Stroke & Seizures | Neurological Emergency Management

Definition & Epidemiology

WHO & AHA/ASA Clinical Criteria

Stroke (Cerebrovascular Accident) is defined as an acute neurological deficit attributable to a focal vascular cause, persisting ≥24 hours or resulting in death. With modern imaging, any acute infarct on DWI-MRI qualifies regardless of symptom duration — effectively rendering the "24-hour rule" a clinical relic.

13.7M

New strokes/year globally

5.5M

Deaths/year (2nd leading COD)

80%

Are ischemic strokes

Classification (TOAST & Bamford)

Etiologic subtypes with clinical bedside differentiation

Subtype (TOAST)	Mechanism	Key Features
Large-Artery Atherosclerosis	Artery-to-artery embolism or in-situ thrombosis of ICA/MCA/Vertebrobasilar	Cortical signs, ≥50% stenosis on CTA/MRA, often stuttering onset
Cardioembolism	AF (most common), valvular disease, LV thrombus post-MI, PFO with DVT	Sudden maximal deficit, hemorrhagic transformation common, multiterritorial infarcts
Small-Vessel (Lacunar)	Lipohyalinosis of perforating arteries (lenticulostriates, pontine perforators)	Pure motor, pure sensory, ataxic hemiparesis, dysarthria–clumsy hand. Infarct <1.5 cm. Normal cortex.
Other Determined	Dissection, vasculitis, hypercoagulable states, moyamoya, sickle cell	Young patients, no traditional risk factors — always investigate
Cryptogenic / ESUS	No identified cause despite comprehensive workup. Embolic Stroke of Undetermined Source.	~25% of ischemic strokes. Prolonged cardiac monitoring often reveals occult AF.

🫀 Cardiology Pearl: In ESUS, implantable loop recorders (ILR) detect AF in ~30% of patients over 3 years (CRYSTAL-AF trial). Always push for prolonged monitoring before labeling cryptogenic.

Intracerebral Hemorrhage (ICH)

• Hypertensive: Basal ganglia (putamen 35%), thalamus (20%), pons (5%), cerebellum (10%)
• Amyloid Angiopathy: Lobar, elderly, recurrent — MRI shows cortical superficial siderosis & microbleeds
• Others: Coagulopathy (warfarin ICH — reverse with 4-factor PCC + Vit K), AVM, tumor bleed, hemorrhagic transformation
• ICH Score: GCS, volume (ABC/2), IVH, infratentorial, age ≥80 → predicts 30-day mortality

Subarachnoid Hemorrhage (SAH)

• Cause: Ruptured berry aneurysm (85%), AVM, perimesencephalic
• Presentation: "Thunderclap headache" — worst headache of life, often during exertion. Neck stiffness develops over hours.
• Sentinel headache: Warning leak in ~30–50% cases, days to weeks prior — frequently missed!
• Grading: Hunt & Hess (I–V), Fisher (CT blood pattern predicts vasospasm)
• Vasospasm: Days 4–14 post-SAH. Nimodipine 60mg q4h × 21 days. Monitor with TCD (MCA velocity >120 cm/s).

Modern definition: Transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia WITHOUT acute infarction (tissue-based, not time-based).

⚡ Emergency Pearl: The ABCD² score (Age, BP, Clinical features, Duration, Diabetes) stratifies 2-day stroke risk post-TIA: Score ≥4 = high risk (8% at 2 days). But from ICU experience — admit all TIAs for urgent workup. The score misses embolic sources.

Dual antiplatelet (aspirin + clopidogrel) for 21 days post-TIA reduces 90-day stroke risk by 32% (CHANCE/POINT trials). Start within 24 hours.

