Epilepsy Surgery and Awake Craniotomy

Quick Answer

What are the key anaesthetic considerations for epilepsy surgery?

Epilepsy surgery requires seamless transitions between general anaesthesia (GA), conscious sedation, and awake cooperative states to enable intraoperative electrocorticography (ECoG) and functional cortical mapping. Key principles:

Preoperative optimisation - Seizure control, antiepileptic drug (AED) management, neuropsychological assessment
Airway security - LMA or endotracheal tube during GA phases; spontaneous ventilation during awake craniotomy
Patient selection - Cooperative patients, language/verbal skills intact, no airway difficulties
Anaesthetic technique - TIVA (propofol/remifentanil) or volatile agents with rapid offset; dexmedetomidine for sedation
Intraoperative management - Scalp blocks for craniotomy, minimal/no sedation during ECoG, seizure preparedness
Emergency readiness - Immediate access to anaesthetic agents, airway equipment, anticonvulsants (midazolam, propofol)

Clinical Pearl: The success of awake craniotomy depends on patient selection above all else. A cooperative, motivated patient with intact language skills and no claustrophobia is essential. Poor candidates include patients with anxiety disorders, severe cough, sleep apnoea, or anticipated difficult airway.

Clinical Overview

Epidemiology of Epilepsy

Global and Australian burden:

Statistic	Finding
Global prevalence	50 million people worldwide [1]
Australia prevalence	250,000 people (1% of population) [2]
Drug-resistant epilepsy	30-40% of all epilepsy cases [3]
Surgical candidates	Only 1-2% of drug-resistant patients referred for surgery [4]
Seizure freedom post-surgery	60-80% for temporal lobe epilepsy [5]
Paediatric epilepsy surgery	Earlier intervention associated with better neurodevelopmental outcomes [6]

Epilepsy syndromes amenable to surgery:

Syndrome	Surgical Approach	Outcome
Mesial temporal sclerosis	Anterior temporal lobectomy	65-80% seizure-free at 1 year [5]
Focal cortical dysplasia	Lesionectomy	50-70% seizure-free [7]
Tumour-related epilepsy	Tumour resection ± margins	70-90% seizure-free [8]
Rasmussen encephalitis	Hemispherectomy	80-90% seizure reduction [9]
Hypothalamic hamartoma	LITT or transcallosal	50-80% improvement [10]

Preoperative Assessment

Patient Selection for Awake Craniotomy

Inclusion criteria:

Domain	Criteria
Age	Typically >12-15 years (cognitive maturity)
Cognitive	Intact language, memory, executive function
Psychological	Motivated, cooperative, emotionally stable
Physical	No severe cough, neck pathology, sleep apnoea
Airway	Predicted easy intubation if required
Anatomy	Tumour/lesion amenable to awake approach

Exclusion criteria (absolute and relative):

Absolute Contraindications	Relative Contraindications
Patient refusal	Moderate anxiety (treatable)
Young age (<10-12 years)	Mild learning difficulties
Language barrier	Morbid obesity (OHS risk)
Profound developmental delay	Chronic cough
Severe psychiatric illness	Severe claustrophobia
Anticipated difficult airway	Long procedure anticipated
Patient too sleepy/encephalopathic	Previous craniotomy scar
Medical instability (cardiac, respiratory)	Posterior fossa location

Preoperative Evaluation

Multidisciplinary assessment:

Assessment	Purpose
Video-EEG telemetry	Localise seizure onset zone
MRI	Structural lesion identification
PET/SPECT	Functional localisation (interictal)
Neuropsychology	Baseline cognitive function
Wada test	Language and memory lateralisation
fMRI	Non-invasive language/motor mapping
MEG	Magnetoencephalography for localisation

Antiepileptic drug management:

Timing	Management
Preoperative	Continue AEDs to prevent withdrawal seizures
Morning of surgery	Give usual AED dose with sip of water
Intraoperative	Continue IV formulations if prolonged NBM
Postoperative	Resume oral/enteral as soon as possible
Free drug levels	Monitor for protein binding interactions

Clinical Pearl: Many AEDs are highly protein-bound (valproate, phenytoin). In the perioperative period, altered protein levels and drug interactions can change free drug concentrations significantly. Monitor clinical effect and consider free levels if available.

