Stroke Iskemik
Published on August 7, 2026
Risk Factors
Hypertension, diabetes mellitus, atrial fibrillation, dyslipidemia, smoking, obesity, prior stroke/TIA, carotid stenosis, hypercoagulable states, sickle cell disease
Etiology
Thrombotic or embolic occlusion of a cerebral artery; subtypes include large artery atherosclerosis, cardioembolism, small vessel (lacunar), cryptogenic, and other determined causes (TOAST classification)
Presentation
Sudden-onset focal neurological deficit: unilateral weakness, speech difficulty, facial droop, visual field loss, sensory loss; onset during rest or activity, any time of day
Classic Exam
Contralateral hemiparesis, hemisensory loss, homonymous hemianopia, aphasia (dominant hemisphere), neglect (non-dominant hemisphere), dysarthria, ataxia (posterior circulation); NIHSS scoring for severity
Diagnostics
Non-contrast CT head (rule out hemorrhage); CT angiography (detect large vessel occlusion); CT perfusion or MRI DWI/perfusion (penumbra assessment); blood glucose mandatory before thrombolysis
Management
IV thrombolysis (alteplase 0.9 mg/kg or tenecteplase 0.25 mg/kg) within the appropriate time window; endovascular thrombectomy for large vessel occlusion up to 24 hours; aspirin 160-325 mg within 24-48 hours if no thrombolysis; blood pressure control; secondary prevention
Keywords
"Sudden onset," "worst headache" (for SAH, not ischemic), "wake-up stroke," "large vessel occlusion," "time is brain," "door-to-needle," "mismatch," "penumbra," "NIHSS," "ASPECTS score"
01Pathophysiology
Ischemic stroke accounts for 80 to 85% of all stroke cases and results from the obstruction of blood flow through a cerebral artery, leading to oxygen and glucose deprivation in the downstream territory. The obstruction can take the form of a thrombus (local clot formation at a site of atherosclerotic plaque) or an embolus (a clot originating elsewhere, most commonly the heart or proximal large arteries).
The ischemic cascade begins within seconds of arterial occlusion. The core of the infarct undergoes irreversible neuronal death due to energy failure, loss of ionic homeostasis, glutamate excitotoxicity, and calcium influx. Surrounding the core is the ischemic penumbra, a region of critically hypoperfused but still viable brain tissue. This penumbra is the therapeutic target: if blood flow is restored in time, these neurons can be salvaged. If not, the penumbra progressively converts into infarcted tissue. This is the basis of the principle "time is brain."
Large vessel occlusion (LVO) involves arteries such as the internal carotid artery (ICA), the M1 segment of the middle cerebral artery (MCA), the anterior cerebral artery, or the basilar artery. LVO produces severe deficits and is the primary indication for endovascular thrombectomy. Small vessel disease (lacunar infarcts) affects the penetrating arterioles supplying the deep brain structures (basal ganglia, thalamus, internal capsule, pons) and is strongly associated with chronic hypertension.
Cardioembolic strokes, most commonly caused by atrial fibrillation, tend to produce larger cortical infarcts because the embolus lodges in a major branch. The clinical presentation directly reflects the vascular territory involved:
Anterior circulation (carotid territory) produces contralateral motor and sensory deficits, aphasia (if dominant hemisphere), neglect (if non-dominant hemisphere), and homonymous hemianopia.
Posterior circulation (vertebrobasilar territory) produces vertigo, diplopia, dysphagia, dysarthria, ataxia, crossed deficits (ipsilateral cranial nerve palsy with contralateral motor deficit), and in severe cases, "locked-in syndrome" from basilar artery occlusion.
