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CVA / STROKE

Master Integrated Clinical Learning Notes (MICL v1.0)

Note: This topic is too large for a single response with full depth. Delivered as two logical parts.

• Part 1 (this response): Big Picture → Clinical Thinking → University Notes → Integrated Learning → PG Markers → Additional PG Concepts → Vascular Syndromes → ICH
• Part 2 (next response on request): Previous Exam Trends → MCQs (100+) → Image-Based Learning → Videos → Memory Section → Common Mistakes → Rapid Revision Sheet → Confidence Ratings

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1. BIG PICTURE (8 Lines)

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2. CLINICAL THINKING FLOWCHART

Patient presents with SUDDEN onset focal neurological deficit
               ↓
    ─────────── FAST RECOGNITION ───────────
    Face drooping | Arm weakness | Speech slurred | Time to call
    (FAST criteria - Cincinnati Stroke Scale prehospital)
               ↓
    ┌────────── KEY HISTORY ──────────────┐
    │ • Exact time of onset (LAST KNOWN WELL)│
    │ • Progression: sudden vs gradual?      │
    │ • H/o AF, HTN, DM, smoking, OCP use   │
    │ • Prior TIA or stroke?                 │
    │ • Anticoagulation use?                 │
    │ • Headache at onset? (SAH → "worst ever")│
    │ • Trauma? (dissection / SDH)           │
    └────────────────────────────────────────┘
               ↓
    ┌────────── PHYSICAL EXAM ───────────────┐
    │ Vitals: BP both arms, SpO2, glucose    │
    │ GCS → NIHSS (0-42 scale, higher = worse)│
    │ Cranial nerves, motor, sensory, cerebellar│
    │ Neck: carotid bruit?                   │
    │ Heart: irregular pulse (AF)? murmur?   │
    └────────────────────────────────────────┘
               ↓
    ┌──────── IMMEDIATE INVESTIGATIONS ─────────┐
    │ 1. Non-contrast CT head (FIRST test - ALWAYS)│
    │    • Excludes hemorrhage before tPA        │
    │ 2. Blood glucose STAT (hypoglycemia mimics)│
    │ 3. ECG (AF detection)                      │
    │ 4. CBC, PT/INR/aPTT, platelets             │
    │ 5. Electrolytes, renal function, LFTs      │
    │ 6. Troponin (coexisting MI)                │
    │ 7. CXR                                     │
    └────────────────────────────────────────────┘
               ↓
    ┌──────── CT HEAD RESULT ─────────────────┐
    │ HEMORRHAGE PRESENT → see ICH pathway    │
    │ NO HEMORRHAGE → Ischemic stroke pathway │
    └─────────────────────────────────────────┘
               ↓
    ┌───── ISCHEMIC STROKE - TIME WINDOW ──────────────────────┐
    │ ≤4.5 hours since onset + no contraindications?           │
    │   → IV Alteplase (tPA) 0.9 mg/kg (max 90 mg)            │
    │   → 10% as bolus, 90% over 60 min                       │
    │ Large Vessel Occlusion (LVO) on CTA?                     │
    │   → Mechanical Thrombectomy up to 24 hrs (select patients)│
    │ tPA window missed / not eligible?                        │
    │   → Aspirin 300 mg within 24-48 hrs                     │
    │   → Dual antiplatelet if minor stroke/TIA (POINT trial) │
    └──────────────────────────────────────────────────────────┘
               ↓
    DIAGNOSIS CONFIRMED → ADMIT TO STROKE UNIT
               ↓
    ┌───── SECONDARY PREVENTION ────────────────────┐
    │ Antiplatelet (aspirin / clopidogrel)          │
    │ Statin (regardless of cholesterol level)     │
    │ Antihypertensive (ACEi/ARB preferred)        │
    │ Anticoagulation if AF (DOAC/warfarin)        │
    │ Carotid endarterectomy if >70% stenosis      │
    └───────────────────────────────────────────────┘
               ↓
    REHABILITATION → Physiotherapy, speech therapy, OT

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3. UNIVERSITY EXAMINATION NOTES

A. DEFINITION

• Stroke / CVA: Sudden onset focal (or global) neurological deficit lasting >24 hours due to vascular cause (WHO definition).
• TIA (Transient Ischemic Attack): Focal neurological deficit resolving within 24 hours (classically <1 hour; tissue-based definition: no infarction on imaging).
• RIND (Reversible Ischemic Neurological Deficit): Deficit resolving in >24 hours but <3 weeks (historical term, less used now).