Anaesthetic Techniques for Epilepsy Surgery

Technique 1: Asleep-Awake-Asleep (AAA)

Indication: Motor/speech mapping requiring patient cooperation

Phase	Technique	Considerations
Asleep 1	GA with LMA/ETT	Propofol/remifentanil TIVA or volatile
Awake	LMA removed, sedation	Scalp block, remifentanil ± dexmedetomidine
Asleep 2	Re-intubation if needed	Continue to completion

Advantages:

Secure airway during craniotomy/dural opening
Patient only awake for essential mapping period
Reduced risk of airway compromise during surgical stimulation

Disadvantages:

Two airway manipulations (risk of laryngospasm, airway oedema)
Disruption between phases
More complex logistics

Technique 2: Monitored Anaesthesia Care (MAC) / Conscious Sedation

Indication: Cooperative patients, shorter procedures, ECoG only

Component	Implementation
Scalp block	Supraorbital, supratrochlear, zygomaticotemporal, auriculotemporal, greater occipital
Wound infiltration	Local anaesthetic by surgeon
Sedation	Remifentanil infusion (0.05-0.1 mcg/kg/min)
Adjunct	Dexmedetomidine (0.2-0.7 mcg/kg/hr)
Airway	Nasal cannula, spontaneous ventilation

Advantages:

Single technique throughout
No airway instrumentation
Continuous patient interaction possible

Disadvantages:

Requires highly cooperative patient
Risk of airway obstruction/respiratory depression
Limited if patient becomes agitated

Technique 3: Asleep with ECoG (No Awake Phase)

Indication: ECoG guidance without functional mapping

Anaesthetic considerations:

Light anaesthetic depth to preserve epileptiform activity
Avoid burst suppression during ECoG recording
Minimal opioids (suppress epileptiform activity)
Consider low-dose volatile (sevoflurane 0.5 MAC) or propofol infusion

Intraoperative Neurophysiology

Electrocorticography (ECoG)

Principle: Direct recording from cortical surface via subdural/grid electrodes or strip electrodes

Purpose in epilepsy surgery:

Define seizure onset zone
Identify eloquent cortex to preserve
Guide extent of resection
Confirm complete resection of epileptogenic tissue

Anaesthetic impact on ECoG:

Agent	Effect on ECoG
Propofol	Suppresses interictal spikes at high doses; minimal effect at <100 mcg/kg/min [11]
Sevoflurane	Activates epileptiform activity at 1.5-2.0 MAC; suppresses at high concentrations [12]
Isoflurane	Minimal effect on epileptiform activity
Nitrous oxide	No significant effect
Opioids	Variable - fentanyl may activate spikes; remifentanil relatively neutral [13]
Dexmedetomidine	Minimal effect on ECoG at sedative doses [14]
Ketamine	Activates epileptiform activity [15]
Etomidate	Activates epileptiform activity [16]
Benzodiazepines	Suppress epileptiform activity
Barbiturates	Marked suppression

Optimal ECoG conditions:

Light anaesthetic depth
Minimal or no benzodiazepines preoperatively
Avoidance of burst suppression
Consider activation techniques if no spontaneous activity (methohexital, alfentanil)

Cortical Mapping

Motor mapping:

Technique	Application	Anaesthetic Implications
Direct cortical stimulation	Identify motor cortex	Patient awake, cooperative
EMG recording	Monitor muscle responses	No muscle relaxation during mapping
Train-of-four	Ensure full recovery	Count ≥4, no fade
Threshold determination	Minimum current to elicit response	Document for surgeon

Speech/language mapping:

Task	Purpose
Object naming	Expressive language (Broca's area)
Reading	Language comprehension
Counting	Speech arrest monitoring
Repetition	Arcuate fasciculus
Comprehension	Receptive language (Wernicke's)

Safety limits for cortical stimulation:

Start at 2-4 mA, increase gradually
Maximum typically 10-16 mA
Stimulus duration 1-4 seconds
Afterdischarge threshold determines safe stimulation level
If afterdischarges occur, irrigate cortex with cold saline

Somatosensory Evoked Potentials (SSEPs)

Use: Localise central sulcus (phase reversal) Anaesthetic considerations:

Avoid high-dose volatile agents (>1 MAC depresses amplitude)
Maintain normothermia (hypothermia prolongs latency)
Ensure no residual neuromuscular blockade
Consider TIVA for consistent signals

Intraoperative Seizure Management

Recognition

Types of intraoperative seizures:

Type	Features	Cause
Subclinical (afterdischarges)	EEG only, no clinical signs	Cortical stimulation
Focal motor	Localised limb movement	Activation of motor cortex
Focal impaired awareness	Confusion, behavioural arrest	Temporal/frontal onset
Generalised tonic-clonic	Whole-body convulsions	Secondary generalisation
Status epilepticus	Prolonged seizure activity	Inadequate treatment

Immediate Management

Stepwise approach:

Step	Action	Dose
1. Stop stimulation	Cease cortical mapping	Immediate
2. Cold saline irrigation	Direct onto cortex	50-100 mL cold saline
3. Propofol bolus	If seizure persists	0.5-1 mg/kg
4. Midazolam	Second-line	2-5 mg IV
5. Secure airway	If consciousness impaired	LMA/ETT
6. Antiepileptic loading	Phenytoin/levetiracetam	Per institutional protocol
7. RSI if needed	For status epilepticus	Standard technique

** airway protection during seizure:**

Turn patient lateral if possible
Suction oropharynx
Insert bite block if not already present
100% oxygen
Monitor SpO2 and EtCO2

Clinical Pearl: The cold saline irrigation technique is remarkably effective for stopping stimulation-induced seizures. Keep a 60 mL syringe with iced saline at the surgical field. Most seizures terminate within 10-30 seconds of irrigation.

Pharmacological Considerations

Antiepileptic Drug Interactions

Enzyme-inducing AEDs:

AED	Enzyme Induction	Anaesthetic Implications
Carbamazepine	CYP3A4, CYP1A2, CYP2C	Increased metabolism of opioids, muscle relaxants, propofol
Phenytoin	CYP2C9, CYP2C19	Reduced effect of non-depolarising NMBAs
Phenobarbital	CYP1A2, CYP2C, CYP3A4	Enhanced metabolism of many drugs

Non-enzyme-inducing AEDs:

AED	Mechanism	Considerations
Sodium valproate	Hepatic enzyme inhibition	Increased free fraction of highly protein-bound drugs; hepatotoxicity risk
Levetiracetam	Minimal interaction	Preferred perioperatively
Lacosamide	Minimal interaction	IV formulation available
Perampanel	Minimal interaction	Once-daily dosing

Anaesthetic Drug Selection

Induction agents:

Agent	Recommendation	Rationale
Propofol	Preferred	Rapid onset/offset; antiemetic; preserves ECoG at low dose
Thiopentone	Acceptable	Anticonvulsant properties; longer context-sensitive half-time
Ketamine	Generally avoid	Proconvulsant; may activate epileptiform activity
Etomidate	Use with caution	Activates epileptiform activity; adrenal suppression

Maintenance:

Technique	Suitability	Notes
TIVA (propofol/remifentanil)	Excellent	Rapid offset; minimal ECoG interference
Desflurane	Good	Rapid emergence; minimal metabolism
Sevoflurane	Good at 0.5-1 MAC	Activates spikes at high concentration
Isoflurane	Good	Minimal epileptogenic effect

Analgesia:

Agent	Use	Notes
Remifentanil	First-line	Ultra-short acting; easily titratable
Fentanyl	Second-line	Longer duration; may activate spikes
Alfentanil	Activation studies	Used to provoke epileptiform activity
Morphine	Postoperative	Long-acting; not for intraoperative use

Sedation adjuncts:

Agent	Dose	Notes
Dexmedetomidine	0.2-0.7 mcg/kg/hr	Excellent - minimal respiratory depression; preserves ECoG
Midazolam	1-2 mg boluses	Avoid preoperatively and during ECoG; useful for seizure treatment
Clonidine	150 mcg oral preop	Anxiolysis without respiratory depression

Regional Anaesthesia for Awake Craniotomy

Scalp Block

Technique:

Nerve	Location	Volume
Supraorbital	Supraorbital notch	2-3 mL
Supratrochlear	Medial orbital rim	2-3 mL
Zygomaticotemporal	Zygomatic arch	2-3 mL
Auriculotemporal	Anterior to tragus	2-3 mL
Greater occipital	2-3 cm lateral to occipital protuberance	3-5 mL
Lesser occipital	2-3 cm lateral to greater occipital	2-3 mL

Local anaesthetic:

Ropivacaine 0.5-0.75% (preferred - less motor block)
Bupivacaine 0.25-0.5%
Add adrenaline 1:200,000 for vasoconstriction (reduce bleeding, prolong block)
Total volume: 20-30 mL

Additional infiltration:

Ring block at proposed incision site
Periosteal infiltration (by surgeon)
Dural local anaesthetic application (by surgeon)

Complications of Scalp Block

Complication	Prevention	Management
Local anaesthetic toxicity	Monitor dose (≤3 mg/kg bupivacaine)	Intralipid 20% 1.5 mL/kg bolus
Intravascular injection	Aspirate before injection	Supportive; lipid emulsion
Horner's syndrome	Avoid deep injection	Usually self-limiting
Facial nerve block	Careful landmarking	Wait for resolution

Postoperative Management

Immediate Postoperative Period

Recovery priorities:

Priority	Actions
Seizure prophylaxis	Continue AEDs; ensure therapeutic levels
Neurological monitoring	Serial GCS, focal deficits, seizure activity
Pain management	Multimodal: paracetamol, NSAIDs, low-dose opioids
Nausea/vomiting	Dexamethasone, ondansetron (avoid drowsiness)
Blood pressure	Avoid hypertension (risk of haemorrhage)
Hydration	Maintain euvolaemia

Postoperative seizures:

Occur in 10-30% of patients in first week [17]
Usually due to inadequate AED levels or surgical irritation
Management: Load with AEDs; check levels; CT if concern for bleed

Specific Complications

Complication	Incidence	Management
Cerebral oedema	5-10%	Dexamethasone; mannitol if severe
Haemorrhage	2-5%	Urgent CT; surgical evacuation if significant
Infection	1-3%	Antibiotics; drainage if abscess
Neurological deficit	10-30% (transient)	Rehabilitation; usually improves
Aphasia	5-15% (dominant temporal)	Speech therapy
Memory impairment	10-20%	Cognitive rehabilitation

Indigenous Health Considerations

Aboriginal and Torres Strait Islander Patients

Disproportionate epilepsy burden:

Health Indicator	Aboriginal vs Non-Aboriginal
Epilepsy prevalence	2-3× higher in remote communities [18]
Hospitalisation rates	3× higher for epilepsy-related admissions
Surgical access	Significantly lower rates of epilepsy surgery referral
Medication adherence	Challenges due to remoteness, cost, cultural factors [19]

Contributing factors:

Higher rates of perinatal brain injury (low birth weight, birth trauma)
Increased traumatic brain injury (assault, falls, motor vehicle accidents)
Higher rates of alcohol-related brain injury
Infectious causes more common in tropical regions (neurocysticercosis, cerebral malaria - travellers)
Lower antenatal care access in remote areas

Cultural considerations in epilepsy surgery:

Domain	Consideration
Communication	Use Aboriginal Liaison Officers (ALOs) and Aboriginal Health Workers (AHWs); interpreter services for language groups
Family involvement	Extended family decision-making; may need to consult multiple family members for consent
Seizure understanding	Cultural beliefs about seizures may differ; some communities attribute to spiritual causes
Consent process	Take time; ensure understanding of awake craniotomy concept; visual aids helpful
Remote location	Most epilepsy surgery in major cities (Sydney, Melbourne, Brisbane); significant travel required
Postoperative care	Need for accommodation near hospital for follow-up; limited local neurosurgical follow-up in remote areas

Practical strategies:

Preoperative engagement - Involve ALO early; explain awake craniotomy with diagrams/videos
Family support - Enable family presence during awake phase if patient wishes and space allows
Continuity of care - Telehealth follow-up to reduce travel burden
AED access - Ensure PBS subsidies understood; consider Webster-pak or similar adherence aids
Cultural safety - Acknowledge traditional healing practices; integrate with Western medicine where appropriate

Māori Health (Aotearoa New Zealand)

Epilepsy in Māori communities:

Indicator	Māori vs Non-Māori
Epilepsy prevalence	Higher rates documented; underdiagnosis concerns [20]
Health literacy	Variable; need culturally appropriate education
Access to surgery	Barriers include geographic (North/South Island concentration of services)

Te Tiriti o Waitangi considerations:

Equity of access to epilepsy surgery services
Māori workforce development in neurosciences
Whānau-centred care approaches

Cultural considerations:

Concept	Application
Whānau	Extended family involvement in decision-making
Manaakitanga	Respectful care; hospitality extended to family
Karakia	Prayer/spiritual practice; offer opportunity preoperatively
Mauri	Life force; maintaining dignity during awake procedure
Tapu/noa	Understanding sacredness of head/brain

Practical approaches:

Whānau consent - Ensure appropriate family members included in consent discussions
Māori Health Worker involvement - Cultural support throughout pathway
Karaka opportunity - Offer karakia before surgery if desired
Communication style - Clear, unhurried explanations; check understanding frequently
Postoperative support - Whānau accommodation; transport assistance

ANZCA Final Examination Focus

High-Yield Topics

Written examination areas:

Topic	Key Points
Patient selection for awake craniotomy	Inclusion/exclusion criteria; psychological assessment
Anaesthetic techniques	AAA vs MAC; advantages/disadvantages
ECoG optimisation	Drug effects; ideal conditions
Cortical mapping	Stimulation parameters; safety limits
Intraoperative seizures	Recognition; stepwise management
AED interactions	Enzyme induction; perioperative management
Scalp block	Anatomy; technique; complications

Viva examination scenarios:

Scenario	Expected Response
Patient unsuitable for awake craniotomy	Identify contraindications; propose alternatives (asleep with ECoG, fMRI-guided)
Intraoperative seizure	Immediate actions; cold saline; propofol/midazolam; airway management
ECoG shows no epileptiform activity	Check anaesthetic depth; consider activation (alfentanil, methohexital)
Patient becomes agitated during awake phase	Sedation escalation; communication; safety; abort if necessary
AED interactions	Knowledge of CYP450 effects on anaesthetic drugs

ANZCA Guidelines and References

Relevant professional documents:

Document	Relevance
ANZCA PS08 (BP)	Recommendations for preoperative assessment
ANZCA PS04	Guidelines for sedation
ANZCA PS03	Guidelines for regional anaesthesia
ANZCA PG07 (BP)	Recommendations on the preoperative management of patients on antiepileptic drugs

Assessment Content

SAQ 1: Awake Craniotomy Anaesthesia (20 marks)

Question:

A 32-year-old right-handed man is scheduled for awake craniotomy for resection of a left frontal low-grade glioma. The lesion is near the motor cortex and speech areas. He is anxious but motivated and has no airway concerns.

a) Describe the patient selection criteria for awake craniotomy and list absolute contraindications. (8 marks)

b) Outline your anaesthetic technique for the "asleep-awake-asleep" approach, including airway management and sedation strategy. (8 marks)

c) How would you manage an intraoperative seizure during cortical mapping? (4 marks)

Model Answer:

a) Patient Selection and Contraindications (8 marks):

Selection criteria (4 marks):

Age typically >12-15 years with cognitive maturity
Intact language and communication skills
Cooperative, motivated, emotionally stable
No severe cough, sleep apnoea, or airway pathology
Predicted easy intubation if required
Understanding of procedure and ability to follow commands

Absolute contraindications (4 marks):

Patient refusal or inability to cooperate
Young age (<10-12 years)
Profound developmental delay or intellectual disability
Severe psychiatric illness (untreated anxiety, psychosis)
Anticipated difficult airway
Language barrier affecting communication
Severe medical instability (cardiac, respiratory)
Patient too encephalopathic or drowsy

b) Anaesthetic Technique (8 marks):

Asleep phase 1 (3 marks):

General anaesthesia with LMA or ETT
TIVA: Propofol 100-150 mcg/kg/min + remifentanil 0.05-0.1 mcg/kg/min
Or volatile (sevoflurane 0.5-1 MAC) if preferred
Standard monitoring plus BIS (target 40-60)

Awake phase (3 marks):

Scalp block with ropivacaine 0.5% (supraorbital, supratrochlear, zygomaticotemporal, auriculotemporal, greater/lesser occipital)
LMA removed after dural opening
Remifentanil infusion continued at 0.03-0.05 mcg/kg/min
Dexmedetomidine 0.2-0.5 mcg/kg/hr for anxiolysis
Spontaneous ventilation with nasal cannula O2
Continuous reassurance and communication

Asleep phase 2 (2 marks):

Re-establish airway (LMA/ETT) if needed for resection completion
Continue TIVA or volatile
Lighten anaesthetic for final ECoG

c) Intraoperative Seizure Management (4 marks):

Immediate actions (2 marks):

Stop cortical stimulation immediately
Irrigate cortex with 50-100 mL cold saline
100% oxygen; ensure airway patency
Protect patient from injury (turn lateral if possible)

Pharmacological treatment (2 marks):

Propofol 0.5-1 mg/kg bolus if seizure persists
Midazolam 2-5 mg IV as second-line
Check and secure airway if consciousness impaired
Consider loading with antiepileptic (phenytoin/levetiracetam)

