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9.1 Acute Stroke, TIA, & Neurovascular Emergencies

Key Takeaways

  • Immediate non-contrast head CT is the essential first-line imaging modality to differentiate ischemic from hemorrhagic stroke prior to initiating any acute thrombolytic therapy.

  • According to Canadian Stroke Best Practice Recommendations, IV tenecteplase or alteplase is indicated within 4.5 hours of clear symptom onset provided blood pressure is controlled <185/110 mmHg and no contraindications exist.

  • Endovascular thrombectomy (EVT) is standard of care for anterior circulation large vessel occlusion within 6 hours, and up to 24 hours in selected patients demonstrating a favorable CT perfusion mismatch.

  • High-risk TIA (ABCD2 score ≥ 4, motor weakness, or speech deficit) requires urgent evaluation within 24 hours, CTA head/neck, and short-term dual antiplatelet therapy (aspirin plus clopidogrel for 21–90 days).

  • A normal non-contrast head CT within 6 hours of thunderclap headache onset has high sensitivity for subarachnoid hemorrhage, but lumbar puncture for CSF xanthochromia remains mandatory if clinical suspicion is high and CT is negative.

Last updated: July 2026

Introduction & Hyperacute Assessment

Acute neurovascular events are medical emergencies where rapid recognition, imaging, and intervention directly dictate long-term functional recovery. In Canada, stroke is a leading cause of adult disability and mortality. The clinical approach to acute neurovascular disease centers on rapid differentiation between ischemic stroke, hemorrhagic stroke, and stroke mimics, followed by time-critical reperfusion therapies.

Initial Triage & Emergency Workup

Upon presentation with hyperacute neurological deficits (onset of focal weakness, facial drooping, speech disturbance, or sensory loss):

  1. Stabilize Airway, Breathing, and Circulation (ABCs): Ensure adequate oxygenation (SpO2≥94%SpO_2 \ge 94\%) and continuous cardiac monitoring.
  2. Check Capillary Blood Glucose Immediately: Hypoglycemia (<2.8 mmol/L<2.8\text{ mmol/L}) is the most critical and easily reversible stroke mimic. Severe hyperglycemia can also exacerbate ischemic brain injury.
  3. Perform Focused Neurological Assessment: Calculate the National Institutes of Health Stroke Scale (NIHSS) score to quantify stroke severity and establish baseline function.
  4. STAT Non-Contrast Computed Tomography (NCCT) Head: NCCT must be performed immediately. The primary objective of hyperacute NCCT is not to visualize early ischemic changes, but to rule out intracranial hemorrhage (ICH) prior to initiating antiplatelet or thrombolytic therapy.
  5. Computed Tomography Angiography (CTA): CTA of the head and neck (from aortic arch to vertex) should be performed concurrently with NCCT in all acute stroke candidates to detect Large Vessel Occlusions (LVO) eligible for Endovascular Thrombectomy (EVT).

Ischemic Stroke Thrombolysis & Endovascular Thrombectomy

Ischemic stroke accounts for approximately 85% of all stroke presentations, resulting from thromboembolic arterial occlusion. Canadian Stroke Best Practice Recommendations (CSBPR) emphasize rapid door-to-needle (DTN target <30 minutes<30\text{ minutes}) and door-to-groin-puncture times.

Intravenous Thrombolysis

Intravenous thrombolysis degrades fibrin clots by activating plasminogen to plasmin. CSBPR recommends Tenecteplase (TNK) 0.25 mg/kg0.25\text{ mg/kg} IV single bolus (maximum 25 mg25\text{ mg}) or Alteplase (tPA) 0.9 mg/kg0.9\text{ mg/kg} IV (10% bolus, 90% infusion over 60 minutes, maximum 90 mg90\text{ mg}). Tenecteplase is increasingly preferred in Canadian stroke centers due to rapid single-bolus administration and superior fibrin specificity.

Thrombolysis ParameterCanadian Best Practice Guidelines
Eligible Time WindowWithin 4.5 hours of clear symptom onset (or last known well time)
Pre-Administration BP TargetSystolic BP <185 mmHg<185\text{ mmHg} and Diastolic BP <110 mmHg<110\text{ mmHg}
Post-Administration BP TargetMaintain BP <180/105 mmHg<180/105\text{ mmHg} for at least 24 hours post-thrombolysis
Antiplatelet / Anticoagulant HoldHold aspirin, heparin, or clopidogrel for 24 hours post-thrombolysis until follow-up CT rules out hemorrhagic transformation

Absolute Contraindications to Intravenous Thrombolysis

  • Active internal bleeding or acute bleeding diathesis.
  • Prior intracranial hemorrhage (ICH) at any time.
  • Known intracranial neoplasm, arteriovenous malformation (AVM), or aneurysm.
  • Severe head trauma or intracranial/intraspinal surgery within the preceding 3 months.
  • Uncontrolled severe hypertension (SBP >185 mmHg>185\text{ mmHg} or DBP >110 mmHg>110\text{ mmHg} unresponsive to acute IV antihypertensive therapy).
  • Platelet count <100×109/L<100 \times 10^9\text{/L}, INR >1.7>1.7, or elevated aPTT.
  • Direct Oral Anticoagulant (DOAC) ingestion within the last 48 hours (unless specific lab assays show no anticoagulant activity or specific reversal agent available).

