Faints, Fits and Funny Turns

Last updated 31 May 2026 · Neurology

📋 Key Information Summary

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"Faints, fits and funny turns" is the common diagnostic triad encountered in primary care and emergency departments — the clinician must distinguish syncope, epileptic seizures, and non-epileptic events (psychogenic, metabolic, structural) through a structured history-first approach.
The single most valuable diagnostic tool is a witness account — always obtain collateral history from bystanders, family, or paramedics; video capture (e.g., smartphone) is increasingly valuable.
Syncope accounts for approximately 50% of presentations; features include prodrome (lightheadedness, nausea, visual greying), brief LOC (<30 seconds), rapid recovery, and pallor at onset.
Epileptic seizures are characterised by abrupt onset without prodrome, cyanosis (not pallor), tonic-clonic activity, post-ictal confusion (minutes to hours), and tongue biting (lateral, not tip).
Febrile seizures affect 2–5% of Australian children aged 6 months to 5 years; simple febrile seizures (<15 min, generalised, single episode in 24 h) are benign and do not require anti-epileptic drugs (AEDs).
Infantile spasms (West syndrome) present with clusters of jackknife spasms, developmental regression, and hypsarrhythmia on EEG — this is a neurological emergency requiring urgent ACTH or vigabatrin within days of onset.
Juvenile myoclonic epilepsy (JME) presents in adolescence with early-morning myoclonic jerks, generalised tonic-clonic seizures, and typical absence; valproate is effective but contraindicated in women of childbearing potential — levetiracetam or lamotrigine are preferred alternatives.
Childhood absence epilepsy presents with frequent brief staring episodes (5–30 seconds) with abrupt onset/offset; ethosuximide is first-line; sodium valproate and lamotrigine are second-line options.
Orthostatic (postural) hypotension is defined as a sustained drop in systolic BP ≥20 mmHg or diastolic BP ≥10 mmHg within 3 minutes of standing — common in the elderly and those on antihypertensives.
Non-epileptic attack disorder (NEAD) / functional neurological disorder (FND) accounts for 20–30% of referrals to epilepsy clinics; features include asynchronous limb movements, eyes closed during event, preserved awareness, and event duration >2 minutes without post-ictal confusion.
Red flags requiring emergency referral: first seizure, status epilepticus (>5 minutes), focal neurological deficit, new headache with seizure, seizure in pregnancy (eclampsia until proven otherwise), suspected cardiac syncope, and syncope during exertion.
Aboriginal and Torres Strait Islander Australians have higher rates of epilepsy-related hospitalisation and lower rates of neurology specialist access, particularly in remote communities — culturally safe assessment pathways and telehealth neurology are critical.
Driving restrictions in Australia: single unprovoked seizure — no driving for 6 months (private) or 12 months (commercial); epilepsy diagnosis — seizure-free ≥12 months on treatment for private licence, ≥10 years seizure-free for commercial licence (Austroads 2022 guidelines).

Introduction & Australian Epidemiology

The presentation of episodic neurological events — encompassing "faints, fits, and funny turns" — is one of the most common and diagnostically challenging scenarios in Australian primary care and emergency medicine. These events span a broad differential including syncope, epileptic seizures, and non-epileptic paroxysmal events (psychogenic, metabolic, cardiac, and structural causes). Misdiagnosis rates remain high, with up to 20–30% of patients initially diagnosed with epilepsy ultimately found to have non-epileptic events, and conversely, some genuine epilepsy being missed.

In Australia, epilepsy affects approximately 250,000 people (≈1% prevalence), with bimodal incidence peaks in children (<5 years) and older adults (>65 years). The annual incidence is approximately 50–70 per 100,000. Syncope accounts for 1–3% of emergency department presentations and up to 6% of acute medical admissions. In Aboriginal and Torres Strait Islander populations, epilepsy prevalence is estimated to be 1.5–3 times higher than in non-Indigenous Australians, with significantly higher rates of epilepsy-related hospitalisation and mortality.

The structured diagnostic approach described in this article — the "Faints, Fits and Funny Turns" model — provides a practical framework for Australian clinicians to systematically evaluate paroxysmal events, initiate appropriate investigations, and ensure timely referral where indicated. The model emphasises history-first diagnosis, targeted investigation, and recognition of at-risk populations.

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Diagnostic pitfall: Up to 20% of patients referred to epilepsy clinics with a diagnosis of "refractory epilepsy" actually have non-epileptic attack disorder (NEAD), medication side-effects, or alternative paroxysmal events. Always consider an alternative diagnosis when seizures fail to respond to appropriate AEDs.

Parameter	Australia-wide	Aboriginal & Torres Strait Islander
Epilepsy prevalence	≈1% (250,000)	1.5–3× higher
Annual incidence	50–70 per 100,000	Estimated 80–150 per 100,000
Febrile seizure prevalence	2–5% of children aged 6 mo–5 yr	Higher, linked to higher burden of infectious disease
Epilepsy-related mortality (SMR)	2–3× general population	Significantly higher; SUDEP and status epilepticus contribute
Neurology access (<12 months)	≈60% of new diagnoses	<30% in remote/very remote areas

Faints, Fits & Funny Turns Diagnostic Model

The diagnostic approach to paroxysmal events follows a systematic framework: (1) Was this a true loss of consciousness? (2) Was the event epileptic or non-epileptic? (3) If non-epileptic, was it syncope, or another cause? The cornerstone is the history, supplemented by targeted examination and investigation.

The Three-Question Diagnostic Framework

Was there true loss of consciousness?

Distinguish pre-syncope (near-fainting) from syncope (complete LOC). Distinguish dizziness (vertigo vs. lightheadedness vs. disequilibrium). Some "funny turns" are near-syncope, not true LOC.

Was the event epileptic or non-epileptic?

