Stroke Management for NEET PG — Complete Guide 2026
Master stroke management for NEET PG 2026: ischemic vs hemorrhagic types, vascular territory syndromes (ACA, MCA, PCA, lacunar), NIHSS, tPA window and criteria, mechanical thrombectomy, BP management, ICH scoring, and secondary prevention.
NEETPGAI EditorialPublished 26 Feb 202618 min read
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This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
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Stroke contributes 2–3 direct questions per NEET PG paper. Master these 10 high-yield areas:
Types — Ischemic (85%, thrombotic/embolic/lacunar) vs hemorrhagic (15%, intracerebral hemorrhage or subarachnoid). Non-contrast CT distinguishes them
MCA syndrome — Contralateral face + arm weakness > leg, aphasia (dominant), hemineglect (non-dominant), gaze deviation toward lesion
ACA syndrome — Contralateral leg weakness > arm, abulia, urinary incontinence (bilateral ACA from ACoA aneurysm)
PCA syndrome — Contralateral homonymous hemianopia with macular sparing; alexia without agraphia (dominant)
Lacunar syndromes — Pure motor (internal capsule), pure sensory (thalamus), ataxic hemiparesis, dysarthria-clumsy hand, sensorimotor. Associated with hypertension and diabetes
NIHSS — 15-item scale (0–42). Guides tPA and thrombectomy decisions
tPA window — IV alteplase within 4.5 hours of symptom onset. BP must be <185/110 before, <180/105 for 24 hr after
Mechanical thrombectomy — Up to 6 hours standard; up to 24 hours for LVO with DAWN/DEFUSE-3 imaging mismatch
BP management — Ischemic without tPA: permissive HTN (treat only if >220/120). With tPA: <185/110. Hemorrhagic: target SBP 140 (INTERACT-2)
Secondary prevention — Aspirin (or DAPT x 21 days for minor stroke), statin, BP control <130/80, DOAC for AF, smoking cessation, carotid endarterectomy for symptomatic stenosis >=70%
Stroke is acute focal neurologic deficit from cerebrovascular cause — and it is the second most tested neurology topic in NEET PG after epilepsy. The student who masters vascular territory mapping, tPA criteria, and ICH scoring has covered 2–3 marks per paper. Pair this guide with daily MCQ practice on the Medicine subject hub, cross-reference the high-yield medicine topics overview, and integrate stroke into your overall study plan so you revise it alongside cardiology risk factors.
Types of stroke
Stroke is an acute neurologic deficit from a vascular cause, classified into ischemic (85%) and hemorrhagic (15%) types with fundamentally different management.
Ischemic stroke (85%)
Ischemic stroke is cerebral infarction from arterial occlusion, further classified by TOAST criteria into five etiologic subtypes:
Large-artery atherosclerosis (20%) — extracranial (ICA, vertebral) or intracranial atherosclerosis
80% from ruptured saccular (berry) aneurysm at Circle of Willis branch points
Most common location: anterior communicating artery (30%)
Classic presentation: "worst headache of my life," thunderclap onset, meningismus
Associated with: autosomal dominant polycystic kidney disease, Ehlers-Danlos type IV, aortic coarctation, smoking, hypertension
Pathophysiology and ischemic penumbra
The ischemic penumbra is the zone of viable but hypoperfused brain tissue surrounding an infarct core — it is salvageable with timely reperfusion, which is the biologic basis for acute stroke therapy.
Cerebral blood flow thresholds (per 100 g brain/min):
Normal: 50 mL
Oligemia: 20–50 mL (no symptoms)
Penumbra: 10–20 mL (electrical failure, cells viable but non-functional)
Infarct core: <10 mL (energy failure, irreversible damage within minutes)
"Time is brain":
1.9 million neurons lost per minute of ischemia
14 billion synapses lost per minute
Every 15-minute delay in reperfusion reduces good outcome by 4%
Ischemic cascade:
ATP depletion → Na/K pump failure → cellular swelling
Blood-brain barrier breakdown → cerebral edema (peaks day 3–5)
Stroke syndromes by vascular territory
Vascular territory localization is the mapping of stroke symptoms to the occluded artery — the most frequently tested concept in NEET PG neurology.