02Classification and Clinical Manifestation
TOAST Classification of Ischemic Stroke Subtypes
Large Artery Atherosclerosis
Mechanism
Atherosclerotic plaque in carotid or intracranial arteries causing thrombosis or artery-to-artery embolism
Typical Presentation
Cortical or large subcortical infarct; stepwise or fluctuating onset
Key Feature
Carotid stenosis >50% on imaging; prior TIA in same territory
Cardioembolism
Mechanism
Emboli from heart (atrial fibrillation, valvular disease, mural thrombus, PFO with paradoxical embolism)
Typical Presentation
Sudden maximal deficit at onset; cortical infarcts, often multiple territories
Key Feature
Atrial fibrillation on ECG; intracardiac thrombus on echocardiography
Small Vessel Occlusion (Lacunar)
Mechanism
Lipohyalinosis or microatheroma of small penetrating arteries
Typical Presentation
Pure motor hemiparesis, pure sensory stroke, ataxic hemiparesis, dysarthria-clumsy hand
Key Feature
Small (<1.5 cm) subcortical infarct on imaging; no cortical signs
Other Determined Etiology
Mechanism
Arterial dissection, vasculitis, hypercoagulable states, sickle cell disease, CVST
Typical Presentation
Variable depending on cause
Key Feature
Identifiable unusual etiology on workup
Cryptogenic
Mechanism
No identifiable cause after full workup
Typical Presentation
Variable
Key Feature
Diagnosis of exclusion; consider occult AF or PFO
Subtype | Mechanism | Typical Presentation | Key Feature |
|---|---|---|---|
Large Artery Atherosclerosis | Atherosclerotic plaque in carotid or intracranial arteries causing thrombosis or artery-to-artery embolism | Cortical or large subcortical infarct; stepwise or fluctuating onset | Carotid stenosis >50% on imaging; prior TIA in same territory |
Cardioembolism | Emboli from heart (atrial fibrillation, valvular disease, mural thrombus, PFO with paradoxical embolism) | Sudden maximal deficit at onset; cortical infarcts, often multiple territories | Atrial fibrillation on ECG; intracardiac thrombus on echocardiography |
Small Vessel Occlusion (Lacunar) | Lipohyalinosis or microatheroma of small penetrating arteries | Pure motor hemiparesis, pure sensory stroke, ataxic hemiparesis, dysarthria-clumsy hand | Small (<1.5 cm) subcortical infarct on imaging; no cortical signs |
Other Determined Etiology | Arterial dissection, vasculitis, hypercoagulable states, sickle cell disease, CVST | Variable depending on cause | Identifiable unusual etiology on workup |
Cryptogenic | No identifiable cause after full workup | Variable | Diagnosis of exclusion; consider occult AF or PFO |
Severity by NIHSS Score
NIHSS Score | Severity |
|---|---|
< 5 | Minor deficit |
5 to 14 | Moderate deficit |
15 to 24 | Severe deficit |
25 to 42 | Very severe deficit |
Per PNPK Stroke 2026, NIHSS is the standard instrument for evaluating the degree of neurological deficit in acute stroke.
03Diagnostic Workup
Non-contrast CT head
Role
Best initial test; rule out hemorrhage, detect early ischemic signs
Class of Recommendation
Class I, Level A
Timing
Within 20 minutes of arrival for reperfusion candidates
CT Angiography (CTA)
Role
Detect LVO (NIHSS ≥ 6 or thrombectomy candidate)
Class of Recommendation
Class I, Level A
Timing
Performed alongside or immediately after non-contrast CT
CT Perfusion (CTP)
Role
Assess penumbra vs. core infarct; guide reperfusion in unknown onset or >6 hours
Class of Recommendation
Class I, Level A
Timing
For patients with LVO and onset >6 hours or unknown onset
MRI with DWI
Role
Alternative to CT; superior for early infarct detection, wake-up stroke (DWI-FLAIR mismatch)
Class of Recommendation
Class I, Level B
Timing
When CT is inconclusive or for wake-up stroke evaluation
MRA / MR Perfusion
Role
Vascular assessment and perfusion when CTA/CTP unavailable or contrast contraindicated
Class of Recommendation
Class I, Level B / Class I, Level A
Timing
As alternative to CTA/CTP
Blood glucose
Role
Mandatory before thrombolysis
Class of Recommendation
Class I, Level B