Key distinguishing features: onset (abrupt vs. gradual), motor activity (rhythmic tonic-clonic vs. asynchronous flailing), colour (cyanosis vs. pallor), duration, post-ictal state, and witness description.

If non-epileptic, what is the cause?

Cardiac syncope (arrhythmia, structural), reflex syncope (vasovagal, carotid sinus), orthostatic hypotension, metabolic (hypoglycaemia, hypoxia), psychogenic (NEAD/FND), or other structural neurological cause.

Key Historical Features — Distinguishing Table

Feature	Epileptic Seizure	Syncope	Non-Epileptic Event (NEAD)
Trigger	Sleep deprivation, alcohol withdrawal, flashing lights, medication non-adherence	Prolonged standing, pain, emotion, micturition, postural change	Emotional stress, interpersonal conflict (may not be apparent)
Prodrome	Aura (déjà vu, epigastric rising, olfactory) — seconds	Lightheadedness, nausea, visual greying, sweating — seconds to minutes	Variable; may describe multiple vague symptoms
Onset	Abrupt, often from any posture	Gradual, typically upright/standing	Variable; can be dramatic
Colour	Cyanosis / dusky	Pale, clammy	Usually normal colour
Motor activity	Rhythmic tonic-clonic, ± focal features	Brief myoclonic jerks (<15 sec), stiffening	Asynchronous, thrashing, pelvic thrusting, waxing/waning
Duration	1–3 min (GTCS); seconds (focal/absence)	<30 seconds typically	>2 min, often 5–20+ min
Eyes	Open, deviated upward or laterally	Open or closed, rolling back	Closed during event (resist eye opening)
Tongue biting	Lateral tongue (highly specific)	Rare; tip of tongue	Tip of tongue or none
Post-event state	Confusion, drowsiness, headache (minutes to hours)	Rapid recovery (<5 min), no confusion	Rapid recovery or emotional distress; no true confusion
Incontinence	Common (urinary); faecal rare	Occasional urinary	Rare (suggests organic if present)

Essential Investigations — First-Line Assessment

Essential

12-lead ECG

All patients presenting with LOC or suspected seizure — look for long QT, Brugada pattern, WPW, hypertrophic cardiomyopathy, AV block, arrhythmia. MBS Item 11707.

Essential

Blood glucose (BGL)

Point-of-care; hypoglycaemia (<4 mmol/L) is a treatable cause of any paroxysmal event.

Essential

FBC, UEC, LFTs, calcium, magnesium, TFTs

Metabolic precipitants: hyponatraemia, hypocalcaemia, renal failure, hepatic encephalopathy, thyroid dysfunction. MBS Item 66832.

Available

Serum prolactin (timing critical)

Drawn 10–20 min post-event; elevated >2× baseline is suggestive of generalised tonic-clonic or complex partial seizure. Normal prolactin does not exclude epilepsy. Useful to confirm vs. NEAD.

Referral

EEG (routine / sleep-deprived / ambulatory)

Routine EEG has ~50% sensitivity for epilepsy (repeat or sleep-deprived increases to ~80%). MBS Item 11000. Refer to neurologist or neurophysiology service. Indicated for first unprovoked seizure, suspected epilepsy, and infantile spasms (urgent).

Referral

MRI Brain

Recommended for all new-onset epilepsy (except typical childhood absence/febrile seizures). MBS Item 63001 (Medicare-eligible). Look for hippocampal sclerosis, cortical dysplasia, tumour, vascular malformation.

Referral

Holter / Event monitor / Implantable loop recorder

For recurrent unexplained syncope with suspicion of arrhythmic cause. Referral to cardiology for cardiac monitoring. MBS Item 11709 (24-hr Holter).

Specialist

Tilt-table test (head-up tilt)

For recurrent syncope of uncertain aetiology; reproduces vasovagal/orthostatic mechanism. Available at major hospitals; referral to cardiology.

When to Refer — Red Flags Requiring Urgent Assessment

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First-ever seizure (any age) — urgent neurology referral within 2 weeks
Status epilepticus (seizure >5 min or recurrent seizures without recovery) — call 000
Seizure in pregnancy — eclampsia until proven otherwise; immediate obstetric + medical emergency
Focal neurological deficit (suggests structural lesion)
Syncope during exertion or with family history of sudden cardiac death <40 years
Prolonged QTc (>460 ms female, >440 ms male) on ECG
Suspected infantile spasms — urgent EEG within 24 hours
Headache + seizure (consider space-occupying lesion, meningitis, cerebral venous sinus thrombosis)

Epilepsy Syndromes

Epilepsy is not a single disease but a heterogeneous group of syndromes classified by seizure type, age of onset, EEG findings, and aetiology. The ILAE 2017 classification organises epilepsy by onset (focal, generalised, unknown) and aetiology (genetic, structural, metabolic, immune, unknown). Australian management aligns with the eTG Neurology guidelines and the Epilepsy Society of Australia consensus statements.

Febrile Seizures

Febrile seizures are the most common seizure disorder of childhood, affecting 2–5% of Australian children aged 6 months to 5 years. They are triggered by fever ≥38°C (typically from viral upper respiratory infection, otitis media, or roseola) in the absence of intracranial infection or prior afebrile seizure.

Type	Criteria	Risk of Epilepsy	Management
Simple febrile seizure	Generalised, <15 min, single episode in 24 h, age 6 mo–5 yr	1–2% (similar to general population)	Reassurance; treat underlying fever; no AEDs required; parental education
Complex febrile seizure	Focal features, >15 min, or >1 episode in 24 h	4–10%	Lower threshold for neuroimaging and EEG; consider neurology referral; no routine AED prophylaxis
Febrile status epilepticus	Febrile seizure >30 min (or serial seizures without recovery)	Higher risk of subsequent epilepsy (10–15%)	Manage as status epilepticus; urgent neurology referral; MRI and EEG recommended

ℹ️

Parental reassurance points: Simple febrile seizures do not cause brain damage, do not indicate meningitis (in the well child), and do not require long-term anticonvulsants. Teach parents seizure first aid (recovery position, time the seizure, do not restrain). Paracetamol and ibuprofen for comfort do not prevent febrile seizures.