B. CLASSIFICATION

┌──────────────────────────────────────────────────┐
│                    STROKE                        │
├────────────────────────┬─────────────────────────┤
│   ISCHEMIC (~80%)      │   HEMORRHAGIC (~20%)    │
├──────────┬─────────────┼──────────┬──────────────┤
│Thrombotic│  Embolic    │  ICH     │    SAH       │
│  (~33%)  │   (~25%)   │  (~15%)  │   (~5%)      │
├──────────┴─────────────┤          │              │
│   Lacunar (~25%)       │          │              │
│   Cryptogenic (>30%)   │          │              │
└────────────────────────┴──────────┴──────────────┘

C. ETIOLOGY & RISK FACTORS

• Carotid/vertebral dissection (leading identified cause in young)
• Antiphospholipid syndrome (lupus anticoagulant, anticardiolipin Ab)
• Protein C, S, Antithrombin III deficiency
• Sickle cell disease, polycythemia
• OCP use + migraine with aura
• Cocaine/amphetamines (vasoconstriction)
• CADASIL (cerebral autosomal dominant arteriopathy)
• Fabry disease (young men, angiokeratoma, renal failure)
• PFO (Patent Foramen Ovale) - paradoxical embolism

D. PATHOPHYSIOLOGY

Cerebral blood flow (CBF) normally = 50 mL/100g/min
               ↓ obstruction
CBF drops to <20 mL/100g/min → PENUMBRA (ischemic but salvageable)
CBF drops to <10 mL/100g/min → CORE INFARCT (irreversible)

ISCHEMIC CASCADE:
ATP failure → Na+/K+ pump fails → Cell swelling (cytotoxic edema)
↓
Glutamate release → NMDA receptor activation → Ca2+ influx
↓
Mitochondrial dysfunction → Free radical generation → Lipid peroxidation
↓
CELL DEATH (irreversible within minutes in core)

FRESH WATER vs OCEAN OF BRAIN ISCHEMIA:
• Penumbra = ischemic but alive → treatment window target
• Collateral circulation determines penumbra size
• "Time is Brain" = 1.9 million neurons/min lost

• Endothelial dysfunction → LDL oxidation → Foam cells → Fibrous plaque → Ulceration → Platelet adhesion → Thrombus → Occlusion or embolism

• HTN → Lipohyalinosis (fibrinoid necrosis of small perforating arteries) → Microinfarct 2-15 mm
• Locations: Basal ganglia, internal capsule, thalamus, pons, corona radiata

E. VASCULAR TERRITORY SYNDROMES ⭐⭐⭐

IPSILATERAL:
• Facial pain & temperature loss (5th nerve nucleus)
• Ataxia, nystagmus (cerebellum/vestibular)
• Horner's syndrome (descending sympathetics)
• Dysphagia, hoarseness (9th, 10th nerve nuclei)
• Palatal weakness

CONTRALATERAL:
• Limb/trunk pain & temperature loss (spinothalamic)
• [Touch and proprioception SPARED - preserved via medial lemniscus]

Memory trick: "DASHING" - Dysphagia, Ataxia, Sensory loss (contralateral), Horner's, Ipsilateral 5th, Nystagmus, Gag reflex loss

F. CLINICAL FEATURES

• Sudden ("like a switch being flicked"), maximal at onset (embolic) or stuttering/progressing (thrombotic)
• No headache typically (vs. hemorrhagic)
• Focal deficits based on territory (see above)
• May have cortical signs (aphasia, neglect, agnosia) - distinguishes from lacunar

• Headache + vomiting (raised ICP) more common
• Rapid deterioration
• Hypertension prominently elevated

• Right-sided weakness + aphasia → Left MCA stroke (dominant hemisphere)
• Left-sided weakness + neglect → Right MCA stroke
• Weakness arm > leg → Internal capsule lacune
• Leg > arm weakness → ACA territory
• Crossed signs (ipsilateral face + contralateral body) → BRAINSTEM

G. DIAGNOSIS

• 0-42; higher = more severe
• <4 = minor; 4-15 = moderate; >20 = severe
• Used for tPA eligibility and prognostication

H. INVESTIGATIONS (Systematic)

ACUTE WORKUP:
• STAT blood glucose (hypoglycemia mimics stroke!)
• CBC, platelets, coagulation (PT/INR, aPTT)
• Metabolic panel (Na, K, creatinine, LFTs)
• Cardiac enzymes (troponin - coexisting ACS)
• ECG (AF, LVH, Q waves)
• SpO2 / ABG if respiratory compromise
• Urine pregnancy test in women of childbearing age

IMAGING:
• Non-contrast CT head (FIRST - always)
• CTA head + neck (if LVO suspected)
• MRI brain DWI (if CT normal, posterior fossa lesion suspected)
• CT Perfusion or MRI perfusion (extended window thrombectomy)

ETIOLOGY WORKUP (after stabilization):
• 12-lead ECG + Holter monitor / prolonged cardiac monitoring (AF)
• Echocardiogram (TTE/TEE - cardiac emboli source)
• Carotid Doppler / duplex (stenosis)
• Fasting lipid profile, HbA1c, fasting glucose
• Young stroke: ANA, APLA (anticardiolipin, lupus anticoagulant),
  protein C, S, antithrombin III, factor V Leiden, homocysteine,
  VDRL (syphilis), HIV, vasculitis screen (ANCA, complement)
• Urine drug screen (cocaine)