Endovascular Thrombectomy (EVT)

EVT involves mechanical intra-arterial clot retrieval using stent retrievers or aspiration catheters. It provides dramatic functional benefits for large vessel occlusions.

  • Indications: Occlusion of the internal carotid artery (ICA) or proximal middle cerebral artery (MCA M1/M2 segment), pre-stroke modified Rankin Scale (mRS) score 0–1, age ≥18\ge 18, and NIHSS ≥6\ge 6.
  • Standard Time Window: Within 6 hours of symptom onset.
  • Extended Time Window (6 to 24 Hours): Select patients presenting between 6 and 24 hours after last known well (including wake-up strokes) are eligible for EVT if CT Perfusion (CTP) or diffusion-weighted MRI demonstrates a small ischemic core with a large salvageable ischemic penumbra (DAWN and DEFUSE-3 trial criteria).

Exam Trap: Do NOT delay EVT administration while waiting to observe clinical response to IV thrombolysis. If a patient is eligible for both IV thrombolysis and EVT, initiate IV tenecteplase/alteplase immediately and simultaneously dispatch the patient to the angiography suite for EVT ("bridge therapy").


Permissive Hypertension & BP Management in Acute Stroke

Blood pressure management in hyperacute ischemic stroke requires balancing perfusion of the ischemic penumbra against the risk of cerebral edema or hemorrhagic transformation.

Management Rules

  1. Patients Eligible for IV Thrombolysis / EVT: Lower BP to <185/110 mmHg<185/110\text{ mmHg} prior to bolus using short-acting IV agents (Labetalol 10–20 mg10\text{--}20\text{ mg} IV, Nicardipine infusion, or Hydralazine). Maintain <180/105 mmHg<180/105\text{ mmHg} for 24 hours.
  2. Patients NOT Eligible for Thrombolysis / EVT: Allow permissive hypertension up to 220/120 mmHg220/120\text{ mmHg} for the first 24 to 48 hours. Do not lower blood pressure unless SBP >220 mmHg>220\text{ mmHg} or DBP >120 mmHg>120\text{ mmHg}, or if acute concomitant end-organ damage is present (e.g., acute aortic dissection, acute myocardial infarction, acute pulmonary edema, or hypertensive encephalopathy). When lowering is required, reduce mean arterial pressure (MAP) by no more than 15% in the first 24 hours.

TIA & Secondary Stroke Prevention

A Transient Ischemic Attack (TIA) is defined as a brief episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction on tissue imaging (neuroimaging negative). TIA represents an urgent warning sign; up to 10% of TIA patients suffer an ischemic stroke within 90 days, with the highest risk occurring in the first 48 hours.

ABCD2 Risk Stratification Score

  • Age ≥60\ge 60 years (1 point)
  • Blood Pressure ≥140/90 mmHg\ge 140/90\text{ mmHg} at initial evaluation (1 point)
  • Clinical Features: Unilateral motor weakness (2 points), Speech impairment without weakness (1 point)
  • Duration of Symptoms: ≥60\ge 60 minutes (2 points), 10–5910\text{--}59 minutes (1 point)
  • Diabetes Mellitus history (1 point)

Patients with high-risk TIA (ABCD2 score ≥4\ge 4, motor weakness, speech deficit, or fluctuating symptoms) require immediate workup within 24 hours at a rapid-access TIA clinic or emergency department.

Acute Secondary Prevention Protocols

  • Dual Antiplatelet Therapy (DAPT): For non-cardioembolic high-risk TIA or minor ischemic stroke (NIHSS ≤3\le 3), initiate Aspirin 81 mg81\text{ mg} + Clopidogrel 75 mg75\text{ mg} daily (following loading doses of Aspirin 160–325 mg160\text{--}325\text{ mg} and Clopidogrel 300–600 mg300\text{--}600\text{ mg}) for 21 to 90 days (based on CHANCE and POINT trials), followed by monotherapy (Clopidogrel or Aspirin). DAPT beyond 90 days increases bleeding risk without incremental benefit.
  • High-Intensity Statin: Initiate Atorvastatin 80 mg80\text{ mg} daily immediately regardless of baseline LDL-C.
  • Vascular Imaging: Perform urgent CTA or carotid Doppler ultrasound. If symptomatic carotid artery stenosis is 70%–99%70\%\text{--}99\%, perform Carotid Endarterectomy (CEA) within 14 days of the index event.
  • Cardioembolic Workup: Holter monitoring to detect occult Atrial Fibrillation. If atrial fibrillation is identified, initiate Direct Oral Anticoagulant (DOAC: Apixaban, Rivaroxaban, Dabigatran, or Edoxaban) therapy. Delay initiation by 3 to 14 days post-stroke depending on stroke size and hemorrhagic risk.

Hemorrhagic Neurovascular Emergencies

Intracerebral Hemorrhage (ICH)

Intracerebral hemorrhage results from rupture of small penetrating arteries damaged by chronic hypertension (Charcot-Bouchard microaneurysms) or amyloid angiopathy.