Middle cerebral artery (MCA) stroke
Most common stroke territory. Supplies lateral surface of cerebral hemispheres (frontal, parietal, temporal lobes) and deep structures via lenticulostriate branches.
Clinical features:
Motor: Contralateral face and arm weakness (face > arm > leg because homunculus lateral)
Sensory: Contralateral face and arm numbness
Language (dominant, usually left):
Superior division (M1) → Broca aphasia (non-fluent, preserved comprehension)
Supplies occipital lobe and inferomedial temporal lobe.
Clinical features:
Contralateral homonymous hemianopia with macular sparing (macula has dual blood supply from MCA)
Alexia without agraphia (left PCA + splenium of corpus callosum) — can write but cannot read
Anton syndrome (bilateral PCA) — cortical blindness with denial of blindness
Memory deficits (hippocampal involvement)
Contralateral sensory loss (if thalamic branches involved)
Lacunar syndromes
Lacunar infarcts are small (<15 mm) deep infarcts in the distribution of small penetrating arteries, caused by lipohyalinosis from chronic hypertension and diabetes.
Classic 5 lacunar syndromes:
Syndrome
Location
Features
Pure motor hemiparesis (most common)
Posterior limb of internal capsule
Face + arm + leg weakness, no sensory/cortical deficit
Pure sensory stroke
Ventral posterolateral thalamus
Contralateral hemisensory loss, no motor deficit
Ataxic hemiparesis
Pons or posterior limb of internal capsule
Ipsilateral ataxia + contralateral leg weakness
Dysarthria-clumsy hand
Pons or genu of internal capsule
Facial weakness + dysarthria + mild hand weakness
Sensorimotor stroke
Thalamocapsular
Combined hemisensory + hemimotor deficit
Key point: Lacunar strokes never cause cortical deficits (no aphasia, neglect, visual field defect) because they spare cortex.
Most sensitive for acute ischemia (positive within minutes)
DWI-FLAIR mismatch (DWI bright, FLAIR not yet positive) indicates stroke <4.5 hours — may guide thrombolysis in wake-up stroke or unknown onset (WAKE-UP trial)
Thrombolysis — IV alteplase (tPA)
IV alteplase is the fibrinolytic agent used for acute ischemic stroke — converting plasminogen to plasmin to dissolve the occluding thrombus.
Dose: 0.9 mg/kg (maximum 90 mg). 10% as bolus over 1 minute; remaining 90% as infusion over 60 minutes.
Inclusion criteria:
Age >=18 years
Clinical diagnosis of acute ischemic stroke
Measurable neurologic deficit
Symptom onset <4.5 hours (last known well)
Non-contrast CT excludes hemorrhage
Absolute contraindications:
Intracranial hemorrhage on CT
Recent intracranial or intraspinal surgery, serious head trauma, or prior stroke within 3 months
Active internal bleeding
Aortic arch dissection
Intra-axial intracranial neoplasm
Platelet count <100,000/microL
INR >1.7 or prolonged aPTT
DOAC use within 48 hours (unless reversal available)
Therapeutic LMWH within 24 hours
BP >185/110 mmHg (not controllable with IV antihypertensives)
Blood glucose <50 mg/dL
Relative contraindications (3–4.5 hour window per ECASS-3):
Age >80 years
NIHSS >25
History of both stroke AND diabetes
Oral anticoagulant use (regardless of INR)
BP management with tPA:
Pre-tPA: BP must be <185/110 mmHg (IV labetalol, nicardipine)
Post-tPA: Maintain <180/105 for first 24 hours
Post-tPA monitoring:
Neurochecks every 15 min for 2 hr, then every 30 min for 6 hr, then hourly
No aspirin or anticoagulation for 24 hours
Repeat CT at 24 hours before starting antithrombotics
Risk of symptomatic ICH: 6% with tPA vs 0.5% without
Tenecteplase: Emerging alternative to alteplase. Single bolus, lower cost, equivalent or superior outcomes in some trials (EXTEND-IA TNK).