I. MANAGEMENT

ISCHEMIC STROKE - ACUTE

STROKE RECOGNITION (FAST/BE-FAST)
     ↓
CALL EMS / ACTIVATE STROKE CODE
     ↓
Door-to-CT: <25 minutes
Door-to-Needle (tPA): <60 minutes (target)
Door-to-Groin (thrombectomy): <90 minutes

• Dose: 0.9 mg/kg IV, max 90 mg; 10% as bolus, 90% over 60 min
• Window: 0-4.5 hours from symptom onset
• Mechanism: Activates plasminogen → plasmin → fibrinolysis

• Age ≥18
• Ischemic stroke with measurable neurological deficit
• Onset <3 hours (standard); 3-4.5 hours (with additional exclusions)

• 0.25 mg/kg IV single bolus (simpler administration than alteplase)
• Non-inferior to alteplase; superior revascularization before thrombectomy in some trials
• Increasingly replacing alteplase in LVO patients being bridged to thrombectomy

• For Large Vessel Occlusion (ICA, M1, M2, basilar artery)
• Window: Up to 24 hours in selected patients (DAWN + DEFUSE-3 trials)
  • 0-6 hours: standard criteria
  • 6-16 hours: DAWN trial criteria
  • 6-24 hours: DEFUSE-3 trial criteria (perfusion imaging guided)
• Stent retrievers (e.g., Solitaire) = first-line device
• Can be done after tPA (bridging therapy) - tPA should NOT be delayed for thrombectomy evaluation

• Maintain SpO2 ≥94%, supplement O2 only if hypoxic
• Normoglycemia (target 140-180 mg/dL) - hyperglycemia worsens outcome
• Avoid hyperthermia (antipyretics if fever)
• DVT prophylaxis (compression stockings initially; avoid heparin first 24 hrs)
• Early mobilization (within 24 hrs if stable)
• Nil by mouth until dysphagia screened (aspiration risk)
• Foley catheter if needed; prevent UTI

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HEMORRHAGIC STROKE - ACUTE (ICH)

• If SBP 150-220 mmHg: acute lowering to SBP 140 mmHg is safe and may improve outcome
• Target SBP <140 mmHg acutely

• Cerebellar hemorrhage >3 cm or deteriorating → surgical evacuation (URGENT)
• Lobar ICH with mass effect in younger patients
• IVH with hydrocephalus → external ventricular drain (EVD)
• Hypertensive pontine/putaminal ICH → generally medical management

• Elderly patients with recurrent LOBAR hemorrhages
• Amyloid deposition in cortical vessels → fragile vessels → bleeding
• MRI gradient echo (GRE/SWI): multiple "microbleeds" (black dots)
• Boston criteria for diagnosis
• NO antiplatelets/anticoagulants (increases rebleed risk)

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SUBARACHNOID HEMORRHAGE (SAH)

• CT head: Hyperdensity in basal cisterns (Fisher grade)
• If CT negative + clinical suspicion: LP after 12 hours → xanthochromia (yellow CSF) ⭐⭐⭐
• CTA or DSA: Aneurysm localization

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J. SECONDARY PREVENTION ⭐⭐⭐

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K. COMPLICATIONS

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L. PREVENTION

• Control HTN (most important intervention in population)
• Anticoagulation for AF (CHA₂DS₂-VASc score guided)
• Statins for atherosclerosis
• Lifestyle modification
• Aspirin for high cardiovascular risk (evidence now controversial)
• Screen + treat carotid stenosis

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4. INTEGRATED LEARNING BOX

Anatomy Integration:

Physiology Integration:

• Cerebral autoregulation: CBF remains constant between MAP 60-160 mmHg. In chronic HTN, curve shifts right → higher baseline needed → explains permissive hypertension in acute stroke
• Penumbra physiology: Viable neurons at CBF 10-20 mL/100g/min; lose electrical function but not structural integrity; glutamate excitotoxicity kills them rapidly
• Cerebral perfusion pressure (CPP) = MAP - ICP → in hemorrhagic stroke with raised ICP, maintaining MAP critical

Biochemistry Integration:

• Troponin I/T: Released in stroke due to catecholamine surge → cardiac stunning (neurogenic cardiac injury) - do not mistake for primary MI
• BNP: Elevated in AF and heart failure → marker of cardioembolic risk
• Homocysteine: Elevated = independent risk factor (cofactor with B6, B12, folate); causes endothelial damage + thrombosis
• Lactate: Elevated in ischemic tissue → metabolic acidosis → cellular death cascade

Pathology Integration:

Pharmacology Integration:

Microbiology Integration:

• Syphilis (Treponema pallidum): Meningovascular syphilis → stroke in young → test VDRL/RPR in young stroke
• HIV: Vasculopathy, hypercoagulable state
• Varicella: Post-varicella vasculopathy → ischemic stroke in children
• TB meningitis → arteritis → ischemic stroke

Radiology Integration:

Medicine Integration:

• AF: CHA₂DS₂-VASc → anticoagulation decision
• Endocarditis → septic emboli → hemorrhagic infarcts (DO NOT anticoagulate)
• Sick sinus syndrome, recent MI (mural thrombus) → cardioembolic stroke
• PAN, SLE → cerebral vasculitis → stroke in young

Surgery Integration:

• Carotid endarterectomy (CEA): ≥70% symptomatic stenosis → significant benefit
• Decompressive hemicraniectomy: Malignant MCA infarction (<60 years)
• Coil embolization vs surgical clipping: SAH - both options; coiling preferred if suitable (ISAT trial)
• Surgical evacuation of cerebellar ICH >3 cm

Pediatrics Integration:

• Sickle cell disease → stroke in children (#1 cause in African-origin children)
• Exchange transfusion + TCD screening prevents stroke in SCA
• AHA 2026 guidelines now include children for alteplase and EVT consideration

OBG Integration:

• OCP → thrombotic stroke (especially with migraine with aura, smoking, age >35)
• Eclampsia/pre-eclampsia → cerebral hemorrhage + PRES (Posterior Reversible Encephalopathy)
• PRES: Headache, seizures, visual loss, altered consciousness; MRI: FLAIR hyperintensity parieto-occipital (vasogenic edema) - REVERSIBLE
• Peripartum cardiomyopathy → cardioembolic stroke
• Antiphospholipid syndrome → recurrent miscarriage + stroke

Psychiatry Integration:

• Post-stroke depression: 30% of patients; SSRIs (fluoxetine - FOCUS trial, modest benefit)
• Emotionalism (pseudobulbar affect): Involuntary crying/laughing
• Vascular dementia: Stepwise cognitive decline, focal deficits, history of stroke

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5. PG HIGH-YIELD MARKERS

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6. ADDITIONAL PG CONCEPTS (University misses these)

1. "Time is Brain" quantified: 1.9 million neurons/minute die in an untreated stroke. Every 10-min improvement in door-to-needle saves ~1 yr life (stat for integrated understanding).
2. DWI+/FLAIR- mismatch: Identifies wake-up strokes potentially within 6-hr window, allowing tPA even without known onset time (MR WITNESS, WAKE-UP trials).
3. ASPECTS score: Alberta Stroke Program Early CT Score - 10-point CT scoring system; ASPECTS <6 = poor outcome with thrombectomy; helps patient selection for EVT.
4. Hemorrhagic transformation types: HI1, HI2 (petechial; acceptable) vs PH1, PH2 (parenchymal hematoma; PH2 = clinical deterioration, "malignant transformation").
5. Cortical spreading depression: Electrophysiological phenomenon in penumbra that may contribute to infarct expansion; basis of migraine-stroke link.
6. Neurogenic stunned myocardium: Stroke (especially insular cortex or SAH) → massive catecholamine release → Takotsubo-like cardiomyopathy + ECG changes (T-wave inversions, QTc prolongation, U waves) + troponin rise. Do NOT confuse with ACS.
7. Malignant MCA infarction: Large MCA territory (>50%) → severe brain edema → herniation → death. Hemicraniectomy within 48 hrs in patients <60 years reduces mortality (HAMLET/DESTINY/DECIMAL trials).
8. Cryptogenic stroke + PFO: 25-30% of strokes labeled cryptogenic. PFO found in 40-50% of young cryptogenic stroke. Transcatheter PFO closure reduces recurrence in selected patients <60 years (CLOSE, REDUCE trials).
9. CADASIL: Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy. NOTCH3 gene mutation. Young adults: recurrent lacunar strokes, migraine with aura, dementia, psychiatric features. No atherosclerosis.
10. Cerebral venous sinus thrombosis (CVST): Thrombosis of dural sinuses → infarction + hemorrhage. Causes: OCP, pregnancy, puerperium, dehydration, hypercoagulable states. Imaging: "Empty triangle sign" on contrast CT (filling defect in superior sagittal sinus). Treatment: Anticoagulation (even with hemorrhage on imaging). ⭐⭐ INI-CET
11. Endpoint difference - tPA vs thrombectomy: tPA works for all clot sizes; thrombectomy specifically for LVO. They are complementary; tPA given first if eligible, then proceed to thrombectomy ("drip and ship" / "mothership" models).
12. Statin in hemorrhagic stroke: Evidence is mixed; generally not started acutely; if patient was on statin pre-stroke, continue.
13. PRES (Posterior Reversible Encephalopathy Syndrome): HTN, pre-eclampsia, immunosuppressants (cyclosporine, tacrolimus) → posterior predominant vasogenic edema on MRI. Clinically: seizures, headache, visual disturbance, confusion. Reversible with BP control / drug discontinuation.
14. Decompressive hemicraniectomy criteria: Age <60, unilateral MCA infarction >50%, NIHSS >15, surgery within 48 hrs - reduces mortality but survivors may have severe disability.
15. Anti-VEGF drugs + stroke: Bevacizumab → arterial thromboembolism risk; important pharmacology link.

