Epilepsy & Seizures

📋 Key Information Summary

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A first unprovoked seizure requires urgent EEG (ideally within 24–48 hours), MRI brain, basic metabolic panel, and assessment of provoking factors (sleep deprivation, alcohol, infection, metabolic derangement).
Epilepsy is diagnosed after ≥2 unprovoked seizures >24 hours apart, or one unprovoked seizure with a high recurrence risk (>60% on EEG with epileptiform discharges).
Seizure classification follows the ILAE 2017 framework: focal (aware/impaired awareness, motor/non-motor), generalised (tonic-clonic, absence, myoclonic, atonic), and unknown onset.
Driving restrictions in Australia after a first unprovoked seizure: minimum 6 months seizure-free for private vehicle (varies by state/territory); 12 months for commercial licences per Austroads Assessing Fitness to Drive.
Antiseizure medication (ASM) should be initiated after a diagnosis of epilepsy, not routinely after a single unprovoked seizure unless EEG or MRI shows high-risk features.
First-line ASMs by seizure type: focal — levetiracetam (Keppra®), carbamazepine (Tegretol®), lamotrigine (Lamictal®); generalised tonic-clonic — valproate or levetiracetam; absence — ethosuximide or valproate; myoclonic — levetiracetam or valproate.
Levetiracetam is the most commonly used first-line ASM in Australia due to broad efficacy, minimal drug interactions, and renal (not hepatic) elimination.
Sodium valproate (Epilim®) is absolutely contraindicated in women of childbearing potential unless enrolled in the Pregnancy Prevention Programme (TGA mandatory) due to high teratogenic risk (neural tube defects, neurodevelopmental effects).
Status epilepticus (≥5 minutes of continuous seizure or ≥2 discrete seizures without recovery) requires immediate benzodiazepines (midazolam IM pre-hospital; IV diazepam or lorazepam in ED), followed by IV levetiracetam, valproate, or phenytoin if seizures persist beyond 20 minutes.
All women with epilepsy planning pregnancy should receive high-dose folate (5 mg daily) at least 1 month before conception, and ASM doses may need adjustment due to altered pharmacokinetics in pregnancy.
Aboriginal and Torres Strait Islander Australians have higher rates of epilepsy and status epilepticus, with barriers including remote access to neurology, delayed EEG availability, and cultural factors affecting medication adherence.
Referral to a neurologist or epilepsy specialist is recommended for all new diagnoses, refractory epilepsy (failure of 2 appropriate ASMs), suspected genetic or structural epilepsy syndromes, and women of childbearing age.

First Seizure Evaluation

A first seizure presentation is a common reason for emergency department attendance and general practice referral in Australia. The key clinical objectives are to confirm the event was a seizure (versus syncope, psychogenic non-epileptic seizures, or other paroxysmal events), identify provoking factors, assess recurrence risk, and determine whether investigation and treatment thresholds have been met.

Provoked vs Unprovoked Seizures

A provoked (acute symptomatic) seizure occurs in close temporal relationship to an acute systemic, metabolic, or toxic insult, or in the context of an acute brain insult (e.g., stroke, traumatic brain injury, CNS infection). Provoked seizures have a low recurrence risk once the provoking factor is resolved and do not, by themselves, constitute epilepsy.

An unprovoked seizure has no identifiable acute precipitant. Unprovoked seizures carry a recurrence risk of approximately 40–50% within 2 years, increasing to >60% if epileptiform discharges are present on EEG.

Feature	Provoked (Acute Symptomatic)	Unprovoked
Timing	Within 7 days of acute insult	No identifiable acute precipitant
Common causes	Hypoglycaemia, hyponatraemia, hypocalcaemia, alcohol withdrawal, drug intoxication/withdrawal, CNS infection, acute stroke, traumatic brain injury, eclampsia	Structural lesion (tumour, cortical dysplasia), genetic predisposition, cryptogenic
Recurrence risk	Low (<10%) if cause fully corrected	40–50% within 2 years
ASM indication	Treat the underlying cause; ASMs rarely needed long-term	Consider ASM if high recurrence risk or after second unprovoked seizure
Driving restriction	Generally 4 weeks if isolated, fully corrected cause	Minimum 6 months seizure-free (private vehicle)

Metabolic Causes to Exclude

All patients presenting with a first seizure require a basic metabolic screen. Seizures secondary to metabolic derangement are provoked and generally do not require long-term ASM therapy.

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Always check: Blood glucose, sodium, calcium (corrected), magnesium, phosphate, renal function, hepatic function, ammonia (if suspected hepatic encephalopathy), and consider toxicology screen. Hypoglycaemia (<3.0 mmol/L) and severe hyponatraemia (<120 mmol/L) are common treatable causes in the Australian emergency setting.

EEG Timing

An EEG should be performed as soon as possible after a first unprovoked seizure, ideally within 24–48 hours. Early EEG has higher sensitivity for detecting epileptiform abnormalities (sensitivity increases from ~30% on routine EEG to ~50–70% if performed within 24 hours). In Australia, EEG is accessible in major hospitals; however, outpatient EEG may have wait times of 2–6 weeks in regional areas.

Routine EEG (MBS Item 11005): 20–30 minute recording; available at most metropolitan hospitals. Can be performed as an inpatient or outpatient.
Sleep-deprived EEG: Improves yield if routine EEG is normal; patient sleeps only 3–4 hours the night before.
Prolonged/ambulatory EEG: Consider if clinical suspicion remains high with normal routine EEG.
Presence of epileptiform discharges on EEG increases 2-year recurrence risk to >60%, supporting early ASM initiation discussion.

