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Vascular Neurology›Condition·Updated Apr 17, 2026·v1

Acute Ischemic Stroke

Acute Ischemic Stroke management centers on rapid identification and reperfusion of salvageable brain tissue. Evaluation requires immediate NCCT to rule out hemorrhage, followed by CTA/CTP to identify large vessel occlusions. First-line treatment is IV Tenecteplase within 4.5 hours, with Mechanical Thrombectomy indicated for LVOs up to 24 hours. Secondary prevention is tailored to the TOAST subtype, emphasizing DAPT for minor strokes and DOACs for atrial fibrillation.

High Evidence113 references·1,037 words·5 min read·v1
StrokeNeurologyEmergency MedicineThrombectomyThrombolysis

Quick Reference

RxDrug of choiceTenecteplase (0.25 mg/kg IV bolus, max 25 mg)
AltAlternativesAlteplase (0.9 mg/kg IV, max 90 mg), Aspirin, Clopidogrel
⊘AvoidAnticoagulants within 24 hours of thrombolysis; SBP >185/110 mmHg during acute reperfusion
DxTest of choiceMRI with DWI (most sensitive); NCCT (fastest for ruling out hemorrhage)
ScKey scoreNIHSS (severity), ABCD2 (TIA risk), mRS (90-day outcome)
→When to referSuspected Large Vessel Occlusion (LVO) for mechanical thrombectomy; Malignant MCA syndrome for neurosurgery
Time is brain; prioritize rapid neuroimaging and reperfusion via thrombolysis or thrombectomy while maintaining strict blood pressure control.
Acute Ischemic Stroke (AIS) is a medical emergency characterized by sudden focal neurological deficits resulting from the interruption of cerebral blood supply. Modern management has shifted from a strictly time-based approach to a tissue-based paradigm, utilizing advanced neuroimaging to identify the ischemic penumbra—functionally impaired but salvageable brain tissue. Rapid reperfusion remains the cornerstone of therapy, achieved through intravenous thrombolysis (IVT) and mechanical thrombectomy (MT).

Overview and Recommendations

Background

  • •Define Acute Ischemic Stroke (AIS) as an episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction confirmed by clinical symptoms or neuroimaging evidence of tissue death.
  • •Recognize the TOAST classification system to guide secondary prevention: Large-Artery Atherosclerosis (LAA), Cardioembolism (CE), Small-Vessel Occlusion (SVO/lacunar), Other Determined Etiology (ODE), and Undetermined Etiology (UDE).
  • •Identify the ischemic penumbra as the primary therapeutic target; this is the zone of functionally impaired tissue maintained by that will progress to irreversible infarction (the core) without rapid reperfusion.
  • •Screen for major modifiable risk factors including , diabetes mellitus, and , which significantly increase the hazard ratio for incident stroke.
  • •Distinguish specialized variants such as Embolic Stroke of Undetermined Source (ESUS), which accounts for 17% of cases and often requires intensive cardiac monitoring to detect occult sources like a patent foramen ovale (PFO).

Evaluation

  • •Suspect AIS in any patient presenting with sudden-onset focal deficits; use the FAST-ED or NIHSS (National Institutes of Health Stroke Scale) to quantify severity and localize the vascular territory.
  • •Obtain a fingerstick glucose immediately to rule out hypoglycemia, the most common metabolic stroke mimic, which can perfectly replicate focal neurological deficits.
  • •Order a non-contrast computed tomography (NCCT) of the head as the first-line imaging modality to exclude and identify early ischemic changes.
  • •Look for the Hyperdense Middle Cerebral Artery Sign (HMCAS) on NCCT, which indicates an erythrocyte-rich thrombus and suggests a high likelihood of large vessel occlusion (LVO).
  • •Perform CT Angiography (CTA) from the aortic arch to the vertex to identify the site of arterial occlusion and evaluate the robustness of collateral vessels.
  • •Utilize CT Perfusion (CTP) or MRI Diffusion-Weighted Imaging (DWI) in patients presenting in the 6–24 hour window or with an unknown time of onset to identify a mismatch between the small infarct core and the larger salvageable penumbra.
  • •Apply the DWI-FLAIR mismatch principle for 'wake-up' strokes: a positive DWI lesion without a corresponding FLAIR signal suggests the stroke occurred within the last 4.5 hours, potentially allowing for thrombolysis.
  • •Calculate the ABCD2 score (Age, Blood pressure, Clinical features, Duration, Diabetes) for patients with (TIA) to risk-stratify for imminent stroke.
  • •Order baseline laboratory tests including coagulation studies, lipid profiles, and the CONUT score (Controlling Nutritional Status) to assess physiological reserve and vascular risk.
  • •Monitor for Early Neurological Deterioration (END), defined as an NIHSS increase of ≥2 points within the first 7 days, which may indicate re-occlusion or hemorrhagic transformation.

