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

EEG - Delta wave

Delta Wave

Denition
-Frequency: <4 Hz
-Physiology: Large‑amplitude, slow oscillatory activity

Mechanism
-2 major neuronal generators:
>Thalamocortical networks→ synchronous, rhythmic delta (particularly in sleep)
>Intrinsic cortical circuits→ focal, polymorphic delta (often pathological)
-Modulators:
>Glial/astrocytic networks influence slow oscillations
*Delta is never generated by purely neuronal mechanisms

Interpretation 
-Depends age, vigilance state, topographic distribution, morphology, reactivity, and clinical context

Age
-Infancy: abundant delta→ physiologic
  ~10 years: <10% of background
-Adults: largely absent in awake state
-Elderly: up to ~1% may persist as physiologic

State
-Delta w/ alertness
>Drowsiness: , often temporal
-Hyperventilation: ↑ generalized delta
-N3 sleep: high‑amplitude, synchronous, generalized delta (“slow‑wave sleep”)

Topography and morphology
-Polymorphic focal delta
>Persistent, non‑reactive, state‑independent→ strong marker of structural lesion (subcortical lesions or large cortical lesions)

-Generalized polymorphic delta
>Suggests diffuse encephalopathy

Rhythmic patterns
-FIRDA (Frontal Intermittent Rhythmic Delta Activity)
>Bilateral, symmetric, intermittent rhythmic delta
>Associated w/ diffuse cerebral dysfunction, ICP, or metabolic encephalopathy
>Benign in children/teens

-TIRDA (Temporal Intermittent Rhythmic Delta Activity)
>Focal, typically unilateral
>Associated w/ TLE, even w/o interictal spikes

-OIRDA (Occipital Intermittent Rhythmic Delta Activity)
>Mainly in children
>Associated w/ CAE and others idiopathic generalized epilepsies

-LRDA (Lateralized Rhythmic Delta Activity)
>Critically ill patients
>IIC pattern

-GRDA  (Generalized Rhythmic Delta Activity)
>Seen in: encephalopaty, sedation,  post‑anoxic injury
>Not epileptiform unless evolving

-SIRPIDs  (Stimulus‑Induced Rhythmic, Periodic, or Ictal‑appearing Discharges)
>Often rhythmic delta following stimulation
>Occur in comatose, septic, or anoxic patients
>Falls under IIC spectrum

-Delta brush pattern
>Fast activity riding on delta
-Seen in: Anti‑NMDA encephalitis (extreme delta brush), premature neonates (physiologic delta brush)

Clinical significance
-Excess generalized delta→ diffuse encephalopathy
-Focal persistent delta→ structural pathology
-Intermittent rhythmic delta→ epilepsy or prior brain injury (location matters)
>Temporal→ TLE
>Occipital→ CAE
>Frontal→ diffuse dysfx

Clinical pearl
-Delta alone is never inherently normal or abnormal — context determines meaning
-Persistent focal polymorphic delta has the highest specificity for structural lesions
-Rhythmic delta is more associated with epilepsy or IIC than polymorphic delta
-Non‑reactive generalized delta in an awake adult→ think encephalopathy

Nodo‑Paranodopathy

Nodo‑Paranodopathy

"My AIN, PAIN"

History
1990s Anti-GM1, paradox of electrical demyelination w/ axonal integrity
2012-2013 Uncini & Kuwabara, term nodopathy
2021 EAN guidelines AIN≠CIPD

Pathophysiology
-AIDP/CIDP = macrophage btw myelin lamellae→ T‑cell recruitment→ segmental demyelination
>Schwann cells shift into iDSc (mimicry)
>AKA macrophage‑associated demyelinating (MAD)-neuropathy
>Demyelination = temporal dispersion + conduction block caused by segmental myelin loss

-NP = Ab-mediated
>Start paranodal loops
>AKA pure antibody‑induced neuropathy (AIN-PAIN)
>Reversible conduction failure (RCF)
  RCF = nodal dysfunction w/o structural injury
Localization
-Node (Kv7)
>NF‑186 (often severe and fulminant)

-Paranode
>NF‑155 (classically tremulous phenotype)
  Triad: Young + ataxic + tremulous
  
>CASPR1
>Contactin‑1 (CNTN‑1) (classically edematous phenotype)
  Triad: Elderly + aggressive + edematous
  Assoc w/ membranous glomerulopathy

-Juxtaparanode (Kv1)
>CASPR‑2
>LGI4
PAIN
-2 types = ganglioside & nodal

Ganglioside Ab
-Usually transient
-Typically produce AIDP presentations
-Often reversible

Nodal Ab
-AIDP/CIDP-like
- AIDP-like: RFC; if early, complete recovery
>Severe cases (like IgG3) activate MAC; irreversible

Acute vs. Chronic
-concept  of IgG class switch
Acute Phase
-Driven by short‑lived plasmablasts
-IgG3 Ab→ ⊕complement (fulminant damage)
Chronic Phase
-Maintained by long‑lived plasma cells
-switch to IgG4 Ab→ ⊖complement; act as functional blockers
*smoldering neuropathy

Therapy
Seropositivity matters for treatment choice
-RTX→ effective IgG4 disorders
-IVIG→ less effective in IgG4
>IVIG relies on complement inh

Consider Ab-test if:
-tremor, ataxia, speed (aggressive), resistance (IVIG), comorbidies (GN), pain

Summary
-First-line
>RTX for NF155, CNTN1, CASPR1 (IgG4/IgG3)
>IVIG/PLEX for ganglioside-mediated AIN, CASPR2

-Second-line
>Combination RTX + IVIG for overlap or refractory cases

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