Neuroimaging

MRI brain with epilepsy protocol is the recommended first-line neuroimaging for all patients with a first unprovoked seizure, except in clearly provoked seizures where the cause is identified and fully corrected. CT head has a role in the acute setting to exclude haemorrhage, space-occupying lesion, or hydrocephalus but has poor sensitivity for cortical dysplasia, hippocampal sclerosis, and low-grade gliomas.

CT head (non-contrast) — MBS Item 56001: Perform acutely in ED if focal neurological signs, persistent altered consciousness, anticoagulation, or suspected structural lesion. Available 24/7 at most Australian hospitals.
MRI brain (epilepsy protocol) — MBS Item 63060/63063: Includes thin coronal T2/FLAIR sequences through the temporal lobes and hippocampi. Requires neurology or neurosurgery referral. Wait times in regional Australia may be 4–8 weeks; urgent inpatient MRI if suspected structural cause.
In children, MRI under general anaesthesia may be required; this is available at paediatric tertiary centres.

Driving Restrictions

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Mandatory notification: In most Australian states and territories, doctors have a legal obligation to notify the relevant driver licensing authority (e.g., VicRoads, Transport NSW, TMR QLD) when a patient has experienced a seizure, regardless of whether it was provoked or unprovoked. The patient must be counselled not to drive until cleared by the licensing authority.

Australian driving restrictions are governed by Austroads Assessing Fitness to Drive (2022 update):

Scenario	Private Vehicle (Car)	Commercial Licence (Heavy Vehicle, Bus, Taxi)
Single provoked seizure (fully resolved cause)	Minimum 4 weeks seizure-free	Minimum 6 months seizure-free
Single unprovoked seizure	Minimum 6 months seizure-free	Minimum 12 months seizure-free (consider specialist review)
Established epilepsy (≥2 unprovoked seizures)	Minimum 12 months seizure-free (or seizure-free with appropriate ASMs)	Generally disqualifying; individual assessment by treating neurologist and licensing authority
Seizures only in sleep	3 years of exclusively nocturnal seizures with no daytime seizures	Generally disqualifying

State-specific legislation varies. For example, in Victoria, mandatory reporting is required under the Road Safety Act 1986, while in NSW it is governed by the Road Transport Act 2013. GPs should document the driving discussion, provide written patient advice, and notify the licensing authority in writing.

Step-by-Step Approach to First Seizure

1

Confirm seizure vs mimic

Detailed eyewitness history, peri-ictal features (tongue biting, cyanosis, post-ictal confusion), differentiate from syncope, panic attack, or psychogenic non-epileptic seizures (PNES).

2

Identify and treat provoking factors

Check glucose, electrolytes, calcium, magnesium, renal/hepatic function, toxicology screen. Treat hypoglycaemia, hyponatraemia, alcohol withdrawal promptly.

3

Acute neuroimaging if indicated

CT head acutely if focal deficit, persistent altered consciousness, anticoagulated, or new headache. Arrange MRI brain (epilepsy protocol) for all unprovoked seizures.

4

EEG within 24–48 hours

Inpatient if available; otherwise urgent outpatient within 1–2 weeks. Sleep-deprived EEG if initial normal and clinical suspicion high.

5

Driving counselling and notification

Advise patient not to drive. Notify state/territory licensing authority. Document discussion in medical record.

6

Referral and follow-up

Refer to neurology for all unprovoked seizures. Arrange outpatient follow-up within 4–6 weeks with EEG and MRI results.

Diagnosis of Epilepsy

Epilepsy is a clinical diagnosis based on the ILAE 2014 operational definition: ≥2 unprovoked seizures occurring >24 hours apart, or one unprovoked seizure with a probability of recurrence ≥60% (e.g., epileptiform EEG abnormalities, structural brain lesion on MRI), or diagnosis of an epilepsy syndrome.

ILAE 2017 Seizure Classification

The ILAE 2017 classification replaces the older terms "partial" and "grand mal/petit mal." Seizure type is classified by onset (focal, generalised, unknown) and then by awareness, motor/non-motor features, and evolution.

Seizure Type	Subtypes	Key Clinical Features	EEG Pattern
Focal aware	Motor (clonic, tonic, automatisms); Non-motor (autonomic, emotional, sensory, cognitive)	Aura only; consciousness preserved; may be mistaken for anxiety, migraines, or TIAs	Focal epileptiform discharges, lateralised rhythmic activity
Focal impaired awareness	Motor or non-motor onset; often evolves to bilateral tonic-clonic	Staring, unresponsiveness, automatisms (lip smacking, hand fumbling), post-ictal confusion	Temporal or frontal sharp waves; may show ictal pattern from one hemisphere
Generalised motor	Tonic-clonic, tonic, clonic, myoclonic, atonic	Bilateral symmetric involvement from onset; tonic-clonic = most common and dramatic; cyanosis, tongue biting, incontinence, post-ictal drowsiness	Generalised spike-and-wave (3 Hz for absence), polyspike-and-wave (myoclonic), diffuse attenuation (tonic)
Generalised non-motor (absence)	Typical, atypical, myoclonic absence, eyelid myoclonia	Brief staring spells (5–30 sec), abrupt onset/offset, no post-ictal confusion; easily provoked by hyperventilation; common in children aged 4–12	Generalised 3 Hz spike-and-wave (typical); hyperventilation activates
Unknown onset	Motor, non-motor, unclassified	When onset cannot be determined clinically or on EEG	Non-localising or insufficient data

Common Epilepsy Syndromes

Epilepsy syndromes are defined by a cluster of clinical and EEG features including seizure type(s), age of onset, EEG pattern, comorbidities, and prognosis. Syndrome identification guides ASM selection and prognosis counselling.