Timing
Immediate, in the emergency department
CBC, renal function
Role
Routine labs; must not delay thrombolysis
Class of Recommendation
Class I, Level B
Timing
Drawn but results not required before thrombolysis initiation (except glucose)
ECG 12-lead
Role
Detect atrial fibrillation, acute MI; must not delay reperfusion
Class of Recommendation
Class I, Level B
Timing
At presentation
Coagulation (PT, INR, aPTT)
Role
Optional at ED; important if anticoagulant use suspected
Class of Recommendation
Class IIa, Level B
Timing
As indicated
Carotid Doppler
Role
Evaluate carotid stenosis in anterior circulation stroke
Class of Recommendation
Class I, Level B
Timing
Post-stabilization
TCD / TCCD
Role
Monitor vasospasm, detect intracranial stenosis, right-to-left shunt (bubble test)
Class of Recommendation
Class I to IIb, Level B
Timing
Post-stabilization, as indicated
DSA (Cerebral Angiography)
Role
Gold standard for vascular anatomy; can proceed to thrombectomy if LVO found
Class of Recommendation
Class I, Level B
Timing
Pre-intervention or when CTA/MRA inconclusive
TTE / TEE
Role
Evaluate cardiac source of embolism
Class of Recommendation
Class IIa, Level B
Timing
During hospitalization
Holter 24-hour ECG
Role
Detect paroxysmal atrial fibrillation in cryptogenic stroke
Class of Recommendation
Class I, Level B
Timing
During hospitalization
Test | Role | Class of Recommendation | Timing |
|---|---|---|---|
Non-contrast CT head | Best initial test; rule out hemorrhage, detect early ischemic signs | Class I, Level A | Within 20 minutes of arrival for reperfusion candidates |
CT Angiography (CTA) | Detect LVO (NIHSS ≥ 6 or thrombectomy candidate) | Class I, Level A | Performed alongside or immediately after non-contrast CT |
CT Perfusion (CTP) | Assess penumbra vs. core infarct; guide reperfusion in unknown onset or >6 hours | Class I, Level A | For patients with LVO and onset >6 hours or unknown onset |
MRI with DWI | Alternative to CT; superior for early infarct detection, wake-up stroke (DWI-FLAIR mismatch) | Class I, Level B | When CT is inconclusive or for wake-up stroke evaluation |
MRA / MR Perfusion | Vascular assessment and perfusion when CTA/CTP unavailable or contrast contraindicated | Class I, Level B / Class I, Level A | As alternative to CTA/CTP |
Blood glucose | Mandatory before thrombolysis | Class I, Level B | Immediate, in the emergency department |
CBC, renal function | Routine labs; must not delay thrombolysis | Class I, Level B | Drawn but results not required before thrombolysis initiation (except glucose) |
ECG 12-lead | Detect atrial fibrillation, acute MI; must not delay reperfusion | Class I, Level B | At presentation |
Coagulation (PT, INR, aPTT) | Optional at ED; important if anticoagulant use suspected | Class IIa, Level B | As indicated |
Carotid Doppler | Evaluate carotid stenosis in anterior circulation stroke | Class I, Level B | Post-stabilization |
TCD / TCCD | Monitor vasospasm, detect intracranial stenosis, right-to-left shunt (bubble test) | Class I to IIb, Level B | Post-stabilization, as indicated |
DSA (Cerebral Angiography) | Gold standard for vascular anatomy; can proceed to thrombectomy if LVO found | Class I, Level B | Pre-intervention or when CTA/MRA inconclusive |
TTE / TEE | Evaluate cardiac source of embolism | Class IIa, Level B | During hospitalization |
Holter 24-hour ECG | Detect paroxysmal atrial fibrillation in cryptogenic stroke | Class I, Level B | During hospitalization |
The best initial test in any patient with suspected acute stroke is a non-contrast CT of the head. The primary purpose is not to confirm ischemia (which may not be visible in the first 6 to 12 hours) but to exclude hemorrhage. A normal CT in the acute phase does not rule out ischemic stroke (Class I, Level A). PNPK Stroke 2026 states that brain imaging with non-contrast CT or MRI DWI should be completed within 20 minutes of arrival for candidates of IV thrombolysis or mechanical thrombectomy.
