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Neurology›Condition·Updated Jul 11, 2026·v1

Ischemic Stroke

Ischemic stroke is a time-sensitive emergency requiring rapid reperfusion with IV thrombolysis (alteplase or tenecteplase) and/or endovascular thrombectomy for large-vessel occlusion. Etiologic classification (TOAST) guides secondary prevention: DAPT for noncardioembolic minor stroke, DOACs for atrial fibrillation, and high-intensity statins for all. Early dysphagia screening, cardiac monitoring, and rehabilitation improve outcomes. The global burden is rising, driven by uncontrolled hypertension, diabetes, and smoking.

High Evidence434 references·2,883 words·12 min read·v1
ischemic strokeacute stroke managementthrombolysisendovascular thrombectomysecondary preventionTOAST classificationNIHSSmodified Rankin Scale

Quick Reference

RxDrug of choiceAlteplase 0.9 mg/kg IV (max 90 mg) within 4.5 hours; tenecteplase 0.25 mg/kg IV bolus is an alternative, especially for LVO.
AltAlternativesTenecteplase 0.25 mg/kg IV bolus; tirofiban 0.4 μg/kg/min for 30 min then 0.1 μg/kg/min for 24 h after thrombolysis; clopidogrel + aspirin for DAPT; DOACs (rivaroxaban, apixaban, edoxaban) for AF.
⊘AvoidThrombolysis if symptom onset >4.5 h (unless favorable imaging), INR >1.7, platelets <100,000, recent major surgery, active bleeding. EVT contraindicated if large core with no penumbra or poor collateral status.
DxTest of choiceNoncontrast CT head (first test to exclude hemorrhage) followed by CTA + CTP (or MRI DWI + PWI) to identify LVO and salvageable tissue.
ScKey scoreNIHSS (severity), ASPECTS (early ischemic changes on CT), modified Rankin Scale (functional outcome), CHA₂DS₂-VASc (AF stroke risk).
→When to referFor EVT: LVO within 24 h with favorable imaging. For carotid revascularization: symptomatic stenosis ≥50% or asymptomatic ≥70%. For PFO closure: cryptogenic stroke with high-risk PFO. For rehabilitation: all patients with residual deficits.
Time is brain: golden-hour thrombolysis (NNT 2.6) and EVT for LVO (NNT 3-10) are the most powerful interventions. Etiology-guided secondary prevention with DAPT, DOACs, and statins reduces recurrence by 50-70%.
Ischemic stroke is CNS infarction due to ischemia, accounting for 87% of strokes. Acute management focuses on reperfusion with thrombolysis and thrombectomy. Etiologic classification guides secondary prevention. This reference covers pathophysiology, diagnosis, acute and long-term management, complications, and special populations.

Overview and Recommendations

Background

  • •Ischemic stroke is defined as brain, spinal cord, or retinal cell death attributable to ischemia, confirmed by neuropathology, neuroimaging, or clinical evidence of permanent injury. It accounts for approximately 87% of the 13.7 million new strokes worldwide each year and is the second-leading cause of death globally, with 3.29 million deaths in 2019 projected to rise to 4.90 million by 2030.
  • •The etiologic classification, large-artery atherosclerosis, cardioembolism, small-vessel occlusion, other determined cause, and cryptogenic (TOAST), is essential because it dictates acute treatment and secondary prevention. Cardioembolic strokes carry the highest 30-day case fatality (28%) and 6-month dependency or death (62%).
  • •The ischemic cascade begins within seconds of flow cessation: cerebral blood flow below 10-15 mL/100 g/min triggers ATP depletion, cytotoxic edema, glutamate excitotoxicity, and calcium-mediated cell death. The penumbra, tissue at risk but still viable, expands at an average rate of 5.4 mL/h in large-vessel occlusion, creating a time-dependent window for reperfusion.
  • •Immunothrombosis amplifies injury: neutrophil extracellular traps (NETs) stabilize thrombi and cause no-reflow after reperfusion. Interleukin-6 levels predict recurrence in large-artery and small-vessel subtypes, and viral transcripts (CMV, EBV) are elevated in stroke blood, suggesting a role for chronic infection in pathogenesis.
  • •The tissue-based definition of transient ischemic attack (TIA), transient neurologic dysfunction without infarction, replaced the time-based definition. After TIA, the pooled risk of subsequent ischemic stroke is 2.4% within 2 days and 4.7% within 90 days, making urgent evaluation and prevention critical.
  • •Key prognostic tools include the (NIHSS) for severity grading and the (mRS) for functional outcome. The dynamic continuum from benign oligemia to leaky core underpins reperfusion decision-making and explains why some patients with large cores still benefit from thrombectomy.

