonsillar descent = classic cutoff for Chiari I, but:
-0–5 mm can still be symptomatic (in small posterior fossa)
-Tonsillar pointing is more predictive of clinical significance than absolute descent
Epidemiology
-Prevalence ↑ dramatically with modern MRI.
-Often incidental (up to 1% of MRIs).
-Association: 
>connective tissue disorders (Marfan, Ehlers-Danlos)→ ligamentous laxity → more craniocervical instability
>Klippel–Feil syndrome
>Craniosynostosis

Types
One falls→ tonsils fall down
Two crowds→ crowded posterior fossa (tonsils + brainstem)
Three out→ herniates OUT into an encephalocele
Four without→ without a cerebellum

Classical 4
The 9 types
Clinical manifestations
- 2/2 CSF flow obstruction
>Headaches (occipital, worsened by coughin/straining/sneezing)
>Tinnitus
 Pulsatile→ abnormal CSF pulsation
 High-Hz→ brainstem-involvement
 Intermittent-pressure→ ICP spikes
>Dizziness/ imbalance
>Visual disturbances
 Episodes of visual obscurations

-Syringomyelia
>paresthesias→ cape-like (dissociated anesthesia)

-Brainstem/ lower cranial nerve signs
>Dysphagia, dysarthria, sleep‑disordered breathing (central OSA), nystagmus, brisk reflexes in lower limbs

-Associated syndromes
>Syringobulbia→ facial numbness, palatal weakness
>Tethered cord syndrome (Chiari II)
>Basilar invagination/ platybasia→ worsens compression

Diagnostic imaging
-bMRI if suspicion
>c-MRI for all cases
>t&l-MRI, if suspect below cervical sx or spinal deformity
-Cine MRI = evaluates CSF flow obstruction; crucial for:
>deciding surgery in borderline cases
>assessing postoperative success

Craniocervical Angles
-Most important chiari displacement
-Other:
>CXA→ predictor of sx
>pB-C2 line→ ventral brainstem compression
>McRae line/ Chamberlain line→ basilar invagination
Management
-Asymptomatic→ observe, avoid activities that ↑ICP (heavy straining)
>Repeat MRI (1y) if >10mm or syringomyelia

-Symptomatic
w/o syrinx→ usual care, if refractory→ surgery
w/ syrinx→ surgery

-Other indications for surgery
>Visual obscurations
>Papilledema
>LOC
>Central OSA→ CPAP

Surgery 
-PFD (post fossa decompress)
>SOC + C1 laminectomy + duraplasty (controversial but ↑ decompression effectiveness)
>Sx pt improve after surgery (>70%)

Ocular neuromyotonia

Ocular Neuromyotonia
Kenneth Ricker (1935–2004) (photo)
Hans Georg Mertens (1921–2006) 

Definition
"intermittent, tonic spasms of one or more of the EOM, resulting in strabismus & paroxysmal diplopia"
-delayed relaxion of EOM makes eye temporarily get 'stuck' after eccentric gaze
- AKA "locking-eye"
Etiology
-MC post-RXT of parasellar area
> 2 monhts to 18 years, mean 5y
-Others: autoimmune disorders (MG & thyroid disease)
-Rare: chemotherapy(cisplatin, 5-FU), Vit B12/D def, thorium myelography, botox injection, alcohol, and cataract surgery

Pathophysiology
-May relate to focal demyelination causing ephaptic transmission
-Eggenberger suggest “reflecting nerve circuit”
-Dysfunction of potassium channels
-Mucopolysaccharide deposition after thyroid-associated orbitopathy

Presentation
-Transient diplopia/strabismus

Neuro-exam
-Prolonged eccentric gaze (1 min)
-Advanced test: electromyography, electrooculography, and videotaping 

Investigation
-bMRI and oMRI w/wo contrast
-TFT

Ddx
-ONM = Triggered by sustained eccentric gaze + brief tonic deviation
-SOM = Torsional micro-oscillations (tremor)
-Cyclic 3rd = Cyclic (predicted) weakness/spasm in a fixed rhythm
-Convergence spasm = Miosis + accommodation
-MG = Fatigues
-Graves = Restrictive pattern + orbital signs
-Decomp phoria = Fatigue‑dependent misalignment without spasm

