Theta wave

Theta wave

Definitions
-Theta frequency: 4–7 Hz
-Theta rhythm: sustained, regular 4–7 Hz oscillation
-Theta activity: any waveform in the 4–7 Hz range, rhythmic or not

Morphology
-Rounded, smooth waveforms
-Broader than alpha
-Less sharply contoured than beta
-Amplitude: 20–100 μV

Neurophysiology
-Generated by cortical and hippocampal networks
-Modulated by 
>Cholinergic input via the ARAS
>Thalamocortical circuits
>Hippocampal oscillations

-Hippocampal theta
>Long‑term potentiation
>Memory encoding & consolidation
>Spatial navigation

Physiological
-N1 sleep
-Drowsiness
>Inc drowsy, dec alert
>Assess reactivity, non‑reactive theta→ c/f encephalopathy
-Meditation / internal attention
-Normal infant EEG (bilateral polymorphic theta)
-Young individuals during syncope
-Centroparietal rhythmic theta (“drowsy syndrome”)

Topographic interpretation
-Frontal theta
>Common in drowsiness
>Excess→ metabolic encephalopathy

-Temporal theta
>Intermittent → benign
>Persistent/asymmetric → structural

-Posterior theta
>Slowed PDR
>Diffuse cortical dysfunction

Clinical correlates
-Persistent gen polymorph theta (adults)→ diffuse cerebral dysfunction
-Dominant theta background in severe illness→ “theta coma”
-Focal persistent theta→ subcortical structural lesion
-Excess theta in elderly→ dementia syndromes
-High‑amplitude theta bursts→ narcolepsy

Medication‑Related Theta
-Sedation: bzd, barbiturates, ASMs
-Typical features: diffuse, symmetric, non‑focal

Age‑Dependent Interpretation
-Children/adolescents
>Theta may dominate waking EEG

-Adults
>Persistent waking theta is abnormal

-Elderly
>Mild theta may be age‑related
>Excess→ neurodegeneration

BEVs
-RMTD
-Midline Theta (Ciganek Rhythm)

qEEG
-Inc theta assoc w/ cognitive slow, red attention, executive dysfx
-Frontal theta excess assoc w/ dementia, TBI, ADHD

Cranial Nerve 0

Cranial Nerve 0 (Terminal Nerve)
Definition
-Collection of microscopic nerve fibers found on the ventral surface of the frontal lobe, close to the olfactory tract

Discovery
-1st described by Felix Pinkus (1913)

Anatomical Course
-Originates from neurons in the nasal mucosa
-Fibers pass through the cribriform plate
-Terminate in areas of the forebrain, especially the hypothalamus and septal nuclei

Functions
-Pheromone detection, sexual behavior
>Terminal nerve provides a direct pathway between nasal cavity & hypothalamic reproductive centers, bypassing classical olfactory circuits
-Reproductive, neurons related to GnRH
-Modulation of autonomic & limbic activity

Clinical Significance
-Developmentally related to migration of GnRH neurons
>Abnormality may lead Kallmann syndrome

Why It Is Called “Cranial Nerve Zero”
-Lies ant to CN I

Important Characteristics
-Very thin and microscopic
-Present in humans and many vertebrates
-Often not visible in routine gross dissection

Dyslipidemia

Dyslipidemia
2026 ACC/AHA Dyslipidemia Guidelines

Screening
Who
-At 19 yo, and every 5y
-At 9–11, 1x s/f FH
≥2y, if FH⊕

How
-Lipid profile (TC, LDL, HDL, TG)
-ApoB
>For high-risk group already in LLT
-Lpa
>At least 1x in life
>FH hx

Follow-up
-Draw lab, repeat 3 mo, repeat every year

CPR Framework
Calculate risk→ Personalize→ Reclassify

Calculate risk
PREVENT-ASCVD
https://professional.heart.org/en/guidelines-and-statements/prevent-calculator
-Age 30–79
-Results: low < 3%, border 3–5, intermediate 5-10, high ≥10

Personalize
-Assess risk enhancers
Reclassify
CAC, coronary artery calcium

Management→ Absolute Goals!
-Primary prevention
*Automatic LLT,  regardless of LDL-C level
 Adults aged 40-75 with diabetes, chronic kidney disease (stage 3 or 4), or HIV!

-Classify "very high-risk"
-2nd prevention
-ASCVD and hyperTG
-If statin-attributed muscle sx

Goals
ApoB
Lpa
-Goal < 75
-Statins do no ↓ Lpa, only PCSK9 



Notes
PCSK9 and Bempedoic acid
non-HDL-C?
Guidelines, baby!


Benign epileptiform variants

Benign Epileptiform Variants

History
-Initially eveything was epileptiform
-Dr. Wilder Penfield discover TLE
-Discovery of BEVs

BEV clues
-No after‑going slow wave = think BEV
-Rhythmic without evolution = benign
-Sleep‑related sharp transients ≠ epilepsy
-Clinical correlation always normal

Variants
Temporal/ focal sharp‑appearing variants
>Wicket waves
>RMTD (Rhythmic mid‑temporal theta of drowsiness)
>TSS (Temporal small sharp spikes)
  BETS (Benign epileptiform transients of sleep)

Generalized spike‑like variants
>6‑Hz phantom spike‑and‑wave

Sleep‑related benign variants
>6–14 Hz positive spikes (Ctenoids)
>BSSS (Benign sporadic sleep spikes)

Rhythmic non‑epileptic patterns
>SREDA
>Lambda waves

Pediatric / Developmental Variants
>Hypnagogic hypersynchrony
>PDR variants


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
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