Stroke Emergency Treatment — Cost, Top Hospitals & Success Rates | MyMedicPlus

<p>Stroke emergency treatment refers to the <strong>time-critical, acute medical and interventional care</strong> delivered within the first hours of stroke onset, aimed at restoring cerebral blood flow, minimising irreversible brain damage, and preventing early neurological deterioration. Stroke is one of the world's leading causes of death and disability, with the World Health Organization estimating that 15 million strokes occur globally each year, resulting in 5 million deaths and 5 million permanent disabilities.</p><p>The fundamental principle of emergency stroke care is encapsulated in the phrase <strong>"Time is Brain"</strong> — coined by neurologist Vladimir Hachinski to convey that during an acute ischemic stroke, approximately <strong>1.9 million neurons are lost every minute</strong> that perfusion is not restored (Saver JL, 2006). This makes acute stroke one of the most time-sensitive emergencies in medicine, comparable only to myocardial infarction (STEMI) in its demand for rapid, systematic treatment.</p><p>Approximately <strong>85% of all strokes are ischemic</strong> — caused by occlusion of a cerebral artery by a thrombus or embolism. The remaining 15% are <strong>hemorrhagic</strong>, caused by rupture of a blood vessel leading to intracerebral haemorrhage (ICH) or subarachnoid haemorrhage (SAH). Emergency treatment differs fundamentally between these two types: ischemic stroke requires rapid restoration of blood flow (thrombolysis or mechanical thrombectomy), while haemorrhagic stroke requires haemostasis, blood pressure control, and in some cases surgical intervention.</p><p>Since the landmark NINDS trial in 1995 demonstrating the efficacy of intravenous tissue plasminogen activator (tPA/alteplase) in ischemic stroke, and the revolutionary mechanical thrombectomy trials of 2015 (MR CLEAN, ESCAPE, EXTEND-IA, SWIFT PRIME, THRACE), emergency stroke care has undergone a transformation. Comprehensive stroke centres (CSCs) now offer 24/7 access to intravenous thrombolysis, endovascular thrombectomy suites, and specialised neurointensive care, resulting in dramatically improved functional outcomes for stroke survivors.</p><p>The FAST acronym — <strong>Face drooping, Arm weakness, Speech difficulty, Time to call emergency services</strong> — is the internationally recognised public awareness tool. Public education on FAST recognition has significantly reduced time from symptom onset to hospital presentation ("onset-to-door time"), a key determinant of treatment eligibility and outcome.</p>

<p>Emergency stroke treatment protocols are designed to rapidly assess and manage the full spectrum of acute cerebrovascular events. Accurate diagnosis — requiring urgent neuroimaging — is essential because treatments that benefit ischemic stroke can be catastrophic in haemorrhagic stroke.</p><h4>Ischemic Stroke Subtypes</h4><ul><li><strong>Cardioembolic Stroke (30-35%):</strong> Caused by thrombus formation in the heart (most commonly in atrial fibrillation) with embolisation to cerebral arteries. Often causes large territorial infarctions with severe deficits.</li><li><strong>Large Vessel Atherosclerotic Stroke (20-25%):</strong> Due to atheromatous plaque rupture or stenosis in major cerebral vessels (ICA, MCA, basilar artery). Frequently involves large vessel occlusion (LVO) amenable to mechanical thrombectomy.</li><li><strong>Small Vessel (Lacunar) Stroke (20-25%):</strong> Occlusion of small perforating arteries causing small, deep infarcts in the basal ganglia, thalamus, and brainstem. Generally associated with hypertension and diabetes; not typically amenable to thrombectomy.</li><li><strong>Cryptogenic Stroke (25-30%):</strong> No definite cause identified despite extensive investigation; may be related to occult paroxysmal atrial fibrillation, patent foramen ovale (PFO), or aortic arch atheroma.</li></ul><h4>Haemorrhagic Stroke Subtypes</h4><ul><li><strong>Intracerebral Haemorrhage (ICH):</strong> Spontaneous bleeding directly into brain parenchyma; most commonly caused by chronic hypertension (hypertensive arteriopathy) or cerebral amyloid angiopathy. Carries a 30-day mortality of 40-50%.