Recognize disabling stroke, interpret urgent imaging, select reperfusion, and prevent early harm with cases that separate the clock from tissue viability.
A normal early head CT does not exclude ischemic stroke, and a small NIH Stroke Scale score does not guarantee a small disability. A person who can lift both arms but suddenly cannot speak may still need immediate reperfusion. The first decision is whether an acute vascular deficit threatens useful brain function, followed by which treatment can safely restore flow.
Start with the lost function and its last normal time
A music teacher stops naming familiar objects during rehearsal and drops a pencil from the right hand. The combination points toward the dominant, usually left, cerebral hemisphere. Ask when someone last observed normal language and strength. Record last known well separately from the time symptoms were discovered, emergency arrival, and treatment. A person found weak at breakfast was not necessarily normal immediately before breakfast.
Sudden unilateral weakness, sensory loss, visual loss, aphasia, neglect, diplopia, or severe new imbalance warrants emergency stroke assessment. Activate the stroke team while assessing airway, breathing, circulation, glucose, and a focused examination. A decreasing level of consciousness can require airway protection; inability to speak alone does not establish inability to understand. Obtain a witness history and medication list in parallel with transport to imaging. [1][2]
Localize the deficit before interpreting the vessel image. These patterns guide examination; vascular territories and language dominance vary.
Anatomic region
Findings that fit
What to check next
Anatomic regionDominant MCA cortex
Findings that fitAphasia with opposite face and arm weakness
What to check nextLanguage comprehension, naming, visual fields, and proximal MCA or ICA patency
Anatomic regionNondominant MCA cortex
Findings that fitOpposite-sided inattention, sensory extinction, and weakness
What to check nextNeglect despite the person's limited awareness of the deficit
Anatomic regionPosterior circulation
Findings that fitDiplopia, dysarthria, ataxia, crossed cranial nerve and limb findings, or impaired consciousness
What to check nextBrainstem examination and vertebrobasilar vessels
Anatomic regionVentral pons with basilar occlusion
Findings that fitQuadriplegia and loss of speech with potentially preserved awareness and vertical gaze
What to check nextUrgent vascular imaging and communication through preserved eye responses
The NIHSS runs from 0 to 42 and standardizes severity and serial examination. It is not a treatment permission score. Aphasia, hemianopia, dominant-hand weakness, or inability to walk can be disabling at a low total. Posterior circulation disease can also be underestimated. Ask what the person can no longer do independently, then document the actual deficit rather than substituting the score for clinical judgment.
Hypoglycemia, seizure, migraine, and functional neurological symptoms can resemble stroke. Correct a low glucose immediately and reexamine. A seizure at onset can accompany an infarct; persistent disabling findings are not automatically postictal. Fever with a seizure also raises infection or encephalitis, so the examination, time course, and imaging must settle the competing explanations. Improvement is reassuring only if the remaining deficit is genuinely nondisabling. [1]
Use each image to answer a different question
Noncontrast CT rapidly identifies hemorrhage and major established infarction. Loss of gray-white distinction, sulcal effacement, or a hyperdense artery may appear early, but a normal scan does not demonstrate normal perfusion. MRI can also exclude hemorrhage in an appropriate rapid pathway; obtaining it should not delay otherwise eligible early intravenous thrombolysis. CTA of the head and neck identifies a treatable occlusion and should be coordinated with, not postponed until after, the thrombolysis decision. [1]
Three distinct imaging questions. Read across a row; one normal result does not answer the other rows.
Question
Useful study
Interpretive limit
QuestionIs there blood or extensive established injury?
Useful studyNoncontrast CT, or a rapid appropriate MRI pathway
Interpretive limitA negative CT can coexist with acute ischemia.
QuestionWhich artery is obstructed?
Useful studyCTA or MRA
Interpretive limitOcclusion anatomy alone does not quantify viable tissue.
QuestionDoes tissue or imaging timing support extended-window treatment?
Useful studyCT/MR perfusion or an eligible MRI diffusion-FLAIR pattern
Interpretive limitSelection depends on a validated protocol and the entire clinical picture.
The ischemic core represents severely injured tissue; the surrounding penumbra has impaired function but potential for rescue. Collateral circulation and elapsed time influence how quickly these regions change. Perfusion software estimates tissue states rather than observing an exact border between living and dead cells. This is why both speed and appropriate imaging matter, and why a single core-volume number should not be treated as universal futility.
