Cns case presentation and discussion and complete viva questions and answers for mbbs medicine practical examination

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CNS CASE PRESENTATION - STROKE (CEREBROVASCULAR ACCIDENT)

MBBS Medicine Practical Examination - Complete Guide


PART 1: CASE PRESENTATION


PRESENTING THE CASE TO THE EXAMINER


"Sir/Ma'am, I would like to present my case."

BIODATA

Name: Mr. Ramesh Kumar Age: 62 years Sex: Male Occupation: Retired government employee Residence: Urban Informant: Patient and wife (history partially obtained from wife as patient has dysphasia) Reliability: Moderately reliable

CHIEF COMPLAINTS

  1. Sudden onset weakness of right side of the body - 3 days
  2. Inability to speak properly - 3 days
  3. Deviation of angle of mouth to the left - 3 days

HISTORY OF PRESENT ILLNESS

The patient was apparently well 3 days back when, at around 8 AM after waking up, he suddenly developed weakness of the right upper and lower limb. The weakness was sudden in onset, progressed to complete inability to move the right side within 30 minutes. There was no preceding headache, vomiting, or loss of consciousness. Simultaneously, the patient developed difficulty in speaking - he could not express himself clearly though he appeared to understand commands (suggesting Broca's/expressive aphasia). The angle of his mouth deviated to the left side.
Positive history:
  • No seizures at onset or afterwards
  • No preceding TIA episodes (no prior transient weakness/vision loss/speech disturbance)
  • No trauma
  • No fever or neck stiffness
Negative history:
  • No recent myocardial infarction
  • No palpitations (no obvious AF)
  • No visual complaints at onset
  • No bladder/bowel involvement initially

PAST HISTORY

  • Hypertension - known for 8 years, on Tab. Amlodipine 5 mg OD, poorly controlled
  • Type 2 Diabetes Mellitus - 5 years, on Tab. Metformin 500 mg BD
  • No prior strokes or TIAs
  • No history of cardiac disease, rheumatic fever, valvular heart disease
  • No history of anticoagulant use

PERSONAL HISTORY

  • Diet: Mixed
  • Appetite: Decreased since illness
  • Sleep: Disturbed
  • Bowel: Constipated since illness
  • Bladder: No incontinence
  • Smoking: 20 pack-year history, stopped 5 years ago
  • Alcohol: Occasional, social
  • No illicit drug use

FAMILY HISTORY

  • Father died of a "brain attack" (stroke) at 70 years
  • Mother: Hypertension
  • No family history of bleeding disorders

SOCIOECONOMIC HISTORY

Middle socioeconomic class. Lives with wife and son. Good support system available for rehabilitation.

SUMMARY OF HISTORY

"To summarize, this is a 62-year-old hypertensive diabetic male with a positive family history of stroke, who presented 3 days ago with sudden onset right-sided hemiplegia and expressive aphasia, consistent with a left-sided cerebrovascular accident likely in the territory of the left middle cerebral artery."

PHYSICAL EXAMINATION


GENERAL EXAMINATION

  • Patient conscious, alert, but anxious
  • Lying in bed with right arm and leg in characteristic posture
  • Oriented to person and place (difficulty in verbal response due to aphasia)
  • Built: Average, mildly obese
  • Nourishment: Adequate
Vitals:
ParameterFinding
Pulse84/min, regular, normal volume, all peripheral pulses palpable
Blood Pressure164/96 mmHg (right arm), measured both arms
Respiratory Rate18/min
Temperature98.6°F (afebrile)
SpO297% on room air
No pallor, cyanosis, jaundice, clubbing, lymphadenopathy, or edema.
Fundus examination (examiner may ask): Hypertensive retinopathy - AV nicking, silver wiring (grade II changes).

NEUROLOGICAL EXAMINATION

(Present in this order: Higher functions → Cranial nerves → Motor → Sensory → Reflexes → Cerebellar → Meningeal signs)

HIGHER MENTAL FUNCTIONS

  • Consciousness: Alert, GCS = 14/15 (E4 V4 M6) - verbal score reduced due to aphasia
  • Orientation: Oriented to person and place, partially to time
  • Speech: Expressive aphasia (Broca's aphasia) - non-fluent speech, difficulty in naming and repetition, comprehension relatively preserved
  • Memory: Difficult to fully assess due to aphasia
  • Attention: Maintained

