Epileptiform Discharge

Epileptiform Discharge
According to IFCN, a waveform can be considered epileptiform if ≥4 of 6 defining features are present:

1️⃣ Physiological field of distribution
-The discharge must have a plausible neurophysiological field.
-It should show:
>A clear phase reversal
>A logical spatial voltage gradient
>Distribution consistent with cortical generators
This helps differentiate true cortical discharges from artifact or benign variants

2️⃣ Morphology: spike or sharp wave
-The waveform must have the morphology of:
>Spike: duration < 70 ms
>Sharp wave: duration 70–200 ms
These reflect synchronous neuronal depolarization

3️⃣ Asymmetry of the waveform
-The ascending limb is steeper and more vertical
-The descending limb is slower and less steep
This asymmetry distinguishes epileptiform discharges from benign rhythmic activity

4️⃣ After-Coming Slow Wave
-A true epileptiform discharge is often followed by a slow wave
-This represents:
>Spike → depolarization
>Slow wave → inhibitory postsynaptic potentials/repolarization
The slow wave reinforces epileptogenic significance

5️⃣ Duration Different from Background
-The waveform should have a clearly different duration from surrounding background rhythms
-It should stand out from alpha, theta, or delta activity
This ensures it is not a fragment of background oscillation

6️⃣ Disruption of Background Activity
-The discharge should interrupt or distort ongoing background rhythms
-There may be:
>Transient attenuation
>Phase resetting
>Background interruption
This indicates abnormal cortical synchronization

Locked-In Syndrome

Locked-In Syndrome

SPT
Communicationg strategies

Low‑Tech AAC
-Early on during acute and subacute rehab
 If look to all directions→ transparent board
 If only up/down→ technique (go by line, and then letter)
>Eye‑blink systems (1 blink = yes, 2 = no)
>Eye-gaze boards (alphabet boards, color-coded grids)
>Partner-assisted scanning
>Simple speech-generating switches, if any movement available (e.g., toe, finger, head, eyelid)

High‑Tech AAC
-Stable eye movement or small residual motor control
>Eye-tracking communication devices (e.g., Tobii Dynavox, EyeLink)
>Brain–Computer Interface (BCI) systems (experimental but promising)
>Speech-generating AAC tablets

Aortic Arch - Anatomy

Aortic Arch - Anatomy

Variants
-Subclavian
>Aberrant R subclavian
>Aberrant R subclavian + carotid vert origin
>Vert origin from supreme intercostal
>R-side arch, L-sided heart

-Arch
>Classic
>Bovine
>Direct Vert 1
>Direct Vert 2


229. Accepted

228. Accepted

Stroke - Anticoagulation

Stroke - Anticoagulation

Coagulation cascade

DOAC
Direct factor Xa inhibitor
-prevent thrombin formation
>Apixaban (Eliquis)
>Rivaroxaban (Xarelto)
>Edoxaban (Lixiana)
>Betrixaban (Bevyxxa)

Direct thrombin inhibitor
>Dabigatran (Pradaxa)

VKA
-Warfarin (Coumadin)→ deplet CS 1972
>Vit K-dependent clotting factors (protein C, protein S, X, IX, VII, II)

Heparin
-Factor Xa inhibitor

UFH
-IV Hep

LMWH
-Enoxaparin (Lvenox), Dalteparin (Fragmin), Tinzaparin (Innohep)

Fondaparinux
(Arixtra)
-IV, if HIT

Parenteral direct thrombin inhibitor
-Argatroban
-Bivalirudin

Consider in stroke
Afib→ DOAC
Mechanical valve stroke→ warfarin
CVST→ heparin transition DOAC/warfarin
Cancer-assocaited stroke→ LMWH or DOAC
APS-related stroke→ warfarin

Reversal agents
Andexanet alfa
>Only given if NSGY indication

TNK
- Cryoprecipitate to replenish fibrinogen
- Tranexamic acid or aminocaproic acid can be administered to prevent further fibrinolysis

Stroke - Dissection

Dissection

Difference IC vs EC
-IMA = Intima, Media, Adventitia
*external elastic lamina

Traumatic vs non-traumatic
-If blunt, full AC (heparin preferred) according to trauma guidelines