</li><li><strong>Subarachnoid Haemorrhage (SAH):</strong> Bleeding into the subarachnoid space, usually from rupture of an intracranial aneurysm. Presents with the classic "thunderclap headache" — described as the worst headache of one's life. Emergency coiling or surgical clipping of the aneurysm is required.</li></ul><h4>Stroke Mimics and TIA</h4><ul><li><strong>Transient Ischaemic Attack (TIA):</strong> Focal neurological deficit lasting <24 hours (usually <60 minutes) with no infarction on MRI. Constitutes a neurological emergency: 10-15% of TIA patients have a disabling stroke within 90 days, with the highest risk in the first 48 hours. Requires urgent assessment and secondary prevention initiation.</li><li><strong>Large Vessel Occlusion (LVO):</strong> Occlusion of the internal carotid artery (ICA), proximal middle cerebral artery (M1/M2 MCA), or basilar artery. LVO causes the most severe strokes and is the primary target for mechanical thrombectomy.</li></ul><p>All suspected stroke presentations must be treated as medical emergencies requiring immediate <strong>911/999 activation and transport to the nearest stroke-capable centre</strong>. Never drive a suspected stroke patient to hospital — ambulance services activate pre-notification protocols that substantially reduce in-hospital treatment times.</p>

<p>Eligibility for specific emergency stroke interventions is determined by a combination of <strong>time from onset, clinical severity, imaging findings, and medical contraindications</strong>. These criteria are based on evidence from pivotal clinical trials and are regularly updated by major stroke societies (AHA/ASA, ESO, ESOC).</p><h4>IV Alteplase (tPA) Eligibility</h4><ul><li><strong>Time window:</strong> Within 4.5 hours of confirmed symptom onset (or last known well time). Extended to 4.5h from the initial 3h window based on ECASS-3 trial evidence.</li><li><strong>Inclusion criteria:</strong> Confirmed ischemic stroke with measurable neurological deficit (NIHSS ≥ 1); age ≥ 18 years; CT head showing no haemorrhage or large established infarct (>1/3 MCA territory).</li><li><strong>Key contraindications:</strong> Active intracranial haemorrhage; recent major surgery or trauma within 14 days; current anticoagulation with INR >1.7 or DOAC use within 48 hours; very high blood pressure (>185/110 mmHg refractory to treatment); history of prior ICH; large established infarct; infective endocarditis.</li><li><strong>Wake-up stroke:</strong> Patients waking with stroke symptoms are eligible if MRI DWI/FLAIR mismatch (WAKE-UP trial) confirms the stroke is acute (occurred within the past 4.5 hours).</li></ul><h4>Mechanical Thrombectomy Eligibility</h4><ul><li><strong>Standard window (0–6 hours):</strong> Confirmed LVO (ICA, M1, M2, basilar); NIHSS ≥ 6; ASPECTS ≥ 6 (small infarct core on CT); eligible for any patient otherwise suitable.</li><li><strong>Extended window (6–24 hours):</strong> DAWN trial criteria (age ≥80, NIHSS ≥10, infarct core <21 mL) or DEFUSE-3 criteria (mismatch ratio ≥1.8, penumbra >15 mL, infarct core <70 mL) on CT/MRI perfusion imaging.</li><li><strong>Basilar artery occlusion (BAO):</strong> Thrombectomy considered in any time window given catastrophic prognosis without treatment (90-day mortality 70-80% without recanalization).</li></ul><h4>Haemorrhagic Stroke Considerations</h4><ul><li><strong>Surgical ICH:</strong> Surgical evacuation considered for cerebellar haemorrhage >3 cm (or causing brainstem compression), lobar haemorrhage with rapid neurological deterioration, or hydrocephalus.</li><li><strong>Aneurysmal SAH:</strong> All confirmed aneurysmal SAH patients are candidates for urgent aneurysm securing (coiling or clipping); timing and modality determined by neurosurgery/interventional neuroradiology consensus.</li></ul><p>Eligibility assessment in the emergency setting must be completed within <strong>30–60 minutes of hospital arrival</strong> (door-to-needle time <60 minutes for tPA; door-to-groin <90 minutes for thrombectomy) to maximise treatment benefit. The treating team performs a rapid neurological examination, urgent CT/CT angiography, and blood tests (including coagulation screen, glucose, FBC) simultaneously.</p>