In ordinary early treatment, do not wait for every laboratory result when there is no reason to suspect a relevant abnormality. Glucose must be checked before thrombolysis. Anticoagulant exposure, bleeding history, thrombocytopenia, or liver disease can make coagulation and platelet results essential. An INR above 1.7 on warfarin or platelets below 100,000/µL generally preclude intravenous thrombolysis. A normal INR does not establish absence of a clinically active direct oral anticoagulant; last dose, renal function, drug-specific testing where available, and the stroke protocol matter.
Unknown onset is a selection problem, not automatic exclusion. WAKE-UP tested alteplase in selected patients with a diffusion-positive lesion without corresponding marked FLAIR signal. Perfusion-based pathways also identify selected patients beyond the conventional clock window. These are defined imaging protocols, not permission to treat every late or wake-up stroke. [3]
Restore flow without turning parallel decisions into delays
Alteplase and tenecteplase promote conversion of plasminogen to plasmin, which degrades fibrin within a thrombus. This explains both their potential to restore flow and their bleeding risk. For an eligible adult with disabling ischemic stroke within 4.5 hours, the 2026 AHA/ASA guideline recommends either tenecteplase or alteplase. The guideline tenecteplase regimen is 0.25 mg/kg, maximum 25 mg, as a single intravenous bolus. Alteplase is 0.9 mg/kg, maximum 90 mg, with 10% given as a bolus and the remainder infused over 60 minutes. Use an actual weight in kilograms, the correct stroke preparation, and an independent medication check. Stroke and myocardial-infarction tenecteplase regimens are not interchangeable. [1][4][5]
Regulatory labeling and guideline recommendations are different documents. The 2025 US TNKase label specifies treatment within 3 hours and provides weight-band dosing, whereas the 2026 stroke guideline supports the 4.5-hour window and the regimen above. Follow the institution's current stroke protocol rather than silently combining parts of different dosing tables. Alteplase labeling also has a narrower US onset window than guideline-supported treatment.
Blood pressure must be below 185/110 mm Hg before intravenous thrombolysis and maintained below 180/105 for the following 24 hours. A titratable intravenous agent can bring an otherwise eligible patient into range. Uncontrolled pressure despite treatment is a reason to withhold thrombolysis, not to administer it and address pressure afterward. Correct severe hypo- or hyperglycemia and reassess the deficit; the initial glucose number is not a permanent exclusion if the metabolic problem is corrected and a disabling stroke remains.
Thrombectomy physically retrieves an occluding thrombus. Eligible large-vessel occlusion patients need immediate endovascular evaluation even while intravenous treatment is being prepared or administered. Do not observe for an hour to see whether the drug works. Selected anterior circulation occlusions remain treatable up to 24 hours, and large-core trials have expanded eligibility: SELECT2 included ICA or proximal MCA occlusion with ASPECTS 3 to 5 or a substantial estimated core. Large infarction increases risk, but it no longer means automatic exclusion. [6]
Basilar occlusion needs its own evidence, not an assumption that every posterior artery behaves like the MCA. BAOCHE supported thrombectomy in selected patients presenting 6 to 24 hours after basilar stroke. The 2026 guideline strongly supports selected basilar occlusion patients with substantial deficits, including NIHSS at least 10, limited established posterior injury, and suitable baseline function within 24 hours. Selection remains individualized for milder deficits and extensive injury. A hospital without thrombectomy capability should arrange an appropriate transfer immediately. [7][1]
Protect the recovering brain during the first day
Reperfusion does not end the emergency. Follow serial neurological examinations and blood pressure closely. New headache, vomiting, reduced consciousness, or worsening weakness after thrombolysis demands immediate evaluation for hemorrhage; stop an ongoing infusion and obtain emergency imaging and the stroke service's bleeding-management pathway. Orolingual angioedema requires urgent airway assessment and treatment. A routine follow-up scan tomorrow is not adequate for deterioration today. [4][5]
Routine antiplatelet and anticoagulant treatment is deferred until 24 hours after intravenous thrombolysis and follow-up CT or MRI has excluded bleeding. Selected procedural situations require specialist decisions, but the standard pathway never means automatic aspirin immediately after the lytic. Without thrombolysis, aspirin is usually started within 24 to 48 hours after hemorrhage is excluded, using a safe route. Full-dose heparin is not routine treatment to reopen an acutely occluded cerebral artery.