SAQ 2: ECoG and Anaesthetic Drugs (20 marks)

Question:

A patient is undergoing epilepsy surgery with intraoperative electrocorticography (ECoG) to localise the seizure focus. The neurophysiologist reports that no epileptiform activity is being recorded.

a) Discuss the effects of common anaesthetic agents on ECoG recordings. (10 marks)

b) What strategies can be used to optimise ECoG recordings intraoperatively? (6 marks)

c) Describe techniques to activate epileptiform activity if none is present spontaneously. (4 marks)

Model Answer:

a) Anaesthetic Effects on ECoG (10 marks):

Suppression of epileptiform activity (4 marks):

Propofol: Suppresses at high doses (>100 mcg/kg/min); minimal effect at sedation doses
Benzodiazepines (midazolam, diazepam): Marked suppression even at low doses
Barbiturates (thiopentone): Pronounced suppression
High-dose volatile agents (>1.5 MAC)

Activation of epileptiform activity (3 marks):

Sevoflurane: Activates at 1.5-2.0 MAC; epileptiform patterns common
Ketamine: Proconvulsant; activates epileptiform activity
Etomidate: Activates spikes and seizures
Enflurane (historical): Marked activation

Neutral/minimal effect (3 marks):

Isoflurane: Minimal effect on epileptiform activity
Nitrous oxide: No significant effect
Remifentanil: Relatively neutral at analgesic doses
Dexmedetomidine: Minimal effect at sedative doses
Alfentanil: Variable; may activate at high doses

b) Optimisation Strategies (6 marks):

Anaesthetic management (3 marks):

Lighten anaesthetic depth before ECoG (BIS 60-80)
Avoid burst suppression patterns
Minimise benzodiazepines preoperatively
Consider low-dose propofol or volatile (0.5 MAC) during recording
TIVA with propofol/remifentanil allows rapid titration

Technical considerations (3 marks):

Ensure adequate oxygenation (hypoxia can suppress)
Maintain normocapnia (hypocapnia reduces cerebral blood flow)
Normothermia (hypothermia affects neuronal activity)
Allow time after anaesthetic reduction (5-10 minutes)
Check electrode placement and impedance

c) Activation Techniques (4 marks):

Pharmacological activation (2 marks):

Alfentanil bolus (10-20 mcg/kg): Brief activation for localisation
Methohexital (0.5-1 mg/kg): Activates epileptiform activity
Etomidate: Can be used but risk of myoclonus

Physiological activation (2 marks):

Reduction of anaesthetic depth
Hyperventilation (can activate in some patients)
Sleep deprivation preoperatively (increases interictal spikes)
Activation through cortical stimulation during mapping

Viva Scenario: Antiepileptic Drug Interactions

Scenario:

You are anaesthetising a 28-year-old woman for temporal lobectomy. She has drug-resistant epilepsy and takes carbamazepine 800 mg BD and levetiracetam 1000 mg BD. She had a previous anaesthetic where she appeared resistant to neuromuscular blockade.

Examiner: "How would her antiepileptic medications affect your anaesthetic management?"

Candidate Response:

"Carbamazepine is an enzyme-inducing antiepileptic drug that induces CYP3A4, CYP1A2, and CYP2C enzymes. This has several implications:

First, carbamazepine increases the metabolism of non-depolarising neuromuscular blocking agents, particularly vecuronium and pancuronium. Rocuronium is less affected but may still require higher doses or more frequent top-ups. I would use neuromuscular monitoring and titrate doses based on TOF response rather than standard dosing.

Second, it increases metabolism of opioids like fentanyl and alfentanil, potentially requiring higher doses or more frequent administration. Remifentanil, metabolised by plasma esterases, is less affected.

Third, propofol metabolism may be increased, though this is less clinically significant than with opioids or muscle relaxants.

Fourth, carbamazepine induces its own metabolism (autoinduction), so patients on long-term therapy have more pronounced effects.

Levetiracetam, which she also takes, has minimal enzyme effects and doesn't significantly interact with anaesthetic agents.

My management strategy would include:

Acceleromyography for precise NMB monitoring
Rocuronium as preferred NMBA (less affected than aminosteroids)
Consider 20-30% higher initial NMBA dose with titration
Remifentanil-based TIVA for intraoperative analgesia
Ensure carbamazepine continued perioperatively to prevent withdrawal seizures"

Examiner: "What about valproate? How would that differ?"