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7. PREVIOUS EXAM TREND (Educational judgment - not confirmed exact data)

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8. HIGH-YIELD MCQs

Standard MCQs (10)

• Blood glucose must be checked before anything. Hypoglycemia is a stroke mimic and must be excluded STAT. If glucose is <50, correcting it may resolve all symptoms.
• A is wrong: aspirin given if tPA not indicated, not before glucose check
• C is wrong: cannot give tPA before excluding hypoglycemia and hemorrhage
• D is wrong: non-contrast CT comes before MRI, and glucose check is even before CT
• Pearl: The single most important STAT test = blood glucose

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• NCCT is fast, available, and primarily rules out hemorrhage before tPA. MRI DWI is more sensitive but takes longer and is not always immediately available.
• Pearl: "CT rules out hemorrhage; MRI detects ischemia"

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• Pre-tPA BP must be <185/110 mmHg. If achievable and maintained, tPA can be given.
• Post-tPA target: <180/105 mmHg for 24 hrs
• D is wrong: persistent uncontrolled BP is a contraindication, but treatable BP is NOT

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• INR >1.7 is a contraindication to tPA
• This is a common exam trap: even therapeutic anticoagulation prevents tPA
• Pearl: tPA absolute contraindication: INR >1.7, platelets <1,00,000, aPTT >40s

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• PCA infarction → contralateral homonymous hemianopia with MACULAR SPARING (macula has dual supply from MCA)
• Right PCA → left visual field loss (left homonymous hemianopia)

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• Pure motor hemiplegia = classic lacunar syndrome; posterior limb of internal capsule (corticospinal tract)
• No cortical signs: no aphasia, no neglect, no hemianopia = subcortical lesion

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• DAWN (16-24 hrs) and DEFUSE-3 (6-16 hrs) trials extended window to 24 hrs in select patients with perfusion mismatch
• Key qualifier: requires CT perfusion or MRI perfusion to identify salvageable tissue

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• Brain = liquefactive necrosis (enzymes from neurons themselves digest tissue → fluid-filled cavity = cystic encephalomalacia)
• All other organs (heart, kidney) = coagulative
• Exception among coagulative: TB → caseous; brain → liquefactive

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• Classic thunderclap headache = SAH until proven otherwise
• CT normal does not rule out SAH (especially after 6-24 hrs from onset)
• LP after 12 hours detects XANTHOCHROMIA reliably (takes time for RBC breakdown)
• Immediate LP may miss xanthochromia; do NOT do LP immediately

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• Nimodipine 60 mg orally every 4 hours for 21 days
• Nimodipine is an L-type Ca2+ channel blocker with selectivity for cerebral vasculature
• Does NOT clearly reverse established vasospasm but prevents it
• Reduces mortality and neurological deficit post-SAH

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NEET PG Level MCQs (10)

• Prior intracranial hemorrhage = ABSOLUTE contraindication to tPA (regardless of time elapsed)
• Minor stroke (NIHSS ≤3) on aspirin - DAPT (aspirin + clopidogrel for 21 days) is correct secondary prevention
• Technically B would be the secondary prevention; C is the immediate decision

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• Hypoglycemia (glucose <50 mg/dL) can mimic focal stroke including pure motor hemiplegia
• Mechanism: focal hypoglycemia preferentially affects vulnerable cortical/subcortical regions
• Pearl: Always check glucose FIRST in any stroke presentation

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• ICH score: Volume >30 mL (+1), IVH (+1), GCS 5-12 (+1), Age ≥80: no (age 78), location: putamen/supratentorial (+0)
• Total = 3 points
• Wait - GCS 9 = 5-12 = 1 point; Volume >30 = 1; IVH = 1; Age <80 = 0; Supratentorial = 0 → Total = 3
• Answer: A (3)

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• INTERACT2 and ATACH-2 trials: SBP 150-220 → reduce to 140 mmHg safe, may improve outcome
• <120 mmHg (aggressive) - ATACH-2 showed HARM at this level
• Unlike ischemic stroke (where permissive HTN protects penumbra), in ICH there is no penumbra - reducing BP is safe and beneficial

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• Empty triangle/delta sign = contrast CT filling defect in superior sagittal sinus = CVST
• Risk factors: OCP, females
• Treatment: ANTICOAGULATION (even in presence of hemorrhage on imaging - counterintuitive)
• Cross-territorial infarction, cortical hemorrhage, venous infarcts = think CVST

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• Amaurosis fugax = transient monocular blindness = TIA of ophthalmic artery
• Ophthalmic artery = first branch of ICA → emboli from ICA plaque
• "Curtain coming down over vision" = classic description
• Management: carotid Doppler; CEA if >70% stenosis

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• SAH → massive catecholamine surge → neurogenic cardiac injury
• Deep T-wave inversions (especially leads V2-V5), QTc prolongation, prominent U waves
• Can also cause atrial/ventricular arrhythmias
• Troponin may rise - do NOT confuse with ACS