CRANIAL NERVE EXAMINATION

NerveFinding
I (Olfactory)Not tested routinely
II (Optic)Visual fields: Right homonymous hemianopia (right side). Visual acuity: Unable to fully assess. Fundus: Hypertensive retinopathy
III, IV, VIConjugate gaze deviation to the LEFT (patient looks towards the lesion side). No ptosis. Pupils 3mm bilaterally, equal and reactive to light
V (Trigeminal)Corneal reflex reduced on right. Jaw jerk normal. Facial sensation impaired on right side
VII (Facial)Right-sided lower motor neuron? NO - Right-sided UPPER motor neuron type facial palsy - forehead sparing, drooping of right nasolabial fold, angle of mouth deviated to LEFT (healthy side), Bell's phenomenon ABSENT (UMN)
VIIIHearing: Not significantly impaired
IX, XUvula deviated to left (right-sided palatal weakness), gag reflex reduced on right
XIRight sternomastoid and trapezius weakness (involvement of right UMN supply)
XIITongue deviates to the RIGHT on protrusion (right-sided tongue weakness - deviates to side of lesion)

MOTOR SYSTEM EXAMINATION

Inspection:
  • Wasting: None (acute presentation)
  • Fasciculations: Absent
  • Posture: Right arm flexed (flexion synergy), right leg extended
  • Involuntary movements: None
Tone:
  • Right upper limb: Increased (spasticity/clasp-knife rigidity)
  • Right lower limb: Increased (spasticity)
  • Left limbs: Normal
Power (MRC grading):
LimbProximalDistal
Right Upper Limb2/51/5
Right Lower Limb2/52/5
Left Upper Limb5/55/5
Left Lower Limb5/55/5
Coordination:
  • Finger-nose test: Unable to perform on right. Normal on left.

REFLEXES

ReflexRightLeft
Biceps (C5,6)Exaggerated (+++)Normal (++)
Triceps (C7)Exaggerated (+++)Normal (++)
Supinator (C5,6)ExaggeratedNormal
Knee jerk (L3,4)Exaggerated (+++)Normal (++)
Ankle jerk (S1,2)Exaggerated (+++)Normal (++)
Plantar (Babinski)EXTENSOR (positive Babinski sign - big toe dorsiflexes)Flexor (normal)
Abdominal reflexesAbsent on rightPresent on left
ClonusPresent at right ankleAbsent

SENSORY SYSTEM

  • All modalities (pain, temperature, light touch, vibration, proprioception) reduced over right side
  • Cortical sensations (two-point discrimination, stereognosis): Impaired on right
  • No sensory level

CEREBELLAR EXAMINATION

  • Gait: Unable to assess (patient bedridden)
  • No nystagmus, dysarthria (masked by aphasia), dysdiadochokinesia not testable on right

MENINGEAL SIGNS

  • Neck stiffness: ABSENT
  • Kernig's sign: ABSENT
  • Brudzinski's sign: ABSENT
(Absence of meningeal signs makes meningitis/SAH less likely)

PART 2: DISCUSSION


SUMMARY OF EXAMINATION FINDINGS

"On neurological examination, this patient has:
  1. Expressive (Broca's) aphasia
  2. Right homonymous hemianopia
  3. Right-sided UMN facial palsy
  4. Right-sided spastic hemiplegia (UMN pattern - tone increased, power reduced, reflexes exaggerated, Babinski positive)
  5. Right-sided hemisensory loss
  6. Gaze deviation to the left
These findings together constitute a LEFT MIDDLE CEREBRAL ARTERY (MCA) TERRITORY INFARCT."

DIAGNOSIS

Working Diagnosis: Left Middle Cerebral Artery Ischemic Stroke
Basis:
  • Sudden onset
  • Right hemiplegia (contralateral to lesion) - UMN pattern
  • Expressive aphasia (left hemisphere dominant for language in right-handed individuals)
  • Right homonymous hemianopia
  • Right hemisensory loss
  • Hypertensive, diabetic, smoker - multiple vascular risk factors
  • Gaze deviation towards lesion side
  • Absence of meningeal signs (against hemorrhage/meningitis)
  • Absence of fever (against meningitis/cerebral abscess)

CLASSIFICATION OF STROKE

TypeFrequencyMechanism
Ischemic stroke~80%Thrombosis, embolism, lacunar
Intracerebral hemorrhage~15%Hypertensive, AVM, amyloid
Subarachnoid hemorrhage~5%Aneurysm rupture
In this patient: Ischemic stroke most likely - No sudden thunderclap headache, no meningeal signs, gradual onset (took 30 min to peak), classic vascular risk factors.

