Neuro-Anesthesia
ICP, cerebral blood flow, SAH, TBI, AVM, neuromonitoring, awake craniotomy, spinal cord protection. ← Back to Q-Bank
Q1. Cerebral blood flow autoregulation
Cerebral autoregulation maintains constant CBF between MAP:
A. 30–90 mmHg
B. 60–150 mmHg (shifted right in chronic hypertension)
C. 90–200 mmHg
D. 40–100 mmHg
E. No autoregulation exists
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Answer: B. Normal CBF ~50 mL/100 g/min, autoregulated MAP 60–150. Chronic HTN shifts curve right (vulnerable to relative hypoperfusion at "normal" BP). Autoregulation impaired by: anesthesia, trauma, ischemia, tumors, hypercapnia.
Q2. CBF and PaCO₂
For every 1 mmHg change in PaCO₂, CBF changes:
A. 0.1 mL/100g/min
B. 1–2 mL/100g/min (linear over 20–80 mmHg)
C. 10 mL/100g/min
D. 50%
E. No relation
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Answer: B. ΔCBF ~1–2 mL/100g/min per mmHg ΔPaCO₂. Useful for transient ICP control (decrease PaCO₂ to 30–35 buys ~30 mins). Effect dissipates 6–8 hr from bicarb buffering. Avoid extreme hyperventilation (CBF can drop to ischemic levels <20).
Q3. Cerebral perfusion pressure
CPP is calculated as:
A. MAP – ICP (or CVP, whichever is greater)
B. MAP + ICP
C. Aortic diastolic – LVEDP
D. MAP – CSF pressure only
E. Mean PA – PCWP
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Answer: A. CPP = MAP – (greater of ICP or CVP). Target 60–70 in TBI. Above 70 increases ARDS risk; below 50 risks ischemia. Spinal cord perfusion pressure = MAP – CSF pressure (relevant for spine surgery, TAAA repair → CSF drainage to 10 mmHg + MAP >90).
Q4. Anesthetic effect on CBF/CMRO₂
Which anesthetic increases both CBF and CMRO₂?
A. Propofol
B. Etomidate
C. Ketamine
D. Sevoflurane
E. Dexmedetomidine
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Answer: C. Ketamine ↑CBF, ↑CMRO₂, ↑ICP — traditionally avoided in patients with ↑ICP (though recent evidence less concerning if PaCO₂ controlled). Nitrous oxide also ↑CBF, ↑CMRO₂. Most other IV anesthetics ↓CBF and ↓CMRO₂. Volatiles ↓CMRO₂ but ↑CBF at >0.5 MAC (uncoupling).
Q5. ICP management
A patient with TBI develops ICP 28 mmHg. Initial measures include all EXCEPT:
A. HOB elevated 30°
B. Head midline (no neck rotation)
C. Hypotonic saline infusion
D. PaCO₂ 35–40 (avoid prolonged hyperventilation)
E. Sedation, analgesia, possibly neuromuscular blockade
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Answer: C. Avoid hypotonic fluids — worsens cerebral edema. Use isotonic crystalloid (NS) or hypertonic saline. Tier 1: HOB ↑, head midline, sedation, normocapnia, normothermia. Tier 2: hyperosmolar therapy (mannitol 0.25–1 g/kg, 3% saline), CSF drainage. Tier 3: paralysis, brief hyperventilation, barbiturate coma. Tier 4: decompressive craniectomy.
Q6. Cushing reflex
A patient with severe ICP elevation classically develops:
A. Hypertension, bradycardia, irregular respirations (Cushing's triad)
B. Hypotension and tachycardia
C. Hypotension and bradycardia
D. Hyperventilation only
E. Fever
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Answer: A. Cushing reflex = late sign of impending brainstem herniation. HTN to maintain CPP, baroreceptor-mediated bradycardia, Cheyne-Stokes or apneustic respirations. Emergency — treat ICP immediately with hyperosmolar therapy, CSF drainage, neurosurgical decompression.