Syndrome	Age of Onset	Key Features	First-Line Treatment	Prognosis
Childhood absence epilepsy	4–10 years	Multiple daily absence seizures; 3 Hz spike-and-wave; normal cognition at onset	Ethosuximide (Zarontin®) or valproate	60–70% remit by adolescence
Juvenile myoclonic epilepsy (JME)	12–25 years	Morning myoclonic jerks, generalised tonic-clonic seizures; photosensitivity; lifelong ASM usually needed	Valproate (males); levetiracetam (females of childbearing age)	Lifelong; >90% seizure-free on ASMs; relapse on withdrawal common
Temporal lobe epilepsy (TLE)	Any age (often childhood–young adult)	Focal impaired awareness seizures with automatisms; epigastric rising aura; MRI may show hippocampal sclerosis	Carbamazepine, lamotrigine, or levetiracetam	60–70% drug-responsive; surgical candidate if refractory
Benign epilepsy with centrotemporal spikes (BECTS / Rolandic)	3–13 years	Focal seizures (hemifacial, oropharyngeal) often nocturnal; centrotemporal spikes on EEG; normal development	Often no ASM needed; carbamazepine or levetiracetam if seizures frequent	Excellent; remits by age 15–16
Lennox-Gastaut syndrome	2–8 years	Multiple seizure types (tonic, atonic, atypical absence); intellectual disability; slow spike-and-wave on EEG	Valproate, clobazam, rufinamide, lamotrigine	Poor; refractory epilepsy with developmental impairment

Red Flags for Secondary Causes

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Urgent investigation required if any of the following are present: New-onset focal neurological deficit, progressive headache, papilloedema, cognitive decline, fever with neck stiffness (meningitis/encephalitis), history of malignancy (brain metastasis), immunosuppression (cerebral abscess, PML, CNS lymphoma), sudden onset "thunderclap" headache (SAH), or new seizures in a patient >40 years old without prior history.

When to Refer to Neurology/Epilepsy Specialist

All patients with a new diagnosis of epilepsy — specialist confirmation and treatment planning (MBS Item 104 for specialist consultation, or MBS Item 99 for telehealth specialist consultation).
Diagnostic uncertainty — suspected psychogenic non-epileptic seizures (PNES), which account for 20–30% of referrals to Australian epilepsy clinics.
Refractory epilepsy — failure of ≥2 appropriate, adequately dosed ASMs (approx. 30% of patients); consider video-EEG monitoring and surgical evaluation.
Women of childbearing age — pre-conception counselling, ASM optimisation, folate planning.
Suspected epilepsy syndrome requiring specialist confirmation (e.g., JME, Dravet syndrome).
Status epilepticus or recurrent cluster seizures.
Consideration of epilepsy surgery — referral to an accredited epilepsy surgical centre (e.g., Royal Melbourne Hospital, Royal Prince Alfred Hospital, Austin Health, Mater Brisbane, Royal Adelaide Hospital).

Antiseizure Medication Initiation

When to Start Antiseizure Medication

ASM initiation is recommended after a confirmed diagnosis of epilepsy (≥2 unprovoked seizures or high recurrence risk after one seizure). The decision is individualised and considers seizure type, epilepsy syndrome, patient preference, comorbidities, reproductive plans, and driving needs.

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Key principles: Start with monotherapy at low dose, titrate gradually to the lowest effective dose. Use the ASM with the best efficacy–tolerability profile for the specific seizure type. The goal is seizure freedom (no seizures, no side effects) — if the first ASM fails, switch to an appropriate alternative monotherapy rather than adding a second agent (unless there are ≥2 seizure types or a defined syndrome requiring polytherapy).

Drug Selection by Seizure Type

Seizure Type / Syndrome	First-Line ASMs	Second-Line / Adjunctive ASMs	ASMs to AVOID
Focal seizures (aware or impaired awareness)	Levetiracetam, carbamazepine, lamotrigine, lacosamide	Clobazam, topiramate, zonisamide, oxcarbazepine, perampanel	Sodium valproate in women of childbearing potential
Generalised tonic-clonic seizures	Sodium valproate, levetiracetam	Lamotrigine, topiramate, perampanel	Carbamazepine, oxcarbazepine, phenytoin, gabapentin (may worsen myoclonic/absence)
Absence seizures	Ethosuximide, sodium valproate	Lamotrigine	Carbamazepine, oxcarbazepine, phenytoin, gabapentin, vigabatrin (may worsen absence)
Myoclonic seizures (JME)	Sodium valproate (males), levetiracetam	Clobazam, topiramate, zonisamide, lamotrigine (partial efficacy)	Carbamazepine, oxcarbazepine, phenytoin, gabapentin, pregabalin (exacerbate myoclonus)
Atonic / tonic seizures (Lennox-Gastaut)	Sodium valproate, clobazam	Rufinamide, lamotrigine, topiramate, cannabidiol (Epidyolex® — TGA Special Access Scheme)	Carbamazepine, oxcarbazepine

First-Line Antiseizure Medications — Drug Cards

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Levetiracetam

Keppra® · Generic available · SV2A ligand

Indications Focal, generalised tonic-clonic, myoclonic seizures; broadest first-line spectrum

Adult dose Start 250 mg PO BD, increase by 250 mg BD every 2 weeks; target 500–1500 mg PO BD

