Acute focal neurologic deficit from arterial occlusion causing brain infarction.
Also known as: CVA, cerebral infarction, brain attack, thromboembolic stroke, large vessel occlusion, LVO
Overview
Acute focal neurologic deficit lasting >24 hours (or imaging-confirmed infarction at any duration) caused by interruption of cerebral arterial blood flow with resulting tissue ischemia and infarction.
Epidemiology
Fourth leading cause of death in the US (CDC 2023) and a leading cause of long-term disability. ~87% of all strokes are ischemic. Incidence rises sharply after age 55, doubling each decade.
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Question 1NeurologyMedium
A 72-year-old man comes to the emergency department 8 hours after the sudden onset of a mild right facial droop and mild weakness of the right arm and leg. He has hypertension and hyperlipidemia, takes no antiplatelet or anticoagulant medication, and has no history of gastrointestinal or intracranial bleeding. Pulse is 76/min and fingerstick glucose is 104 mg/dL. He is fully alert with fluent speech; he holds the right arm and the right leg against gravity with mild drift in each, and the National Institutes of Health Stroke Scale score is 3. ECG and continuous telemetry since arrival show normal sinus rhythm. Noncontrast CT of the head shows no hemorrhage, and diffusion-weighted MRI shows a small acute infarct in the left corona radiata. Which of the following is the most appropriate antithrombotic strategy?
AAspirin plus clopidogrel for 21 days, then aspirin alone
BAspirin alone, started now and continued indefinitely
CApixaban alone, started now and continued indefinitely
DIntravenous heparin for 5 days, then aspirin alone
EAspirin plus clopidogrel for 12 months, then aspirin alone
Reveal answer & full explanation
Correct answer: A — Aspirin plus clopidogrel for 21 days, then aspirin alone
AAspirin plus clopidogrel for 21 days, then aspirin alone✓
BAspirin alone, started now and continued indefinitely
CApixaban alone, started now and continued indefinitely
DIntravenous heparin for 5 days, then aspirin alone
EAspirin plus clopidogrel for 12 months, then aspirin alone
Why Aspirin plus clopidogrel for 21 days, then aspirin alone is correct
Sudden focal deficits with a small acute infarct on diffusion-weighted imaging and no hemorrhage on CT make this an acute ischemic stroke, and an NIHSS score of 3 with sinus rhythm makes it a minor noncardioembolic stroke
For minor ischemic stroke with an NIHSS score of 3 or less, or high-risk TIA with an ABCD2 score of 4 or more, aspirin plus clopidogrel is started early, ideally within 12 to 24 hours of symptom onset; at 8 hours he is well inside that window
CHANCE and POINT each cut 90-day recurrent stroke by roughly a quarter to a third compared with aspirin alone, and the benefit is concentrated in the first 2 to 3 weeks, when recurrence risk peaks
Guidelines accept 21 to 90 days of the pair, and 21 days is the usual choice because the 21-day course in CHANCE added no excess major bleeding, whereas in the 90-day course in POINT the ischemic benefit was confined to the early weeks while major bleeding kept accruing
He is antithrombotic-naive with no gastrointestinal or intracranial bleeding history, so he has no feature that would make a second antiplatelet agent unsafe
The second agent is then dropped and a single antiplatelet agent is continued indefinitely; typical dosing is an aspirin load of 160 to 325 mg with a clopidogrel load of 300 to 600 mg, then aspirin 81 mg plus clopidogrel 75 mg daily
Why the others are wrong
Aspirin alone, started now and continued indefinitely - aspirin monotherapy is exactly the comparator arm that CHANCE and POINT beat, and it is the right therapy only after the second agent comes off; with no bleeding history to weigh against it, starting one agent today forfeits the first 3 weeks, when recurrence risk is highest and two agents carry a Class 1 recommendation (the trap is the reflex to give aspirin and stop there)
Aspirin plus clopidogrel for 12 months, then aspirin alone - the right two drugs for a duration no stroke guideline supports: past the first weeks the reduction in recurrent stroke flattens while major bleeding keeps accumulating, so the second agent comes off between day 21 and day 90; 12 months of dual therapy belongs to coronary stenting (the trap is importing the post-stent DAPT duration into stroke)
Apixaban alone, started now and continued indefinitely - oral anticoagulation is the answer when the mechanism is cardioembolic, and his ECG and continuous telemetry show sinus rhythm with a small deep infarct; anticoagulation does not lower early recurrence in noncardioembolic stroke and it raises symptomatic intracranial hemorrhage (the trap is treating an acute arterial thrombus the way a cardioembolic clot is treated)
Intravenous heparin for 5 days, then aspirin alone - early heparin was once the reflex for a fresh infarct, which is why it tempts while he is still inside the first day; trials of early heparin and heparinoids found that any fall in early recurrence was offset by more intracranial and extracranial bleeding with no better outcome, so guidelines advise against urgent anticoagulation to prevent early recurrence or halt worsening, and the first weeks belong to dual antiplatelet therapy (the trap is reaching for an anticoagulant to stop an evolving stroke)