Infantile Spasms (West Syndrome)

Infantile spasms are a severe epilepsy syndrome presenting between 3 and 12 months of age. The classic triad is (1) clusters of epileptic spasms (jackknife flexion/extension spasms), (2) developmental arrest or regression, and (3) hypsarrhythmia on EEG (chaotic, high-amplitude slow waves with multifocal sharp waves).

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Neurological emergency: Infantile spasms require urgent diagnosis and treatment within days, not weeks. Delayed treatment (>2–3 weeks from onset) is associated with significantly worse developmental outcomes. If suspected, arrange urgent EEG (within 24 hours) and refer immediately to paediatric neurology.

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ACTH (Tetracosactide)

Synacthen® · First-line for infantile spasms

Paediatric dose 0.5 mg (40 IU) IM daily for 2 weeks, then taper over 2–4 weeks

Route IM injection

Duration 4–6 weeks total course

Key adverse effects Hypertension, infection risk, irritability, Cushing syndrome, adrenal suppression

PBS status ⚑ Authority Required

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Vigabatrin

Sabril® · First-line for tuberous sclerosis complex (TSC)-associated spasms

Paediatric dose 50 mg/kg/day PO BD, titrate up to 100–150 mg/kg/day

Route Oral (granules or tablets)

Key adverse effects Concentric visual field constriction (irreversible in ~30%), sedation, MRI signal changes

Monitoring Baseline and serial visual field assessment (older children); MRI at 3–6 months

PBS status ⚑ Authority Required

Juvenile Myoclonic Epilepsy (JME)

JME is one of the most common genetic generalised epilepsy syndromes, accounting for 5–10% of all epilepsy. Onset is typically between 12 and 18 years. The hallmark is early-morning myoclonic jerks (especially of the upper limbs), often triggered by sleep deprivation, fatigue, or alcohol. Most patients also experience generalised tonic-clonic seizures (GTCS), and up to 30% have absence seizures. EEG shows bilateral synchronous 4–6 Hz polyspike-and-wave discharges.

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Lifelong treatment consideration: JME typically requires lifelong AED therapy. Withdrawal of medication results in seizure recurrence in 80–90% of patients. Patients must be counselled about medication adherence, sleep hygiene, and avoidance of alcohol excess and seizure precipitants.

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Sodium Valproate (Valproic acid)

Epilim® · First-line for JME in males

Adult dose 500 mg PO BD–TDS, titrate to 1000–2000 mg/day in divided doses

Paediatric dose 20–40 mg/kg/day PO BD–TDS

Key adverse effects Teratogenicity (neural tube defects, neurodevelopmental effects), weight gain, tremor, hepatotoxicity (rare), pancreatitis, thrombocytopenia

Monitoring FBC, LFTs at baseline and 3-monthly; valproate levels (therapeutic 350–700 micromol/L)

PBS status ✔ PBS General Benefit

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Levetiracetam

Keppra® · First-line alternative for women of childbearing potential with JME

Adult dose 500 mg PO BD, titrate to 1000–3000 mg/day

Paediatric dose 10–20 mg/kg/day PO BD, titrate to 40–60 mg/kg/day

Key adverse effects Behavioural/psychiatric (irritability, depression, aggression in ~15%), somnolence

Renal adjustment Dose reduce if eGFR <50 mL/min; 50% dose if eGFR 30–50; 25% if eGFR <30

PBS status ✔ PBS General Benefit

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Lamotrigine

Lamictal® · Second-line for JME (especially women of childbearing potential)

Adult dose 25 mg PO OD for 2 weeks → 50 mg OD for 2 weeks → increase by 50 mg every 1–2 weeks to 100–200 mg/day BD

Key adverse effects Serious rash (SJS/TEN risk, especially with rapid titration or concomitant valproate), headache, nausea

⚠ Critical safety Slow titration mandatory — SJS risk highest in first 8 weeks. Double the dose interval if used with valproate.

PBS status ✔ PBS General Benefit

Childhood Absence Epilepsy (CAE)

Childhood absence epilepsy typically presents between ages 4 and 10 years with frequent (up to 100/day) brief staring episodes lasting 5–30 seconds with abrupt onset and offset, no post-ictal confusion, and often subtle automatisms (eye blinking, lip smacking). Hyperventilation for 3–5 minutes reliably provokes absence seizures and is a useful bedside test. EEG shows classical 3 Hz generalised spike-and-wave discharges. Prognosis is generally good — 65–70% remit by adolescence.

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Ethosuximide

Zarontin® · First-line for childhood absence epilepsy

Paediatric dose 20 mg/kg/day PO OD–BD, titrate to 30–40 mg/kg/day (max 1500 mg/day)

Route Oral (capsules or syrup)

Key adverse effects GI upset (nausea, vomiting, abdominal pain — minimised with food/slow titration), headache, rare blood dyscrasias

Monitoring FBC at baseline and periodically; ethosuximide levels if suboptimal response

PBS status ⚑ Authority Required

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Sodium Valproate

Epilim® · Second-line for CAE (if ethosuximide not tolerated or unavailable)

Paediatric dose 20–30 mg/kg/day PO BD–TDS, titrate to 30–40 mg/kg/day

Note Effective but carries greater adverse effect burden; avoid in adolescent females where possible

PBS status ✔ PBS General Benefit

Status Epilepticus — Emergency Management

Status epilepticus is defined as a seizure lasting ≥5 minutes, or ≥2 seizures without return to baseline consciousness. It is a medical emergency with significant morbidity and mortality. Australian treatment follows the Epilepsy Society of Australia / ANZ guidelines.