Paediatric dose ≥4 years: 10 mg/kg PO BD, titrate to 20–40 mg/kg/day in 2 divided doses

Renal adjustment eGFR 50–80: max 1000 mg BD; 30–50: 250–750 mg BD; <30: 250–500 mg BD; HD: 500–1000 mg post-dialysis

Key adverse effects Behavioural/psychiatric (irritability, aggression, depression — 5–15%); somnolence; rarely haematological

Drug interactions Minimal hepatic metabolism; no CYP450 interactions — major advantage

PBS status ✔ PBS General Benefit

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Sodium Valproate

Epilim® · Generic available · Multiple mechanisms

Indications Generalised tonic-clonic, absence, myoclonic seizures; JME; broadest efficacy

Adult dose Start 200 mg PO BD, titrate to 600–2000 mg/day in 2–3 divided doses; target trough 50–100 mg/L

Paediatric dose ≥1 month: 10 mg/kg/day, titrate to 20–40 mg/kg/day in 2–3 divided doses

Renal/hepatic Hepatically metabolised; avoid in severe hepatic impairment. Contraindicated in urea cycle disorders.

Key adverse effects Weight gain, tremor, hair loss, hepatotoxicity (rare, idiosyncratic), pancreatitis, thrombocytopenia. TERATOGENIC — neural tube defects 5–10%, neurodevelopmental effects (IQ reduction).

TGA mandatory requirement Women of childbearing potential MUST be enrolled in the Valproate Pregnancy Prevention Programme; annual review; effective contraception required.

PBS status ✔ PBS General Benefit

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Carbamazepine

Tegretol® · Generic available · Sodium channel blocker

Indications Focal seizures (first-line); generalised tonic-clonic seizures; trigeminal neuralgia

Adult dose Start 100 mg PO BD with food; titrate by 100–200 mg/day every 1–2 weeks; target 200–800 mg PO BD

Paediatric dose <1 year: 50–100 mg BD; 1–5 years: 100–200 mg BD; 5–12 years: 200 mg BD–600 mg/day; ≥12 years: adult dosing

Key adverse effects Dizziness, diplopia, ataxia, hyponatraemia (SIADH), rash (including SJS — HLA-B*1502 risk in SE Asian ancestry, HLA-A*3101 in European). Hepatic enzyme inducer.

Drug interactions Potent CYP3A4 inducer; significant interactions with oral contraceptives, warfarin, DOACs, corticosteroids, many other medications.

Pharmacogenomics HLA-B*1502 testing recommended before initiation in patients of SE Asian, Han Chinese, or Indian ancestry (available via pathology in Australia). HLA-A*3101 testing in European-ancestry patients where feasible.

PBS status ✔ PBS General Benefit

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Lamotrigine

Lamictal® · Generic available · Sodium channel blocker

Indications Focal seizures; generalised tonic-clonic seizures; absence seizures (adjunctive); well tolerated; preferred in women of childbearing age

Adult dose (monotherapy) Start 25 mg PO OD for 2 weeks → 50 mg OD for 2 weeks → 50 mg BD for 1 week → then increase by 50 mg/day every 1–2 weeks; target 100–200 mg PO BD

Adult dose (with valproate) Start 25 mg PO every other day for 2 weeks → 25 mg OD for 2 weeks → then increase slowly; dose reduced ~50% due to valproate interaction

Paediatric dose ≥2 years: 0.5 mg/kg/day (with enzyme inducers) or 0.15 mg/kg/day (with valproate); titrate over 6–8 weeks

Key adverse effects Serious rash (SJS/TEN) — risk highest with rapid titration, concomitant valproate, or in children. Must follow slow titration schedule. Headache, nausea, insomnia, dizziness.

Pregnancy Lowest teratogenic risk of all ASMs; preferred ASM in pregnancy. Dose requirements increase 50–100% by third trimester due to increased clearance.

PBS status ✔ PBS General Benefit

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Ethosuximide

Zarontin® · Succinimide

Indications Absence seizures — first-line (equal to valproate for absence; fewer adverse effects)

Adult dose Start 500 mg PO OD; titrate by 250 mg every 4–7 days; target 750–1500 mg/day in 1–2 divided doses

Paediatric dose 3–6 years: start 250 mg PO OD; titrate to 20–40 mg/kg/day in 1–2 divided doses

Key adverse effects GI upset (nausea, vomiting, anorexia), drowsiness, headache. Rare: blood dyscrasias, SLE-like syndrome.

PBS status ✔ PBS General Benefit

Titration and Monitoring

Start low, go slow: All ASMs should be initiated at a low dose and titrated gradually to minimise adverse effects and identify the lowest effective dose.
Baseline investigations before starting ASM: FBC, LFTs, renal function, electrolytes. For carbamazepine/phenytoin: consider HLA testing. For valproate: pregnancy test in women of childbearing age; weight; counselling re: teratogenicity.
Therapeutic drug monitoring (TDM): Not routinely needed for levetiracetam or lamotrigine. Indicated for: phenytoin (narrow therapeutic index: 10–20 mg/L), carbamazepine (4–12 mg/L), valproate (50–100 mg/L), and when non-adherence, toxicity, drug interactions, pregnancy, or renal/hepatic changes alter pharmacokinetics.
Follow-up: Review at 4–6 weeks after initiation, then 3-monthly until stable, then 6–12-monthly. Assess seizure frequency, adverse effects, driving status, mood/cognition, and adherence at every visit.
When to switch or add: If seizures persist at maximum tolerated monotherapy dose, consider switching to an alternative appropriate ASM (preferred) or adding a second ASM if seizures are close to controlled and the patient is tolerating treatment.