INVESTIGATIONS

Immediate (Emergency)

  1. Non-contrast CT Brain - FIRST investigation; to exclude hemorrhage (appears as hyperdense area within 6 hours; ischemic infarct appears hypodense after 24-48 hours)
  2. MRI Brain (DWI - Diffusion Weighted Imaging) - Most sensitive for early ischemic stroke (shows restricted diffusion within minutes to hours)
  3. 12-lead ECG - Atrial fibrillation? Evidence of MI?
  4. Blood glucose (exclude hypoglycemia mimicking stroke)
  5. Complete blood count (CBC)
  6. Coagulation profile: PT, aPTT, INR
  7. Renal function tests (BUN, creatinine)
  8. Electrolytes (Na, K)
  9. Cardiac enzymes (Troponin I/T)
  10. Serum lipid profile

To Determine Etiology

  1. 2D Echocardiogram - Valvular disease, thrombus, patent foramen ovale
  2. Carotid Doppler ultrasound - Carotid stenosis/plaques
  3. MR Angiography (MRA) or CT Angiography (CTA) - Vascular occlusion site
  4. Holter monitoring (24-48 hours) - Paroxysmal AF
  5. HbA1c - Glycemic control assessment
  6. Fasting lipid profile

Expected Results in This Patient

  • CT brain: Normal in first 6-24 hours OR may show early MCA sign (hyperdense MCA)
  • MRI DWI: Bright signal in left MCA territory (restricted diffusion)
  • ECG: May show left ventricular hypertrophy (due to hypertension)
  • Blood glucose: Elevated (uncontrolled DM)

MANAGEMENT

A. ACUTE MANAGEMENT (First 24-72 hours)

1. ABC and Supportive Care
  • Ensure airway (position patient, suction if needed)
  • O2 supplementation only if SpO2 <94%
  • IV access - two large bore peripheral lines
  • Cardiac monitoring and continuous pulse oximetry
  • Nil by mouth initially (dysphagia risk - NGT if needed)
  • Foley catheter for urinary output monitoring
2. Blood Pressure Management
  • In ischemic stroke patients NOT receiving thrombolysis: Allow permissive hypertension (do NOT lower BP unless >220/120 mmHg) - brain needs collateral perfusion
  • If eligible for tPA: Lower BP to <185/110 mmHg before administration
  • Avoid abrupt BP lowering - can worsen ischemia
3. Blood Glucose
  • Target: 140-180 mg/dL
  • Treat hypoglycemia (<60 mg/dL) immediately - it mimics stroke
  • Avoid hyperglycemia (worsens infarct)
4. Thrombolytic Therapy (IV rt-PA / Alteplase)
  • Indication: Ischemic stroke within 4.5 hours of symptom onset
  • Dose: 0.9 mg/kg IV (max 90 mg); 10% as bolus, 90% over 60 min
  • NIHSS should be documented before administration
Contraindications to tPA:
  • Hemorrhage on CT
  • BP >185/110 mmHg (refractory)
  • Platelet count <100,000/mm³
  • INR >1.7 or on anticoagulants
  • Recent surgery (<14 days)
  • Prior stroke or head trauma within 3 months
  • Blood glucose <50 or >400 mg/dL
  • Known intracranial hemorrhage, AVM, or tumor
5. Mechanical Thrombectomy
  • Indication: Large vessel occlusion (LVO), within 6-24 hours if mismatch criteria met
  • Highly effective for proximal MCA/ICA/basilar artery occlusion
6. Antiplatelet Therapy
  • Aspirin 300 mg stat (if no hemorrhage on CT and thrombolysis not given/completed >24 hrs)
  • Do NOT give aspirin within 24 hours of tPA

B. SECONDARY PREVENTION

CategoryTreatment
AntiplateletAspirin 75-100 mg/day OR Clopidogrel 75 mg/day OR Dual (Aspirin + Clopidogrel for 21 days if minor stroke/TIA)
AnticoagulationWarfarin or NOAC (Apixaban/Rivaroxaban) if AF detected
StatinHigh-intensity statin (Atorvastatin 40-80 mg)
AntihypertensivesACE inhibitor + Thiazide diuretic (post-acute phase)
Diabetes controlOptimize glycemic control (target HbA1c <7%)
LifestyleSmoking cessation, diet modification, regular exercise

C. REHABILITATION

  • Physiotherapy (early mobilization - Day 1-2 if stable)
  • Occupational therapy (ADL retraining)
  • Speech therapy (for aphasia and swallowing)
  • Psychological support
  • Prevention of complications: DVT prophylaxis, pressure sores, aspiration pneumonia

COMPLICATIONS

Early (Days to weeks):
  • Cerebral edema (peak at 3-5 days) - malignant MCA infarction
  • Hemorrhagic transformation
  • Aspiration pneumonia (most common cause of early death)
  • DVT and pulmonary embolism
  • Urinary tract infection
  • Pressure sores
Late:
  • Post-stroke depression (very common, ~30%)
  • Spasticity and contractures
  • Epilepsy (post-stroke seizures)
  • Vascular dementia
  • Recurrent stroke (risk ~10% in first year)