Vascular Territory Syndromes

Bedside localization — the art of clinical neurology

MCA (Most Common)

• Contralateral hemiparesis (face & arm > leg)
• Contralateral hemianesthesia
• Homonymous hemianopia
• Dominant: Broca's (frontal) / Wernicke's (temporal) aphasia
• Non-dominant: Hemispatial neglect, anosognosia
• Gaze preference TOWARD the lesion

ACA

• Contralateral leg > arm weakness
• Abulia (bilateral), akinetic mutism
• Urinary incontinence
• Grasp reflex, alien hand syndrome

PCA

• Contralateral homonymous hemianopia with MACULAR SPARING
• Visual agnosia, prosopagnosia
• Alexia without agraphia (dominant)
• Thalamic pain syndrome (Déjerine–Roussy)

Vertebrobasilar / Posterior Fossa

• Wallenberg (PICA): Ipsi facial pain/temp loss + contra body pain/temp loss, dysphagia, vertigo, Horner's, ipsi cerebellar ataxia
• Basilar Tip: Decreased LOC, bilateral motor signs, "top of the basilar" — coma, pupillary abnormalities
• Locked-in (Ventral Pons): Quadriplegia + anarthria. CONSCIOUSNESS PRESERVED. Communicate via vertical eye movements.
• Cerebellar: Ataxia, vertigo, headache — can herniate rapidly! Surgical emergency if hydrocephalus develops.

Acute Ischemic Stroke — Time-Critical Management

"Time is Brain" — 1.9 million neurons lost per minute of ischemia

Minutes 0–10: Door to Assessment

• ABC stabilization, IV access × 2 large-bore
• NIHSS scoring (baseline), glucose check (MUST rule out hypoglycemia!)
• STAT NCCT head — hemorrhage exclusion (door-to-CT <25 min target)
• Labs: CBC, coag, renal, troponin, HbA1c — but do NOT wait for labs to give tPA (except glucose & known coagulopathy)

≤60

Door-to-Needle ≤60 min: IV Alteplase (tPA)

• 0.9 mg/kg (max 90 mg): 10% bolus over 1 min, remainder infused over 60 min
• Window: ≤4.5 hours from last known well (ECASS-III extended window criteria)
• BP must be <185/110 before, <180/105 for 24h after thrombolysis
• Tenecteplase (TNK) 0.25 mg/kg emerging as single-bolus alternative — easier in field/smaller EDs

🚨 Key Contraindications: Active bleeding, plt <100k, INR >1.7, recent surgery (14d), GI bleed (21d), prior ICH, BP uncontrolled >185/110, glucose <50.

≤24h

Mechanical Thrombectomy — Large Vessel Occlusion (LVO)

• ≤6 hours: All LVO with NIHSS ≥6, ASPECTS ≥6 (MR CLEAN, EXTEND-IA, ESCAPE, SWIFT PRIME, REVASCAT)
• 6–24 hours: Selected patients with perfusion mismatch (DAWN, DEFUSE-3 criteria)
• Target: ICA, M1-MCA, basilar artery occlusions. M2 and anterior vertebral emerging.
• NNT = 2.6 for good outcome — one of the most powerful interventions in medicine

ICU

Post-Acute / ICU Management

• BP: Permissive hypertension (up to 220/120) if no thrombolysis. Post-tPA: <180/105 × 24h
• Glucose: Target 140–180 mg/dL. Hypoglycemia is more dangerous than mild hyperglycemia
• Swallow screen before ANY oral intake (aspiration pneumonia kills more than the stroke itself)
• DVT prophylaxis: SCDs immediately, enoxaparin at 24–48h post-imaging stability
• Malignant MCA: Age <60 with >50% territory infarct → decompressive hemicraniectomy (DECIMAL, DESTINY, HAMLET — NNT 2)
• Temperature: Treat fever aggressively (each 1°C rise = 2× worse outcome)

Secondary Prevention

Evidence-based long-term risk reduction

Antithrombotics

• Non-cardioembolic: Aspirin 75–325mg OR clopidogrel 75mg. DAPT × 21d for minor stroke/TIA.
• Cardioembolic (AF): DOACs preferred over warfarin (NOAC trials). Start at 4–14 days post-stroke based on infarct size (1-3-6-12 day rule).

Risk Factor Control

• BP: Target <130/80 (SPRINT). Start/resume at 24–72h post-stroke.
• LDL: <70 mg/dL (high-intensity statin ± ezetimibe). TST trial: <70 superior to 90–110.
• Carotid stenosis ≥70%: CEA within 2 weeks (NASCET benefit lost if delayed).
• PFO closure: Age <60 with cryptogenic stroke + high-risk PFO features (CLOSE, RESPECT, REDUCE trials).