Non-traumatic
-If EC: ASA vs DAP vs AC = same benefit
-If IC: no data

Observations
-wait 1y for pregnancy

MS - Diagnosis

Multiple Sclerosis - Diagnosis
"Multiple Sclerosis," 1955
Douglas McAlpine (1890–1981)
Nigel Compston (1918–1986)
Charles Lumsden (1913–1974)

History - dx criteria
-Allison and Millar 1954
-McAlpine 1957, 1965
-Schumacher 1965
-McDonald and Halliday 1977
-Poser 1983
-McDonald (International) criteria 2001, 2005, 2010, 2017, 2024

Considerations
-MS remains dx of exclusion
-20% misdx
-MS dx→ DIS + biological ± DIT (optional)

Questions
Q1 Does the patient have a syndrome compatible with MS?
Q2 Is there any better explanation?
Q3 Does the patient meet DIS?
Q4 Is there biological evidence supporting MS?

Q1 Compatible presentation?
-ON
-TM
-Brainstem syndrome
-Cerebellar syndrome
-Classic CIS
-Progressive
-Incidental lesions

Q2 Better explanation?
-Migraine
>Tiny T2 lesion
-Vascular disease
>MVD: HTN, DM, smoking
-NMOSD, MOGAD
-Spinal dural AVF
-Metabolic or infectious myelopathies

Q3 DIS?
Definition
≥1 T2 lesion in ≥2 of the 5 locations

PISCO
Periventricular, Infratentorial, Spinal cord, Cortical/juxtacortical, Optic nerve

How to confirm ON
-OCT: ≥6 µm pRNFL difference or ≥4 µm GCIPL difference
-VEP: P100 latency prolongation
-MRI: intrinsic ON lesions, w/o chiasmal/perineuritis features

Q4 Biological evidence or DIT?
DIT
-Not req
>substituted by DIS + paraclinical markers
-Definition
>New T2 lesion
>New Gd+ lesion
>Simultaneous Gd+ and non‑enhancing lesions

Biological evidence
-CSF Markers
>OCBs
>kFLC

-MRI Markers
>CVS
>PRLS

Reverse algorithm



OBSERVATIONS

RIS/CIS to MS
-RIS at 10y→ 50-51%
-CIS at 20y→ 60-70%

Higher-misdx-risk
≥50 yo individuals 
-Should have bMRI and more 1 of below
>Spinal cord lesion
>Select‑6 CVS
>Positive CSF marker

Unified framework
Relapsing MS→ RRMS; Progressive MS→ PPMS or SPMS
-RRMS→ Clinical relapse or DIT + DIS (or CSF OCB/kFLC)
-PPMS→ 1 year progression + DIS + CSF OCB/kFLC
-SPMS→ Relapsing MS + progression

Investigation
OCB-CSF
≥2 OCBs in CSF that are NOT in serum = POSITIVE
-Think: “2 = MS”

kFLC
-High kFLC index = intrathecal IgG production = MS‑supportive
-kFLC index ≥6.1 = positive (supports MS)

CVS
-MS lesion = vein in the middle
≠mimics: migraine or MVD
-SELECT-6: ≥6 lesions, and at least 6 of them show a CVS
>Use susceptibility-based imaging (2/2 inside vein deoxyHb)
  SWI (prefer clinical), T2* EPI (research) FLAIR* (FLAIR combined with T2*/SWI)
  Look for a dark vein running through the lesion center
TIP: 3D FLAIR (s/f lesion), switch SWI (is CVS?), switch FLAIR* to confirm; lesion in 2-planes
PRLS
-Iron-ring lesions = chronic active MS lesions
>Iron‑laden microglia
-Criteria: ≥1 PRL lesion (SP99.7%)
*≥4 PRLS associated w/ ↑ disability (research)
>Use susceptibility-based imaging
  SWI (prefer), T2*
  Look for dark paramagnetic rim around a FLAIR-bright lesion
TIP: FLAIR (s/f lesion), switch to SWI, exclude other causes (CVS, hemosiderin from trauma, MCB, calcification); s/f periventricular first; lesion in 2-planes


ESUS

ESUS (Embolic Stroke of Undetermined Source)