PART 3: COMPLETE VIVA QUESTIONS AND ANSWERS


SECTION A - DEFINITION AND CLASSIFICATION

Q1. Define stroke. A: Stroke is defined as a rapidly developing clinical syndrome of focal (or global) neurological disturbance due to a vascular cause, lasting more than 24 hours or leading to death, with no apparent cause other than vascular origin. (WHO definition). If symptoms resolve within 24 hours, it is called a Transient Ischemic Attack (TIA). Note: Modern definition considers tissue-based criteria - TIA has no permanent infarction on imaging even if symptoms last >24 hrs.
Q2. How is stroke classified? A:
  • Ischemic stroke (80%): Thrombotic (large vessel, small vessel/lacunar), Embolic (cardiogenic, artery-to-artery)
  • Hemorrhagic stroke (20%):
    • Intracerebral hemorrhage (ICH) - 15%
    • Subarachnoid hemorrhage (SAH) - 5%
Q3. What is a TIA? A: A TIA (Transient Ischemic Attack) is a brief episode of focal neurological dysfunction of vascular origin lasting typically <1 hour, with complete recovery and no evidence of infarction on imaging. It is a medical emergency (stroke risk is highest in the days after TIA - up to 10% risk within 2 days). It should be assessed using the ABCD2 score.
Q4. What are lacunar infarcts? A: Lacunar infarcts are small infarcts (<15 mm) in the deep white matter, basal ganglia, thalamus, or brainstem, caused by occlusion of small penetrating arteries (lenticulostriate, thalamoperforating). They are strongly associated with hypertension and diabetes. Classic lacunar syndromes include: pure motor hemiplegia (posterior limb of internal capsule), pure sensory stroke (thalamus), sensorimotor stroke, ataxic hemiparesis, dysarthria-clumsy hand syndrome.

SECTION B - ETIOLOGY AND RISK FACTORS

Q5. What are the risk factors for stroke? A:
  • Non-modifiable: Age (>55 years, risk doubles each decade), sex (males > females), race, family history, prior stroke/TIA
  • Modifiable:
    • Hypertension (most important, accounts for ~50% attributable risk)
    • Atrial fibrillation (5-fold increased risk)
    • Diabetes mellitus
    • Hyperlipidemia
    • Smoking
    • Obesity
    • Physical inactivity
    • Excessive alcohol use
    • Oral contraceptive pills (especially + smoking + migraine with aura)
    • Carotid artery stenosis
    • Cardiac disease (heart failure, valvular disease, PFO)
Q6. What are cardiac causes of embolic stroke? A:
  • Most common: Atrial fibrillation (AF) - 50% of cardioembolic strokes
  • Rheumatic heart disease with mitral stenosis
  • Infective endocarditis
  • Prosthetic heart valves
  • Acute MI with mural thrombus
  • Left ventricular aneurysm
  • Cardiomyopathy with reduced EF
  • Patent foramen ovale (PFO) - paradoxical embolism
  • Left atrial myxoma (rare but important)
Q7. How does AF cause stroke? A: In AF, the irregular atrial contraction leads to blood stasis in the left atrial appendage, resulting in thrombus formation. This thrombus can embolize to the cerebral circulation causing embolic stroke. The risk is highest in non-valvular AF with CHA2DS2-VASc score >2.

SECTION C - PATHOPHYSIOLOGY

Q8. What is the ischemic penumbra? A: After arterial occlusion, two zones are created:
  • Core: CBF <10-12 mL/100g/min - irreversibly infarcted tissue within minutes
  • Penumbra: CBF 12-23 mL/100g/min - ischemic but potentially salvageable tissue if reperfusion occurs in time
The penumbra is the therapeutic target of thrombolysis and thrombectomy. Normal CBF is ~55 mL/100g/min.
Q9. Why does UMN facial palsy spare the forehead? A: The forehead (frontalis muscle) receives bilateral cortical innervation (from both hemispheres). Therefore, even if one hemisphere is damaged (as in stroke), the contralateral hemisphere still provides cortical input to the forehead via the intact corticobulbar tract. Hence, in UMN (supranuclear) facial palsy, only the lower face is affected. In LMN (nuclear/infranuclear) facial palsy, the entire face including forehead is involved.
Q10. Why does the tongue deviate towards the side of the lesion in UMN lesions (for stroke)? A: In UMN lesions, the tongue deviates TOWARDS the side of the WEAKNESS (the same side as the hemiplegia), which is the OPPOSITE side to the brain lesion. The genioglossus muscle pushes the tongue forward; the weaker side cannot push effectively, so the tongue deviates to the weak/affected side. This is in contrast to LMN lesions where the tongue also deviates to the weak side (same principle). In UMN stroke affecting the left hemisphere, the right side is weak, and the tongue deviates to the right.
Q11. Why does conjugate gaze deviation occur, and which direction does it deviate in stroke? A: The frontal eye field (FEF) in each hemisphere drives the eyes AWAY from that hemisphere (contralaterally). In a left hemispheral stroke:
  • The left FEF is damaged
  • The right FEF is unopposed
  • Eyes are driven to the LEFT (towards the side of the lesion)
  • The patient "looks towards the lesion" This is contrasted with pontine lesions where the eyes deviate AWAY from the lesion (towards the hemiplegia side).