Once hemorrhage is excluded, the next step depends on clinical severity. For patients with NIHSS ≥ 6 or clinical suspicion of LVO, CTA is performed to identify the site of occlusion. CTA covers both extracranial and intracranial arteries and is the most commonly used imaging selection tool for thrombectomy.
CT perfusion becomes critical when the time of onset is unknown (wake-up stroke) or the patient presents beyond 6 hours from last known well. CTP differentiates salvageable penumbra from irreversible core infarct by mapping cerebral blood flow, cerebral blood volume, and mean transit time. This mismatch between core and penumbra is the basis for extending the reperfusion window to 24 hours in selected patients.
MRI with DWI is the most sensitive modality for detecting acute ischemia, even within minutes of onset. In wake-up strokes, the DWI-FLAIR mismatch pattern (DWI positive, FLAIR negative) suggests the infarct is likely less than 4.5 hours old, making the patient a potential thrombolysis candidate (Class IIa, Level B-R).
Critically, PNPK Stroke 2026 emphasizes that multimodal imaging must never delay reperfusion therapy (Class III, Level B). Blood glucose is the only lab result that must be available before initiating thrombolysis.
04Management and Treatment
Pre-hospital
Intervention
Stabilize ABC; avoid aggressive BP lowering; avoid antiplatelet/anticoagulant; crystalloid only if dehydrated; avoid glucose-containing fluids (unless hypoglycemia)
Details
Preparation and departure for referral ≤ 30 minutes from decision
Class
Class I, Level A
IV Thrombolysis (onset < 4.5 h)
Intervention
Alteplase 0.9 mg/kg (max 90 mg): 10% IV bolus over 1 min, remainder infused over 60 min
Details
For disabling deficit regardless of NIHSS score
Class
Class I, Level A
IV Thrombolysis (onset < 4.5 h)
Intervention
Tenecteplase 0.25 mg/kg (max 25 mg): single IV bolus
Details
Alternative to alteplase
Class
Class I, Level A
IV Thrombolysis (4.5 to 9 h)
Intervention
Consider if perfusion imaging (CTP or MRI perfusion) shows salvageable penumbra
Details
Alteplase with imaging guidance
Class
Class IIa, Level B-R
IV Thrombolysis (4.5 to 24 h, LVO, no EVT access)
Intervention
Tenecteplase 0.25 mg/kg may be considered if penumbra present on perfusion imaging
Details
For LVO patients who cannot undergo thrombectomy
Class
Class IIb, Level B-R
Wake-up stroke
Intervention
Thrombolysis considered if MRI shows DWI-FLAIR mismatch
Details
Alteplase
Class
Class IIa, Level B-R
Thrombectomy (EVT)
Intervention
For LVO (ICA, M1) within 24 hours; patient ≥ 18 years, pre-stroke mRS 0-1, NIHSS > 5
Details
Stent retriever, aspiration, or combination device; target mTICI 2b/3
Class
Class I, Level A
EVT for basilar occlusion
Intervention
NIHSS ≥ 10, PC-ASPECTS ≥ 6, mRS 0-1, within 24 hours
Details
Class I, Level B
Class
EVT for large core (ASPECTS 3-5)
Intervention
Ages 18 to 80, mRS 0-1, ICA/M1 occlusion, within 0-24 hours
Details
Per RESCUE-Japan LIMIT, SELECT2, ANGEL-ASPECT trials
Class
Class I, Level A
Bridging therapy
Intervention
IV thrombolysis should be started immediately for eligible patients even if EVT is planned; do not wait for thrombolysis response before proceeding to EVT
Details
Simultaneous preparation of angiography suite
Class
Class I, Level B
Antiplatelet (no thrombolysis)
Intervention
Aspirin 160-325 mg within 24-48 hours of onset
Details
Class I, Level A
Class
Aspirin after thrombolysis
Intervention
Delay aspirin until 24 hours post-thrombolysis unless withholding poses known risk
Details
Class I, Level A
Class
Dual antiplatelet (DAPT)
Intervention
Aspirin + clopidogrel for 21 days in minor stroke (NIHSS < 5) or TIA, then switch to monotherapy
Details
Can extend to 90 days if intracranial stenosis 70-99%
Class
Class II, Level B
Anticoagulation for AF
Intervention
DOAC preferred over warfarin for non-valvular AF; initiate within 48 hours for mild stroke, 7 days for moderate/severe
Details
Aspirin is not a substitute for anticoagulation in AF (Class III)
Class
Class I, Level A
BP management (pre-thrombolysis)
Intervention
Must be < 185/110 mmHg before starting thrombolysis
Details
Class I
Class
BP management (post-thrombolysis)