Definition
1st description 2014
-Specific subset of cryptogenic stroke
>No major CE factors
  >Embolic Stroke of Undetermined Source
    >17% of IS

Diagnostic
Basic
-bMRI & vessel (CTA/ MRA)

Advanced
Vascular
-Vessel wall MRI (black-blood sequence)
>Eval of high-risk A-A, although no significant stenosis

-T1-fat suppression
>if c/f dissection

-DSA
>highly c/f vasculitis

Cardiac
≠TTE, TEE, Cardiac CT, and Cardiac MRI
If PFO→ LE and UE dopplers; pelvic MR venography

-TCD-HIT

Rhythm monitoring
MCOT/ ILR

Labs
Hypercogulable panel
>repeat in 3mo for confirmation
Autommine work-up

Others
CAP CT scan w/ IV contrast
PET CT scan
Age-appropriate cancer screening, fu w/ PCP
>CEA
>CA19-9
Therapy
-ASA
>DOAC not superior to ASA
  >NAVIGATE ESUS and RE-SPECT ESUS

DBS - Intro

DBS Programming - Intro
Neurophys
-DBS activate axons
-DBS ↓excessive synchronization in motor network
-DBS activates multiple populations

Parts
-Brain electrode
-IPG/Battery
-Patient programmer
-Clinician programmer

Brain electrodes
Medtronic
-3389 ring (0.5mm spacing)
-3387 ring (1.5mm spacing)
-Segmented (Sensight), 0.5 or 1.5mm spacing

Abbott (formerly St. Jude)
-Segmented, 0.5 or 1.5mm spacing

Boston Scientific
-8 ring contacts
-Segmented 8 contact (Cartesia)
-Segmented 16 contacts (Cartesia X & HX)
-all 0.5mm spacing
IPG
Medtronic
-Activa
>PC (primary cell, dual channel)
>SC (primary cell, single channel)
>RC (rechargeable, dual channel)
-Percept PC (primary cell, dual channel, sensing)
-Percept RC (rechargeable, dual channel, sensing)

Abbott
-Infinity 5 (primary cell, dual channel, small)
-Infinity 7 (primary cell, dual channel, large)
-Liberta RC (rechargeable, dual channel)

Boston Scientific
-Vercise (rechargeable, dual channel)
-Vercise Gevia (rechargeable, dual channel, wand)
-Vercise Genus R16 or P32 (rechargeable, 2-4 leads, Bluetooth)
-Vercise Genus P16 or P32 (primary cell, 2-4 leads, Bluetooth)
Clinician programmer
-Medtronic tablet (Samsung)
-Abbott tablet (iPad)
-Boston Scientific tablet (Surface)
Patient programmer
-Medtronic (Samsung smartphone or remote)
-Abbott (iPad mini)
-Boston Scientific (remote; Gevia-gray; Genus-black)

Adjustable parameters
-Amplitude (2-3 mA or V)
>Spread of stimulation
-Pulse width (60-90 μs)
>Time linger in tissue
-Frequency (130-180 Hz)
>Least important
>↑Hz (180)→ tremor; ↓Hz→ gait

Nomenclature
General
-Leads vs Electrodes vs Contact
-Negative contact = cathode
>active contact; most neural activation
-Positive contact = anode
>current return; some neural activation
-Contact labelling
-Therapy impedance and current
Medtronic Percept
Ring
>0–3(L); 8–11(R)
Segmented
>0, 1A, 1B, 1C, 2A, 2B, 2C, 3
>8, 9A, 9B, 9C, 10A, 10B, 10C, 11
*Segments labeled counter-clockwise
 L brain: A (ant), B (lat), C (med)
 R brain: A (ant), B (med), C (lat)
*Multiple current source, so each contact assigned its own amplitude

Abbott
-U/L: 1, 2A, 2B, 2C, 3A, 3B, 3C, 4
-R: 9, 10A, 10B, 10C, 11A, 11B, 11C, 12
*Segment A usually implanted anterior (but can rotate)
*Segments labeled clockwise
 L brain: A (ant), B (med), C (lat) 
 R brain: A (ant), B (lat), C (med)
*Single current source, so one amplitude split between contacts