<p>Emergency stroke treatment requires rapid triage to the correct intervention based on stroke type, vessel occlusion site, time from onset, and patient eligibility. The following describes the key treatment modalities available at comprehensive stroke centres.</p><h4>Intravenous Thrombolysis</h4><ul><li><strong>IV Alteplase (tPA):</strong> The gold-standard thrombolytic for ischemic stroke. Dose: 0.9 mg/kg (maximum 90 mg), administered as 10% bolus over 1 minute followed by 90% infusion over 60 minutes. Dissolves the occluding clot by activating plasminogen to plasmin, restoring arterial perfusion. Approved within 4.5 hours of onset.</li><li><strong>Tenecteplase (TNK):</strong> A newer, fibrin-specific thrombolytic with a simpler single-bolus administration. EXTEND-IA TNK trial demonstrated non-inferiority (and potential superiority in LVO patients) vs alteplase. Increasingly adopted as preferred agent for LVO patients prior to thrombectomy.</li></ul><h4>Mechanical Thrombectomy (Endovascular Treatment)</h4><ul><li><strong>Stent Retriever Devices:</strong> Self-expanding stent-like devices (Solitaire, Trevo) deployed within the thrombus and retracted under suction to mechanically extract the clot en masse. Achieve successful recanalisation (mTICI 2b/3) in 60-80% of cases.</li><li><strong>Direct Aspiration First Pass Technique (ADAPT):</strong> Large-bore aspiration catheter advanced directly to the clot face; negative suction applied to aspirate the thrombus. Faster than stent retrieval in some centres.</li><li><strong>Combined Technique:</strong> Stent retriever combined with simultaneous proximal aspiration for improved clot capture, used when first-pass fails.</li></ul><h4>Haemorrhagic Stroke Management</h4><ul><li><strong>Blood Pressure Control:</strong> INTERACT-2 and ATACH-2 trials: target systolic BP <140 mmHg within 1 hour for ICH using IV labetalol or nicardipine to reduce haematoma expansion.</li><li><strong>Anticoagulation Reversal:</strong> For warfarin-associated ICH: vitamin K + 4-factor PCC (prothrombin complex concentrate); for DOAC-associated ICH: idarucizumab (reverses dabigatran), andexanet alfa (reverses apixaban/rivaroxaban).</li><li><strong>Surgical Evacuation:</strong> Craniotomy or minimally invasive surgery (MIS-ICH) for selected haematoma locations; most beneficial for cerebellar ICH causing brainstem compression.</li><li><strong>Aneurysm Securing (SAH):</strong> Endovascular coiling (first-line, less invasive) or surgical clipping of the ruptured aneurysm to prevent re-haemorrhage.</li></ul><h4>Supportive Emergency Care</h4><ul><li><strong>Airway management:</strong> Oxygen for hypoxia (SpO2 <94%); intubation for NIHSS >20 with impaired airway protection.</li><li><strong>Glucose management:</strong> Hyperglycaemia (>11 mmol/L) worsens infarct outcomes; insulin infusion targeting 6–10 mmol/L.</li><li><strong>Fever management:</strong> Hyperthermia dramatically worsens ischemic injury; paracetamol for temperature >37.5°C.</li><li><strong>DVT prophylaxis:</strong> Pneumatic compression stockings from admission; pharmacological VTE prophylaxis initiated after 24–48 hours in ischemic stroke.</li></ul>

<p>The evidence supporting emergency stroke interventions represents some of the most clinically impactful trial data in modern medicine. Rapid, appropriate treatment dramatically changes the trajectory of stroke recovery — the difference between full recovery and permanent disability often measured in minutes.</p><h4>Benefits of IV Thrombolysis (tPA)</h4><ul><li><strong>Absolute risk reduction in poor outcome:</strong> NINDS trial demonstrated that tPA reduced the proportion of patients with major disability or death by ~30% at 3 months vs placebo. Number Needed to Treat (NNT) ≈ 6 — meaning for every 6 patients treated, one additional patient achieves independent functional outcome.</li><li><strong>Time dependency:</strong> The earlier tPA is given, the greater the benefit. Benefit is maximal within the first 90 minutes (NNT ≈ 4), decreasing progressively to 4.5 hours. Every 15-minute reduction in door-to-needle time is associated with improved functional outcome and reduced mortality.</li><li><strong>Functional independence:</strong> Patients treated with tPA are 30% more likely to achieve functional independence (modified Rankin Scale ≤2) at 3 months compared to placebo-treated patients.</li></ul><h4>Benefits of Mechanical Thrombectomy</h4><ul><li><strong>Transformative efficacy in LVO:</strong> The 2016 HERMES meta-analysis of all five pivotal thrombectomy trials demonstrated a 46% relative reduction in severe disability (mRS 3-6) and a 20% absolute increase in functional independence at 90 days compared to medical treatment alone.