Additional high-yield points
The deficit, not the clock, is what keeps him from a thrombolytic: he is 8 hours out, past the standard 4.5-hour window, and the 2026 AHA/ASA guideline allows IV thrombolysis from 4.5 to 9 hours only when automated perfusion imaging shows salvageable penumbra, but at any time point a mild nondisabling deficit is rated no benefit for IV thrombolysis and short-course dual antiplatelet therapy is given instead; thrombectomy is the reperfusion option the clock still allows out to 24 hours but it applies to a large-vessel occlusion rather than a small deep infarct like his, and when a thrombolytic is given a single tenecteplase 0.25 mg/kg bolus up to 25 mg is an accepted alternative to an alteplase infusion, with only one thrombolytic ever given
MATCH and SPS3 are the trials behind the bleeding ceiling on dual therapy, and SPS3 enrolled only recent lacunar infarcts; both began the pair weeks to months after the index event and continued it for 18 months to about 3 years, so they bound how long two agents are given rather than whether the short course is started, and a small deep infarct with an NIHSS score of 3 or less still gets the 21-day course
Short-course dual antiplatelet therapy applies to patients who did not receive thrombolysis; after IV thrombolysis antiplatelet agents are withheld for 24 hours and a follow-up head CT is obtained first
Ticagrelor plus aspirin for 30 days (THALES) is an alternative short course, and CYP2C19 loss-of-function carriers derive less benefit from clopidogrel (CHANCE-2), but ticagrelor carries a weaker recommendation and is not a co-equal first choice
Prolonged rhythm monitoring to hunt occult atrial fibrillation belongs to cryptogenic and embolic strokes rather than to a clear small-vessel lacune like this one; wherever atrial fibrillation is found the regimen becomes an oral anticoagulant, with the start timed to infarct size, within a few days for a small infarct and later for a large one, and never as an urgent heparin infusion
Carotid endarterectomy within 2 weeks is added to antiplatelet therapy for a cortical stroke ipsilateral to 70 to 99 percent internal carotid stenosis; a small deep infarct like this one is small-vessel disease, not a carotid lesion
The rest of secondary prevention is high-intensity statin therapy, blood pressure below 130/80 mm Hg, and glycemic and smoking-cessation management
Question 2NeurologyMedium
A 65-year-old man with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) has had a fourth lacunar stroke in 3 years despite aspirin therapy. MRI of the brain shows extensive white matter lesions. Which of the following is the most appropriate management strategy?
ABlood pressure control plus antiplatelet
BEscalation to high-dose aspirin therapy
CDual antiplatelet with clopidogrel-aspirin
DWarfarin anticoagulation therapy
ELong-term nimodipine prophylaxis
Reveal answer & full explanation
Correct answer: A — Blood pressure control plus antiplatelet
ABlood pressure control plus antiplatelet✓
BEscalation to high-dose aspirin therapy
CDual antiplatelet with clopidogrel-aspirin
DWarfarin anticoagulation therapy
ELong-term nimodipine prophylaxis
Why blood pressure control plus antiplatelet is correct
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is caused by a NOTCH3 mutation and is a hereditary small vessel disease causing recurrent lacunar strokes and subcortical dementia.
The cornerstone of management is aggressive blood pressure control (target <130/80), which is the most important intervention.
Antiplatelet therapy (aspirin) and smoking cessation are also recommended.
Why the others are wrong
Dual antiplatelet with clopidogrel-aspirin — No proven benefit of dual antiplatelet therapy in CADASIL, and the microbleed burden raises hemorrhage risk; over-treatment trap.
Warfarin anticoagulation therapy — No proven benefit; anticoagulation is not standard of care in CADASIL and increases bleeding risk; confused-with-cardioembolic-stroke trap.
Long-term nimodipine prophylaxis — Nimodipine is a 21-day course after aneurysmal subarachnoid hemorrhage to limit delayed cerebral ischemia; it has no established role in CADASIL, does not prevent lacunar infarcts, and lacks the antiplatelet half of the correct strategy; right-drug-wrong-disease trap.
Escalation to high-dose aspirin therapy — recurrence despite aspirin invites the idea that the dose was too low, but trials comparing low and high aspirin doses show no added stroke protection at higher doses, only more gastrointestinal toxicity, and recurrent lacunes in CADASIL reflect progressive small vessel disease, where aggressive blood pressure control is the cornerstone; aspirin-failure-dose-escalation trap.
Additional high-yield points
Genetic counseling is recommended for family members given the autosomal dominant inheritance.
Prognosis involves progressive cognitive decline and disability.