Boston Scientific
Ring
>U/L: 1–8
>R: 1–8 (old 9–16)
Segmented
>L: 1, 2A, 2B, 2C, 3A, 3B, 3C, 4 (previously 1, 2/3/4, 5/6/7, 8)
>R: same as Left (previously 9, 10/11/12, 13/14/15, 16)
*Segments labeled counter-clockwise
 L brain: A (ant), B (lat), C (med)
 R brain: A (ant), B (med), C (lat)
*Multiple current source, so each contact assigned its own amplitude

Segment leads - orientation
-Stereotactic marker for determining orientation of segments
-Leads typically implanted with segment A facing anterior
>Medtronic: proximal marker (triangle down) aligned with segment A; distal marker (triangle up) aligned with B
>Boston, Abbot: vertical marker aligned with segment A
-Repeat X-ray or CT for orientation
Contact configuration
-monopolar, double monopolar, fractionated monopolar, wide bipolar, narrow bipolar, double bipolar
First Programming
-2-4wks after procedure 2/2 micro-lesioning effect
-For PD, hold meds
-Check surgical sites
-Monopolar mapping
>Explain side effects
>Choose 130hz and 60us, adjust amplitude
>Amplitude jumps 0.5 if paresthesias 0.1
>Neuro-exam, including speechs for every change in amplitude
Side effect map
Vim
-Muscle contraction→ Lat
-Dysarthria→ Lat/Posteromedial
-Paresthesia→ Post
-Ataxia→ Ventral
-No side effect >5mA→ Sup/Ant
STN
-Paresthesia→ Medial/Post
-Muscle contraction→ Lat/Ant
-Dysarthria→ Lat/Ant
-Mood→ Inf/Med
-Autonomic→ no specific region
>Diplopia→ anteromedial
-Dyskinesia→ at the site!
-No side effect >5mA→ Sup/Ant
GPi
-Muscle contractions→ PostMed
-Dysarthria→ PostMed
-Phosphenes→ DeepMed
-Dyskinesia→ at the site!
-Bradykinesia→ Med
-FOG→ Med
-No side effect >5mA→ Ant/Lat/Dorsal
*High stimulation can worse tremor, dystonia
Electrode position
-bMRI
Tips
-Always save old settings
-Teach patient
>patient programmer
>DBS do's and don'ts
-Fu every mo for 6mo
-Refer to monopolar map, redo if needed
-If no benefit after 2 sessions, do imaging for lead position

Future adjustments
-ET→ Taper off after stimulation
-PD→ Meds for NMS
>STN→ med red 2/2 DKN
>GPi→ can maintain same regimen
-DTN→  retain pre-op meds

Warnings
-Diathermy (‘deep heating’)
-Electrical or radiofrequency therapeutic devices (keep away from head/chest)
-Electrocautery (surgery)
-Lithotripsy
-MRI (heating effect)
-TMS, ECT
-Magnetic fields
-Metal/theft detectors (airport report pacemaker and request pat down)
-Store refrigerators, industrial microwave ovens
-Arc welding equipment, high voltage power lines
-Effect on other medical devices (external defibrillation, cardiac pacemakers)

IPG longevity
PCs→ 3-5y

Impedance
>10,000ohm→ break along contact
 Will not affect stimulation if that contact is unused
-3000-5000→ not problem (but ↑V if CV mode)
-Segments can have ‘high’ bipolar impedance (>10,000 ohm) but not a problem if monopolar impedances wnl
-Low impedance (10-100)→ short in circuit
>Stimulation will be applied to all shorted contacts even if they are not “turned on”
>Quick battery drain if stimulation applied between two shorted contacts (one +, the other -) so do not do

Refine parameters
-If low side effect thresholds, try bipolar or directional:
>Use most optimal contact as negative in bipolar configuration
>Perform monopolar mapping for each segment on the best level
-If unable to achieve benefit with single contact, try double-monopolar stimulation using two adjacent contacts
>Double monopolar if high side effects thresholds (or fractionate current to avoid side effects)
>Double bipolar if low side effects threshold
-Establish best contact first, before changing PW and frequency
>Lower PW if side effects
>Increase frequency for tremor
>Increase PW for more benefit (can also increase amplitude)