Pressure targets depend on treatment. Without reperfusion or another hypertensive emergency, routine early reduction is generally avoided below 220/120 mm Hg. Treat hypotension and hypovolemia. After successful thrombectomy, forcing systolic pressure below 140 mm Hg can be harmful; use the stroke team's target rather than a universal intensive goal. Correct hypoglycemia, manage persistent hyperglycemia, and avoid intensive glucose targets that provoke low glucose. Treat fever and investigate its cause. [1][8]
Screen swallowing before food, fluid, or oral medication. Provide oxygen for hypoxemia, not automatically for a normal saturation. Use stroke-unit care, appropriate venous-thrombosis prevention, and rehabilitation assessment. Large hemispheric and cerebellar infarctions can swell and threaten adjacent structures. Declining consciousness, new pupillary findings, or worsening brainstem signs require urgent repeat imaging and neurocritical or neurosurgical assessment; apparent initial stabilization does not eliminate this risk.
Choose prevention from the stroke mechanism
A minor noncardioembolic stroke with nondisabling symptoms is not simply a smaller version of the thrombolysis pathway. In appropriate patients with NIHSS 3 or less who did not receive intravenous thrombolysis, early aspirin plus clopidogrel for 21 days followed by a single agent reduces early recurrence. Bleeding risk persists with prolonged dual treatment, so do not convert this short course into an indefinite prescription. Disabling low-score stroke still requires a reperfusion assessment. [9][10]
Identify atrial fibrillation, symptomatic cervical arterial disease, intracranial atherosclerosis, and small-vessel risk factors through targeted vascular imaging, cardiac evaluation, and monitoring. Noncardioembolic stroke generally calls for antiplatelet therapy; atrial fibrillation often calls for oral anticoagulation. A symptomatic severe ipsilateral carotid stenosis needs timely revascularization assessment, not indefinite medication-only management by default. Address blood pressure, lipids, diabetes, smoking, physical activity, medication access, and rehabilitation goals. [11]
Anticoagulation timing after an AF-associated infarct depends on infarct size, bleeding or hemorrhagic transformation, stability, and the selected drug. ELAN studied earlier treatment stratified by imaging-defined severity; OPTIMAS found initiation within 4 days noninferior to initiation at 7 to 14 days in its trial population. These findings replace a rigid waiting rule with individualized timing, not with immediate anticoagulation for every infarct. Document the planned start and the imaging or clinical findings that could change it. [12][13]
Cases: decide what the findings permit now
Use the exact deficit, timing, imaging, medication exposure, and treatment already given. Each case asks for one decision at that point in care.
Case 1
Show answer and explanations for case 1
A. Aspirin alone because a normal early CT excludes clinically important ischemia and therefore removes the need for reperfusion assessment (Why this does not fit)
A normal early CT does not exclude ischemia. Aspirin alone would forgo a reperfusion opportunity in this disabling presentation.
B. Intravenous heparin to dissolve the arterial thrombus while avoiding the hemorrhagic risk associated with stroke thrombolysis (Why this does not fit)
Heparin is not routine acute cerebral reperfusion treatment and adds bleeding risk without the established benefit of eligible thrombolysis.
C. Carotid endarterectomy before any reperfusion assessment (Why this does not fit)
No culprit cervical carotid stenosis has been demonstrated. Immediate management must address the acute disabling deficit.
D. Intravenous thrombolysis with a guideline-supported stroke regimen while vascular imaging proceeds (Best answer)
This is an early disabling ischemic syndrome with hemorrhage excluded and no supplied exclusion. Either recommended thrombolytic may be selected under the stroke protocol.
Takeaway: A normal early CT can permit thrombolysis by excluding hemorrhage even before the infarct becomes visible.
A. Wait for the routine 24-hour post-alteplase scan before deciding whether the documented proximal occlusion still needs endovascular treatment (Why this does not fit)
That scan helps guide later antithrombotics; it is not a prerequisite for urgent thrombectomy.
B. Start warfarin immediately to prevent further clot enlargement while waiting to see whether alteplase restores flow through the M1 segment (Why this does not fit)
Warfarin does not promptly reopen this M1 occlusion and is not the acute treatment decision.
C. Proceed immediately with thrombectomy evaluation and treatment if eligible (Best answer)
A proximal occlusion with a disabling deficit needs prompt EVT. Starting alteplase does not justify a wait for improvement.
D. Observe for one hour to judge alteplase response (Why this does not fit)
Waiting wastes potentially salvageable tissue and is not required before EVT in an eligible patient.
Takeaway: Intravenous thrombolysis and thrombectomy preparation should proceed without an observation delay between them.
A. Continue aspirin plus clopidogrel indefinitely because the early benefit of dual therapy should persist as long as both agents are taken (Why this does not fit)
The benefit is concentrated early; indefinite dual treatment exposes him to bleeding without the same established benefit.