0–5 min

Stabilisation: ABC approach, high-flow oxygen, IV access, BGL check. If hypoglycaemic: IV glucose 50 mL 50% (adults) or 2–4 mL/kg 10% dextrose (children). Thiamine 300 mg IV if alcohol dependency suspected.

5–20 min (First-line)

Benzodiazepines: Midazolam 10 mg IM (preferred pre-hospital) OR Diazepam 10–20 mg IV (max 5 mg/min) OR Lorazepam 4 mg IV. Paediatric: Midazolam 0.2 mg/kg IM (max 10 mg) or Diazepam 0.5 mg/kg PR (max 20 mg). If IV access: Lorazepam 0.1 mg/kg IV (max 4 mg).

20–40 min (Second-line)

Second-line AED: Levetiracetam 60 mg/kg IV (max 4500 mg) over 15 min OR Sodium valproate 40 mg/kg IV (max 3000 mg) over 10 min OR Phenytoin 20 mg/kg IV at max 50 mg/min (with cardiac monitoring). Paediatric doses adjusted per weight.

>40 min (Refractory)

ICU admission, anaesthesia: Propofol 1–2 mg/kg bolus then 1–10 mg/kg/hr OR Midazolam 0.2 mg/kg bolus then 0.1–2 mg/kg/hr OR Thiopentone 3–5 mg/kg bolus then 3–5 mg/kg/hr. Continuous EEG monitoring essential. Treat underlying cause aggressively.

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Pre-hospital management: Ambulance Victoria, NSW Ambulance, and Queensland Ambulance protocols recommend midazolam IM (10 mg adults, 0.2 mg/kg children) as the preferred first-line pre-hospital treatment for status epilepticus when IV access is not available. Community-administered buccal midazolam (0.5 mg/kg, max 10 mg) is available for carers of patients with known epilepsy.

Syncope & Orthostatic Intolerance

Syncope is a transient loss of consciousness (TLOC) due to global cerebral hypoperfusion, characterised by rapid onset, short duration, and spontaneous complete recovery. It accounts for approximately 1–3% of emergency department attendances in Australia and becomes increasingly common with age. Syncope must be distinguished from other causes of TLOC (seizure, metabolic, structural) and from non-TLOC mimics (drop attacks, falls, presyncope).

Classification of Syncope

Low Risk

Reflex (Vasovagal) Syncope

Most common cause (~60% of syncope). Triggered by pain, emotion, prolonged standing, warm environment, Valsalva. Classic prodrome: nausea, sweating, visual greying, pallor. Brief LOC (<30 sec). Rapid full recovery. Benign prognosis.

Setting: Reassurance, education, lifestyle measures

Moderate Risk

Orthostatic Hypotension

Defined as sustained systolic BP drop ≥20 mmHg or diastolic BP drop ≥10 mmHg within 3 min of standing. Common causes: dehydration, medications (antihypertensives, diuretics, alpha-blockers, antidepressants, levodopa), autonomic neuropathy (diabetes, Parkinson disease), prolonged bed rest.

Setting: GP review, medication review, specialist if recurrent

High Risk

Cardiac Syncope

Arrhythmic (bradycardia, SVT, VT, long QT, Brugada, WPW) or structural (aortic stenosis, HCM, PE, aortic dissection, cardiac tamponade). Associated with significant mortality if untreated. Features: syncope during exertion, supine syncope, sudden onset without prodrome, family history of sudden death <40 yr, abnormal ECG.

Setting: Emergency admission, cardiology referral, telemetry

San Francisco Syncope Rule / Canadian Syncope Risk Score

Risk stratification tools help identify high-risk patients requiring admission. The Canadian Syncope Risk Score (CSRS) outperforms older tools and is increasingly used in Australian EDs. High-risk features include: abnormal ECG, history of heart disease, syncope during exertion, syncope while supine, family history of sudden cardiac death, and elevated troponin.

Orthostatic Intolerance — Spectrum of Disorders

Condition	Mechanism	Key Features	Management
Orthostatic hypotension	Failure of BP autoregulation on standing	BP drop ≥20/10 mmHg within 3 min; lightheadedness, visual blurring on standing	Medication review, fluid/salt intake, compression stockings, fludrocortisone or midodrine if severe
Postural orthostatic tachycardia syndrome (POTS)	Excessive heart rate increase on standing without BP drop (autonomic dysregulation)	HR increase ≥30 bpm (≥40 in teens) within 10 min of standing, with symptoms (palpitations, lightheadedness, fatigue, brain fog); predominantly young women	Exercise programme (recumbent → upright), increased fluid (2–3 L/day) and salt (6–10 g/day), compression garments; pharmacotherapy: ivabradine, midodrine, low-dose beta-blocker
Carotid sinus hypersensitivity	Exaggerated baroreceptor reflex → bradycardia ± vasodilation	Syncope triggered by head turning, tight collar, shaving; predominantly elderly males; diagnosed by carotid sinus massage (supervised)	Avoid triggers; dual-chamber pacemaker if cardioinhibitory type with recurrent syncope

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Fludrocortisone

Florinef® · Mineralocorticoid for orthostatic hypotension

Adult dose 50–200 micrograms PO OD in the morning

Key adverse effects Hypokalaemia, hypertension, oedema, headache

Monitoring BP, serum potassium, weight; titrate to symptom response

PBS status ✔ PBS General Benefit

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Midodrine

Gutron® · Alpha-1 agonist for orthostatic hypotension

Adult dose 2.5–10 mg PO TDS (morning, midday, late afternoon — avoid after 6 PM due to supine hypertension)

Contraindications Supine hypertension, urinary retention, pheochromocytoma, severe cardiac disease

PBS status ⚑ Authority Required

Non-Pharmacological Management of Reflex Syncope

Education & Reassurance

Explain the benign nature of vasovagal syncope. Recognise prodromal symptoms. Avoid prolonged standing, hot environments, dehydration.