</li><li><strong>Extended window results:</strong> DAWN trial: 73% of thrombectomy-treated patients achieved functional independence (mRS 0-2) vs 36% with medical care alone (NNT = 2.8) in the 6–24 hour window — among the most impressive NNTs in stroke medicine.</li><li><strong>Basilar artery occlusion:</strong> ATTENTION and BAOCHE trials (2022) confirmed thrombectomy significantly improves outcomes in BAO even beyond 6 hours, addressing one of the last therapeutic frontiers in stroke.</li></ul><h4>System-Level Benefits</h4><ul><li><strong>Stroke unit care:</strong> Admission to a specialised stroke unit (vs general medical ward) reduces death or dependency by 18% (Stroke Unit Trialists' Collaboration); equivalent in magnitude to thrombolysis.</li><li><strong>Reduced long-term care costs:</strong> Successful acute stroke treatment dramatically reduces lifetime care costs — each disability-free year gained is associated with approximately $50,000–$100,000 in avoided long-term care expenditure.</li></ul><p>For families and caregivers, the most profound benefit of successful acute stroke treatment is the <strong>preservation of the patient's independence, dignity, and quality of life</strong> — outcomes that no number of statistics can adequately capture.</p>

<p>Emergency stroke interventions carry real procedural and treatment risks, all of which must be weighed against the substantial risk of permanent disability or death from untreated acute ischemic stroke. For eligible patients, <strong>the risk-benefit ratio strongly favours treatment</strong> in the vast majority of cases.</p><h4>Risks of IV Thrombolysis (tPA)</h4><ul><li><strong>Symptomatic Intracranial Haemorrhage (sICH):</strong> The most feared complication. Occurs in 6-8% of patients treated with tPA vs 1% in controls (NINDS trial). Higher risk with severe stroke (NIHSS >20), large infarct volume, hyperglycaemia, or elevated blood pressure at time of treatment. Despite this risk, overall functional outcomes are better with tPA than without in eligible patients.</li><li><strong>Haemorrhagic Transformation:</strong> Conversion of ischemic infarct to haemorrhagic infarct; asymptomatic forms are common (30-40%) on follow-up imaging and do not necessarily worsen outcomes.</li><li><strong>Orolingual Angioedema:</strong> Occurs in 1-5% of tPA recipients, particularly those on ACE inhibitors. Usually mild and self-limiting, but can be severe and require airway management.</li><li><strong>Systemic Bleeding:</strong> Access site haemorrhage, GI bleeding, and haematuria are uncommon but possible; the 36-hour no-anticoagulation/antiplatelet window reduces this risk.</li></ul><h4>Risks of Mechanical Thrombectomy</h4><ul><li><strong>Vascular Access Complications:</strong> Groin haematoma, femoral artery pseudoaneurysm, or AV fistula at the puncture site; occurring in 2-5% of cases.</li><li><strong>Vessel Injury:</strong> Arterial dissection, perforation, or vasospasm during catheter navigation; serious but rare (<1% for perforation).</li><li><strong>Clot Fragmentation / Distal Embolisation:</strong> During clot retrieval, clot fragments can embolise to previously unaffected territories; risk reduced with modern aspiration techniques.</li><li><strong>Intracranial Haemorrhage:</strong> Reperfusion haemorrhage post-thrombectomy occurs in 4-9% of patients, with sICH in approximately 4-7%.</li><li><strong>Contrast Nephropathy:</strong> Use of iodinated contrast for angiography can impair renal function, particularly in pre-existing CKD.</li></ul><h4>Risks of Haemorrhagic Stroke Treatment</h4><ul><li><strong>Aggressive BP Lowering:</strong> Rapid systolic BP reduction to <130 mmHg (as tested in ATACH-2) was associated with higher renal adverse events without mortality benefit; current guidelines target <140 mmHg.</li><li><strong>Surgical Risks (ICH Evacuation):</strong> Craniotomy carries perioperative risks including re-bleeding, infection, and anaesthetic complications; reserved for selected cases where benefit outweighs risk.</li></ul><p>All emergency stroke treatments are delivered by specialist teams with the expertise to rapidly identify, manage, and mitigate these complications. The overriding clinical message is that for eligible patients, <strong>the risk of not treating far exceeds the risk of treating</strong> — particularly in the critical early hours when brain salvage is possible.</p>