B. Begin therapeutic heparin immediately, then transition to warfarin even though no atrial fibrillation or other anticoagulation indication has been identified (Why this does not fit)
There is no AF or other supplied anticoagulation indication, and urgent heparin is not routine treatment for this infarct.
C. No prevention because the deficit is too small (Why this does not fit)
Even a small infarct can precede recurrent stroke and warrants mechanism-appropriate prevention.
D. Aspirin plus clopidogrel for 21 days, then a single antiplatelet (Best answer)
He meets the described minor nondisabling noncardioembolic pathway without IVT. A short course balances early prevention against continued bleeding risk.
Takeaway: Minor nondisabling noncardioembolic stroke can warrant short DAPT; define eligibility rather than relying only on the score.
A. Use short dual antiplatelet therapy instead because every stroke with NIHSS 3 or less is nondisabling, regardless of which function has been lost (Why this does not fit)
The minor nondisabling antiplatelet pathway does not describe this disabling aphasia.
B. Wait for arm or leg weakness to appear before considering reperfusion because isolated language loss does not qualify as a disabling neurologic deficit (Why this does not fit)
Language loss already establishes important focal dysfunction; weakness is not required.
C. The aphasia is disabling despite the low NIHSS, so assess and treat with IVT if eligible (Best answer)
Loss of functional language is substantial disability even when relatively few scale points are assigned.
D. NIHSS below 4 automatically means no thrombolysis (Why this does not fit)
A numeric cutoff alone does not determine whether the remaining deficit is disabling.
Takeaway: A low NIHSS cannot substitute for an assessment of disability.
A. Stop the infusion, obtain urgent brain imaging, and activate the stroke hemorrhage-management pathway (Best answer)
The abrupt deterioration could represent symptomatic intracranial hemorrhage and requires immediate evaluation and treatment preparation.
B. Complete the alteplase infusion and wait for the scheduled next-day CT because the baseline scan excluded intracranial hemorrhage before treatment began (Why this does not fit)
A routine future scan is inadequate for a new potentially life-threatening complication.
C. Give aspirin now to treat presumed persistent ischemia (Why this does not fit)
Adding an antiplatelet before excluding post-lytic hemorrhage could worsen bleeding.
D. Attribute the new headache and worsening weakness to anxiety because the first CT was normal and therefore excludes a treatment-related hemorrhage (Why this does not fit)
The pretreatment scan cannot exclude a hemorrhage developing during treatment.
Takeaway: New neurological deterioration during thrombolysis is an emergency, even after a reassuring baseline scan.
A. Omit medication review and bleeding-history assessment while the laboratory tests are pending because only the final test values determine thrombolysis eligibility (Why this does not fit)
The history is essential for deciding whether a pending result is necessary before IVT.
B. Replace IVT with heparin until the laboratory results return (Why this does not fit)
Heparin is neither a safe holding strategy nor equivalent acute reperfusion treatment.
C. Do not delay otherwise eligible IVT solely for routine results when relevant abnormalities are not suspected (Best answer)
Rapid treatment is appropriate after the necessary assessment; suspicion of an abnormal result would change the laboratory requirement.
D. Wait for the complete metabolic panel, troponin, platelet count, and every coagulation result before IVT in all patients, even when no relevant abnormality is suspected (Why this does not fit)
This blanket rule creates avoidable delay and does not distinguish tests essential for this patient's eligibility.
Takeaway: Laboratory urgency is determined by what could change eligibility, not by a universal demand that every result return.
A. Withhold IV thrombolysis at this INR and continue urgent thrombectomy evaluation (Best answer)
Therapeutic warfarin activity above the IVT threshold does not automatically prohibit EVT.
B. Give standard IV thrombolysis because the platelet count is normal, treating that result as sufficient to override the elevated INR from therapeutic warfarin (Why this does not fit)
Normal platelets do not remove the anticoagulation-related bleeding concern.
C. Give a half-dose thrombolytic as a validated substitute (Why this does not fit)
Arbitrary dose reduction is not an established solution to this exclusion.
D. Abandon every reperfusion option because any recent warfarin exposure excludes both intravenous thrombolysis and mechanical thrombectomy by the same rule (Why this does not fit)
A contraindication to one reperfusion method does not necessarily exclude another.
Takeaway: Separate IVT exclusions from endovascular eligibility.
A. Early ischemic stroke remains possible; continue eligible reperfusion and vascular assessment (Best answer)
CT can exclude hemorrhage before ischemic tissue change becomes conspicuous.