Counter-Pressure Manoeuvres

Leg crossing with muscle tensing, squatting, handgrip, lower-body muscle tensing — effective at aborting episodes when prodrome is recognised.

Physical Counter-Pressure Training

Tilt-training (progressive standing against a wall) — limited evidence but may help selected patients.

Increased Fluid & Salt Intake

2–3 litres of fluid per day, increase dietary salt (unless contraindicated by hypertension, heart failure, or renal disease).

Non-Epileptic Events

Non-epileptic events encompass a broad range of paroxysmal episodes that mimic epileptic seizures but do not have an epileptic basis. The most common and clinically significant category is non-epileptic attack disorder (NEAD), also termed functional seizures or dissociative seizures within the functional neurological disorder (FND) spectrum. NEAD accounts for 20–30% of referrals to Australian epilepsy monitoring units.

Non-Epileptic Attack Disorder (NEAD) / Functional Seizures

NEAD is a condition in which patients experience episodes that resemble epileptic seizures but are not caused by epileptic brain activity. It is a genuine, involuntary neurological condition — not "faking" or malingering. The mechanism involves altered brain network function (aberrant default mode network activation) rather than cortical hypersynchrony. Psychiatric comorbidities (depression, anxiety, PTSD, dissociation) are common but are not always present and do not fully explain the condition.

Feature	Favouring NEAD	Favouring Epilepsy
Eyes	Closed during event; resist forced eye opening	Open; may be deviated
Motor pattern	Asynchronous, side-to-side head movement, pelvic thrusting, opisthotonus, waxing/waning	Rhythmic, symmetric tonic-clonic or sustained tonic/postural
Duration	>2 min (often 5–30+ min)	GTCS typically 1–3 min; focal seizures seconds–1 min
Incontinence	Rare	Common (urinary)
Tongue biting	Tip of tongue or absent	Lateral tongue (highly specific)
Post-event	Rapid recovery or emotional distress; no true confusion	Confusion, drowsiness, headache; Todd paresis possible
EEG during event	Normal background (no epileptiform discharges)	Ictal epileptiform activity
Prolactin (10–20 min post)	Normal	Elevated >2× baseline (GTCS, complex partial — but normal does not exclude)
Trigger	Emotional stress, interpersonal conflict, fatigue	Sleep deprivation, medication non-adherence, alcohol withdrawal

Gold Standard: Video-EEG Monitoring

The definitive diagnostic test is video-EEG telemetry capturing a typical event, demonstrating normal EEG during a convulsive episode (confirming NEAD) or ictal epileptiform discharges (confirming epilepsy). This is available at major Australian tertiary epilepsy centres (Royal Melbourne, Royal Prince Alfred, Westmead, Royal Brisbane, Royal Adelaide). Medicare Item 11020 covers prolonged EEG monitoring. Referral should be made via the treating neurologist.

⚠️

Diagnostic communication matters: The diagnosis of NEAD should be delivered positively, not as a diagnosis of exclusion. Use language such as: "We have found the cause of your episodes — they are not epileptic seizures but are a type of brain network dysfunction that we can treat. This is good news because it means we can stop antiepileptic medications and start targeted treatment." Refer for psychology (CBT, trauma-focused therapy) and physiotherapy (motor retraining for FND). Avoid saying "it's all in your head."

Other Non-Epileptic Paroxysmal Events

Condition	Typical Age	Key Features	Investigation / Management
Breath-holding spells (cyanotic)	6 mo – 5 yr	Triggered by anger/frustration/cry → apnoea → cyanosis → brief LOC (10–30 sec) ± brief stiffening/myoclonus. Self-resolving. Iron deficiency common comorbidity.	Reassurance; check FBC/ferritin; iron supplementation if deficient; no AEDs needed
Pallid breath-holding (reflex anoxic seizures)	6 mo – 5 yr	Triggered by pain/startle → vagal cardiac inhibition → bradycardia/asystole → pallor → LOC → brief stiffening. Provoked by trivial head bump or surprise.	ECG to exclude long QT; reassure parents; atropine-resistant; usually self-resolving by school age
Benign paroxysmal vertigo of childhood	2 – 8 yr	Brief (seconds–minutes) episodes of vertigo, ataxia, nystagmus, pallor, ± vomiting. No LOC. Normal neurological examination. Migraine equivalent.	Reassurance; often evolves into migraine in later childhood/adolescence
Paroxysmal kinesigenic dyskinesia (PKD)	Childhood – adolescent	Brief (seconds) episodes of dystonia/choreoathetosis triggered by sudden movement. No LOC. Precipitated by standing, walking, surprise. Excellent response to low-dose carbamazepine.	Low-dose carbamazepine (25–100 mg PO OD–BD) — dramatic response confirms diagnosis
Benign nocturnal myoclonus (sleep myoclonus)	Infants – any age	Brief jerking of limbs during drowsiness or NREM sleep. Normal examination, normal EEG. Often alarming to parents.	Reassurance only; no investigation or treatment needed
Hyperekplexia (startle disease)	Neonatal – infantile	Exaggerated startle response to auditory/tactile stimuli → generalised stiffness. Neonatal hypertonia. GLRA1 gene mutation. Risk of sudden infant death if severe.	Clonazepam 0.01–0.05 mg/kg/day; genetic testing (GLRA1, GLRB, SLC6A5)
Metabolic causes	Any age	Hypoglycaemia, hyponatraemia, hypocalcaemia, hypoxia, uraemia, hepatic encephalopathy — can all produce paroxysmal neurological events including seizures, altered consciousness, movement disorders	BGL, UEC, calcium, LFTs, ABG — treat underlying cause

Treatment of NEAD / Functional Seizures

Positive Diagnosis & Explanation

Explain the diagnosis confidently using positive signs (eyes closed, asynchronous movements, normal EEG during event). Validate the condition as real and involuntary. Provide written information (e.g., from FND Australia).

