Epilepsy Monitoring Unit (EMU)

Epilepsy Monitoring Unit (EMU)


How to restart ASM

Lamotrigine
- if < 7d, LMT can be restarted fully no risk of SJS

Stroke - Antiplatelet drugs

Antiplatelet drugs

COX inhibitors

Glycoprotein IIb/IIIa inhibitors
-Integrilin
ADP receptor/P2Y12 inhibitors

-Cangrelor drip

-Prasugrel→ black-box of ICH in pts w/ previous stroke/ TIA

Phosphodiesterase inhibitors

Epileptogenic Zone

Epileptogenic Zone
“Area of cortex that is necessary and sufficient for initiating seizures and whose removal (or disconnection) is necessary for complete abolition of seizures”
Hans Lüders, 1993

History
1884-1935 (Sir John Hughlings Jackson & Victor Horseley)
-1st cortical resections for EPI
-Szs originate from a specific cortical region that can be surgically targeted

Early–Mid 20th Century: Penfield & Jasper
-ECoG to map, now epileptic activity can be recorded & localized

1966: Tailarach & Bancaud
-sEEG based definition

1993: Lüders
-EZ, hypothetical concept

2000s–present
-Focal view to network model

Concepts
EZ
-Minimum amount of cortex to achieve SF
-Inferered it by combining multiple zones

Seizure onset zone (SOZ)
-Szs is actually generated as measured by EEG

Ictal onset zone (IOZ)
-Szs actually begin, as recorded on sEEG
>Often smaller than the EZ
>Sometimes only part of true epileptogenic network

Potential ictal onset zone
-Might be involved in szs onset but are not definitively proven due to limited data
>Common in sEEG when sampling is incomplete

Irritative zone
-Generates interictal epileptiform discharges as defined by EEG
>Usually larger than true EZ
>Helps guide electrode placement but is not sufficient for surgical targeting

Epileptic lesion zone
-Structural abnormality seen on neuroimaging believed to be source of szs
>Not all lesions are epileptogenic, and some EZs occur without visible lesions

Early spread zone
-Region involved immediately after szs onset
>Helps distinguish primary onset from rapid spread
>Spread zones are not necessarily part of EZ

Symptomatogenic zone
-Activation produces clinical sx of szs
>Sx often reflect spread, not onset
>Not removed if overlaping essential function

Eloquent cortex
-Damage causes major, permanent deficits
>Avoid resecting, unless absolutely necessary

Non-eloquent cortex
-Resection is less likely to cause major functional impairment
>Most resections target this area

Putative epileptogenic zone (Resection margins)
-Estimated EZ based on all available data
-Area planed to be removed
-Practical, clinically actionable version of theoretical EZ

Musician's Dystonia

Musician's Dystonia
"When I try to move the fourth finger of my right hand, my whole body seems to contort."
Robert Schumann (1810–1856)

Musician's history
-Robert Schumann (1810–1856) – Composer / Pianist
-Leon Fleisher (1928–2020) – Pianist
-Gary Graffman (1928–2025) – Pianist
-David Leisner (b. 1953) – Classical Guitarist / Composer
-Reinhard Goebel (b. 1952) – Baroque Violinist
-Glenn Gould (1932–1982) – Pianist 
-Joachim‑Ernst Berendt (1922–2000) – Jazz Critic / Saxophonist
-Billy McLaughlin (b. 1953) – Fingerstyle Guitarist

Definition
-Focal task-specific DTN of the musicians' arm (FTSDma)
-1st describe was William Gowers

Epidemiology
-Onset: typically 3rd–5th decade
-Often after ~30 yrs / ≥10,000 h of playing
>Early musical training (<10 yo, Suzuki method) may be protective
-Male predominance
-High-risk instruments: piano, guitar, violin, brass, woodwinds

Phenomenology
-If not visible, record & see slow-motion
-Hand & OMD (can affect speech, eating, drinking)
-FHD divided in 4 types
G1 Precision→ 2&3
G2 Power→ 3&4&5
G3 Precision→1&2
G4 Proximal
G1 - Precision
1) Pianist, isolated dystonic extension of the second digit (Ia pattern)
2) Guitarist, dystonic extension of 2 and flexion of 3 (pattern Ib)
3) Pianist, dystonic flexion of 2 (pattern Ic)
4) Pianist, dystonic flexion of 2 and extension of 3, (pattern Id)
5) Banjo player, dystonic flexion of 2 and 3 appears mild (pattern Ie)
6) Irish accordion player, extension of 3
7) Guitarist, dystonic extension of 2 and 3 (pattern Ig)

G2 - Power
1) Violinist, dystonic flexion of 4 and 5 (pattern IIa)
2) Pianist, dystonic flexion of the left third and fourth finger (pattern IId)
3) Pianist, dystonia affecting fingers 3-5 (pattern IIc)
4) Piccolo player, dystonic flexion of the left third finger at the middle phalanx (pattern IId)
*Botox at the flexor digitorum superficialis of 3
5) Pianist, extension of 3 and flexion of 4 and 5
6) Violinist, flexion of 4 (likely lumbrical-mediated)
7) Flexion of the 3rd finger (likely lumbrical-mediated) (pattern IIf)
8) Extension of 4 and 5
9) Jazz guitarist, flexion of 5 (pattern IIi)

G3 - Precision
1) Flexion/adduction of the thumb and extension of 2 while playing (pattern IIIa)
2) Flexion/adduction of the thumb and flexion of 2 while writing, producing a pincer-like posture of the thumb and index finger holding the pen (pattern IIIb)
3) Flexion of the thumb (particularly the distal phalanx) while playing (pattern IIIc)
4) Hybrid banjo/guitar, extension of the thumb and flexion/adduction of 2 while playing (pattern IIId)
5) Banjo player, dystonic extension of the thumb while playing (pattern IIIe)

G4 - Proximal
1) Pianist, isolated extension of the wrist as soon as his left hand touches the keyboard (pattern Va)
2) Guitarist, pronation of the wrist, which spread to the task of writing (pattern Vb)
3) Tennis coach, wrist flexion dystonia which spread to occur when he held his arms up (pattern Vc)
4) Percussionist, ulnar deviation of the left wrist while playing with “soft mallets” in a fast roll (pattern Vd)
5) Violinist, subtle loss of vibrato 2/2 biceps activation (VIa)
6) Violinist, dystonia of the bow arm (pattern VII)
*Botox injection
7) Athletics, dystonia of the throwing arm causes the ball to fly wildly off target (pattern EA)

Scales
-Tubiana & Chamagne Scale

Pathophysiology
-Maladaptive sensorimotor plasticity
-Power hand mismatch→ hand is evolutionarily designed to stabilize and exert force onto an object, rather than engaging in precision kinetics

Observations
-Manipulandum DTN→ instrument-specific
-Overflow DTN→ spread to adjacent muscles
-Can progress from focal→ segmental DTN
>Initially task‑specific, but may lose task specificity
-High spread risk in woodwind players (speech/swallowing involvement)

Differential Dx
-Overuse syndromes
-Entrapment neuropathies (e.g., ulnar neuropathy)
>Neuropathy may coexist but is rarely the primary cause
-Functional movement disorder

Treatment Options
-Non-pharm
>Pedagogical: relearning, changing technique, temporary switch
>Sensory: glove
>Constrain-induced technique

-Botox
>US-guided, selective
>Low-doses

-TMS: transient effects, not durable

-Surgery:
>VoA thalamotomy (Japan reports benefit)
>DBS: experimental, protocol-driven only

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
-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
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