Q7. Mannitol mechanism
Mannitol reduces ICP via:
A. Direct vasoconstriction
B. Osmotic shift of water out of brain into intravascular space → reduced cerebral edema
C. Decreased CSF production
D. Decreased CMRO₂
E. β-blockade
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Answer: B. Mannitol 0.25–1 g/kg IV bolus. Onset 5–10 min, duration 4–6 hr. Side effects: diuresis (volume depletion), hyperosmolarity, hyperkalemia transient → then hypokalemia. Reverse osmotic gradient with prolonged use (mannitol can cross damaged BBB → cerebral edema rebound). Hypertonic saline alternative — better hemodynamics, useful in hypovolemia.
Q8. SAH grade
Hunt and Hess grading of aneurysmal SAH:
A. Grade 1: asymptomatic; Grade 5: deep coma, decerebrate, moribund
B. Grade 1: severe headache, Grade 5: minimal symptoms
C. Grade 1: vasospasm
D. Numeric only — no clinical correlation
E. Time-based grading
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Answer: A. Hunt and Hess: 1 = asymptomatic/mild headache, 2 = moderate HA + CN palsy, 3 = drowsy/mild deficit, 4 = stupor + hemiparesis, 5 = deep coma/decerebrate. Higher grade = worse outcome. WFNS uses GCS-based. Fisher scale grades on CT for vasospasm risk.
Q9. Vasospasm in SAH
Cerebral vasospasm after SAH peaks at:
A. Day 0–1
B. Days 3–14
C. Day 30
D. 6 weeks
E. Never
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Answer: B. Peak vasospasm days 3–14 post-SAH. Prophylaxis: nimodipine 60 mg PO q4h × 21 days (improves outcome). Detection: transcranial Doppler (FVMCA >120 cm/s or FV ratio MCA:ICA >3 suggests spasm), CT angiography. Treatment: induced HTN, intra-arterial vasodilators (verapamil, milrinone), transluminal angioplasty for large vessels.
Q10. AVM embolization anesthesia
Anesthetic priority during AVM embolization includes:
A. Routine general anesthesia
B. Induced hypotension at time of glue injection (esmolol, adenosine, vasodilators) to prevent distal embolization
C. Hypertension throughout
D. Avoid all anticoagulation
E. Hypothermia
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Answer: B. Induced hypotension during glue injection prevents systemic spread of cyanoacrylate. Methods: short-acting β-blockers, vasodilators, transient asystole with adenosine, rapid ventricular pacing. Heparinization typically maintained during procedure. Post-embolization: monitor for normal perfusion pressure breakthrough (NPPB) — sudden vasodilation in chronically hypoperfused brain → edema/hemorrhage.
Q11. Awake craniotomy
The primary indication for awake craniotomy is:
A. Posterior fossa lesions
B. Resection of lesions near eloquent cortex (motor, language, memory) for intraoperative cortical mapping
C. Pediatric tumors
D. Aneurysm clipping
E. CSF shunt
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Answer: B. Awake craniotomy for tumors near eloquent cortex (Broca's, Wernicke's, motor strip). Technique: asleep-awake-asleep, or monitored anesthesia care. Local + scalp block, dexmedetomidine + propofol/remifentanil titration. Be ready for seizures (have midazolam, propofol), hypertension, brain swelling, air embolism if dural sinus opened.
Q12. Acute spinal cord injury
For acute traumatic spinal cord injury, the most evidence-based intervention is:
A. High-dose methylprednisolone (NASCIS protocol)
B. Maintain MAP >85 mmHg × 5–7 days, avoid hypoxia, surgical decompression as indicated
C. Hypothermia therapy
D. Mannitol bolus
E. Magnesium infusion
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Answer: B. MAP >85 × 5–7 days improves neurologic outcome. Steroids have fallen out of favor (NASCIS criticized — no longer recommended by AANS). Avoid hypoxia, hypotension. Surgical decompression within 24 hr improves outcomes (STASCIS).