Mechanical thrombectomy
Mechanical thrombectomy is endovascular retrieval of the occluding clot using a stent-retriever or aspiration device — the standard of care for large-vessel occlusion in eligible patients.
Standard window: within 6 hours of symptom onset
Indication: LVO of ICA or M1 MCA (also considered for M2, basilar, vertebral)
Early securing (coiling or clipping) within 24 hours
Nimodipine 60 mg PO q4h for 21 days (reduces vasospasm and delayed cerebral ischemia)
Maintain euvolemia (avoid HHH therapy routinely)
Hunt and Hess scale for prognosis
Secondary prevention
Secondary prevention after ischemic stroke requires five pillars: antiplatelet, statin, BP control, risk-factor modification, and source-specific therapy (anticoagulation for AF, carotid revascularization for symptomatic stenosis).
Antiplatelet therapy:
Aspirin 75–325 mg daily — start within 24–48 hours (hold 24 hr after tPA)
Clopidogrel 75 mg — alternative in aspirin intolerance
Dual antiplatelet therapy (DAPT):
Minor stroke (NIHSS <=3) or high-risk TIA: aspirin + clopidogrel for 21 days (CHANCE, POINT), then aspirin alone
21 days is the window — longer increases bleeding without ischemic benefit
Statin therapy:
High-intensity statin (atorvastatin 80 mg or rosuvastatin 40 mg)
SPARCL trial: atorvastatin 80 mg reduced recurrent stroke by 16%
LDL target <70 mg/dL (or <55 for very high risk per 2019 ESC)
DOAC preferred over warfarin for non-valvular AF (apixaban, rivaroxaban, dabigatran, edoxaban)
Warfarin for mechanical valves or moderate-severe mitral stenosis
Start timing: 1-3-6-12 day rule based on infarct size (small infarct 3 days, large 6–12 days) — earlier now with small strokes (ELAN, TIMING trials)
Carotid endarterectomy (CEA):
Symptomatic stenosis 70–99%: CEA within 2 weeks (NASCET)
Symptomatic stenosis 50–69%: CEA considered (less benefit)
Asymptomatic stenosis >=60%: controversial; CEA may be considered in select patients
Carotid artery stenting: alternative in high surgical risk
Lifestyle:
Smoking cessation (largest modifiable risk)
Mediterranean diet
Physical activity 150 min/week
Alcohol moderation
Transient ischemic attack (TIA)
TIA is a transient episode of neurologic dysfunction caused by focal ischemia WITHOUT acute infarction on imaging (AHA 2013 tissue-based definition) — a medical emergency predicting imminent stroke.
Anticoagulation if AF detected (ambulatory monitoring required)
Sources and references
American Heart Association / American Stroke Association — 2019 Guidelines for the Early Management of Patients With Acute Ischemic Stroke (Stroke, 2019) — the global reference for stroke protocols.
Harrison's Principles of Internal Medicine, 21st Edition (Loscalzo et al., 2022) — Chapters on Cerebrovascular Disease.
Adams and Victor's Principles of Neurology, 11th Edition (Ropper et al., 2019) — detailed stroke syndromes and neuroanatomy.
Goyal M, Menon BK, et al. — HERMES collaboration meta-analysis (Lancet 2016; 387:1723-1731) — thrombectomy within 6 hours.
API Textbook of Medicine, 11th Edition (Munjal et al., 2019) — Indian-context stroke epidemiology and management.
Frequently asked questions
How many stroke questions appear in NEET PG?
Cerebrovascular disease contributes 2-3 direct questions per NEET PG paper across medicine and neurology. Vascular territory syndromes, tPA inclusion and exclusion criteria, and hemorrhagic stroke management are the three most frequently tested subtopics based on 2019-2025 pattern analysis.
What is the difference between ischemic and hemorrhagic stroke?