SECTION D - CLINICAL FEATURES AND SYNDROMES

Q12. What are the features of complete MCA territory infarction? A:
  • Contralateral hemiplegia (face and upper limb > lower limb)
  • Contralateral hemisensory loss
  • Contralateral homonymous hemianopia
  • Conjugate gaze deviation towards lesion side
  • Left MCA (dominant hemisphere): Aphasia (Broca's or Wernicke's depending on division)
  • Right MCA (non-dominant hemisphere): Contralateral neglect, anosognosia, constructional apraxia
  • Severe malignant MCA infarction can cause life-threatening cerebral edema
Q13. Differentiate ACA, MCA, and PCA infarcts:
FeatureACAMCAPCA
Motor weaknessLeg > armArm + face > legMinimal or absent
Sensory lossLeg > armArm + face > legContralateral hemisensory
Visual defectNoneHomonymous hemianopiaHomonymous hemianopia (macular sparing)
SpeechTranscortical motor aphasiaBroca's/Wernicke's (left)Alexia without agraphia
OtherAbulia, grasp reflexNeglect (right MCA)Thalamic pain, visual agnosia
Q14. What is the lateral medullary syndrome (Wallenberg syndrome)? A: Caused by infarction of the lateral medulla due to PICA (Posterior Inferior Cerebellar Artery) or vertebral artery occlusion. Features include:
  • Ipsilateral: Facial pain and temperature loss (V), Horner's syndrome (ptosis, miosis, anhidrosis), cerebellar signs, dysphagia, dysarthria
  • Contralateral: Pain and temperature loss in the limbs and trunk (spinothalamic)
  • Dissociated sensory loss (crossed pattern - hallmark)
  • Vertigo, nystagmus, hiccup
  • Motor power is PRESERVED (pyramidal tracts spared)
Q15. What is Broca's aphasia vs Wernicke's aphasia?
FeatureBroca's (Expressive)Wernicke's (Receptive)
LocationInferior frontal gyrus (Broca's area, F2, dominant)Superior temporal gyrus (Wernicke's area, T1)
SpeechNon-fluent, effortful, telegraphicFluent, pressured but paraphasic
ComprehensionRelatively preservedSeverely impaired
RepetitionImpairedImpaired
NamingImpairedImpaired
Patient aware?Yes - frustratedNo - unaware
Common inMCA superior division infarctMCA inferior division infarct

SECTION E - DIAGNOSIS AND INVESTIGATIONS

Q16. What is the FIRST investigation in a suspected stroke? A: Non-contrast CT (NCCT) of the brain. It is done IMMEDIATELY to:
  1. Exclude intracerebral hemorrhage (appears as hyperdense/bright white area)
  2. Exclude other structural causes (tumor, subdural hematoma)
  3. Determine eligibility for thrombolysis (must exclude hemorrhage first) Note: CT is normal in the first 6-24 hours in ischemic stroke.
Q17. What does CT brain show in ischemic stroke? A:
  • 0-6 hours: Often normal; may show early signs:
    • Hyperdense MCA sign (thrombus in MCA)
    • Loss of gray-white matter differentiation
    • Sulcal effacement
    • Insular ribbon sign (loss of insular cortex demarcation)
  • 12-24 hours: Hypodensity in infarcted area
  • 24-48 hours: Well-defined hypodense area corresponding to vascular territory
  • 1-2 weeks: Fogging effect (isodense)
  • Weeks-months: Encephalomalacia (cavitation/cystic area)
Q18. Why is MRI DWI preferred over CT in acute stroke? A: MRI Diffusion Weighted Imaging (DWI) detects restricted diffusion (reduction in Brownian motion of water molecules in ischemic cells) within MINUTES of stroke onset. It shows bright signal on DWI and dark signal on ADC map. It is far more sensitive than CT in the hyperacute phase (first 6 hours) and for small infarcts, lacunar infarcts, and posterior fossa (brainstem/cerebellum) infarcts where CT has poor resolution. However, CT is more readily available and faster in emergencies.
Q19. What is the NIHSS and why is it important? A: The National Institutes of Health Stroke Scale (NIHSS) is a standardized 15-item neurological assessment tool that quantifies stroke severity. It scores level of consciousness, gaze, visual fields, facial palsy, limb motor, limb ataxia, sensory, language, dysarthria, and extinction/inattention. Total score 0-42. It is used to:
  • Guide thrombolysis eligibility (score 4-22 typically eligible)
  • Monitor progression
  • Predict outcome
  • Research standardization
Q20. What investigations help determine the etiology of stroke? A:
  • ECG and Holter: AF detection
  • 2D Echo: Cardiac source of embolism
  • Carotid Doppler: Atherosclerotic stenosis
  • CT/MR Angiography: Large vessel disease, dissection
  • Lipid profile: Hyperlipidemia
  • HbA1c: Glycemic control
  • Thrombophilia screen (young stroke): Protein C, S deficiency; Antiphospholipid antibody syndrome; Factor V Leiden; Homocysteine
  • Vasculitis screen: ANA, ANCA, anti-dsDNA, VDRL (syphilis)
  • TTE/TEE: Paradoxical embolism (PFO)