Intervention
Maintain < 180/105 mmHg for 24 hours
Details
Class I
Class
BP management (no reperfusion, no comorbidity)
Intervention
No urgent lowering needed in first 48-72 hours
Details
Class IIb, Level C
Class
Edema / herniation
Intervention
Mannitol, hypertonic saline as first-line medical therapy; decompressive craniectomy within 48 hours for malignant MCA infarcts (age > 6 years)
Details
Class I, Level A (surgery)
Class
CSVT
Intervention
UFH or LMWH in the acute phase, even with hemorrhagic infarction; followed by oral anticoagulant for 3-6 months
Details
Class I, Level B
Class
Phase | Intervention | Details | Class |
|---|---|---|---|
Pre-hospital | Stabilize ABC; avoid aggressive BP lowering; avoid antiplatelet/anticoagulant; crystalloid only if dehydrated; avoid glucose-containing fluids (unless hypoglycemia) | Preparation and departure for referral ≤ 30 minutes from decision | Class I, Level A |
IV Thrombolysis (onset < 4.5 h) | Alteplase 0.9 mg/kg (max 90 mg): 10% IV bolus over 1 min, remainder infused over 60 min | For disabling deficit regardless of NIHSS score | Class I, Level A |
IV Thrombolysis (onset < 4.5 h) | Tenecteplase 0.25 mg/kg (max 25 mg): single IV bolus | Alternative to alteplase | Class I, Level A |
IV Thrombolysis (4.5 to 9 h) | Consider if perfusion imaging (CTP or MRI perfusion) shows salvageable penumbra | Alteplase with imaging guidance | Class IIa, Level B-R |
IV Thrombolysis (4.5 to 24 h, LVO, no EVT access) | Tenecteplase 0.25 mg/kg may be considered if penumbra present on perfusion imaging | For LVO patients who cannot undergo thrombectomy | Class IIb, Level B-R |
Wake-up stroke | Thrombolysis considered if MRI shows DWI-FLAIR mismatch | Alteplase | Class IIa, Level B-R |
Thrombectomy (EVT) | For LVO (ICA, M1) within 24 hours; patient ≥ 18 years, pre-stroke mRS 0-1, NIHSS > 5 | Stent retriever, aspiration, or combination device; target mTICI 2b/3 | Class I, Level A |
EVT for basilar occlusion | NIHSS ≥ 10, PC-ASPECTS ≥ 6, mRS 0-1, within 24 hours | Class I, Level B | |
EVT for large core (ASPECTS 3-5) | Ages 18 to 80, mRS 0-1, ICA/M1 occlusion, within 0-24 hours | Per RESCUE-Japan LIMIT, SELECT2, ANGEL-ASPECT trials | Class I, Level A |
Bridging therapy | IV thrombolysis should be started immediately for eligible patients even if EVT is planned; do not wait for thrombolysis response before proceeding to EVT | Simultaneous preparation of angiography suite | Class I, Level B |
Antiplatelet (no thrombolysis) | Aspirin 160-325 mg within 24-48 hours of onset | Class I, Level A | |
Aspirin after thrombolysis | Delay aspirin until 24 hours post-thrombolysis unless withholding poses known risk | Class I, Level A | |
Dual antiplatelet (DAPT) | Aspirin + clopidogrel for 21 days in minor stroke (NIHSS < 5) or TIA, then switch to monotherapy | Can extend to 90 days if intracranial stenosis 70-99% | Class II, Level B |
Anticoagulation for AF | DOAC preferred over warfarin for non-valvular AF; initiate within 48 hours for mild stroke, 7 days for moderate/severe | Aspirin is not a substitute for anticoagulation in AF (Class III) | Class I, Level A |
BP management (pre-thrombolysis) | Must be < 185/110 mmHg before starting thrombolysis | Class I | |
BP management (post-thrombolysis) | Maintain < 180/105 mmHg for 24 hours | Class I | |
BP management (no reperfusion, no comorbidity) | No urgent lowering needed in first 48-72 hours | Class IIb, Level C | |
Edema / herniation | Mannitol, hypertonic saline as first-line medical therapy; decompressive craniectomy within 48 hours for malignant MCA infarcts (age > 6 years) | Class I, Level A (surgery) | |
CSVT | UFH or LMWH in the acute phase, even with hemorrhagic infarction; followed by oral anticoagulant for 3-6 months | Class I, Level B |
Acute Stabilization. At the emergency department, the first goal is stabilizing airway, breathing, and circulation while simultaneously performing rapid neurological assessment with NIHSS. PNPK Stroke 2026 states the standard is to complete ED management within 1 hour with a multidisciplinary team (Class I, Level B). Identify stroke type and cause as quickly as possible, then determine definitive therapy.
