Stroke Management for NEET PG — Complete Guide 2026

Version 1.0 — Published February 2026

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:

1. Large-artery atherosclerosis (20%) — extracranial (ICA, vertebral) or intracranial atherosclerosis
2. Cardioembolic (25%) — atrial fibrillation (most common), post-MI mural thrombus, valvular disease, patent foramen ovale, infective endocarditis
3. Small-vessel occlusion (lacunar) (25%) — hypertensive lipohyalinosis, diabetic microangiopathy
4. Other determined etiology (5%) — dissection, vasculitis, hypercoagulable state, MELAS, moyamoya
5. Undetermined (cryptogenic) (25%) — no cause identified or multiple possible causes

Thrombotic vs embolic:

Hemorrhagic stroke (15%)

Hemorrhagic stroke is bleeding into the brain parenchyma (intracerebral hemorrhage, 10%) or subarachnoid space (subarachnoid hemorrhage, 5%).

Intracerebral hemorrhage (ICH) causes:

• Hypertension (50%) — basal ganglia (putamen most common), thalamus, pons, cerebellum
• Cerebral amyloid angiopathy — lobar hemorrhages in elderly, recurrent
• AVM, cavernoma — young patients
• Anticoagulation — warfarin-associated
• Tumor hemorrhage — metastatic melanoma, choriocarcinoma, renal cell carcinoma, thyroid

Subarachnoid hemorrhage (SAH):

• 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:

1. ATP depletion → Na/K pump failure → cellular swelling
2. Glutamate release → NMDA receptor activation → calcium influx
3. Mitochondrial dysfunction → free radical generation
4. Apoptosis and necrosis
5. 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)
  • Inferior division → Wernicke aphasia (fluent, impaired comprehension)
  • Large MCA → global aphasia
• Neglect (non-dominant, usually right): Contralateral hemineglect
• Visual: Contralateral homonymous hemianopia (optic radiations affected)
• Eyes: Gaze deviation TOWARD the lesion (ipsilateral gaze preference)

Anterior cerebral artery (ACA) stroke

Supplies medial surface of frontal and parietal lobes (leg representation).

Clinical features:

• Contralateral leg weakness > arm (legs are medial on homunculus)
• Contralateral sensory loss in leg
• Abulia, apathy (frontal lobe)
• Urinary incontinence (if bilateral ACA from anterior communicating artery aneurysm rupture)
• Transcortical motor aphasia (dominant)

Posterior cerebral artery (PCA) stroke

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:

Key point: Lacunar strokes never cause cortical deficits (no aphasia, neglect, visual field defect) because they spare cortex.

Vertebrobasilar stroke syndromes

Wallenberg syndrome (lateral medullary / PICA territory):

• Ipsilateral: Horner syndrome, facial pain/temperature loss (CN V), palatal/vocal cord paralysis (CN IX, X), cerebellar ataxia, nystagmus, vertigo
• Contralateral: body pain/temperature loss (spinothalamic)
• No limb weakness, no tongue weakness

Medial medullary syndrome (vertebral artery):

• Ipsilateral tongue weakness (CN XII)
• Contralateral arm and leg weakness (pyramidal)
• Contralateral loss of vibration/proprioception (medial lemniscus)

Locked-in syndrome (bilateral basilar / ventral pons):

• Quadriplegia + aphonia + aphagia
• Preserved consciousness and vertical eye movements (midbrain spared)

Top-of-the-basilar syndrome:

• Bilateral occipital + bilateral thalamic strokes
• Cortical blindness, amnesia, visual hallucinations, vertical gaze palsy

Initial evaluation — NIHSS, CT, and MRI

The first hour after stroke onset determines treatment options, and rapid evaluation with NIHSS and imaging is the standardized approach.

NIHSS (National Institutes of Health Stroke Scale):

• 15-item standardized neurologic examination
• Score range 0–42
• Severity: 0 = no stroke, 1–4 = minor, 5–15 = moderate, 16–20 = moderate-severe, 21–42 = severe
• Items: level of consciousness, gaze, visual fields, facial palsy, motor (4 limbs), ataxia, sensory, language, dysarthria, extinction/inattention

Non-contrast CT head (first imaging):

• Goal: Exclude hemorrhage (all hyperdense bleeds visible immediately)
• Early ischemic signs (may be subtle):
  • Hyperdense MCA sign (acute thrombus in MCA)
  • Insular ribbon sign (loss of grey-white differentiation)
  • Obscuration of lentiform nucleus
  • Sulcal effacement
• ASPECTS score — 10-point score of MCA territory; score <=6 suggests large infarct (poor thrombectomy outcome)