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Other: hypercoagulable states (antiphospholipid syndrome, malignancy), oral contraceptives + smoking in women >35, cocaine/methamphetamine use, recent MI with mural thrombus, PFO (paradoxical embolism)
Pathophysiology
Occlusion of a cerebral artery by thrombus (in-situ atherosclerosis) or embolus (cardioembolic or artery-to-artery) reduces regional cerebral blood flow below the threshold for neuronal function (~20 mL/100 g/min) and then below the threshold for cellular integrity (~10 mL/100 g/min). The irreversibly infarcted core is surrounded by an ischemic penumbra of stunned but viable tissue maintained by collateral flow. Reperfusion within the therapeutic window can salvage the penumbra; without it the infarct expands.
Dominant (left) MCA aphasias: Broca (nonfluent, effortful speech, comprehension intact, poor repetition; inferior frontal gyrus, superior division) vs Wernicke (fluent, paraphasic, poor comprehension, often unaware; superior temporal gyrus, inferior division) vs global (both; proximal M1) vs conduction (poor repetition only; arcuate fasciculus)
Classic findings
Sudden onset focal deficit referable to a single vascular territory; NIHSS quantifies severity (0-42).
Differential diagnosis
Hemorrhagic stroke (ICH) — Indistinguishable clinically — non-contrast head CT differentiates; headache, vomiting, and rapidly declining consciousness more common with ICH
TIA — Same clinical syndrome but symptoms resolve completely, usually <1 hour; no infarction on imaging
Seizure with Todd paralysis — Postictal focal weakness lasting minutes to ~48 h; witnessed convulsion or tongue bite favor this
Hypoglycemia — Can mimic any focal deficit; fingerstick glucose mandatory before tPA — D50 if <60 mg/dL
Complex migraine (hemiplegic migraine) — Younger patient, headache prominent, spreading march of symptoms over minutes, prior similar episodes
Conversion disorder / functional — Inconsistent exam, non-anatomic distribution, normal imaging — diagnosis of exclusion
Brain tumor / abscess — Subacute progression over days-weeks; CT/MRI with contrast diagnostic
Bell palsy — Isolated peripheral CN VII palsy involving the forehead; central facial sparing involves lower face only
Diagnostic workup
Diagnostic criteria
Clinical syndrome of acute focal neurologic deficit with hemorrhage excluded on non-contrast CT (often normal in the first hours); infarction is confirmed by MRI DWI restriction or later CT hypodensity, or by a deficit persisting >24 h.
Labs
Fingerstick glucose immediately (rule out hypoglycemia)
CBC, platelets, PT/INR, PTT, BMP, troponin
Lipid panel, A1c — for secondary prevention
Pregnancy test in women of childbearing age
Imaging
Non-contrast head CT within 20 min of arrival — excludes hemorrhage (essential before tPA)
CT angiography head and neck — identifies large vessel occlusion candidates for thrombectomy
CT perfusion or MR diffusion/perfusion — quantifies core vs penumbra in the extended window (DAWN, DEFUSE-3); under AHA/ASA 2026, ASPECTS on CT can also select 6-24 h candidates, so a perfusion mismatch is not required for everyone
MRI with DWI — most sensitive for acute infarction (positive within minutes)
Carotid duplex, transthoracic or transesophageal echo, telemetry/Holter (AFib detection) for etiology; if cryptogenic or embolic-appearing (ESUS), ≥30-day ambulatory monitor or implantable loop recorder to find paroxysmal AFib (EMBRACE, CRYSTAL-AF) rather than empiric anticoagulation (NAVIGATE ESUS, RE-SPECT ESUS)
Early non-contrast CT is often normal in the first hours (clear hypodensity evolves over ~6-24 h); early ischemic signs include loss of gray-white differentiation, insular ribbon sign, sulcal effacement, and the hyperdense MCA sign (acute intraluminal thrombus suggesting LVO, prompting CTA)
Diagnostic algorithm
flowchart TD
A[Acute focal deficit<br/>Last known well documented] --> B[Glucose + NIHSS]
B --> C[Non-contrast head CT<br/>≤20 min]
C --> D{Hemorrhage?}
D -->|Yes| E[Hemorrhagic pathway<br/>BP control, reverse anticoag]
D -->|No| F{"Disabling deficit, no contraindications,<br/>and ≤4.5 h or 4.5-9 h with perfusion penumbra?"}
F -->|Yes| G[IV tenecteplase 0.25 mg/kg<br/>or alteplase 0.9 mg/kg]
F -->|No| H[No thrombolysis]
G --> I[CTA head/neck]
H --> I
I --> J{LVO present?}
J -->|Yes, ≤24 h + favorable imaging| K[Mechanical thrombectomy]
J -->|No| L[Stroke unit admission<br/>workup etiology]
K --> L
L --> M["Swallow screen, then aspirin within 24-48 h<br/>(24 h after IVT); DAPT if minor stroke"]
Acute ischemic stroke triage — time-critical pathway from arrival to reperfusion therapy.