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Never abruptly cease ASMs. Sudden withdrawal can precipitate status epilepticus. When discontinuing ASM therapy (after ≥2 years seizure-free and specialist review), taper over 2–6 months (minimum 2–3 months for barbiturates and benzodiazepines).

Emergency Seizure Management

Acute Generalised Convulsive Seizure

Most generalised tonic-clonic seizures are self-limiting (duration 1–3 minutes). Immediate management focuses on airway protection, injury prevention, and monitoring. Pharmacological intervention is required if the seizure persists >5 minutes.

Status Epilepticus — Definition

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Status epilepticus is defined as: (1) Convulsive status epilepticus (CSE): ≥5 minutes of continuous generalised convulsive seizure activity OR ≥2 discrete seizures without full recovery of consciousness between seizures. (2) Non-convulsive status epilepticus (NCSE): Prolonged altered consciousness/confusion without prominent motor features — requires EEG for diagnosis. CSE is a neurological emergency with mortality of 15–20% in adults if untreated beyond 30 minutes.

Pre-Hospital Algorithm (0–5 minutes)

0

Seizure begins — start timer

Position on side (recovery position). Protect head. Do not restrain. Do not insert anything into mouth. Remove dangerous objects. Note time of onset.

5 min

First-line benzodiazepine

Midazolam 10 mg IM (preferred pre-hospital; does not require IV access). Or diazepam 10–20 mg PR if midazolam not available. For children: midazolam 0.2 mg/kg IM (max 10 mg) or diazepam 0.5 mg/kg PR (max 20 mg).

Emergency Department Algorithm (5–30 minutes)

5 min

Initial assessment

ABCs. Establish IV access. Check BGL. Apply continuous pulse oximetry. Send bloods: glucose, FBC, UEC, LFTs, calcium, magnesium, ASM levels, VBG, lactate. Administer oxygen if SpO₂ <94%.

5 min

IV benzodiazepine (if not already given IM)

Diazepam 10 mg IV (given over 2–3 minutes; may repeat once after 5 minutes) OR lorazepam 4 mg IV (may repeat once after 5 min). Paediatric: diazepam 0.2 mg/kg IV (max 10 mg) or lorazepam 0.1 mg/kg IV (max 4 mg).

20 min

Second-line ASM (established status epilepticus)

If seizure persists after 2 doses of benzodiazepine, give ONE of the following:
IV Levetiracetam 60 mg/kg (max 4500 mg) over 15 min — preferred (safest profile) OR
IV Sodium valproate 40 mg/kg (max 3000 mg) over 5–10 min — avoid in women of childbearing age, hepatic disease, suspected metabolic disorder OR
IV Fosphenytoin 20 mg PE/kg at max 150 mg PE/min — risk of hypotension, arrhythmia; cardiac monitoring required. Contraindicated with suspected cardiac conduction abnormality.

40 min

Refractory status epilepticus — ICU admission

If seizures continue despite second-line ASM, proceed to rapid sequence intubation (RSI) and continuous IV infusion of:
Midazolam infusion 0.2 mg/kg bolus, then 0.05–2 mg/kg/hr OR
Propofol 2 mg/kg bolus, then 2–10 mg/kg/hr (caution: propofol infusion syndrome if >48 hrs or >5 mg/kg/hr) OR
Thiopentone 3–5 mg/kg bolus, then 3–5 mg/kg/hr
Continuous EEG monitoring is essential. Aim for burst suppression or seizure cessation on EEG.

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Hypoglycaemia correction: If BGL <3.0 mmol/L, administer IV glucose immediately — 50 mL of 50% glucose (25 g) IV bolus in adults, or 2–5 mL/kg of 10% glucose in children. Do not wait for lab confirmation if point-of-care glucose is low. Thiamine 100 mg IV should be given before glucose if alcohol misuse or malnutrition suspected (Wernicke's prevention).

Post-Status Epilepticus Management

Admit to HDU/ICU for at least 24 hours monitoring.
Continuous EEG monitoring if available — NCSE may persist without clinical signs in 15–20% of cases.
Identify and treat precipitant: infection, metabolic derangement, ASM non-adherence, alcohol withdrawal, intracranial pathology.
Review and optimise ASM regimen. MRI brain when clinically stable.
Referral to neurology/epileptology for all patients with status epilepticus.

Seizure First Aid — Patient Education

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Stay with the person

Time the seizure. Keep calm. Reassure bystanders.

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Protect from injury

Place on side when convulsions cease. Cushion head. Remove sharp objects.

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Do NOT restrain or put anything in the mouth

Restraint increases injury risk. Bite injuries are self-limited.

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Call 000 if: seizure >5 min, repeated seizures, injury, pregnancy, diabetes, first known seizure, or post-ictal confusion >30 min

Provide EMS with seizure duration, medications, medical history, and allergy information.

Women with Epilepsy

Epilepsy management in women requires particular attention to hormonal interactions, contraception efficacy, teratogenic risk, pregnancy planning, and breastfeeding. Up to 50% of pregnancies in women with epilepsy are unplanned, making proactive counselling at every consultation essential.

Contraception and ASM Interactions

Enzyme-inducing ASMs reduce the efficacy of hormonal contraception, increasing unintended pregnancy risk. Non-enzyme-inducing ASMs have no clinically significant interaction with contraception.

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Enzyme-inducing ASMs reduce hormonal contraception efficacy: Carbamazepine, phenytoin, phenobarbitone, topiramate (>200 mg/day), oxcarbazepine, eslicarbazepine, and rufinamide. Lamotrigine has a bidirectional interaction with the combined oral contraceptive pill (COC reduces lamotrigine levels by ~50%; lamotrigine does not significantly affect COC efficacy).