Gradual AED Withdrawal

If the patient is on AEDs and diagnosis is confirmed on video-EEG, gradually taper medications under neurology supervision. Do not stop abruptly — precipitated withdrawal seizures may occur even in NEAD patients.

Psychological Therapy

CBT is the best-evidenced therapy for NEAD. Trauma-focused therapy if PTSD is comorbid. Mindfulness-based approaches, ACT (acceptance and commitment therapy), and EMDR may be beneficial. Referral to clinical psychologist with FND experience.

Physiotherapy & Functional Motor Rehabilitation

Physiotherapy targeting functional movement symptoms is evidence-based for FND. Focus on automatic/voluntary motor retraining, distraction techniques, and graded activity.

✅

Prognosis: With appropriate diagnosis and treatment, approximately 50–70% of patients with NEAD experience significant reduction in event frequency. Early diagnosis (<12 months from onset) is associated with better outcomes. Multidisciplinary care (neurology, psychology, psychiatry, physiotherapy, occupational therapy) produces the best results. FND Australia and Epilepsy Action Australia provide patient support resources.

Special Populations

🤰 Pregnancy

Epilepsy in pregnancy: All women with epilepsy should be reviewed by a neurologist pre-conception. Folate 5 mg/day (PBS authority) should be commenced ≥3 months before conception.

Valproate is absolutely contraindicated in pregnancy (teratogenic — neural tube defects, neurodevelopmental effects). Switch to levetiracetam or lamotrigine pre-conception under specialist guidance.

Seizure in pregnancy = eclampsia until proven otherwise. Manage with IV magnesium sulphate (4 g loading dose, then 1–2 g/hr maintenance) per ANZCA/ANZOG guidelines. Immediate obstetric emergency — call for senior obstetric and anaesthetic review.

AED levels change in pregnancy: Lamotrigine clearance increases 2–3× (requires dose increases and therapeutic drug monitoring). Levetiracetam levels also decrease. Free (unbound) phenytoin monitoring is essential.

Breastfeeding: Most AEDs are compatible with breastfeeding. Levetiracetam and lamotrigine are considered low-risk. Monitor infant for sedation and poor feeding.

PBS Note: Sodium valproate is now restricted under TGA pregnancy prevention programme (RMP mandatory for women of childbearing potential).

👶 Paediatrics

Febrile seizures are the most common seizure type in children (see Epilepsy Syndromes section). Simple febrile seizures do not require AEDs or EEG.

Infantile spasms require urgent recognition and treatment — developmental outcomes depend on speed of diagnosis (see above).

Neonatal seizures are often subtle (eye deviation, lip smacking, cycling movements) and require urgent neonatal assessment, EEG, and metabolic workup. Phenobarbitone remains first-line in the neonatal period (20 mg/kg IV loading).

Childhood absence epilepsy — ethosuximide first-line (see above). Hyperventilation in clinic is a useful provocative test.

Breath-holding spells — reassure parents; check ferritin; iron supplementation if ferritin <30 microg/L may reduce frequency.

Driving restrictions for adolescents: Private licence — seizure-free ≥6 months. Discuss in adolescence transition planning.

👴 Elderly

First seizure in the elderly has a different differential from young adults — consider stroke, intracranial tumour, subdural haematoma, metabolic derangement, medication toxicity (tramadol, bupropion, antidepressants, theophylline). Lower threshold for neuroimaging (CT/MRI).

Syncope is more common in the elderly due to polypharmacy, autonomic dysfunction, cardiac disease, and carotid sinus hypersensitivity. Medication review is essential — deprescribe where possible.

Orthostatic hypotension — measure lying/standing BP in all elderly patients presenting with falls or LOC. Ask patients to stand for 3 minutes before recording BP.

AED selection: Start low, go slow. Lamotrigine and levetiracetam are preferred in the elderly due to favourable side-effect profiles and fewer drug interactions. Avoid enzyme-inducing AEDs (carbamazepine, phenytoin) if possible due to drug interactions with warfarin, DOACs, statins.

Carotid sinus massage should only be performed in a monitored setting (risk of prolonged asystole). Positive if >3 sec asystole or >50 mmHg systolic BP drop.

🫘 Renal Impairment

Uraemia itself lowers seizure threshold; seizures in CKD/dialysis patients require metabolic workup (calcium, magnesium, sodium, glucose, BSL, drug levels).

Levetiracetam: Dose reduce by 50% if eGFR 30–50 mL/min; by 75% if eGFR <30. Supplemental dose after dialysis (250–500 mg).

Valproate: No renal dose adjustment needed (hepatically metabolised) but protein binding may be altered in uraemia — monitor free levels if hypoalbuminaemic.

Phenytoin: Free fraction increases in CKD (reduced albumin binding). Measure free phenytoin levels. Standard total phenytoin levels are unreliable.

Gabapentin/Pregabalin: Significant renal clearance — dose reduce per eGFR. Often used adjunctively for neuropathic pain and can lower seizure threshold if withdrawn abruptly.

🫁 Hepatic Impairment

Valproate: Avoid in significant hepatic impairment (hepatotoxicity risk). Contraindicated in urea cycle disorders. LFT monitoring required at baseline, 3 months, 6 months, then annually.

Phenytoin/Carbamazepine: Enzyme-inducing AEDs — hepatic metabolism affected by liver disease; lower doses needed. Carbamazepine also induces its own metabolism (auto-induction).

Levetiracetam and lamotrigine are generally preferred in hepatic impairment — levetiracetam (renally cleared) requires no hepatic dose adjustment; lamotrigine requires slower titration but is otherwise well tolerated.

Hepatic encephalopathy can mimic or trigger paroxysmal neurological events — always consider in cirrhotic patients with altered consciousness.