Q13. Autonomic dysreflexia
A spinal cord injury patient at T6 develops sudden BP 220/120 with headache, flushing above the lesion, and pallor below the lesion during bladder catheterization. Initial management:
A. β-blocker IV
B. Identify and remove noxious stimulus (e.g., bladder distention), sit patient up, loosen clothing; nitrate or hydralazine if persistent
C. Vasopressin
D. Sodium nitroprusside infusion as first line
E. Calcium gluconate
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Answer: B. Autonomic dysreflexia (lesion at T6 or above) — noxious stimulus below lesion → unopposed sympathetic outflow → severe HTN. Bradycardia reflex above intact baroreceptor reflex. Remove stimulus first (distended bladder, fecal impaction). Then nitrate, hydralazine, nicardipine. Avoid pure β-blocker (unopposed α). Spinal anesthesia preferred for procedures in chronic SCI.
Q14. CSF formation
CSF is produced primarily by:
A. Pacchionian granulations
B. Choroid plexus in the lateral, third, and fourth ventricles
C. Arachnoid villi
D. Pia mater
E. Sagittal sinus
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Answer: B. CSF formed by choroid plexus (~500 mL/day, total volume ~150 mL — turns over 3–4× daily). Reabsorbed via arachnoid villi/Pacchionian granulations into superior sagittal sinus. Communicating hydrocephalus → ↓absorption; non-communicating → obstruction at ventricles.
Q15. Posterior fossa surgery — sitting position risks
The major risks of sitting position for posterior fossa craniotomy include:
A. Venous air embolism, paradoxical embolism through patent foramen ovale, hypotension, pneumocephalus, quadriplegia from cervical flexion
B. Only PE risk
C. Only positional eye injury
D. Hemodilution
E. Hypothermia only
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Answer: A. Sitting position complications: VAE (more sensitive monitoring with precordial Doppler/TEE), paradoxical AE through PFO (screen with bubble study preop), hypotension (avoid hypovolemia), quadriplegia from cervical flexion ("two-finger rule" mandible to sternum), pneumocephalus.
Q16. EEG patterns under anesthesia
EEG under volatile anesthesia at 1–2 MAC shows:
A. Beta waves
B. Slower-frequency higher-amplitude waves; >2 MAC → burst suppression → electrocortical silence
C. No change
D. Theta waves only
E. Spikes throughout
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Answer: B. Volatile dose-dependent: ≤1 MAC → higher frequency; 1–2 MAC → slowing; >2 MAC → burst suppression; even higher → electrocortical silence. Ketamine increases theta. Nitrous → fast activity. Methohexital (alone among barbiturates) activates epileptic foci.
Q17. Carotid endarterectomy — neuro monitoring
The most reliable monitor for cerebral ischemia during carotid endarterectomy under general anesthesia is:
A. Pulse oximetry
B. EEG continuous + processed (or SSEP + TCD); cerebral oximetry as adjunct
C. Heart rate alone
D. EtCO₂
E. Mean arterial pressure alone
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Answer: B. Under GA: EEG (raw or processed), SSEP, TCD, cerebral oximetry — none perfect alone. Under regional (awake CEA): direct neurologic exam is the gold standard. GALA trial: no difference in outcome between GA and regional.
Q18. Triple-H therapy
For symptomatic vasospasm after SAH, triple-H therapy traditionally involves:
A. Hyperventilation, hypothermia, hyperoxia
B. Hypertension, hemodilution, hypervolemia (now mainly induced hypertension with euvolemia)
C. Hyponatremia, hypocalcemia, hypoglycemia
D. Hyperventilation, hypocapnia, hypothermia
E. Hypertension and intracranial pressure monitoring
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Answer: B. Traditional triple-H (hypertension, hemodilution, hypervolemia) — modern approach focuses on induced hypertension with euvolemia (avoid pulmonary edema, hyponatremia). Aneurysm must be secured first.