ASM	Effect on Contraception	Recommended Contraception
Levetiracetam, valproate, ethosuximide, gabapentin, pregabalin, lacosamide, zonisamide, clobazam	No significant interaction	Standard contraceptive options including combined oral contraceptive pill, progestogen-only pill, implant, IUD, depot
Carbamazepine, phenytoin, phenobarbitone, oxcarbazepine, eslicarbazepine	Reduced efficacy of hormonal contraception (COC, POP, implant, depot)	Levonorgestrel IUD (Mirena®) — most reliable; or copper IUD; if using COC, use ≥50 µg ethinyloestradiol with continuous use (no pill-free week); or double-dose progestogen; barrier methods as adjunct
Lamotrigine + COC	COC reduces lamotrigine levels by ~50% (risk of breakthrough seizures); lamotrigine does not affect COC efficacy	Monitor lamotrigine levels when starting/stopping COC. Consider IUD or progestogen-only alternatives. If COC used, consider increasing lamotrigine dose during active pill phase.
Topiramate >200 mg/day	Reduces COC efficacy	IUD, barrier methods, or alternative non-hormonal methods

Pregnancy Planning and Teratogenic Risk

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Sodium valproate is absolutely contraindicated in pregnancy. The TGA mandates that all women of childbearing potential prescribed valproate must be enrolled in the Valproate Pregnancy Prevention Programme. This includes: annual specialist review, documented pregnancy test before each prescription, acknowledgement of teratogenic risk signed by patient and prescriber, and effective contraception documented at every prescription. Valproate carries a 5–10% risk of major congenital malformations (neural tube defects, cardiac defects, hypospadias) and a 30–40% risk of neurodevelopmental disorders (autism spectrum disorder, reduced IQ) when used in pregnancy.

Teratogenic Risk by ASM

ASM	Major Congenital Malformation Risk	Neurodevelopmental Risk	Pregnancy Recommendation
Valproate	5–10% (dose-dependent; >1500 mg/day highest risk)	30–40% risk of ASD, IQ reduction 7–10 points	CONTRAINDICATED in pregnancy. Switch to alternative ASM before conception if possible.
Phenobarbitone	6–7%	Increased risk of cognitive effects	Avoid if possible; use lowest effective dose
Phenytoin	~6%	Some evidence of neurodevelopmental risk	Avoid if possible; switch to levetiracetam or lamotrigine
Carbamazepine	~4.5% (neural tube defect risk ~0.5–1%)	Limited evidence of neurodevelopmental risk at low doses	Acceptable if needed; lowest effective dose; folic acid 5 mg/day
Lamotrigine	~2–3%	No evidence of neurodevelopmental harm	Preferred ASM in pregnancy. Monitor levels — clearance increases 50–100% by third trimester.
Levetiracetam	~2%	No evidence of neurodevelopmental harm	Preferred ASM in pregnancy. Minimal protein binding; no teratogenic signal in large registries.

Folate Supplementation

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All women with epilepsy of childbearing potential should receive folic acid 5 mg daily (high-dose, PBS-subsidised — authority required for 5 mg tablets). Start at least 1 month before conception and continue through the first trimester (ideally throughout pregnancy). Standard 0.5 mg folate is inadequate for women on ASMs. Some experts recommend continuing 5 mg daily throughout pregnancy, particularly for those on enzyme-inducing ASMs.

Pre-Conception Checklist

Review ASM regimen — switch from valproate to levetiracetam or lamotrigine where possible, ideally ≥3 months before conception.
Commence folic acid 5 mg daily — at least 1 month before conception.
Optimise seizure control — seizure freedom before pregnancy reduces perinatal risk more than ASM changes.
Document baseline ASM levels (especially lamotrigine) for comparison during pregnancy.
Ensure effective contraception during transition to pregnancy-safe ASM regimen.
Counsel regarding: seizure risk during pregnancy (~25–30% may have increased seizure frequency, often due to non-adherence or pharmacokinetic changes); risks of seizures vs risks of ASM; management during labour and delivery.
Referral to maternal-fetal medicine or combined obstetric-epilepsy clinic at tertiary centre.

Antenatal Monitoring

Lamotrigine and levetiracetam levels: Check at baseline pre-pregnancy, then monthly during pregnancy and at 2-weekly intervals from 28 weeks. Dose may need to be increased 50–100% to maintain pre-pregnancy levels. Check levels again at 2–4 weeks postpartum (levels fall rapidly; dose reduction needed to avoid toxicity).
Obstetric ultrasound: Detailed morphology scan at 18–20 weeks (fetal anomaly screening — particularly neural tube defects for those on valproate or carbamazepine historically).
Fetal monitoring: Low threshold for fetal monitoring if seizure occurs in pregnancy; CTG monitoring during labour if seizure occurs in third trimester.

Labour, Delivery, and Postnatal

Continue ASMs throughout labour (oral or via NG if vomiting). Consider IV preparation if prolonged labour and oral intake impaired (levetiracetam IV, valproate IV available; carbamazepine has no IV formulation).
Seizures during labour: IV lorazepam 4 mg or diazepam 10 mg.
Vitamin K 1 mg IM for the neonate (standard) — ASMs that induce enzymes may reduce neonatal vitamin K-dependent clotting factors.
Breastfeeding is encouraged for all ASMs. Levetiracetam, lamotrigine, and carbamazepine are compatible. Monitor infant for drowsiness, poor feeding, or rash.
Postnatal dose adjustments: lamotrigine dose may need rapid reduction post-delivery; monitor levels at 2 and 6 weeks postpartum.
Psychosocial support: screen for postnatal depression (higher risk in women with epilepsy); ensure safe infant care practices (bathing supervision, avoid co-sleeping if uncontrolled seizures).