IV Thrombolysis. For patients presenting within 4.5 hours of onset with a disabling deficit, IV thrombolysis is indicated regardless of the NIHSS score (Class I, Level A). However, thrombolysis is not recommended for patients with non-disabling deficits (Class III, Level B-R). Two agents are available:
Alteplase is given at 0.9 mg/kg (maximum 90 mg). Ten percent of the total dose is administered as an IV bolus over 1 minute, followed by the remaining 90% infused over 60 minutes via syringe pump.
Tenecteplase is given at 0.25 mg/kg (maximum 25 mg) as a single IV bolus. This is increasingly recognized as a practical alternative, particularly in settings preparing for bridging to thrombectomy.
For patients in the 4.5 to 9 hour window, thrombolysis can be considered when perfusion imaging demonstrates salvageable penumbra (Class IIa, Level B-R). Beyond 9 hours or with unknown onset, the decision must rely on advanced imaging; thrombolysis based on non-contrast CT alone beyond 4.5 hours is not recommended (Class III, Level B).
For wake-up strokes, a DWI-FLAIR mismatch on MRI can identify patients likely within the treatable window. If MRI is unavailable, CT perfusion can guide the decision.
Endovascular Thrombectomy (EVT). EVT is recommended for LVO involving the anterior circulation (ICA intracranial segment or M1 MCA) within 24 hours of last known well, provided the patient meets all four eligibility criteria: patient criteria (age ≥ 18, pre-stroke independence), symptom criteria (disabling deficit, NIHSS > 5), occlusion criteria (confirmed LVO accessible to intervention), and brain parenchyma criteria (assessed by ASPECTS, CT perfusion, or MRI).
For ASPECTS ≥ 6, EVT is strongly recommended with robust trial evidence. For ASPECTS 3 to 5 (large core ischemic stroke), EVT is still recommended based on multiple RCTs (RESCUE-Japan LIMIT, SELECT2, ANGEL-ASPECT, TESLA, TENSION, LASTE). For ASPECTS 0 to 2, EVT is not routinely recommended and can only be considered very selectively within 6 hours at experienced centers (Class III, Level C).
For basilar artery occlusion, EVT is recommended within 24 hours if NIHSS ≥ 10, PC-ASPECTS ≥ 6, and pre-stroke mRS 0-1 (Class I, Level B). For NIHSS 6 to 9 with PC-ASPECTS ≥ 6, EVT can be considered (Class IIb, Level B).
PNPK Stroke 2026 explicitly states: do not wait for the clinical response to IV thrombolysis before proceeding to EVT (Class I, Level B). Thrombolysis and angiography suite preparation should occur simultaneously.
The target for successful thrombectomy is reperfusion graded as mTICI 2b/3 (Class I, Level A).