<p>Following emergency stroke treatment, patients require structured in-hospital monitoring and then a carefully planned transition to secondary prevention and rehabilitation. The acute hospital phase typically lasts 3–7 days, followed by rehabilitation and long-term neurological follow-up.</p><h4>Acute In-Hospital Monitoring (0–72 hours)</h4><ul><li><strong>Neurological observations:</strong> Hourly NIHSS assessments for the first 24 hours post-thrombolysis; continuous BP monitoring (target <180/105 mmHg post-tPA); pulse oximetry; 12-lead ECG on admission.</li><li><strong>Follow-up neuroimaging:</strong> CT or MRI brain at 24 hours post-tPA to detect haemorrhagic transformation; MRI brain/DWI to define infarct volume and guide prognosis.</li><li><strong>Cardiac monitoring:</strong> Continuous telemetry for at least 24–72 hours to detect paroxysmal atrial fibrillation (detected in an additional 10–15% of cryptogenic stroke patients on prolonged monitoring).</li><li><strong>Dysphagia screening:</strong> Bedside swallow assessment before any oral intake; nil-by-mouth and NG feeding if unsafe swallow detected.</li></ul><h4>Subacute In-Hospital Phase (72 hours – discharge)</h4><ul><li><strong>Secondary prevention initiation:</strong> Antiplatelet therapy (aspirin 300 mg daily for 2 weeks, then 75 mg) initiated at 24 hours post-tPA if no haemorrhagic transformation; anticoagulation for AF-related stroke deferred 4–14 days depending on infarct size.</li><li><strong>High-intensity statin therapy:</strong> Atorvastatin 40–80 mg daily initiated during admission regardless of baseline LDL.</li><li><strong>Blood pressure management:</strong> Target <130/80 mmHg for long-term secondary prevention; commonly not aggressively treated in first 24–72 hours post-stroke (permissive hypertension).</li></ul><h4>Post-Discharge Follow-Up</h4><ul><li><strong>Neurology outpatient review:</strong> At 2–4 weeks post-discharge for medication review, neurological assessment, imaging review, and secondary prevention optimisation.</li><li><strong>Cardiac workup:</strong> Echocardiogram to assess LV function and identify cardioembolic source; prolonged cardiac Holter or implantable loop recorder for paroxysmal AF detection in cryptogenic stroke.</li><li><strong>Carotid imaging:</strong> Duplex ultrasound or CTA of carotid arteries to identify significant stenosis requiring carotid endarterectomy (CEA) or stenting.</li><li><strong>Rehabilitation referral:</strong> Immediate referral to stroke rehabilitation team; early mobilisation within 24–48 hours shown to improve outcomes (AVERT trial at low-medium frequency).</li></ul><p>Patients and families should be educated about <strong>recurrent stroke warning signs</strong> and instructed to call emergency services immediately if FAST symptoms recur, as the same treatment principles apply in the event of a second event.</p>

<p>Emergency stroke treatment involves significant healthcare costs, primarily driven by the acute intervention (thrombolysis, thrombectomy), intensive care requirements, extended hospital admission, and the long-term care burden of stroke disability. Understanding these costs is important for healthcare systems and patients planning care.</p><h4>Acute Treatment Costs (United States)</h4><ul><li><strong>IV Alteplase (tPA) drug cost:</strong> Approximately $2,500–$5,000 per course depending on dose and supplier. When factoring professional fees and monitoring, total thrombolysis episode cost is $5,000–$15,000.</li><li><strong>Mechanical Thrombectomy:</strong> Procedural costs $15,000–$40,000 including interventional suite use, catheter and device costs, anaesthesia, and professional fees. Device costs alone (stent retrievers, aspiration systems) are $3,000–$8,000 per procedure.</li><li><strong>Neuroimaging:</strong> Emergency CT head and CTA (CT angiography) $500–$3,000; MRI brain with DWI $2,000–$5,000; CT perfusion $1,500–$4,000.</li><li><strong>ICU / Stroke Unit admission:</strong> $3,000–$8,000/day; average acute stroke hospitalisation cost in the US $30,000–$100,000 depending on severity, interventions, and complications.</li></ul><h4>International Cost Comparisons</h4><ul><li><strong>United Kingdom (NHS):</strong> Stroke treatment is fully funded by the NHS; average acute stroke admission cost approximately £6,000–£12,000 (GBP).