Therapy
-Carbamazepine & oxcarbazepine
*lower dose
-Others: gabapentin, phenytoin, lacosamide
-Tx hypovitamins
-If refractory, surgery→ binocular fusion w/ strabismus surgery
-Behavioral change, if pt has a AM clock to one side change to other

Videos

ONM
-Nasopharyngeal CA, ttx w/ cisplatin + 5-FU, 9y later transient diplopia
*Worse w/ prolonged eccentric gaze
-Tx CBZ

ONM
-Midbrain glioma, RXT 20y before, now R CN III palsy
-ONM observed during ptosis surgery
ONM
-Full resolution within 1y
-Difficult to atrtibute only to ONM
>Pt does not have tonic spasm
ONM
-Remote hx of pituitary macroadenoma
-Referral for intermittent diplopia for several years

Neurobowl - 2026

Neurobowl - 2026

1️⃣ Video w/ FBDS
A definitive serum diagnostic study was performed. 
Her serum demonstrated _____   ____
LGI-1 antibody

This patient likely has what electrolyte abnormality?
Hyponatremia

2️⃣ Pt w/ clivus chordoma, treated w/ surgery and radiation. 5y later, p/w R CN VI palsy, which was not really palsy was myotonia
Ocular neuromyotonia
-Tx CBZ/OXC

3️⃣ Severe R&L M1 stenosis
This patient's diagnosis is ______ syndrome
-moyamoya
-RNF213 gene

4️⃣ 66yo woman w/ small prior stroke and acute onset dysarthria and dysphagia
-Pseudobulbar palsy
-Foix-Chavany-Marie syndrome

5️⃣ Video w/ stroke pt w/ mouth and genital ulcers
This pt most likely diagnosis is ____
-Behcet
-Cascade sign aka waterfall sign
6️⃣ Hands dark rash, uveitis, and headaches
-VKH (Vogt-Koyanagi-Harada) syndrome
-BEE→ Brain, Ear, Eye
-T-cell autoimmunity targeting melanocytes

7️⃣ Video w/ pt closing and having difficult to open hand
She reproted that did not worse with sustained activity
-Myotonia congenita
8️⃣ 11yo boy w/ abnormal movements occuring when going to the chalkboard 
PKD
-PRRT2

9️⃣ This best term for this patient's clinical symptoms is _______
Amusia
"tone-deafness"
Does not recognized tones, you can try happy birthday

1️⃣0️⃣
Brain abscess p/w aphasia
Tongue w/ telangiectasia
Intrapulmonary shunt
Osler Weber Rendu syndrome
Hereditary hemorrhagic telangiectasia

Neurobowl - 2025

Neurobowl - 2025

1️⃣ Stroke, bMRI w/ WMD, skin biopsy w/ lipoma
CADASIL
Notch3

2️⃣ Hemichorea
Subthalamic nucleus (Nucleus of Luys)

3️⃣ JME
EEG: Generalized 4Hz spike-and-wave discharges induced by photic stimulation

4️⃣ Thetered cord
Spinal cord ends around L1/2

5️⃣ West Nile virus

6️⃣ TGA

7️⃣ Frey's syndrome
Cause by parotidectomy
Damage auriculotemporal nerve, which conveys autonomic fibers from the glossopharyngeal nerve

8️⃣ Post-LP headache 2/2 epidural
Pneumocephalus
Intracranial hypotension

9️⃣ Meige syndrome

1️⃣0️⃣ Peter Brueghel

1️⃣1️⃣ Melkersson-Rosenthal syndrome
-Lingua plicata 

1️⃣2️⃣ Pseudogout
Rhomboid-shaped crystals
Polarized light

1️⃣3️⃣ I-CAA
Inflammatory-CAA

1️⃣4️⃣ Vogt Koyangi Harada disease
T-cell-mediated autoimmunity targeting melanocytes

Neurobowl - 2024

Neurobowl - 2024

1️⃣ Silas Weir Mitchell
-Discoverer of the phantom limb

2️⃣ ⁠Right sciatic nerve causing a foot drop

3️⃣ Left dorsal pons
4️⃣ 8 and a half syndrome
1 + 1/2 + CN 7 = 8 and 1/2

5️⃣ Nitrous oxide leading to a myelopathy

6️⃣ Dural AV fistula

7️⃣ DYT1 Dystonia, not dopamine responsive 
-TorsinA
-Showing a child w/ leg involvement, and significant improvement after DBS
8️⃣ Cheiro oral syndrome