Antiplatelet Therapy. For patients who did not receive thrombolysis, aspirin 160 to 325 mg should be given within 24 to 48 hours of onset (Class I, Level A). In patients who received thrombolysis, aspirin is delayed until 24 hours unless withholding it creates a known risk.
Dual antiplatelet therapy (aspirin + clopidogrel) is used for 21 days in minor stroke (NIHSS < 5) or high-risk TIA, then transitioned to single-agent therapy. DAPT may be extended to 90 days for symptomatic intracranial atherosclerotic stenosis of 70 to 99% (Class IIa, Level B).
Ticagrelor (loading 180 mg, then 90 mg twice daily) plus aspirin for 30 days is slightly superior to aspirin alone for preventing recurrent stroke (Class II, Level B). Addition of cilostazol (100 mg twice daily) to aspirin or clopidogrel for 15 to 180 days after non-cardioembolic stroke can reduce recurrent ischemic events (Class II, Level B).
Anticoagulation. Routine anticoagulation in acute ischemic stroke is not recommended for improving neurological outcomes or early secondary prevention (Class III, Level A). For patients with atrial fibrillation, DOACs (dabigatran, apixaban, edoxaban, rivaroxaban) are preferred over warfarin for non-valvular AF (Class I, Level A). Anticoagulation can be started within 48 hours for mild strokes and 7 days for moderate to severe strokes (Class II, Level B). Aspirin is not an acceptable substitute for anticoagulation in AF (Class III, Level B).
Neuroprotectants, vasodilators, albumin, and hemodilution are not recommended as routine therapy due to lack of consistent clinical evidence (Class III, Level A).
05Differential Diagnosis and Distractors
Hemorrhagic stroke (ICH)
Why It Is Similar
Sudden focal neurological deficit; identical presentation clinically
Key Discriminator
Non-contrast CT shows hyperdense lesion (acute blood) in ICH; CT is normal or shows hypodensity in ischemic stroke
Subarachnoid hemorrhage
Why It Is Similar
Sudden onset; can have focal deficits if complicated by vasospasm
Key Discriminator
"Thunderclap headache," meningismus, blood in subarachnoid space on CT; ischemic stroke typically lacks severe headache
Hypoglycemia
Why It Is Similar
Sudden onset of focal deficits including hemiparesis and confusion
Key Discriminator
Blood glucose is low; deficits resolve with glucose correction; this is why glucose must be checked before thrombolysis
Todd's paralysis (postictal)
Why It Is Similar
Unilateral weakness following a seizure mimics acute stroke
Key Discriminator
History of witnessed seizure preceding the deficit; weakness resolves within hours; EEG may show postictal changes
Complex migraine with aura
Why It Is Similar
Unilateral sensory or motor symptoms, visual disturbance, aphasia
Key Discriminator
Gradual onset ("marching" spread over minutes), history of similar episodes, complete resolution, younger patient, headache follows the aura
Brain tumor / abscess
Why It Is Similar
Focal neurological deficit, may present acutely if hemorrhage into tumor
Key Discriminator
Subacute progression of symptoms over days to weeks; CT shows ring-enhancing lesion or mass with surrounding edema rather than vascular territory infarct
Cerebral venous sinus thrombosis
Why It Is Similar
Headache, focal deficits, seizures, can mimic stroke in young patients
Key Discriminator
Headache is often progressive (not thunderclap); hemorrhagic infarcts not conforming to arterial territories; "empty delta sign" on contrast CT; confirmed with CTV or MRV
Conversion disorder (functional)
Why It Is Similar
Sudden weakness or sensory loss mimicking stroke
Key Discriminator
Deficits do not follow anatomical patterns; "give-way" weakness on exam; Hoover sign positive; normal imaging
Differential | Why It Is Similar | Key Discriminator |
|---|---|---|
Hemorrhagic stroke (ICH) | Sudden focal neurological deficit; identical presentation clinically | Non-contrast CT shows hyperdense lesion (acute blood) in ICH; CT is normal or shows hypodensity in ischemic stroke |
Subarachnoid hemorrhage | Sudden onset; can have focal deficits if complicated by vasospasm | "Thunderclap headache," meningismus, blood in subarachnoid space on CT; ischemic stroke typically lacks severe headache |