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• Hemorrhagic transformation is most common with CARDIOEMBOLIC strokes
• Mechanism: embolus → occlusion → infarction → embolus fragments/lyses → reperfusion → hemorrhage into already damaged vessels
• Petechial hemorrhage within infarcted zone = HI1/HI2 pattern on CT

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• tPA converts plasminogen → plasmin → dissolves fibrin in the clot → arterial recanalization → reperfusion of ischemic penumbra
• The penumbra is electrically silent but structurally viable → time-sensitive rescue
• KEY: tPA does NOT help once the core infarct is established (no penumbra)

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• LVO (M1 MCA) + CT perfusion showing large penumbra + small core = ideal thrombectomy candidate
• Time window 6-24 hrs: DAWN/DEFUSE-3 criteria
• This is the paradigm shift in stroke management: perfusion imaging identifies salvageable tissue regardless of time window

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INI-CET Level MCQs (10)

• Neck manipulation → ICA dissection → intimal tear → thrombus → embolic stroke + Horner's syndrome (sympathetic chain runs along ICA)
• Carotid dissection = leading IDENTIFIED cause of stroke in young
• Ipsilateral Horner's + contralateral hemiplegia = ICA dissection
• Treatment: Anticoagulation or antiplatelet (both debated; CADISS trial)

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• Pontine hemorrhage = "flame-shaped" or "basin-shaped" hyperdensity in the pons
• Classic triad: Coma + pinpoint pupils (bilateral pontine sympathetic disruption) + hyperthermia
• Extremely poor prognosis; typically no surgery
• Bilateral pinpoint pupils are DIAGNOSTIC of pontine lesion

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• Idarucizumab (Praxbind) = specific, humanized monoclonal antibody fragment that reverses dabigatran
• Dabigatran is a direct thrombin inhibitor
• Protamine reverses heparin; 4F-PCC reverses warfarin/Xa inhibitors; vitamin K reverses warfarin
• Pearl for INI-CET: Know specific antidotes: Dabigatran → Idarucizumab; Xa inhibitors → Andexanet alfa; Warfarin → Vitamin K + 4F-PCC

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• DWI becomes positive within MINUTES - TRUE
• FLAIR becomes positive AFTER DWI (typically >6 hrs) - FALSE for statement 2
• DWI+/FLAIR- = likely within 6 hours (WAKE-UP trial used 4.5 hrs for tPA eligibility) - TRUE (roughly)
• This mismatch identifies "wake-up strokes" for thrombolysis

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• Classic Wallenberg (lateral medullary syndrome) = PICA occlusion
• PICA supplies lateral medulla
• AICA infarction: similar but adds ipsilateral deafness (cochlear nucleus) + facial nerve palsy

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• Antiphospholipid syndrome (APS): recurrent thrombosis + pregnancy loss + APLA antibodies
• OCP further increases thrombotic risk
• Treatment: Long-term anticoagulation (warfarin with INR 2-3, or higher target 3-4 if arterial)
• Discontinue OCP; switch contraception

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• ASPECTS = 10 points; each MCA territory subdivision = 1 point
• Score 0 = entire MCA territory infarcted; Score 10 = normal
• ASPECTS ≤6 = extensive early ischemic changes → poor thrombectomy outcome
• Many trials used ASPECTS ≥6 as inclusion criterion for EVT
• Recent trials (SELECT2, RESCUE-Japan) show even ASPECTS 0-5 may benefit in selected cases

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• Delayed cerebral ischemia (DCI) = vasospasm occurs Day 4-14 post-SAH (peak Day 7)
• TCD: raised velocities in MCA >120 cm/s = vasospasm
• Rebleeding is an EARLY complication (Day 1)
• Prevention: Nimodipine; treatment of established vasospasm: "Triple H" therapy (hypertension, hypervolemia, hemodilution - less evidence now) + endovascular papaverine/balloon angioplasty

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• Anticoagulation is CONTRAINDICATED in CAA (increases rebleed risk dramatically)
• CAA: APOE ε4 allele is a risk factor - TRUE
• Cortical/leptomeningeal amyloid deposition - TRUE
• SWI microbleeds (cortical/subcortical) - TRUE
• No proven treatment to prevent recurrence except avoiding antithrombotics

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• Destructive frontal lesion → eyes deviate TOWARD the lesion side (look toward stroke)
• Destructive pontine lesion → eyes deviate AWAY from the lesion (look away from brainstem lesion)
• Memory: "Frontal lesion looks at hemiplegia" (toward lesion side); "Pontine lesion looks away from hemiplegia" (away from lesion)

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Clinical Case MCQs (5)

• "Wake-up stroke" = unknown onset time (last known well = midnight)
• Last known well = midnight → >6 hours from earliest possible onset
• AHA guidelines: DWI+/FLAIR- mismatch on MRI can guide tPA in wake-up strokes
• If MRI shows restricted diffusion on DWI but no FLAIR signal = likely within 4.5-6 hrs
• WAKE-UP trial: MRI-guided tPA in unknown onset stroke → better functional outcomes