Catamenial Epilepsy

Seizure exacerbation in relation to the menstrual cycle occurs in approximately 10–40% of women with epilepsy. Two patterns are recognised: perimenstrual (catamenial type 1 — seizure clustering around menses due to declining progesterone and oestrogen ratio) and periovulatory (catamenial type 2 — seizure clustering around ovulation due to oestrogen surge). Management options include: clobazam 10–20 mg/day for 10–14 days perimenstrually ("luteal-phase rescue"); hormonal strategies (levonorgestrel IUD, combined oral contraceptive pill); or ASM dose adjustment guided by specialist.

Special Populations

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Paediatric Epilepsy

Febrile seizures (simple: <15 min, generalised, age 6 months–5 years) do not require ASM; counsel parents regarding recurrence risk (~30%). Complex febrile seizures warrant EEG and neurology referral.

Neonatal seizures are often subtle (apnoea, eye deviation, cycling movements) and require urgent EEG and neuroimaging. Phenobarbitone remains first-line in neonates; levetiracetam increasingly used.

Dravet syndrome should be suspected in previously well infant with prolonged febrile seizures (often >15 min) in the first year of life. Genetic testing (SCN1A) available in Australia. Avoid sodium channel blockers (carbamazepine, lamotrigine, phenytoin) — these exacerbate seizures in Dravet syndrome.

First-line ASMs in children: levetiracetam or valproate for generalised seizures; carbamazepine, levetiracetam, or oxcarbazepine for focal seizures. Avoid carbamazepine in suspected generalised epilepsy (may worsen absence/myoclonic seizures).

Paediatric neurology referral (MBS Item 104 or telehealth MBS Item 99) recommended for all new paediatric epilepsy diagnoses, suspected genetic syndromes, developmental regression, or refractory epilepsy.

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Elderly Patients (≥65 years)

Epilepsy incidence is highest in the elderly (up to 100 per 100,000/year in those >65 years), primarily due to cerebrovascular disease, neurodegenerative disease, and brain tumours.

Seizure presentations in the elderly are frequently subtle — isolated confusion, falls, or transient unresponsiveness may be the only manifestation. High index of suspicion required.

Preferred ASMs: levetiracetam (renally cleared, no drug interactions) and lamotrigine (well tolerated, cognitive sparing). Start at very low doses and titrate slowly.

Avoid phenytoin (complex pharmacokinetics, osteoporosis risk, drug interactions), phenobarbitone (sedation, falls, cognitive impairment), and carbamazepine (hyponatraemia risk, drug interactions) when possible.

Falls risk assessment is essential. Polypharmacy review — ASMs may interact with anticoagulants (warfarin, DOACs), antihypertensives, and other CNS-active medications.

Bone health: long-term enzyme-inducing ASMs (phenytoin, carbamazepine) increase osteoporosis risk. Consider DEXA scan, calcium/vitamin D supplementation, and bisphosphonates as indicated.

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Renal Impairment

Levetiracetam: Requires dose reduction. eGFR 50–80 mL/min: max 1000 mg BD. eGFR 30–50: 250–750 mg BD. eGFR <30: 250–500 mg BD. Haemodialysis: supplemental dose 500–1000 mg post-dialysis (highly dialysable, ~50% removed per session).

Valproate: No dose adjustment required (highly protein-bound, not dialysed).

Carbamazepine: No dose adjustment, but monitor for accumulation of active metabolite (carbamazepine-10,11-epoxide) in renal impairment.

Lamotrigine: No dose adjustment required. Not significantly renally cleared.

Phenytoin: No dose adjustment, but free fraction increases in renal failure (hypoalbuminaemia). Measure free phenytoin level if monitoring.

Gabapentin/pregabalin: Significant renal clearance — dose reduction required by eGFR. Gabapentin: eGFR 30–60: 300 mg BD–TDS; eGFR 15–30: 300 mg OD; eGFR <15: 300 mg every other day.

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Hepatic Impairment

Valproate: CONTRAINDICATED in severe hepatic impairment and active liver disease. Hepatotoxicity is a rare but serious idiosyncratic reaction — monitor LFTs at baseline, 1 month, 3 months, 6 months, and annually.

Carbamazepine, phenytoin, phenobarbitone: All hepatically metabolised. Use with caution; dose reduction may be required. Monitor drug levels.

Levetiracetam: Preferred in hepatic impairment — minimal hepatic metabolism; no dose adjustment.

Lamotrigine: Hepatically metabolised (glucuronidation). Use with caution in severe hepatic impairment; dose reduction of ~50% recommended. Monitor levels.

Avoid highly protein-bound ASMs in severe hepatic impairment (increased free fraction). Monitor both total and free drug levels for phenytoin and valproate if used.

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Immunocompromised Patients

New seizures in immunocompromised patients (HIV, transplant recipients, chemotherapy) should raise suspicion for CNS infection (toxoplasmosis, cryptococcal meningitis, PML, CMV encephalitis) or CNS lymphoma/malignancy.

Urgent MRI with contrast, CSF analysis (if safe), and HIV/torch serology if not already known.