Ischemic stroke (85 percent of cases) is caused by thrombotic or embolic occlusion of a cerebral artery. Hemorrhagic stroke (15 percent) is intracerebral hemorrhage from hypertension, amyloid angiopathy, AVM, or aneurysm. Non-contrast CT is the first imaging to differentiate them. Management diverges completely — thrombolysis in ischemic, BP control and reversal of coagulopathy in hemorrhagic.
What is the tPA window for ischemic stroke?
IV alteplase (tPA) is indicated within 4.5 hours of symptom onset (last known well) for eligible patients aged 18 years or older. The original 3-hour window was extended to 4.5 hours after the ECASS-3 trial. For patients in the 4.5-9 hour window or with wake-up stroke, DWI-FLAIR mismatch on MRI may guide extended-window thrombolysis.
What is the window for mechanical thrombectomy?
Mechanical thrombectomy is indicated up to 6 hours from symptom onset for all eligible large vessel occlusions (ICA, M1 MCA). The window extends to 24 hours for patients with favorable imaging (DAWN and DEFUSE-3 criteria: small core infarct with large penumbra). Thrombectomy is performed in addition to IV tPA if the patient qualifies for both.
How do I localize stroke to a vascular territory?
MCA stroke: contralateral face and arm weakness greater than leg, aphasia (dominant), neglect (non-dominant). ACA stroke: contralateral leg weakness greater than arm, abulia. PCA stroke: contralateral homonymous hemianopia with macular sparing. Lacunar: pure motor, pure sensory, ataxic hemiparesis, dysarthria-clumsy hand. Vertebrobasilar: crossed deficits, cerebellar signs, brainstem syndromes.
What is the BP target in acute ischemic stroke?
For ischemic stroke patients NOT receiving tPA, do not treat BP unless greater than 220/120 mmHg (permissive hypertension maintains cerebral perfusion). For patients receiving tPA, BP must be less than 185/110 before thrombolysis and maintained less than 180/105 for 24 hours after. For hemorrhagic stroke, target SBP 140 mmHg (INTERACT-2 trial).
What is the NIHSS and why is it used?
NIHSS (National Institutes of Health Stroke Scale) is a 15-item clinical scale (score 0-42) quantifying stroke severity. NIHSS less than 4 is mild, 4-15 moderate, 16-20 severe, greater than 20 very severe. A minimum NIHSS of 4 typically qualifies for tPA (though isolated severe aphasia may qualify below this). NIHSS also predicts outcome and guides thrombectomy eligibility.
What is the ICH score?
The ICH score predicts 30-day mortality after intracerebral hemorrhage using 5 components (0-6 points): GCS (3-4 = 2 points, 5-12 = 1, 13-15 = 0), hemorrhage volume greater than 30 mL (1), intraventricular extension (1), infratentorial location (1), age 80 years or older (1). Score 0 = 0 percent mortality; score 5 = 100 percent. Widely used in emergency triage.
What is a TIA?
A transient ischemic attack (TIA) is a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia WITHOUT acute infarction on imaging (tissue-based definition, AHA 2013). Most TIAs resolve in under 1 hour. ABCD2 score predicts early stroke risk: Age over 60, BP over 140/90, Clinical features (weakness, speech), Duration, Diabetes. High-risk TIA requires admission and urgent workup.
What is the secondary prevention after ischemic stroke?
Start antiplatelet (aspirin 75-100 mg daily; add clopidogrel for 21 days after minor stroke or high-risk TIA per CHANCE and POINT trials), high-intensity statin (atorvastatin 80 mg, SPARCL trial, LDL target less than 70), BP control (target less than 130/80), diabetes control, anticoagulation if atrial fibrillation (DOACs preferred over warfarin for non-valvular AF), and smoking cessation.
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This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
Written by: NEETPGAI Editorial Team
Reviewed by: Pending SME Review
Last reviewed: February 2026
This article is reviewed by qualified medical professionals for clinical accuracy and exam relevance. For corrections or updates, contact the editorial team.