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• AF → cardioembolic → large vessel occlusion likely
• High NIHSS (16) suggests LVO
• tPA should be given if eligible (within 4.5 hrs, no contraindications)
• Simultaneous CTA to identify LVO for thrombectomy
• tPA + thrombectomy = "bridging therapy" = best outcomes in LVO
• BP 170/100 is below the 185/110 threshold → can give tPA

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• Puerperium = highest risk period for CVST
• Multiple cortical infarcts crossing vascular territories = venous infarction
• If CT showed empty delta sign → confirms CVST
• Treatment: ANTICOAGULATE (even if hemorrhagic infarcts present)
• Peripartum cardiomyopathy is possible (C) but typically single territory infarct

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• BP >185/110 = relative contraindication to tPA; can be TREATED and tPA given
• Use IV labetalol 10-20 mg bolus OR nicardipine infusion to lower BP
• Target <185/110 before tPA, then <180/105 for 24 hrs after
• D is wrong: treatable hypertension is NOT an absolute contraindication

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• Major surgery within 14 days = RELATIVE contraindication to tPA (risk of bleeding at surgical site)
• Most guidelines: surgery within 14 days (some use 3 months for intracranial/spinal surgery specifically)
• Consider thrombectomy if LVO present and bleeding risk from surgery site acceptable
• Pearl: Post-surgical strokes are a common clinical scenario MCQ; always remember surgical exclusion criteria

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Image-Based MCQs (5)

• Hyperdense MCA sign (also "hyperdense dot sign" for distal branches)
• Represents acute thrombus in MCA - fresh clot is hyperdense on CT
• This sign indicates LVO → patient may benefit from thrombectomy
• Seen in embolic strokes; sensitivity low (~25-35%) but highly specific

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• Acute ischemia: DWI hyperintense + ADC hypointense = RESTRICTED DIFFUSION
• "Bright on DWI, Dark on ADC" = ACUTE (hours to ~10 days)
• Chronic: DWI dark (T2 blackout), ADC bright (free water/gliosis)
• This is the most tested MRI MCQ in stroke

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• Hypertensive ICH: most common site = putamen (via lenticulostriate arteries)
• Hyperdense lesion = fresh blood (40-80 HU)
• Clinical: severe hypertension + acute onset neurological deficit + headache/vomiting
• Metastasis: ring-enhancing on contrast; abscess: ring enhancement + surrounding edema + fever

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• Empty delta/triangle sign = filling defect surrounded by contrast in sagittal sinus = CVST
• Also called "cord sign" on non-contrast CT (hyperdense thrombosed sinus)
• Treatment: ANTICOAGULATION
• Associated with OCP, pregnancy, puerperium, dehydration

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• Chronic hypertension → small vessel disease → periventricular white matter changes + lacunae
• Binswanger disease = hypertensive subcortical encephalopathy
• CAA: lobar hemorrhages + cortical microbleeds, not predominantly periventricular
• CADASIL: NOTCH3 mutation, autosomal dominant, younger patients, characteristic temporal pole involvement on MRI

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9. IMAGE-BASED LEARNING

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10. FREE VIDEO RECOMMENDATIONS

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11. MEMORY SECTION

Mnemonic - FAST (Prehospital Stroke Recognition):

Mnemonic - BE-FAST (extended):

Mnemonic - Wallenberg Syndrome "DASHING":

Mnemonic - tPA Contraindications "BRAIN BLEED":

Comparison Table - Ischemic vs Hemorrhagic Stroke:

Comparison Table - Fresh water / SAH vs Stroke:

Visual Memory - Artery territories (simple):

          ACA = LEG
         /
 ←  BRAIN  → MCA = FACE + ARM + SPEECH (dominant)
         \
          PCA = VISION (posterior)
          
BRAINSTEM = CROSSED SIGNS (ipsilateral face + contralateral body)

One-line Memory Rules:

• "DWI bright, ADC dark = ACUTE stroke" ⭐
• "Brain = liquefactive necrosis (only organ)" ⭐
• "Worst headache of life = SAH until proven otherwise" ⭐
• "PCom aneurysm = CN III palsy (blown pupil)" ⭐
• "Nimodipine prevents vasospasm in SAH" ⭐
• "Permissive hypertension in ischemic stroke" ⭐
• "Empty triangle sign = CVST" ⭐
• "Anticoagulate CVST even if there is hemorrhage" ⭐
• "Cerebellar ICH >3 cm = surgical emergency" ⭐
• "Crossed signs = brainstem lesion" ⭐