Preferred ASMs: levetiracetam or lacosamide (no drug interactions with immunosuppressants). Avoid carbamazepine, phenytoin, and phenobarbitone (enzyme induction reduces tacrolimus, cyclosporine, and other immunosuppressant levels — risk of transplant rejection).

Lamotrigine may be used but levels may be affected by immunosuppressant changes.

Antiretroviral interactions: many ARVs interact with enzyme-inducing ASMs. Consult HIV specialist pharmacist. Levetiracetam is the safest ASM choice in HIV-positive patients.

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Australians experience a higher burden of epilepsy, status epilepticus, and epilepsy-related mortality compared to non-Indigenous Australians. Contributing factors include higher rates of traumatic brain injury, CNS infections (particularly in remote communities), perinatal complications, substance use (including petrol sniffing-related brain injury in some communities), and limited access to neurological services. Culturally safe, trauma-informed care is essential.

Epidemiology

Epilepsy prevalence is 1.5–2 times higher in Aboriginal and Torres Strait Islander Australians. Status epilepticus admissions are significantly higher. Epilepsy-related mortality is disproportionately elevated, particularly in remote and very remote communities. Children have higher rates of convulsive status epilepticus.

Access to specialist services

Neurology and epilepsy specialist services are concentrated in metropolitan centres. Remote and very remote communities may have no resident neurologist. Telehealth (MBS Item 99) is essential for specialist access — ensure availability of Aboriginal Health Worker or health practitioner support during telehealth consultations. EEG availability is limited in many remote health services; mobile EEG services and store-and-forward EEG interpretation can improve access. MRI requires transfer to a regional or metropolitan centre.

Medication adherence and supply

Remote community pharmacies may have limited ASM stock (particularly levetiracetam liquid formulations, lacosamide, ethosuximide). Use Remote Area Aboriginal Health Services (RAAHS) Section 100 supplies where available. Long-acting depot formulations may be considered where daily adherence is challenging (note: no long-acting ASMs exist; medication administration by health staff may be needed). Aboriginal Health Workers can support supervised medication administration in community settings.

Driving and geographic isolation

Driving restrictions have disproportionate impact in remote communities where alternative transport is limited or non-existent. Licence suspension may affect access to essential services, employment, and cultural activities. Support patient with practical transport solutions and community liaison during restriction periods.

Cultural considerations

Seizures may be understood differently in some cultural contexts — avoid dismissal of cultural explanations; integrate Western medical management with culturally respectful explanations. Ensure family and community involvement in care planning where desired. "Sorry Business" and cultural obligations may affect appointment attendance and medication supply — flexible scheduling and medication planning ahead of known absences. Young males in remote communities may present later due to reluctance to seek healthcare; community-based seizure education programs can improve early recognition.

Specific clinical considerations

HLA testing: Higher prevalence of HLA-B*1502 in some Aboriginal communities — consider HLA-B*1502 testing before carbamazepine in all Aboriginal and Torres Strait Islander patients. Alcohol-related epilepsy: Higher rates of alcohol-related brain injury and withdrawal seizures in some communities — ensure alcohol withdrawal protocols are available in remote health centres. CSF infections: Higher rates of bacterial meningitis and neurocysticercosis in some regions — consider in new-onset seizure with fever or focal signs. Petrol sniffing: In communities with historical or ongoing petrol sniffing (lead encephalopathy, solvent-induced brain injury), chronic epilepsy management may be complex; ensure neurological follow-up via visiting specialist or telehealth.

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Key practice points for Aboriginal and Torres Strait Islander epilepsy care: Use Aboriginal Health Workers and practitioners as key members of the epilepsy care team. Ensure culturally appropriate seizure first aid education is provided to families and community members. Prioritise telehealth specialist access for all new diagnoses and refractory epilepsy. Consider medication supply chain and remote pharmacy limitations when selecting ASMs. Discuss driving restrictions sensitively and explore practical alternatives. Incorporate Yarning and storytelling approaches in patient education where appropriate.

📚 References

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2. Fisher RS, Acevedo C, Arzimanoglou A, et al. ILAE official report: a practical clinical definition of epilepsy. Epilepsia. 2014;55(4):475–482.
3. Australasian Chapter of Sexual Health Medicine, RACP. Epilepsy guidelines for Australian clinical practice. Epilepsy Society of Australia; 2023.
4. Austroads. Assessing Fitness to Drive. 4th ed. Sydney: Austroads; 2022. Available from: austroads.com.au.
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6. Glauser T, Shinnar S, Gloss D, et al. Evidence-based guideline: treatment of convulsive status epilepticus in children and adults. Neurology. 2016;86(20):1936–1947.
7. Tomson T, Battino D, Bonizzoni E, et al. Comparative risk of major congenital malformations with eight different antiepileptic drugs: a prospective cohort study of the EURAP registry. Lancet Neurol. 2018;17(6):530–538.
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9. Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG). Antiepileptic medication use during pregnancy. Clinical Guideline C-Obs 51. Melbourne: RANZCOG; 2023.
10. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Epilepsy and neurological conditions. Canberra: AIHW; 2023.
11. Beghi E, Giussani G, Sander JW. The natural history and prognosis of epilepsy. Epileptic Disord. 2015;17(3):243–253.
12. Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: position paper of the ILAE Commission for Classification and Terminology. Epilepsia. 2017;58(4):512–521.
13. Medicines and Healthcare Products Regulatory Agency (MHRA). Valproate Pregnancy Prevention Programme: toolkit for healthcare professionals. London: MHRA; 2023.
14. Panayiotopoulos CP. A Clinical Guide to Epileptic Syndromes and Their Treatment. 2nd ed. London: Springer; 2010.
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