Clinical meaning
Acute ischemic stroke results from arterial occlusion (most commonly middle cerebral artery territory) causing cerebral ischemia. The ischemic core receives <10-12 mL/100g/min blood flow and undergoes irreversible necrosis within minutes (excitotoxic cell death from glutamate release, calcium influx, and mitochondrial failure). Surrounding the core is the ischemic penumbra — functionally impaired but structurally intact tissue receiving 12-22 mL/100g/min. The penumbra represents salvageable brain tissue that is the TARGET of acute stroke treatment. Without reperfusion, the penumbra progressively recruits into the infarct core over hours ('time is brain' — 1.9 million neurons die per minute of untreated large vessel occlusion). Reperfusion strategies: (1) IV alteplase (tPA): within 4.5 hours of symptom onset; dose 0.9 mg/kg (max 90 mg), 10% as bolus, 90% infused over 60 minutes. (2) Mechanical thrombectomy: endovascular clot retrieval for large vessel occlusion (LVO) in anterior circulation, up to 24 hours from symptom onset IF perfusion imaging shows salvageable penumbra (DAWN and DEFUSE-3 trials extended the window). CT perfusion or MRI diffusion-perfusion mismatch identifies the penumbra: the mismatch between the infarcted core (irreversible) and the hypoperfused tissue (salvageable) guides treatment decisions beyond traditional time windows. Reperfusion injury occurs when restored blood flow generates reactive oxygen species (ROS) and inflammatory mediators, potentially worsening edema and causing hemorrhagic transformation. The NIHSS (National Institutes of Health Stroke Scale) quantifies stroke severity and guides treatment decisions: NIHSS ≥6 suggests LVO — activate thrombectomy pathway.