SECTION F - TREATMENT

Q21. What are the eligibility criteria for IV tPA (Alteplase)? A:
  • Inclusion: Ischemic stroke with measurable neurological deficit (NIHSS 4-22 typically); onset within 4.5 hours; age >18 years; NCCT showing no hemorrhage
  • Key Contraindications:
    • Hemorrhage on CT
    • BP >185/110 mmHg (refractory to treatment)
    • Recent surgery within 14 days (major); within 3 months (head/spine)
    • Active bleeding or coagulopathy (INR >1.7, platelets <100,000)
    • Recent MI or stroke within 3 months
    • Blood glucose <50 or >400 mg/dL
    • Seizure at onset with postictal deficit
    • Prior intracranial hemorrhage
Q22. What is the dose of alteplase in stroke? A: 0.9 mg/kg body weight, maximum 90 mg total.
  • 10% (0.09 mg/kg) given as IV bolus over 1 minute
  • Remaining 90% infused over 60 minutes
  • Monitor closely for bleeding complications; ICH can occur in 6%
Q23. Why is BP management in acute ischemic stroke different? A: In acute ischemic stroke:
  • Normal autoregulation is lost in the ischemic penumbra
  • CBF becomes PRESSURE-DEPENDENT (pressure-passive)
  • Lowering BP reduces perfusion pressure and extends infarction into penumbra
  • Therefore, permissive hypertension is allowed: do NOT treat unless BP >220/120 mmHg (if no thrombolysis)
  • If giving tPA: Lower BP to <185/110 mmHg first, then maintain <180/105 during infusion
  • After 24-48 hours: Gradually normalize BP
Q24. What is mechanical thrombectomy? A: Mechanical (endovascular) thrombectomy is the removal of a clot from a large intracranial vessel (ICA, MCA M1, basilar artery) using a mechanical device (stent-retriever or aspiration catheter) via a femoral approach. Indications:
  • Large vessel occlusion confirmed on CTA/MRA
  • Within 6 hours of onset (up to 24 hours if DWI-perfusion mismatch criteria met - DAWN/DEFUSE 3 trials)
  • NIHSS >6 (significant deficit)
  • Premorbid mRS 0-1 (good functional status)
  • It significantly reduces disability (NNT ~2.6 for good outcome)
Q25. What antiplatelet agent is used in ischemic stroke prevention? A:
  • Acute phase (within 24-48 hrs of non-thrombolyzed stroke): Aspirin 300 mg stat, then 75-100 mg/day
  • Long-term: Aspirin 75 mg OD OR Clopidogrel 75 mg OD
  • For high-risk TIA/minor stroke (ABCD2 score ≥4): Dual antiplatelet (Aspirin + Clopidogrel) for 21 days, then monotherapy
  • Cardioembolic stroke (AF): Anticoagulation preferred - Warfarin (INR 2-3) or NOAC (Apixaban, Rivaroxaban, Dabigatran)
  • Statins are given regardless of cholesterol level in ischemic stroke
Q26. When do you anticoagulate in AF-related stroke? A: The timing of anticoagulation after cardioembolic stroke depends on stroke size (risk of hemorrhagic transformation):
  • TIA/minor stroke: Anticoagulate early (within 48-72 hours)
  • Moderate stroke: Delay 5-7 days
  • Large stroke: Delay 14 days
  • Use NOAC (preferred over warfarin) unless valvular AF (mechanical valve/rheumatic MS) where warfarin is indicated