Treatment
First-line
tPA dosing — alteplase 0.9 mg/kg IV (max 90 mg), 10% as bolus over 1 min, remainder over 60 min, if within 4.5 h of last known well and no contraindications (NINDS, ECASS III); 4.5-9 h from last known well or wake-up stroke only if automated perfusion imaging shows salvageable penumbra (EXTEND; AHA/ASA 2026); mild nondisabling deficits get DAPT, not thrombolysis
Tenecteplase 0.25 mg/kg IV single bolus (max 25 mg) — recommended equally with alteplase within 4.5 h (AHA/ASA 2026; FDA-approved for stroke 2025); the single bolus simplifies transfer and bridging to thrombectomy
Mechanical thrombectomy (AHA/ASA 2026) for ICA or M1 occlusion with NIHSS ≥6 and prestroke mRS 0-1: recommended at 0-6 h with ASPECTS 3-10 and at 6-24 h with ASPECTS ≥6, and in selected large-core patients (age <80, no significant mass effect) at 6-24 h with ASPECTS 3-5; reasonable in selected patients at 0-6 h with ASPECTS 0-2 (age <80, no significant mass effect). Not every large infarct qualifies, and every candidate needs urgent stroke-team assessment; basilar artery occlusion with NIHSS ≥10 within 24 h also benefits (ATTENTION, BAOCHE); give IV thrombolysis first if eligible, without delaying thrombectomy
BP target: <185/110 before tPA; <180/105 for 24 h after tPA; otherwise permissive HTN <220/120 unless end-organ injury
Aspirin 325 mg within 24-48 h (delay 24 h after tPA)
DVT prophylaxis (mechanical immediately; chemical after 24 h if no hemorrhage)
Second-line / adjunct
Dual antiplatelet therapy (aspirin + clopidogrel) in patients not given IV thrombolysis: minor noncardioembolic stroke (NIHSS ≤3) or high-risk TIA (ABCD2 ≥4) started within 24 h (CHANCE, POINT), and it may also be used for NIHSS 4-5 or started up to 72 h (INSPIRES; AHA/ASA 2026); usually 21 days (up to 90), then single antiplatelet
Anticoagulation for cardioembolic stroke from AFib: DOAC (apixaban, rivaroxaban, dabigatran, edoxaban) preferred over warfarin (warfarin if mechanical valve or moderate-severe mitral stenosis); start early by infarct size, within ~48 h for minor/moderate stroke and ~day 6-7 for large infarcts (ELAN, OPTIMAS); no urgent heparin bridge
Carotid endarterectomy or stenting if ipsilateral carotid stenosis 70-99% (symptomatic) — within 2 weeks
Hemorrhagic transformation (especially after tPA, large infarct, or reperfusion)
Cerebral edema with herniation (large MCA or cerebellar stroke, peaks days 2-5): malignant MCA infarct → decompressive hemicraniectomy for deterioration within 48 h despite medical therapy, strongest evidence if ≤60 y (osmotherapy and hyperventilation are only a bridge); cerebellar infarct → EVD for obstructive hydrocephalus and suboccipital decompressive craniectomy for brainstem compression or deterioration
Aspiration pneumonia (screen swallow before any oral intake)
BE-FAST: Balance, Eyes, Face, Arm, Speech, Time — public stroke recognition mnemonic.
tPA absolute contraindications: ICH ever, recent (<3 mo) head trauma/stroke/intracranial surgery, active bleeding, platelets <100k, INR >1.7, BP >185/110 refractory to treatment.
Wake-up strokes with favorable MRI mismatch (DWI positive, FLAIR negative — 'WAKE-UP' trial) may still be tPA candidates.
Posterior circulation stroke is frequently misdiagnosed as labyrinthitis; HINTS exam (Head Impulse, Nystagmus, Test of Skew) distinguishes central from peripheral vertigo.
Young stroke workup: hypercoagulable panel, vasculitis serologies, drug screen, echo with bubble study for PFO, vertebral artery dissection imaging.
References
AHA/ASA 2026 — 2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke (Prabhakaran et al., Stroke 2026;57:e316-e436)
NINDS Trial — Tissue Plasminogen Activator for Acute Ischemic Stroke (NINDS rt-PA Study Group, NEJM 1995)
ECASS III — Thrombolysis with Alteplase 3 to 4.5 Hours after Acute Ischemic Stroke (Hacke et al., NEJM 2008)
DAWN Trial — Thrombectomy 6 to 24 Hours after Stroke with a Mismatch (Nogueira et al., NEJM 2018)
DEFUSE 3 — Thrombectomy for Stroke at 6 to 16 Hours with Selection by Perfusion Imaging (Albers et al., NEJM 2018)
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