Seizures — Definition & ILAE Classification

2017 ILAE Operational Classification

A seizure is a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain. Epilepsy requires: ≥2 unprovoked seizures >24h apart, OR 1 unprovoked seizure + ≥60% recurrence risk over 10 years, OR an epilepsy syndrome diagnosis.

Focal Onset

• Aware (old: simple partial) — consciousness preserved
• Impaired awareness (old: complex partial) — temporal lobe most common; automatisms (lip smacking, fumbling)
• Focal to bilateral tonic-clonic (old: secondary generalized) — Jacksonian march pattern
• Motor vs Non-motor onset subclassification

Generalized Onset

• Tonic-clonic (GTC): Tonic phase (10–30s) → clonic phase (30–60s) → postictal state
• Absence: Typical (3Hz spike-wave, childhood) vs Atypical (slower, refractory)
• Myoclonic: Brief shock-like jerks. JME — morning myoclonus + GTC + absences
• Atonic: "Drop attacks" — sudden loss of postural tone

Unknown Onset

• Unwitnessed seizures
• Epileptic spasms
• Behavior arrest (insufficient information)
• Reclassify when more data available

Etiology — Think Age-Stratified

From ICU/ER clinical experience — the differential changes with age

Age Group	Common Etiologies
Neonates	HIE, intracranial hemorrhage, pyridoxine deficiency, inborn errors of metabolism, cortical dysplasia
Infants & Children	Febrile seizures (most common 6mo–5yr), genetic epilepsies (Dravet, West syndrome), CNS infections, birth injury
Adolescents/Young Adults	JME, idiopathic generalized epilepsy, trauma, substance abuse, brain tumors (low-grade gliomas)
Adults 40–60	Tumors (primary & metastatic), alcohol withdrawal, metabolic (uremia, hepatic encephalopathy, hyponatremia), vascular
Elderly >60	STROKE is #1 cause, neurodegeneration (Alzheimer's), subdural hematoma, metabolic, medication-induced

🧠 ER Pearl: Always check: Glucose, Na⁺, Ca²⁺, Mg²⁺, BUN/Cr, ammonia, toxicology screen, and pregnancy test. Seizure workup is incomplete without metabolic screening.

Status Epilepticus — ICU Emergency

Defined: ≥5 min continuous seizure activity OR ≥2 seizures without recovery between. Mortality 20%.

0–5m

Phase 1 — Stabilization

• ABC, O₂, monitor, IV access, check glucose
• Benzodiazepine: IV lorazepam 0.1 mg/kg (max 4mg, repeat ×1) OR IM midazolam 10mg if no IV
• Terminates SE in ~65% of cases (VA Cooperative Study)

5–20m

Phase 2 — Established SE (Urgent AED)

• Fosphenytoin 20 mg PE/kg IV (max 150 mg PE/min) — cardiac monitor mandatory (QT prolongation, bradycardia risk)
• OR Levetiracetam 60 mg/kg IV (max 4500mg, infused over 15 min) — fewer drug interactions, safer cardiac profile
• OR Valproate 40 mg/kg IV (max 3000mg) — avoid in hepatic disease, pregnancy, mitochondrial disease
• ESETT trial: All three equally effective (~47% success in established SE)

>30m

Phase 3 — Refractory SE → ICU Intubation

• Intubate + continuous IV anesthetic: Midazolam drip (0.2 mg/kg/h) OR Propofol (2–5 mg/kg load, 30–200 µg/kg/min)
• Continuous EEG monitoring — target burst suppression for 24–48h
• Pentobarbital for super-refractory SE (hemodynamic instability expected — vasopressors ready)
• Investigate underlying cause aggressively: MRI brain, LP (autoimmune encephalitis!), toxicology

🏥 ICU Pearl: Always consider autoimmune encephalitis (anti-NMDA receptor, anti-LGI1) in refractory SE — young women with psychiatric symptoms → ovarian teratoma screen. Early IVIG/plasma exchange can be life-saving.