SECTION G - DIFFERENTIALS AND COMPLICATIONS

Q27. What are the differentials of acute stroke? A:
  1. Hypoglycemia (most important mimic - always check blood glucose urgently)
  2. Todd's paralysis (post-ictal paresis after seizure)
  3. Hemiplegic migraine
  4. Brain tumor with sudden decompensation
  5. Subdural/epidural hematoma
  6. Hypertensive encephalopathy
  7. Encephalitis/meningitis
  8. Multiple sclerosis (acute demyelination)
  9. Complex partial seizure
  10. Conversion disorder (functional neurological disorder)
Q28. What is hemorrhagic transformation of infarction? A: Ischemic infarcts can undergo hemorrhagic transformation (petechial or confluent hemorrhage into the infarcted area) in 10-40% of cases. Types:
  • HI1/HI2: Petechial hemorrhage (Hemorrhagic Infarct) - usually asymptomatic
  • PH1/PH2: Parenchymal Hematoma - PH2 (>30% of infarct volume) is clinically significant, worsens outcomes Risk factors for hemorrhagic transformation: Large infarct, cardioembolic cause, thrombolysis, anticoagulation, hyperglycemia.
Q29. What is malignant MCA infarction? A: Large MCA territory infarction (>50% of MCA territory) causes massive cerebral edema peaking at 3-5 days. The edema causes:
  • Progressive decrease in consciousness
  • Herniation (uncal, transtentorial)
  • Mortality up to 80% with medical treatment alone
  • Treatment: Decompressive hemicraniectomy (removal of skull flap to allow brain expansion) - significantly reduces mortality and disability, especially in patients <60 years performed within 48 hours (DESTINY, HAMLET, DECIMAL trials).
Q30. What are the signs of raised intracranial pressure (ICP) in stroke? A:
  • Decreasing level of consciousness (most important early sign)
  • Headache (worsening, positional)
  • Vomiting (projectile)
  • Bradycardia + hypertension + irregular respiration = Cushing's triad (late, ominous sign)
  • Papilledema (fundus)
  • Third nerve palsy (uncal herniation - fixed dilated pupil)
  • False localizing sixth nerve palsy

SECTION H - IMPORTANT CLINICAL QUESTIONS

Q31. How do you differentiate UMN from LMN facial palsy?
FeatureUMN Facial PalsyLMN Facial Palsy
CauseStroke, brain tumorBell's palsy, parotid tumor, mastoiditis
ForeheadSPAREDINVOLVED
Furrowing foreheadPossibleNot possible
Bell's phenomenonAbsentPresent (eyes roll up on attempted eye closure)
TasteNormalLost (anterior 2/3) if chorda tympani involved
HyperacusisAbsentPresent (if stapedius involved)
LacrimationNormalMay be abnormal
Q32. What is the ABCD2 score? A: The ABCD2 score predicts 2-day stroke risk after TIA:
FactorScore
Age ≥601
BP ≥140/90 mmHg1
Clinical features: Unilateral weakness2, Speech disturbance only
Duration: 10-59 min1, ≥60 min
Diabetes1
Total 0-7. Score ≥4 = high risk, admit and urgent investigation.
Q33. What is the CHA2DS2-VASc score? A: Used to assess stroke risk in non-valvular AF to guide anticoagulation:
FactorScore
Congestive heart failure1
Hypertension1
Age ≥752
Diabetes1
Stroke/TIA/thromboembolism2
Vascular disease (MI, PAD)1
Age 65-741
Sex category (Female)1
Anticoagulate if score ≥2 (male) or ≥3 (female). Consider if score 1 (male) or 2 (female).
Q34. Name the FAST sign in stroke: A: Used for public awareness and emergency triage:
  • F - Face drooping (ask patient to smile - uneven?)
  • A - Arm weakness (ask patient to raise both arms - one drifts?)
  • S - Speech difficulty (slurred or strange speech?)
  • T - Time to call emergency services
Q35. What is a "stroke unit" and why is it important? A: A stroke unit is a specialized inpatient ward with dedicated multidisciplinary staff (neurologists, nurses, physiotherapists, occupational therapists, speech therapists, dieticians) trained in stroke care. Evidence shows stroke unit care reduces death and dependency by ~20% compared to general ward care - one of the most effective stroke interventions. Benefits include early recognition of complications, early rehabilitation, standardized protocols.

SECTION I - DRUGS USED IN STROKE

Q36. Which drugs are used in secondary prevention of ischemic stroke? A:
  • Antiplatelets: Aspirin, Clopidogrel, Dipyridamole
  • Anticoagulants (AF): Warfarin, Apixaban, Rivaroxaban, Dabigatran, Edoxaban
  • Statins: Atorvastatin 40-80 mg (LDL target <70 mg/dL or <1.8 mmol/L)
  • Antihypertensives: ACE inhibitors (Ramipril/Perindopril + Indapamide most studied - PROGRESS trial)
  • Diabetes management: Metformin, newer agents (GLP-1 agonists may have cardiovascular benefits)
Q37. What is the role of statins in stroke? A: High-intensity statins are recommended for ALL ischemic stroke/TIA patients regardless of baseline LDL:
  • Reduce recurrent stroke risk by ~20%
  • Pleiotropic effects: anti-inflammatory, plaque stabilization, endothelial protection
  • Target LDL <70 mg/dL (1.8 mmol/L) or ≥50% reduction from baseline
  • Caution: Statins should NOT be started acutely for hemorrhagic stroke (theoretical risk of worsening bleeding)
Q38. Name neuroprotective agents in stroke. A: Despite decades of research, NO neuroprotective agent has proven clinical benefit in human stroke trials. Multiple agents (glutamate antagonists, calcium channel blockers, free radical scavengers, growth factors) have failed in Phase 3 trials. The main reason is the narrow therapeutic window and difficulty translating animal data to humans. The only proven "neuroprotection" remains early reperfusion.