Evaluation

  • •Suspect ischemic stroke in any patient with acute onset of focal neurologic deficits, unilateral weakness, sensory loss, aphasia, hemianopia, ataxia, or vertigo, especially when onset is witnessed and maximal at onset. Nonfocal symptoms (headache, altered consciousness) are more common in women and increase the risk of misdiagnosis.
  • •Ask about the exact time of symptom onset or last known well, which determines eligibility for thrombolysis. In wake-up stroke (15-25% of cases), the median time from last seen well to arrival is 288 minutes, and advanced imaging is required to select candidates for reperfusion.
  • •Examine using the NIHSS to quantify severity: mild (0-4), moderate (5-14), severe (≥15). Perform a focused neurologic exam including cranial nerves, motor/sensory function, coordination, and language. Assess for stroke mimics: postictal Todd paresis, migraine aura, hypoglycemia, functional disorder.
  • •Order a noncontrast CT head immediately to exclude intracerebral hemorrhage. CT angiography (CTA) identifies large-vessel occlusion (LVO), the trigger for endovascular thrombectomy. CT perfusion (CTP) or MRI perfusion quantifies ischemic core and penumbra; the Target Mismatch profile (core <70 mL, mismatch >10 mL, ratio >1.2) selects patients for late-window treatment.
  • •MRI with diffusion-weighted imaging (DWI) is the gold standard for diagnosis, with ~93% sensitivity within 12 hours. A negative DWI does not rule out stroke, posterior circulation ischemia has 5-fold higher odds of being DWI-negative. The DWI-FLAIR mismatch (DWI hyperintense, FLAIR negative) identifies patients with unknown onset who benefit from thrombolysis.
  • •Obtain routine labs: CBC, creatinine, glucose, coagulation profile, troponin. Point-of-care glucose excludes hypoglycemic mimic. Consider GFAP testing (portable device) to distinguish hemorrhage from ischemia when CT is equivocal, GFAP <30 pg/mL with NIHSS >6 has 100% NPV for intracerebral hemorrhage.
  • •Diagnostic criteria are clinical: acute focal deficit with imaging evidence of infarction or, if imaging is negative, a clinical syndrome consistent with stroke. The tissue-based definition means any clinical syndrome with infarction on imaging is stroke, regardless of symptom duration.
  • •Also consider alternative diagnoses: seizure (EEG, hyperperfusion on rTmax), migraine with aura (gradual spread, headache, normal DWI), CNS tumor (subacute onset, mass effect), CNS infection (fever, CSF pleocytosis). In young adults, screen for Fabry disease, CADASIL, and patent foramen ovale.
  • •Perform cardiac monitoring (telemetry for ≥24 hours) to detect atrial fibrillation. In cryptogenic stroke, implantable loop recorder detects paroxysmal AF in 21% vs 7.5% with conventional monitoring and reduces recurrence (HR 0.32).
  • •Assess dysphagia before any oral intake using a bedside swallow screen. The Predictive Swallowing Score (age, NIHSS, lesion location, aspiration risk, oral impairment) stratifies risk; score ≥8 predicts persistent dysphagia at 7 days with 96% probability.