</li><li><strong>India:</strong> Thrombolysis available at major centres for $500–$1,500 (tPA drug + facility); thrombectomy $5,000–$15,000 at private hospitals with interventional neuroradiology capability.</li><li><strong>Thailand:</strong> Thrombectomy $8,000–$20,000 at JCI-accredited centres; acute stroke admission $3,000–$10,000.</li><li><strong>Turkey:</strong> Complete thrombectomy and stroke unit care available at $5,000–$12,000 at major centres.</li></ul><h4>Long-Term Cost Considerations</h4><ul><li><strong>Cost-effectiveness of intervention:</strong> Both tPA and thrombectomy are highly cost-effective by health economic standards (ICER well below $50,000/QALY); successful treatment prevents enormous downstream costs of chronic disability and institutionalised care.</li><li><strong>Secondary prevention costs:</strong> Ongoing medications (antiplatelets $5–$20/month; DOACs $300–$500/month; statins generic $5–$20/month) are a continuing but modest cost relative to disability prevention.</li><li><strong>Insurance considerations:</strong> Emergency stroke treatment is generally covered by major health insurance plans, Medicare (US), and universal healthcare systems. Ensure your nearest stroke centre is in-network before a crisis occurs.</li></ul>

<p>Not all stroke patients are eligible for thrombolysis or mechanical thrombectomy. Contraindications, late presentation, or unavailability of interventional facilities mean that a substantial proportion of patients receive supportive medical management alone. It is critical to understand that <strong>no validated alternative therapy can replicate the brain-saving effects of reperfusion</strong> in large vessel occlusion ischemic stroke.</p><h4>Medical Management Without Reperfusion</h4><ul><li><strong>Aspirin 300 mg loading dose:</strong> For ischemic stroke patients not eligible for thrombolysis or as adjunct after thrombectomy (initiated 24 hours post-tPA). Reduces 14-day risk of recurrent stroke by approximately 30% (IST and CAST trials).</li><li><strong>Dual antiplatelet therapy (DAPT):</strong> Aspirin + clopidogrel for 21 days (POINT and CHANCE trials) for minor ischemic stroke or high-risk TIA reduces 90-day recurrence risk by 25-32% compared to aspirin alone.</li><li><strong>Stroke unit admission:</strong> Even without acute intervention, care in a dedicated stroke unit (monitoring, early mobilisation, dysphagia management, early secondary prevention) reduces death or dependency by 18%.</li></ul><h4>Neuroprotection Research</h4><ul><li><strong>Neuroprotective agents:</strong> Decades of research into drugs that protect ischemic brain tissue (NMDA antagonists, free radical scavengers, anti-inflammatory agents) have failed to demonstrate efficacy in phase III trials. No approved neuroprotective agent exists as of 2026. Research continues with agents such as NA-1 (nerinetide) and minocycline.</li><li><strong>Cooling (Therapeutic Hypothermia):</strong> Promising in animal models; human trials have not demonstrated consistent benefit in ischemic stroke. Not currently recommended outside clinical trials.</li></ul><h4>Telemedicine (Telestroke)</h4><ul><li><strong>Telestroke networks:</strong> Where no neurologist is immediately available (rural or remote hospitals), telemedicine consultation platforms enable vascular neurologists to review CT scans and assess eligibility for thrombolysis remotely, substantially expanding access to acute stroke treatment. Telestroke-guided tPA has demonstrated equivalent safety and outcomes to in-person assessment.</li></ul><h4>Prevention as the Ultimate Alternative</h4><ul><li><strong>Primary prevention:</strong> Blood pressure control, anticoagulation for AF, smoking cessation, diabetes management, and a healthy lifestyle prevent up to 90% of strokes (INTERSTROKE study). The most powerful 'alternative' to emergency stroke treatment is preventing the stroke from occurring in the first place.</li></ul><p>The key message remains: for patients who are eligible and present within the treatment window, <strong>no alternative treatment approach matches the clinical efficacy of IV thrombolysis and mechanical thrombectomy</strong>. Seeking emergency care at the earliest possible moment after stroke symptom onset is the single most important action a patient or bystander can take.</p>