Anti-Seizure Medication Selection

Pragmatic approach based on seizure type, comorbidities, and interactions

Seizure Type	First Line	Alternatives	Avoid
Focal ± bilateral GTC	Levetiracetam, Lamotrigine	Oxcarbazepine, Lacosamide, Zonisamide	—
Generalized TC	Valproate (M), Lamotrigine (F)	Levetiracetam, Perampanel	Carbamazepine, Phenytoin (may worsen)
Absence	Ethosuximide, Valproate	Lamotrigine	Carbamazepine, Phenytoin, Gabapentin
JME	Valproate (M), Levetiracetam	Lamotrigine (caution — may worsen myoclonus)	Carbamazepine, Phenytoin
Post-stroke seizures	Levetiracetam, Lacosamide	Lamotrigine, Zonisamide	Enzyme inducers (phenytoin, carbamazepine — interact with anticoagulants)

⚕️ Prescribing Pearl: In women of childbearing age — avoid valproate (teratogenicity NTD risk 5–10%, neurodevelopmental harm). Lamotrigine and levetiracetam are safer. Always discuss contraception.

The Stroke–Seizure Nexus

When two emergencies collide — the clinical overlap that demands attention

Post-Stroke Seizures

• Early (<7 days): 2–6% of ischemic, up to 16% of hemorrhagic strokes. Due to acute metabolic disruption, glutamate excitotoxicity, blood–brain barrier breakdown.
• Late (>7 days): 3–5% over 5 years. Gliotic scarring creates epileptogenic focus. This defines post-stroke epilepsy.
• Risk factors: Cortical involvement (strongest predictor), hemorrhagic stroke, large infarct volume, severe initial NIHSS
• Management: Early seizures — treat acutely, no long-term AED unless recurrent. Late seizures — start AED (levetiracetam preferred — minimal drug interactions with antithrombotics)

Seizures Mimicking Stroke

• Todd's Paralysis: Postictal focal deficit lasting minutes to 72 hours. Can perfectly mimic acute stroke — imaging is critical!
• Incidence: ~13% of focal seizures have postictal motor deficits
• Key differentiators: Witnessed seizure activity, gradual resolution (stroke is sudden onset), no acute infarct on DWI-MRI
• Danger: Unnecessary tPA given for Todd's paralysis → hemorrhagic complication. When in doubt — MRI DWI is the gold standard.

Stroke Causing Seizures Causing More Stroke — The Vicious Cycle

• Seizures increase cerebral metabolic demand by 200–300% during ictal activity
• In penumbral tissue post-stroke, this metabolic surge can convert salvageable tissue to infarction
• Seizures can cause transient hypertension → risk of hemorrhagic transformation
• Prolonged seizures → lactic acidosis → further neuronal injury
• Clinical implication: Aggressive seizure control in acute stroke is neuroprotective. Consider continuous EEG monitoring in obtunded stroke patients — up to 20% have non-convulsive seizures.

🫀 Cardiology Intersection: Both stroke and seizures can cause troponin elevation (neurogenic stunned myocardium / Takotsubo cardiomyopathy). Don't automatically blame the heart — check echo before catheterization. SAH + seizures → inverted T-waves + QT prolongation mimicking STEMI. I've seen cath labs activated unnecessarily.

The ER Diagnostic Dilemma — A Decision Framework

Feature	Stroke	Seizure + Todd's
Onset	Sudden, maximal at onset	May have witnessed ictal activity, gradual onset of deficit
Consciousness	Usually preserved (unless basilar/large territory)	Often impaired ictal/postictal
Positive phenomena	Rare (some hemorrhagic)	Common — jerking, twitching, automatisms
Progression of deficit	Stable or stepwise worsening	Resolving over minutes to hours
Tongue bite	Absent	Lateral tongue bite highly specific for GTC
Incontinence	Uncommon acutely	Common with GTC
DWI-MRI	Restricted diffusion (acute infarct)	Normal or reversible changes
EEG	Focal slowing	Epileptiform discharges, postictal slowing