Management

  • •Administer Tenecteplase 0.25 mg/kg (maximum 25 mg) as a single IV bolus for eligible patients within 4.5 hours of symptom onset; it is preferred over alteplase for its higher fibrin specificity and ease of administration.
  • •Initiate Mechanical Thrombectomy (MT) for patients with LVO (ICA or M1/M2 segments of the MCA) within 6 hours of onset, or up to 24 hours if perfusion imaging shows salvageable tissue.
  • •Maintain blood pressure <185/110 mmHg prior to thrombolysis and <180/105 mmHg for at least 24 hours following treatment to minimize the risk of .
  • •Optimize post-recanalization blood pressure: for patients with successful reperfusion (mTICI 2c/3), target a systolic blood pressure (SBP) of 90–120 mmHg using Clevidipine 1–2 mg/hr IV titration.
  • •Start Dual Antiplatelet Therapy (DAPT) with Aspirin 100 mg and Clopidogrel 75 mg daily for 21–90 days in patients with minor stroke (NIHSS ≤3) or high-risk TIA who did not receive thrombolysis.
  • •Initiate anticoagulation for -related strokes; early initiation (within 4 days) is generally safe for minor-to-moderate strokes, while larger infarcts may require a 7–14 day delay.
  • •Administer high-intensity statins (e.g., Atorvastatin 80 mg daily) for all patients with evidence of atherosclerosis, regardless of baseline LDL levels.
  • •Manage hyperglycemia by maintaining blood glucose between 140–180 mg/dL; avoid aggressive correction to <110 mg/dL due to the risk of secondary brain injury from hypoglycemia.
  • •Refer for urgent decompressive hemicraniectomy in patients <60 years old with malignant MCA syndrome (large-volume infarct with midline shift) within 48 hours of onset.
  • •Avoid the use of prophylactic anticonvulsants; however, treat clinical seizures promptly with agents like Levetiracetam 500–1000 mg BID.
  • •Delay non-cardiac surgery for at least 3 months post-stroke whenever possible to reduce the risk of perioperative recurrent events.
  • •Screen for and treat stroke-associated pneumonia (SAP) and dysphagia; maintain NPO status until a formal swallow evaluation is completed.

Board Review — High Yield

  • •Hyperdense MCA sign — A high-attenuation signal on NCCT representing an acute thrombus in the M1 segment.
  • •DWI-FLAIR Mismatch — Presence of a DWI lesion without FLAIR signal, indicating a stroke duration <4.5 hours.
  • •Penumbra — Ischemic tissue that is functionally silent but structurally intact, salvageable by reperfusion.
  • •ABCD2 Score — Used to predict the 2-day risk of stroke after a TIA; a score of 6-7 indicates high risk.
  • •Malignant MCA Syndrome — Rapidly progressive cerebral edema following large MCA territory infarcts; requires hemicraniectomy.
  • •Tenecteplase vs. Alteplase — Tenecteplase is more fibrin-specific and has a longer half-life, allowing for bolus dosing.
  • •Todd's Paralysis — A focal neurological deficit following a seizure; a key stroke mimic.
  • •mTICI Score — The standard for grading reperfusion after thrombectomy; mTICI 2b, 2c, and 3 are considered successful.

Deep Dive — Evidence Details

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