Management

  • •Initiate intravenous thrombolysis within 4.5 hours of symptom onset: alteplase 0.9 mg/kg (max 90 mg), 10% as bolus, remainder over 60 minutes. Alternatively, tenecteplase 0.25 mg/kg IV bolus (max 25 mg) is noninferior and preferred in patients with LVO. Golden-hour thrombolysis doubles the odds of excellent recovery (NNT 2.6).
  • •For patients presenting 4.5-24 hours after onset with favorable penumbral imaging (core <70 mL, mismatch ratio >1.2), thrombolysis remains beneficial: alteplase improved functional independence in posterior circulation stroke (89.6% vs 72.6%; aRR 1.16). Tenecteplase 0.25 mg/kg also improves reperfusion without excess sICH.
  • •Perform endovascular thrombectomy (EVT) for anterior circulation LVO (ICA, M1-MCA) with ASPECTS ≥6 within 6 hours (NNT 3-10). For ASPECTS 3-5, EVT still improves independent ambulation (RR 1.9) and survival (RR 0.9). EVT is also effective up to 24 hours in patients selected by DAWN/DEFUSE-3 criteria.
  • •For medium-vessel occlusion (M2-MCA, PCA), EVT is not routinely recommended, the ESCAPE-MeVO trial showed no benefit and possible harm (sICH 5.4% vs 2.2%). Individualize for severe deficits and favorable anatomy.
  • •Maintain systolic BP >140 mm Hg during EVT to support collateral flow; after successful reperfusion, target SBP <160 mm Hg. Intensive BP lowering (<120 mm Hg) worsens functional outcomes and quality of life.
  • •After thrombolysis, start antiplatelet therapy at 24 hours if no hemorrhagic transformation. For noncardioembolic minor stroke/TIA, initiate dual antiplatelet therapy (DAPT) within 24-72 hours: clopidogrel 300 mg load + aspirin 100-300 mg, continue for 21-90 days. In CYP2C19 loss-of-function carriers, use ticagrelor 180 mg load + aspirin instead.
  • •Tirofiban infusion (0.4 μg/kg/min for 30 min, then 0.1 μg/kg/min for 24 h) after thrombolysis improves excellent functional outcome (65.9% vs 54.9%; RR 1.20) without increasing sICH. Consider in patients with high-risk noncardioembolic stroke.
  • •For cardioembolic stroke due to atrial fibrillation, start a DOAC (e.g., rivaroxaban 20 mg daily, apixaban 5 mg BID, edoxaban 60 mg daily) within 48 hours to 14 days depending on infarct size. Use the 1-2-3-4-day rule: day 1 after TIA, day 2 after mild stroke (NIHSS 0-7), day 3 after moderate (8-15), day 4 after severe (≥16).
  • •Initiate high-intensity statin (atorvastatin 40-80 mg daily) within 24 hours. Immediate intensive statin (80 mg for 21 days then 40 mg) does not reduce 90-day stroke but improves functional outcome (OR 0.83). Add ezetimibe or PCSK9 inhibitor if LDL ≥70 mg/dL on maximally tolerated statin.
  • •Target blood pressure <130/80 mm Hg for long-term secondary prevention. In the first 72 hours after successful reperfusion, permit mild hypertension (SBP 140-180 mm Hg) to maintain penumbral perfusion.
  • •Avoid non-dihydropyridine CCBs (diltiazem, verapamil) in acute phase. Avoid adding antiplatelet to anticoagulation in AF patients without compelling indication (increases major bleeding without net benefit). Avoid switching a failing DOAC to warfarin, prefer DOAC-to-DOAC or dose adjustment.
  • •Refer for carotid revascularization (CEA or stenting) in symptomatic stenosis ≥50% or asymptomatic ≥70% with favorable anatomy. CREST-2 showed stenting plus medical management reduced 4-year stroke/death (2.8% vs 6.0%; NNT 31).
  • •Refer for PFO closure in selected young patients with cryptogenic stroke and high-risk PFO (RoPE score ≥7, large shunt). Closure reduces recurrent stroke (RR 0.42) but increases new-onset AF (RR 4.59); Amplatzer device preferred.
  • •Monitor for complications: hemorrhagic transformation (sICH 2-8%), malignant cerebral edema (midline shift >11 mm within 20 hours), post-stroke seizures (3% acute, 10-15% late). Use levetiracetam 500-1500 mg/day for seizures; do not use primary prophylaxis.
  • •Discharge criteria: stable neurologic status, no active bleeding, controlled blood pressure, ability to swallow safely (or feeding tube in place), and follow-up plan for rehabilitation and secondary prevention. Arrange early rehabilitation (within 30 days) including physical, occupational, and speech therapy.

Board Review — High Yield

  • •Time is brain, Every 30-minute reduction in door-to-needle time increases odds of mRS 0-1 by 1.8%; golden-hour thrombolysis NNT = 2.6.
  • •TOAST classification, Five subtypes: large artery, cardioembolic, small vessel, other, undetermined. Cardioembolic has highest mortality (28% at 30 days).
  • •Core vs penumbra, Core is irreversibly infarcted; penumbra is salvageable. Target mismatch: core <70 mL, mismatch >10 mL, ratio >1.2 for late-window treatment.
  • •DWI-FLAIR mismatch, DWI hyperintense, FLAIR negative indicates stroke within ~4.5 hours; used to select unknown-onset patients for thrombolysis (WAKE-UP trial).
  • •DAPT for minor stroke, Clopidogrel + aspirin within 24-72 hours reduces 90-day stroke recurrence (HR 0.68-0.79). In CYP2C19 LoF carriers, ticagrelor + aspirin is superior.
  • •DOAC over warfarin, For AF-related stroke, DOACs reduce intracranial hemorrhage (0.5% vs 0.7% for rivaroxaban). Early initiation (day 3-4) is optimal.
  • •EVT for large core, ASPECTS 3-5 still benefits from EVT: improved independent ambulation (RR 1.9) and survival (RR 0.9).
  • •Post-stroke epilepsy, 11% at 5 years; early EEG with epileptiform activity raises risk to 42%. SeLECT-EEG model outperforms clinical scores.
  • •Stroke-heart syndrome, 11% develop ACS, 8.8% new AF within 4 weeks. Telemetry for ≥24 hours is mandatory.
  • •Dysphagia screening, Perform before any oral intake; Predictive Swallowing Score ≥8 predicts failure at day 7 with 96% probability.

Deep Dive — Evidence Details

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