Hypoglycemia | Sudden onset of focal deficits including hemiparesis and confusion | Blood glucose is low; deficits resolve with glucose correction; this is why glucose must be checked before thrombolysis |
Todd's paralysis (postictal) | Unilateral weakness following a seizure mimics acute stroke | History of witnessed seizure preceding the deficit; weakness resolves within hours; EEG may show postictal changes |
Complex migraine with aura | Unilateral sensory or motor symptoms, visual disturbance, aphasia | Gradual onset ("marching" spread over minutes), history of similar episodes, complete resolution, younger patient, headache follows the aura |
Brain tumor / abscess | Focal neurological deficit, may present acutely if hemorrhage into tumor | Subacute progression of symptoms over days to weeks; CT shows ring-enhancing lesion or mass with surrounding edema rather than vascular territory infarct |
Cerebral venous sinus thrombosis | Headache, focal deficits, seizures, can mimic stroke in young patients | Headache is often progressive (not thunderclap); hemorrhagic infarcts not conforming to arterial territories; "empty delta sign" on contrast CT; confirmed with CTV or MRV |
Conversion disorder (functional) | Sudden weakness or sensory loss mimicking stroke | Deficits do not follow anatomical patterns; "give-way" weakness on exam; Hoover sign positive; normal imaging |
06Traps and High-Yield Pearls
The single most tested concept in ischemic stroke is the time-dependent treatment algorithm. Exam vignettes will manipulate the onset time, imaging findings, and available resources to test whether you can correctly determine the next best step.
Trap 1: Delaying thrombolysis for lab results. PNPK Stroke 2026 is unambiguous: the only lab result required before initiating thrombolysis is blood glucose. Waiting for CBC, coagulation, or renal function is incorrect unless there is a known reason (e.g., known anticoagulant use requiring INR check). Many students lose points by selecting "wait for labs" when the correct answer is "give alteplase now."
Trap 2: Skipping thrombolysis and going straight to thrombectomy. PNPK Stroke 2026 states that IV thrombolysis must be given to all eligible patients, including those who also qualify for EVT. The decision to skip thrombolysis and proceed directly to EVT is not routine and must be based on balanced clinical and operational considerations on a case-by-case basis (Class I, Level C). The default answer on an exam is to give thrombolysis first while preparing the angiography suite.
Trap 3: Using non-contrast CT alone beyond 4.5 hours. If a patient presents beyond the 4.5 hour window (or with unknown onset), thrombolysis based on non-contrast CT alone is not recommended (Class III, Level B). Advanced imaging (CT perfusion or MRI with DWI/perfusion) is required to demonstrate salvageable tissue.
Trap 4: Giving aspirin as a substitute for anticoagulation in atrial fibrillation. This is explicitly listed as Class III (not recommended). The correct secondary prevention for cardioembolic stroke with AF is a DOAC or warfarin, not aspirin.
Trap 5: Confusing ASPECTS scoring direction. ASPECTS starts at 10 (normal) and decreases by 1 point for each region showing early ischemic changes. ASPECTS ≥ 6 generally indicates a small core and favors thrombectomy. ASPECTS 3 to 5 represents moderate core (still may benefit from EVT based on recent RCTs). ASPECTS 0 to 2 represents very large core where EVT is generally not recommended routinely.
Trap 6: Blood pressure management before thrombolysis. The BP must be below 185/110 mmHg before starting thrombolysis and maintained below 180/105 mmHg for 24 hours afterward. If you cannot lower the BP below threshold, thrombolysis is contraindicated. However, in patients who are not candidates for thrombolysis or thrombectomy and have no acute comorbidity, aggressive BP lowering in the first 48 to 72 hours is unnecessary (Class IIb, Level C).
The core competency being tested across all ischemic stroke questions is the ability to rapidly triage a patient into the correct treatment pathway based on three variables: time from onset (or last known well), severity of deficit (NIHSS), and imaging findings (hemorrhage excluded, LVO present or absent, penumbra assessable). Master this decision tree and you will answer the majority of ischemic stroke questions correctly.