B. A normal early noncontrast CT excludes hemorrhage and acute ischemia with equal certainty, so no further urgent stroke imaging or reperfusion assessment is needed (Why this does not fit)
Early ischemia may not yet be visible on noncontrast CT.
C. Wait until the next day for the infarct to become visible on CT before treating, because visible tissue injury is required to confirm an acute ischemic stroke (Why this does not fit)
Waiting for radiographic evolution would waste the treatment window.
D. The scan proves a psychiatric cause of weakness (Why this does not fit)
A negative early CT does not establish a functional or psychiatric diagnosis.
Takeaway: Read an early CT for what it can establish, without asking it to exclude invisible early ischemia.
A. Exclude endovascular thrombectomy whenever ASPECTS is below 6, regardless of occlusion site, time window, baseline function, or current large-core evidence (Why this does not fit)
That categorical cutoff reflects an older limitation and ignores newer randomized evidence.
B. Assume a large ischemic core guarantees full functional recovery after thrombectomy and removes the need to discuss hemorrhagic or procedural risk (Why this does not fit)
Eligibility and average benefit do not guarantee an individual outcome or eliminate hemorrhage and procedural risks.
C. Give IV heparin as an equivalent replacement for EVT (Why this does not fit)
Heparin has no equivalent evidence for mechanical reperfusion of this occlusion.
D. Consider thrombectomy under the current large-core selection protocol (Best answer)
SELECT2 and subsequent guideline recommendations support treatment in selected patients with this degree of established injury.
Takeaway: Large core changes risk and selection; it does not automatically establish futility.
A. Never prescribe antiplatelet therapy after intravenous thrombolysis because prior lytic treatment creates a permanent contraindication to all later antiplatelet use (Why this does not fit)
Antiplatelet treatment can be started later when the safety assessment and stroke mechanism support it.
B. Defer routine aspirin until 24 hours after IVT and follow-up CT or MRI excludes hemorrhage (Best answer)
This is the standard safety interval in the uncomplicated post-lytic pathway.
C. Give aspirin immediately because neurological findings improved, using clinical improvement as proof that no post-thrombolysis bleeding complication is present (Why this does not fit)
Clinical improvement does not establish absence of bleeding risk or replace the follow-up safety assessment.
D. Start heparin now and aspirin tomorrow (Why this does not fit)
Substituting another antithrombotic defeats the same safety precaution without a supplied indication.
Takeaway: The reperfusion sequence needs a post-IVT safety interval before routine antithrombotics.
A. Earlier initiation can be reasonable in selected stable patients, with timing individualized to infarct size and bleeding findings (Best answer)
ELAN and OPTIMAS support earlier strategies in eligible populations rather than a single mandatory delay for every stroke.
B. Require every patient with an AF-associated ischemic stroke to wait exactly 14 days before starting a DOAC, regardless of infarct size, stability, or bleeding findings (Why this does not fit)
A fixed universal delay is inconsistent with the trial evidence and individual risk assessment.
C. Require a DOAC within one hour of arrival for every AF-associated ischemic stroke, before completing acute reperfusion decisions or evaluating bleeding risk (Why this does not fit)
Earlier trial strategies are not a mandate for immediate anticoagulation before acute treatment and bleeding assessment.
D. Aspirin and clopidogrel permanently replace anticoagulation for all AF strokes (Why this does not fit)
Antiplatelets are not an equivalent general substitute for indicated AF anticoagulation.
Takeaway: Write an individualized anticoagulation plan tied to infarct extent, stability, and bleeding assessment.
A. Prescribe long-term anticoagulation solely because symptomatic carotid plaque is present, even without atrial fibrillation or another established indication for anticoagulation (Why this does not fit)
Carotid atherosclerosis without another indication is not a reason to replace antiplatelet therapy with routine anticoagulation.
B. Use indefinite dual antiplatelet therapy as a guaranteed substitute for evaluating severe symptomatic carotid stenosis for a potentially appropriate revascularization procedure (Why this does not fit)
Long-term DAPT is not routine prevention and does not remove the need to assess a suitable symptomatic carotid lesion.
C. Stop prevention once the neurological symptoms resolve (Why this does not fit)
Recovery does not eliminate recurrent stroke risk or the significance of the carotid stenosis.
D. Arrange timely carotid revascularization assessment alongside antiplatelet and vascular risk-factor treatment (Best answer)
Symptomatic severe carotid disease is a potentially treatable recurrence mechanism and warrants specialist assessment.
Takeaway: Prevention should address the demonstrated mechanism as well as blood pressure, lipids, diabetes, smoking, and rehabilitation.