CT angiography:

• Confirms large-vessel occlusion (LVO)
• Required for thrombectomy decision

CT perfusion:

• Quantifies core infarct and penumbra
• Extended window thrombectomy (6–24 hours): identifies mismatch

MRI with DWI:

• 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)
• NIHSS >=6
• ASPECTS >=6
• Pre-stroke modified Rankin Scale <=1 (baseline independence)

Extended window: 6–24 hours

• DAWN criteria (2017, 6–24 hours): Clinical-core mismatch (NIHSS vs infarct core volume on CTP/MRI)
• DEFUSE-3 criteria (2018, 6–16 hours): Core <70 mL, mismatch ratio >=1.8, mismatch volume >=15 mL

Outcomes:

• NNT for functional independence ~2.6 (HERMES meta-analysis) — among the strongest effect sizes in medicine
• Combined with tPA (bridging therapy) for eligible patients

BP management in acute stroke

Blood pressure management in acute stroke is nuanced and differs by stroke type — mismanagement can extend infarct or promote rebleeding.

Ischemic stroke, NOT receiving tPA:

• Permissive hypertension (helps perfuse penumbra)
• Treat only if BP >220/120 mmHg
• Target gradual reduction (10–15% in first 24 hours)

Ischemic stroke, receiving tPA:

• Pre-tPA: BP <185/110 (labetalol 10–20 mg IV, nicardipine infusion)
• Post-tPA: <180/105 for 24 hours

Hemorrhagic stroke (ICH):

• INTERACT-2 and ATACH-2 trials: Target SBP 140 mmHg (aggressive lowering did not worsen outcomes but did not improve primary outcome either)
• Use IV labetalol, nicardipine, hydralazine
• Avoid sodium nitroprusside (may increase ICP)

After acute phase (72 hours):

• Start or resume antihypertensives
• Long-term target: <130/80 mmHg (SPRINT, SPS3)

Hemorrhagic stroke management

Intracerebral hemorrhage management focuses on stopping hematoma expansion, reversing coagulopathy, and managing elevated ICP.

Initial management:

1. Airway, breathing, circulation
2. BP control: target SBP 140 mmHg
3. Reverse anticoagulation:
   • Warfarin → 4-factor PCC + vitamin K
   • Dabigatran → idarucizumab
   • Factor Xa inhibitors (apixaban, rivaroxaban) → andexanet alfa or 4-factor PCC
   • Heparin → protamine sulfate
4. Reverse thrombocytopenia if platelets <100,000
5. ICU admission for Q1 hourly neuro checks, ICP monitoring
6. Surgical evacuation for cerebellar hemorrhage >3 cm with brainstem compression, lobar hemorrhage with mass effect; controversial for deep hemorrhages

ICH score (prognosis):

30-day mortality by ICH score: 0 = 0%, 1 = 13%, 2 = 26%, 3 = 72%, 4 = 97%, 5 = 100%.

Subarachnoid hemorrhage management:

• Urgent CT angiography to identify aneurysm
• 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)

BP control:

• Long-term target: <130/80 mmHg
• SPS3 trial in lacunar stroke: tighter target (<130) reduced recurrent stroke

Atrial fibrillation with stroke:

• 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.

ABCD2 score (predicts 2-day stroke risk):

2-day stroke risk: Score 0–3 = 1%, 4–5 = 4%, 6–7 = 8%.

Management:

• High-risk TIA (ABCD2 >=4): admit, urgent workup (MRI, vessel imaging, echocardiography)
• Start DAPT x 21 days (CHANCE, POINT) if high-risk
• Statin, BP control
• Anticoagulation if AF detected (ambulatory monitoring required)

Sources and references

1. 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.
2. Harrison's Principles of Internal Medicine, 21st Edition (Loscalzo et al., 2022) — Chapters on Cerebrovascular Disease.
3. Adams and Victor's Principles of Neurology, 11th Edition (Ropper et al., 2019) — detailed stroke syndromes and neuroanatomy.
4. ECASS-3 Investigators — NEJM 2008; 359:1317-1329 — landmark trial extending tPA window to 4.5 hours.
5. Goyal M, Menon BK, et al. — HERMES collaboration meta-analysis (Lancet 2016; 387:1723-1731) — thrombectomy within 6 hours.
6. 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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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.