  • Clinical Presentation: Sudden focal neurological deficit accompanied by headache, vomiting, rapid elevation of BP, and declining level of consciousness.
  • Acute Interventions:
    • BP Reduction: Rapidly lower SBP to a target of 130–140 mmHg130\text{--}140\text{ mmHg} using IV labetalol or nicardipine (avoiding SBP <110 mmHg<110\text{ mmHg}).
    • Anticoagulation Reversal:
      • Warfarin: IV Vitamin K 10 mg10\text{ mg} + 4-factor Prothrombin Complex Concentrate (PCC).
      • Dabigatran: Idarucizumab 5 g5\text{ g} IV.
      • Factor Xa Inhibitors (Apixaban/Rivaroxaban): Andexanet alfa or 4-factor PCC (50 units/kg50\text{ units/kg}).
      • Heparin: Protamine sulfate.
    • Neurosurgical Consultation: Indicated for cerebellar hemorrhage >3 cm>3\text{ cm} with neurological deterioration, brainstem compression, or hydrocephalus.

Subarachnoid Hemorrhage (SAH)

Subarachnoid hemorrhage is most commonly caused by rupture of a saccular ("berry") aneurysm in the Circle of Willis (most frequent site: Anterior Communicating Artery).

  • Clinical Features: Sudden, catastrophic "thunderclap" headache ("worst headache of my life"), reaching peak intensity within seconds, accompanied by vomiting, meningismus (nuchal rigidity, Kernig/Brudzinski signs), photophobia, and transient loss of consciousness.
  • Diagnostic Algorithm:
    1. Non-Contrast Head CT: Highly sensitive (>95%>95\%) within the first 6 hours of headache onset.
    2. Lumbar Puncture (LP): If NCCT is negative or equivocal and clinical suspicion remains high, LP is mandatory. Inspect CSF for xanthochromia (yellowish discoloration of CSF supernatant caused by bilirubin from RBC breakdown), which requires 12 hours from headache onset to reliably develop. Spectrophotometry or centrifuge visual inspection confirms SAH.
    3. Cerebral Angiography (CTA or Digital Subtraction Angiography): Performed to identify the ruptured aneurysm.
  • Complications & Management:
    • Vasospasm Prevention: Oral Nimodipine 60 mg60\text{ mg} q4h for 21 days improves neurological outcomes by preventing delayed cerebral ischemia.
    • Aneurysm Repair: Endovascular coiling or surgical clipping within 24–72 hours to prevent rebleeding.
    • Hydrocephalus: Managed with External Ventricular Drain (EVD).

Clinical Scenario: A 48-year-old female presents to the ED with a severe, instantaneous headache that began 8 hours ago. Her non-contrast CT head is completely normal. The candidate must recognize that a normal CT at 8 hours DOES NOT rule out subarachnoid hemorrhage. The mandatory next step is a lumbar puncture to assess for xanthochromia.

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Acute Ischemic Stroke & TIA Diagnostic and Treatment Pathway
Test Your Knowledge

A 64-year-old male presents to the emergency department 2 hours after the sudden onset of right-sided arm weakness and expressive aphasia. His past medical history is significant for hypertension. Capillary blood glucose is 6.2 mmol/L. Non-contrast CT head reveals no acute intracranial hemorrhage or early ischemic changes. His blood pressure is 192/108 mmHg. Which of the following is the most appropriate next step in management?

A

Administer IV tenecteplase immediately without lowering blood pressure

B

Administer IV labetalol to reduce blood pressure below 185/110 mmHg, then administer IV thrombolysis

C

Withhold thrombolysis and allow permissive hypertension up to 220/120 mmHg for 24 hours

D

Initiate dual antiplatelet therapy with aspirin and clopidogrel immediately

Test Your Knowledge

A 58-year-old female experiences a 30-minute episode of left-sided facial drooping and hand weakness that completely resolves prior to arrival at the emergency clinic. Her blood pressure is 152/94 mmHg and capillary glucose is 5.8 mmol/L. Non-contrast head CT is normal. Her calculated ABCD2 score is 5. According to current secondary stroke prevention guidelines, which antiplatelet regimen is most appropriate?

A

Aspirin 81 mg daily monotherapy indefinitely

B

Clopidogrel 75 mg daily monotherapy indefinitely

C

Aspirin 81 mg plus Clopidogrel 75 mg daily for 21 to 90 days, followed by single antiplatelet monotherapy

D

Aspirin 81 mg plus Warfarin with target INR 2.0 to 3.0

Test Your Knowledge

A 42-year-old male presents to the emergency room describing a sudden, explosive headache that began 10 hours ago during physical exertion. He reports nausea and photophobia. On examination, he has neck stiffness. Non-contrast head CT performed 10 hours after symptom onset shows no evidence of subarachnoid blood. What is the most appropriate next step to rule out subarachnoid hemorrhage?

A

Perform a lumbar puncture and evaluate CSF for xanthochromia

B

Discharge home with oral NSAIDs and primary care follow-up

C

Repeat the non-contrast head CT in 24 hours

D

Order an unenhanced MRI of the brain

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