Q19. Brain death criteria
Apnea testing for brain death requires:
A. PaCO₂ rise to >60 mmHg or ≥20 mmHg above baseline without respiratory effort
B. PaCO₂ <30 with no breath
C. Hypoxia with no breath
D. Heart rate fall
E. Just observation for 5 min
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Answer: A. Apnea test: pre-oxygenate, disconnect from ventilator, maintain O₂ via tracheal catheter, observe for ≥10 min for respiratory effort; abort if hemodynamically unstable. PaCO₂ rise >60 or ≥20 above baseline without effort = positive. Prerequisites: known irreversible cause, normothermia, normotension, no drugs/electrolyte issues, exclude confounders. Ancillary tests: cerebral angiography (gold standard), TCD, EEG, nuclear flow study.
Q20. Hyperglycemia and brain injury
Hyperglycemia worsens outcomes after stroke and TBI because:
A. Anaerobic metabolism of glucose in ischemic tissue → lactic acidosis → exacerbates neuronal injury
B. Direct neurotoxicity of glucose
C. Hyperglycemia causes vasospasm
D. Insulin resistance only
E. No effect on outcome
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Answer: A. Hyperglycemia (>180–200) → anaerobic glycolysis → ↑lactate → ↑tissue acidosis in ischemic penumbra. Target 140–180 perioperatively. Avoid hypoglycemia (worsens injury, no clear utility of NICE-SUGAR tight control here).
Q21. Spinal cord stimulator indications
Spinal cord stimulator is indicated for all EXCEPT:
A. Failed back surgery syndrome
B. CRPS I and II
C. Refractory chronic angina
D. Acute postoperative pain
E. Lower extremity ischemic pain
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Answer: D. SCS for chronic refractory pain: post-laminectomy syndrome, CRPS, refractory angina, peripheral vascular disease, neuropathic pain. Contraindications: localized infection, coagulopathy, sepsis, spina bifida, psychological inability to use device, somatoform disorder.
Q22. Status epilepticus management
Generalized status epilepticus first-line treatment is:
A. Phenytoin alone
B. IV benzodiazepine (lorazepam 4 mg or midazolam 10 mg IM) → if refractory: phenytoin/fosphenytoin 20 mg/kg or valproate or levetiracetam
C. Propofol bolus
D. Magnesium
E. Mannitol
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Answer: B. Lorazepam IV (or midazolam IM if no IV). 2nd: phenytoin/fosphenytoin, valproate, levetiracetam. Refractory (>30 min): intubate, propofol/midazolam infusion or pentobarbital, EEG guidance to burst suppression. Identify cause (CT, labs).
Q23. Methohexital and ECT
Methohexital is preferred for electroconvulsive therapy because it:
A. Suppresses seizures
B. Lengthens or has minimal effect on seizure duration
C. Has α-blocking properties
D. Eliminates oral secretions
E. Causes tachycardia
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Answer: B. Methohexital (and etomidate, ketamine) preserve or prolong seizure. Other barbiturates and propofol shorten it. Seizure must last ≥25–30 sec for ECT efficacy. Pre-treat with glycopyrrolate (prevent oral secretions/bradycardia), succinylcholine (prevent musculoskeletal injury), labetalol/esmolol (sympathetic surge).
Q24. Postoperative cognitive dysfunction
Risk factors for postoperative cognitive dysfunction include:
A. Advanced age, lower education, preexisting cognitive impairment, depression, sensory deficits, alcohol abuse, major surgery
B. Outpatient surgery only
C. Young age
D. Healthy diet
E. Daily exercise
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Answer: A. POCD/postoperative delirium: more common in elderly, frail, those with baseline cognitive impairment, polypharmacy. Risk reduction: avoid benzos and anticholinergics, minimize opioids (multimodal), depth-of-anesthesia monitoring (BIS) to avoid deep anesthesia, regional anesthesia when appropriate, early mobilization. There is mixed evidence on TIVA vs. inhalation.
Q25. Perioperative stroke timing
Elective non-cardiac surgery after a recent stroke is highest risk in the first:
A. 24 hours
B. 1 week
C. 3 months (defer ≥6 months — 9 months if possible)
D. 5 years
E. Lifetime
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Answer: C. Recent stroke <3 months → highest perioperative stroke risk. Risk levels off ~9 months. Defer elective non-cardiac surgery ≥6 months (preferably 9 months) after stroke. Key risk factors: advancing age, renal disease, prior TIA/stroke.