🛡️ Immunocompromised

HIV: Seizures may result from CNS opportunistic infection (toxoplasmosis, cryptococcal meningitis, PML, TB meningitis), CNS lymphoma, or HIV encephalopathy. Lower threshold for MRI with contrast. Consider drug interactions between AEDs and antiretrovirals (enzyme-inducing AEDs reduce ART efficacy).

Transplant recipients: Calcineurin inhibitors (tacrolimus, cyclosporine) can cause PRES (posterior reversible encephalopathy syndrome) — seizures, visual disturbance, hypertension, MRI white matter changes. Immediate BP management and medication adjustment.

Chemotherapy: High-dose methotrexate, cytarabine, busulfan, and intrathecal agents can cause seizures. Prophylactic levetiracetam may be considered during high-risk protocols.

AED–drug interactions: Levetiracetam and valproate have the fewest drug interactions. Avoid enzyme-inducing AEDs (carbamazepine, phenytoin, phenobarbitone) with immunosuppressants and antiretrovirals.

Driving & Seizure — Australian Requirements

Australian driving regulations for patients with seizures are governed by the Austroads and National Transport Commission Assessing Fitness to Drive Guidelines (2022 edition). All Australian states and territories adopt these national standards, though notification requirements to transport authorities vary by jurisdiction.

Scenario	Private Vehicle (Car Licence)	Commercial Vehicle (Truck/Bus/Taxi)
Single unprovoked seizure (no diagnosis of epilepsy)	No driving for 6 months from the event (or until cause identified and treated)	No driving for 12 months
Diagnosed epilepsy — seizure-free on treatment	Seizure-free for 12 months (or 12 months from commencement/change of AED)	Seizure-free for ≥10 years (may be individual assessment)
AED withdrawal (planned)	No driving for 6 months after last AED dose	No driving for 12 months
Seizures occurring only in sleep (nocturnal-only epilepsy)	May drive if seizure-free for 12 months while awake (seizures only during sleep in preceding 12 months)	Individual assessment
Reflex anoxic seizures / simple febrile seizures	Generally no restriction (considered benign, predictable triggers)	Individual assessment
NEAD / Functional seizures	No driving during active events; restriction may be lifted sooner than epilepsy once diagnosis confirmed — individual assessment	Individual assessment; generally more conservative

⚠️

Mandatory notification: In most Australian states (NSW, VIC, QLD, SA, WA, TAS, NT, ACT), clinicians are required to notify the relevant transport authority (e.g., VicRoads/Department of Transport, Transport NSW, TMR QLD) if a patient is unfit to drive due to epilepsy or seizures. Failure to notify may carry legal liability. Always document the driving restriction conversation in the medical record. See Austroads Assessing Fitness to Drive 2022.

SUDEP (Sudden Unexpected Death in Epilepsy)

SUDEP affects approximately 1 in 1000 people with epilepsy per year. Risk factors include: uncontrolled GTCS, nocturnal seizures, young adults (20–45 years), polytherapy with subtherapeutic AED levels, prone sleeping position, and alcohol/substance misuse. The Australian Epilepsy Mortality Register has documented that many SUDEP deaths are associated with medication non-adherence. All patients with epilepsy should be counselled about SUDEP risk, nocturnal seizure precautions (supine avoidance, seizure alarm devices for nocturnal seizures), and the critical importance of medication adherence.

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Australians experience a significantly higher burden of epilepsy and seizure-related morbidity compared to non-Indigenous Australians. Epilepsy-related hospitalisation rates are 1.5–3 times higher, and access to specialist neurology services is substantially lower, particularly in remote and very remote communities. Febrile seizures in Indigenous children are more common, linked to higher rates of infectious disease burden including otitis media, respiratory infections, and skin infections. Neurocysticercosis, while rare, must be considered in communities with high rates of taeniasis.

Remote access barriers

Many remote communities (>70% of the NT, large parts of WA, QLD, SA) have no resident neurologist or EEG service. Telehealth neurology (via Royal Flying Doctor Service or state-based telehealth platforms) is essential. EEG availability may require transfer to regional or tertiary centres, leading to delays in diagnosis.

Medication adherence & supply

AED supply in remote communities depends on community-controlled health service pharmacy stock. Long-acting depot or once-daily formulations (e.g., levetiracetam XR, valproate CR) may improve adherence. Remote Area Aboriginal Health Workers (AHWs) play a critical role in medication support and monitoring.

Cultural safety & communication

Stigma around epilepsy exists in some communities. Communication should use culturally appropriate language, visual aids, and involve family and community Elders where appropriate. Understand sorry business and cultural obligations that may affect appointment attendance. Use interpreters when English is not the first language (many remote communities speak English as a second, third, or fourth language).

Febrile seizures & infectious burden

Higher rates of febrile illness in Indigenous children (OM, pneumonia, skin infections, rheumatic fever) contribute to higher febrile seizure rates. Effective treatment of underlying infections, improved housing, and health promotion are key preventive strategies. Rheumatic fever prophylaxis (bicillin) may reduce febrile episodes.

Head injury & acquired brain injury

Aboriginal and Torres Strait Islander Australians have higher rates of traumatic brain injury (TBI) — a significant risk factor for post-traumatic epilepsy. Assault-related TBI is disproportionately represented. FASD (fetal alcohol spectrum disorder) is also more prevalent and may be associated with seizure susceptibility. Post-TBI seizure prophylaxis and long-term AED management require coordinated care.

Telehealth & workforce solutions

Telehealth neurology consultations, EEG interpretation services (electronic transmission of EEG data), and remote seizure education programmes (e.g., Epilepsy Foundation Australia partnerships with Aboriginal health organisations) are key to improving access. Aboriginal Health Practitioners and Aboriginal Liaison Officers can facilitate culturally safe neurological assessment and follow-up.