9️⃣ X linked adrenoleukodystrophy
-accumulation of VLCFAs
-defect ABCD1→ impair peroxisomal β‑oxidation→ VLCFAs accumulate

1️⃣0️⃣ Myokymia and 
1️⃣1️⃣ Radiation plexitis
- lung cancer w/ radiation 8y before
- now brachial plexus distribution myokymia

1️⃣2️⃣ ALS with Stephen Hawking

1️⃣3️⃣ Locked in syndrome
Movie: The Diving Bell and the Butterfly
1️⃣4️⃣ Marginal mandibular branch of the facial nerve injured during surgery

1️⃣5️⃣ Eastchester Clapping Sign
-Hemispatial neglect
-Eastchester High School
1️⃣6️⃣ Dermoid cyst
Epidermoid cyst→ Restricts on diffusion; not T1-bright
Lipoma→ Pure fat, usually no calcifications or heterogeneous contents
Arachnoid cyst→ CSF intensity across all sequences, no fat
Teratoma→ Contains fat + soft tissue + calcifications; more complex

1️⃣7️⃣ Facioscalpohumeral dystrophy and 
1️⃣8️⃣ Beevor sign
“movement of umbilicus in supine attempting to flex the head”
1️⃣9️⃣ Post fixational blindness in bitemporal hemianopia


Kahoot

Kahoot!
-QoD

AIS Guideline 2018-2026

AIS Guideline 2018-2026

What Really Changed?
Based on Prabhakaran et al. (2026)
2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association

IVT
Thrombolytic Agent
2018: Alteplase only (standard 0.9 mg/kg)
2026: Tenecteplase (0.25 mg/kg) or alteplase — both Class I recommended
*Tenecteplase 1st-line, if LVO bridging therapy, patients requiring rapid workflow, difficult IV access or prehospital administration
NIHSS and Disability
2018: NIHSS severity emphasized
2026: Any disabling deficit should receive IVT — NIHSS alone should not delay therapy
Ex: aphasia, hemianopia, dominant-hand weakness

Non-disabling stroke
2026: IVT not recommended; DAPT preferred
Extended Window
2018: Mainly MRI DWI–FLAIR mismatch (“wake‑up stroke”)
2026: Perfusion-based IVT up to 9 hours, including wake-up/unknown onset strokes
-CTP
-bMRI D/H: DWI lesion involving <1/3 of MCA territory with no FLAIR signal changes
Contraindication
-prior ICH, DOAC exposure, and stroke within the past 3-months are now relative contraindications
sICH after IVT
EVT
Time Window
2018: 0–6 hrs standard; 6–24 hrs selective (DAWN/DEFUSE‑3)
2026: 0–24 hrs broadly accepted with imaging selection

Large Core Infarcts
2018: Mostly excluded
2026: ASPECTS 3–5 recommended; even 0–2 reasonable in select cases (Class IIb)
>Supported by RESCUE‑Japan, SELECT2, ANGEL‑ASPECT data

Posterior Circulation
2018: No strong recommendation
2026: Class I recommendation for basilar artery thrombectomy (≤24 hrs)
>Supported by ATTENTION & BAOCHE

Pre-stroke Disability
2026: mRS 2 patients now included

Pediatric EVT (NEW)
≥6 years: Class IIa
<6 years: Class IIb selected cases
First formal pediatric interventional guidance
Pediatric AIS
Imaging
-MRI/MRA preferred, but if MRI cannot be obtained within 25 minutes, use CT/CTA to evaluate for LVO

Treatment
-IV alteplase: May be safe, but efficacy remains unclear
-EVT in pediatric LVO (see above)

Early BMT
Glycoprotein IIb/IIIa inhibitors
-No established benefit for IV tirofiban
-IV abciximab is discouraged

Oral anticoagulation
-Early initiation reasonable for mild strokes with Afib

Post‑EVT BP management
-Avoid intensive SBP <140 immediately after thrombectomy

DAPT
-Now recommended for patients presenting within 72h, NIHSS ≤5, and suspected atherosclerotic disease
https://live.avomd.io/algo/01542d1291e749fca1

Remaining gaps
-EVT for NIHSS ≤6
-Optimal intra‑arterial thrombolysis dosing
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