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12. COMMON MISTAKES

1. Giving tPA without checking blood glucose - hypoglycemia must be excluded first; classic exam trap.
2. Treating hypertension aggressively in ischemic stroke - permissive HTN protects penumbra; only treat if >220/120 without tPA, or >185/110 before tPA.
3. Saying ICH is treated with tPA - absolute contraindication; often confused in rushed MCQ reading.
4. Missing the INR >1.7 contraindication for tPA - even "therapeutic" anticoagulation precludes tPA.
5. Confusing Wallenberg (PICA) with AICA: PICA = no hearing loss; AICA = adds ipsilateral deafness + facial nerve palsy.
6. Saying brain infarction is coagulative necrosis - brain is the exception: LIQUEFACTIVE necrosis.
7. LP immediately in suspected SAH - must wait 12 hours for xanthochromia to develop; immediate LP may be negative.
8. Confusing nimodipine "treating" vs "preventing" vasospasm - it PREVENTS vasospasm and neurological deficits but does not clearly reverse established vasospasm.
9. Anticoagulating CAA patients - contraindicated; lobar bleeds will recur.
10. Dexamethasone for stroke edema - harmful in stroke (increases glucose, no benefit); steroids are for TUMOR or abscess edema, NOT stroke.

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13. RAPID REVISION SHEET

CVA/STROKE - ONE PAGE RAPID REVISION

DEFINITION: Sudden focal neurological deficit >24 hrs from vascular cause

TYPES: Ischemic 80% (thrombotic/embolic/lacunar) | ICH 15% | SAH 5%

#1 MODIFIABLE RISK FACTOR: Hypertension
#1 CARDIAC CAUSE OF EMBOLIC STROKE: Atrial fibrillation
#1 CAUSE OF ICH: Hypertension → putamen (#1 site)
#1 SITE OF ICH IN ELDERLY LOBAR: Cerebral amyloid angiopathy

FIRST TEST: Non-contrast CT head (exclude hemorrhage before tPA)
MOST SENSITIVE IMAGING FOR ACUTE ISCHEMIA: MRI DWI (positive within minutes)
DWI bright + ADC dark = ACUTE INFARCT

tPA:
• Dose: 0.9 mg/kg IV (max 90 mg); 10% bolus + 90% over 60 min
• Window: ≤4.5 hours
• BP must be <185/110 before; <180/105 during/after 24 hrs
• Absolute CI: Prior ICH, ICH on CT, INR >1.7, platelets <1L, surgery within 14 days

PERMISSIVE HYPERTENSION in ischemic stroke:
• Do NOT lower BP unless >220/120 (no tPA) or >185/110 (pre-tPA)

MECHANICAL THROMBECTOMY: LVO, up to 24 hrs (DAWN/DEFUSE-3 trials)

VASCULAR SYNDROMES:
• MCA (dominant): Hemiplegia (face+arm>leg) + aphasia + hemianopia
• MCA (non-dominant): Hemiplegia + neglect + anosognosia
• ACA: Leg > arm weakness
• PCA: Hemianopia + macular SPARING
• PICA (Wallenberg): DASHING + ipsilateral Horner's
• BRAINSTEM: Crossed signs (ipsilateral face + contralateral body)

LACUNAR (Fisher's 5):
Pure Motor (#1) → Internal capsule / pons
Pure Sensory → VPL thalamus
Ataxic Hemiparesis → Pons
Dysarthria-Clumsy Hand → Pons
Sensorimotor → Thalamus + capsule

BRAIN NECROSIS TYPE: Liquefactive (only organ; all others coagulative)

ICH MANAGEMENT:
• SBP target: <140 mmHg (INTERACT2)
• Cerebellar ICH >3 cm: SURGICAL EMERGENCY
• Warfarin reversal: Vitamin K + 4F-PCC
• Dabigatran reversal: Idarucizumab
• NO tPA, NO aspirin acutely

SAH:
• Cause: Berry aneurysm (85%) → Anterior communicating #1 > PCom #2
• PCom aneurysm → CN III palsy (blown pupil, ptosis, down-out eye)
• CT: Basal cistern hyperdensity
• CT negative → LP after 12 hrs → Xanthochromia (yellow CSF)
• Vasospasm: Day 4-14 → Nimodipine 60 mg PO q4h × 21 days
• Rebleed: first 24 hrs → secure aneurysm ASAP

CVST:
• Risk: OCP, puerperium, dehydration
• Sign: Empty delta/triangle sign on contrast CT
• Treatment: ANTICOAGULATE (even if hemorrhage present)

CHA₂DS₂-VASc ≥2 (men) or ≥3 (women) → Anticoagulate for AF

SECONDARY PREVENTION:
• Antiplatelets + statin (ALL ischemic stroke) + antihypertensive + anticoagulate (if AF)
• CEA if ipsilateral stenosis ≥70%

STROKE MIMICS: Hypoglycemia (#1 important) | Todd's palsy | Complex migraine

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14. CONFIDENCE RATING

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Part 2 (available on request): Will cover Extended PYQ analysis with individual topic breakdown, 10 more clinical case MCQs, 10 assertion-reason MCQs, complete memory map diagrams, inter-subject integration scenarios (e.g., stroke + MI + pharmacology combined case), and updated 2026 AHA guideline deep-dive including tenecteplase data and pediatric stroke updates.