SECTION J - IMPORTANT EXAM POINTS TO REMEMBER

Q39. What is the "golden hour" / time window concept in stroke? A:
  • "Time is brain" - approximately 1.9 million neurons die every minute of stroke
  • IV tPA window: Within 4.5 hours of symptom onset
  • Mechanical thrombectomy: Within 6-24 hours (LVO with salvageable tissue)
  • Door-to-needle time (for tPA): Target <60 minutes
  • Door-to-groin puncture time (for thrombectomy): Target <90 minutes
Q40. What are the signs that help you localize a stroke lesion to the cortex vs. internal capsule?
FeatureCortical (MCA territory)Internal Capsule (Lacunar)
AphasiaYes (if left hemisphere)No
Visual field defectHemianopiaUsually absent
Sensory lossPresentOnly if capsule extends to thalamus
Cortical signsNeglect, apraxia, agnosiaAbsent
Face involvedYes, prominentlyYes
SeverityUsually severeOften incomplete, can be very dense
CauseEmbolism/large vesselSmall vessel/hypertensive

TIPS FOR THE VIVA

  1. Always start with: "This is a case of left/right-sided MCA territory ischemic stroke" - be definitive
  2. When asked about facial palsy - always immediately say "forehead spared - UMN"
  3. Babinski sign = extensor plantar = UMN lesion - say this clearly
  4. CT before tPA - never give tPA without excluding hemorrhage
  5. "Time is brain" - mention it, it impresses examiners
  6. If asked about young stroke (<45 years) - think: dissection, APS, PFO, vasculitis, CADASIL, cocaine use
  7. Always discuss rehabilitation as part of management
  8. Know the difference between stroke syndromes (MCA vs ACA vs PCA vs posterior fossa)
  9. Mention NIHSS - shows you know current clinical practice
  10. FAST acronym - important for the community medicine aspect

Sources: Adams and Victor's Principles of Neurology, 12th Edition | Neuroanatomy through Clinical Cases, 3rd Edition | Fuster and Hurst's The Heart, 15th Edition | Bradley and Daroff's Neurology in Clinical PracticeHere is your complete CNS case presentation guide. Here's a quick orientation to what's included:

What This Contains

Part 1 - Full Case Presentation
  • Realistic case: 62-year-old hypertensive diabetic male with left MCA stroke
  • Complete history (presenting complaints, HPI, past history, social/family)
  • Full neurological examination with expected findings, organized in standard examination order (Higher functions → Cranial nerves → Motor → Sensory → Reflexes → Cerebellum → Meningeal)
  • Summary statement in examiner-ready format
Part 2 - Discussion
  • Diagnosis with clinical basis
  • Stroke classification table
  • Investigations (acute + etiological) with expected results
  • Complete management (ABC, BP management, tPA criteria/dose, thrombectomy, secondary prevention, rehabilitation)
  • Complications
Part 3 - 40 Viva Questions and Answers covering:
  • Definitions and classification
  • Etiology and risk factors (including CHA2DS2-VASc, ABCD2 scores)
  • Pathophysiology (penumbra, UMN vs LMN facial palsy, gaze deviation, tongue deviation)
  • Vascular syndromes (MCA, ACA, PCA, Wallenberg)
  • Aphasia types (Broca's vs Wernicke's)
  • CT scan findings at each time point
  • tPA eligibility, dose, and contraindications
  • BP management rationale in acute stroke
  • Mechanical thrombectomy, antiplatelets, anticoagulation
  • Differentials (including hypoglycemia - most important mimic)
  • Hemorrhagic transformation, malignant MCA, raised ICP
  • Drugs in secondary prevention
  • 10 practical exam tips

Do the same for cvs case presentation and discussion for ms ,mr,as,ar

Finding Sources
Finding Sources
Finding Sources
Finding Sources
Braunwald's Heart Disease is the gold standard. Let me read all four valvular disease sections in parallel.
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Good overview content. Now let me read the core chapters (block 10) from Braunwald's for detailed clinical features, murmurs, and management of all four lesions.
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Finding Sources
Finding Sources
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