ℹ️

Resources: RHDAustralia (rhdaustralia.com.au) provides resources on neurological complications of rheumatic fever. The Australian Indigenous HealthInfoNet (healthinfonet.ecu.edu.au) provides epidemiological data on epilepsy in Indigenous Australians. The Epilepsy Foundation Australia offers culturally adapted seizure first aid resources. Royal Flying Doctor Service provides emergency and specialist outreach neurology in remote communities.

Quick Reference — First-Line Treatment Summary

Childhood Absence Epilepsy

Ethosuximide

Until remission (typically 2 yr seizure-free)

Sodium valproate or lamotrigine if second-line

Juvenile Myoclonic Epilepsy (males)

Sodium valproate

Lifelong

Levetiracetam preferred in women of childbearing potential

Juvenile Myoclonic Epilepsy (females)

Levetiracetam or lamotrigine

Lifelong

Avoid valproate — teratogenic; TGA pregnancy prevention programme

Infantile Spasms

ACTH (Synacthen) or vigabatrin

4–6 week course (ACTH); ongoing (vigabatrin)

TSC → vigabatrin first-line; otherwise ACTH preferred

Febrile Seizure (simple)

Nil (reassurance)

N/A

Treat fever source; no AEDs; parental education

Status Epilepticus (pre-hospital)

Midazolam 10 mg IM

Single dose; call 000

Paeds: midazolam 0.2 mg/kg IM (max 10 mg)

Status Epilepticus (hospital, 2nd-line)

Levetiracetam 60 mg/kg IV

Single dose over 15 min

Alternatives: valproate 40 mg/kg IV, phenytoin 20 mg/kg IV

Orthostatic Hypotension

Fludrocortisone 50–200 mcg PO OD

Ongoing

First: medication review, fluids, salt, compression; add midodrine if refractory

NEAD / Functional Seizures

CBT + physiotherapy (no AED)

Ongoing; review at 3–6 months

Gradual AED withdrawal under neurology; positive diagnosis communication

Eclampsia

Magnesium sulphate 4 g IV

Loading dose, then 1–2 g/hr maintenance

Obstetric emergency; monitoring for respiratory depression; calcium gluconate at bedside

📚 References

1. Fisher RS, Cross JH, French JA, et al. Operational classification of seizure types by the International League Against Epilepsy (ILAE) and the Bureau for Epilepsy. Epilepsia. 2017;58(4):522–530.
2. 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.
3. Epilepsy Society of Australia. Consensus guidelines for the management of epilepsy in adults. Sydney: ESA; 2023.
4. Austroads and National Transport Commission. Assessing Fitness to Drive: Medical Standards for Licensing and Clinical Management Guidelines. 4th ed. Sydney: Austroads; 2022.
5. Shen W, Sheldon RS, Benditt DG, et al. 2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope. J Am Coll Cardiol. 2017;70(5):e39–e110.
6. Thavendiranathan P, Detsky AS, Cusimano RJ, et al. Does this patient with a seizure have epilepsy? The Rational Clinical Examination. JAMA. 2006;295(16):1942–1949.
7. National Institute for Health and Care Excellence (NICE). Epilepsies: diagnosis and management (NG217). London: NICE; 2022 (updated 2024).
8. Engel J Jr. A proposed diagnostic scheme for people with epileptic seizures and with epilepsy: report of the ILAE Task Force on Classification and Terminology. Epilepsia. 2001;42(6):796–803.
9. Dworetzky BA, Baslet G. Psychogenic nonepileptic seizures: a guide for patients and families. Neurology. 2018;91(10):e1013–e1017.
10. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander health performance framework: epilepsy and neurological conditions. Canberra: AIHW; 2023.
11. Royal Australian College of General Practitioners (RACGP). Management of first seizure in adults: Clinical guide. Melbourne: RACGP; 2023.
12. Pellock JM, Dodson WE, Bourgeois BFD, eds. Pediatric Epilepsy: Diagnosis and Therapy. 4th ed. New York: Demos Medical; 2021.
13. Benbadis SR, LaFrance WC Jr, Papandonatos GD, et al. Interrater reliability of EEG-video monitoring. Neurology. 2009;73(11):876–881.
14. Scheffer IE, Hirsch E, Lagae L, et al. Panayiotopoulos syndrome: a consensus view. Dev Med Child Neurol. 2020;62(7):792–798.
15. Epilepsy Foundation Australia. Epilepsy in Aboriginal and Torres Strait Islander communities: position statement. Melbourne: Epilepsy Foundation; 2023.
16. Devinsky O, Hesdorffer DC, Thurman DJ, Lhatoo S, Richerson G. Sudden unexpected death in epilepsy: epidemiology, mechanisms, and prevention. Lancet Neurol. 2016;15(10):1075–1088.

for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.

Preventive health

Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction

Paracetamol ± NSAID; manual therapy

2–6 weeks

Provocable on palpation; no red flags

Thoracic compression fracture

Paracetamol; ± calcitonin; DXA + osteoporosis Rx

6–12 weeks healing

Elderly; osteoporosis; acute onset

ACS (posterior MI)

Aspirin 300 mg, GTN, heparin; urgent PCI

Time-critical

ECG, troponin; CV risk factors

Aortic dissection

IV labetalol; urgent CT aortogram; surgery (Type A)

Time-critical

Tearing pain; BP differential >20 mmHg

Vertebral osteomyelitis

IV antibiotics (vancomycin + ceftriaxone initially); ID consult

6 weeks IV antibiotics

Fever, elevated CRP, IV drug use

Biliary colic / cholecystitis

Paracetamol ± morphine; lap cholecystectomy

Surgical within 72 h (cholecystitis)

RUQ/infrascapular; post-prandial; RUQ US

📚 References

1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.

for PBS-listed medicines at participating pharmacies.

Cultural safety

Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.

Medication adherence

Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.

Specific conditions

Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.

Referral pathways

Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).

for PBS-listed medicines at participating pharmacies.

Cultural safety

Medication adherence

Specific conditions

Referral pathways

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).