Med2Date β€” Clinical Guidelines
Home Clinical Examination The Nervous System

The Nervous System

Last updated 31 May 2026 Β· Neurology

πŸ“‹ Key Information Summary

πŸ“‹
  • A systematic neurological examination follows a consistent order: inspection β†’ cranial nerves β†’ motor β†’ sensory β†’ coordination β†’ gait β†’ higher cortical functions to avoid missing subtle findings.
  • Neurological history is the single most important part of the assessment β€” the history alone lateralises and localises the lesion in the majority of cases before any examination is performed.
  • Key history domains include headache (SOCRATES, thunderclap, red flags), weakness (distribution, onset, progression), seizures (focality, aura, postictal state), dizziness/vertigo, speech disturbance, visual symptoms, sphincter dysfunction, gait, and memory/cognition.
  • Cranial nerves I–XII are examined systematically; fundoscopy is essential for papilloedema assessment and forms part of every complete neurological examination.
  • Upper motor neurone (UMN) signs include increased tone (spasticity), hyperreflexia, upgoing plantars (Babinski positive), clonus, and an extensor pattern of weakness.
  • Lower motor neurone (LMN) signs include decreased tone, hyporeflexia/areflexia, fasciculation, muscle wasting, and a segmental or nerve-root pattern of weakness.
  • Motor power is graded using the Medical Research Council (MRC) scale 0–5; always compare sides and document systematically.
  • Sensory examination maps light touch, pin-prick (spinothalamic), vibration, and joint-position sense (dorsal columns); a sensory level suggests myelopathy.
  • Cerebellar signs β€” dysdiadochokinesia, intention tremor, past-pointing, nystagmus, and ataxic gait β€” suggest ipsilateral cerebellar or vestibulocerebellar pathology.
  • Romberg test differentiates sensory ataxia (positive β€” falls with eyes closed) from cerebellar ataxia (positive with eyes open and closed).
  • Higher cortical functions screening includes speech (fluency, comprehension, repetition, naming), orientation, memory (registration and recall), attention, and visuospatial function.
  • Gait assessment β€” observe walking, heel-to-toe (tandem), turning, and toe/heel walking; characteristic patterns include hemiplegic, parkinsonian, ataxic, steppage, and waddling gaits.
  • Red-flag findings requiring urgent neuroimaging or specialist referral include: new papilloedema, progressive unilateral weakness, saddle anaesthesia with sphincter dysfunction, acute speech disturbance, and thunderclap headache.

Introduction & Australian Context

Neurological conditions account for a substantial burden of disease in Australia. According to the Australian Institute of Health and Welfare (AIHW), diseases of the nervous system contribute significantly to years lived with disability, with stroke, dementia, epilepsy, migraine, and multiple sclerosis among the most prevalent chronic neurological diagnoses. An estimated 441,000 Australians live with stroke aftermath, over 400,000 with dementia, and approximately 250,000 with epilepsy.

A comprehensive neurological history and systematic examination remain the cornerstone of clinical neurology. Neuroimaging and electrophysiology are adjuncts that complement β€” but never replace β€” a careful bedside assessment. In the Australian primary-care setting, a methodical neurological examination allows the general practitioner to localise a lesion (cortex, brainstem, spinal cord, nerve root, peripheral nerve, neuromuscular junction, muscle), formulate a differential diagnosis, determine urgency of referral, and identify red flags mandating same-day hospital assessment.

This article provides a step-by-step guide to performing a complete neurological examination in the Australian clinical setting, covering neurological history, cranial nerves I–XII, motor system, sensory system, cerebellar function, higher cortical functions, and gait analysis. It is written in Australian English and references Australian guidelines and PBS-listed medications where relevant.

πŸ₯
Examination sequence tip: Perform the examination in a consistent order every time so it becomes second nature. A recommended sequence is: general inspection β†’ stance and gait (if ambulant) β†’ cranial nerves β†’ upper limbs (tone, power, reflexes, coordination) β†’ lower limbs (tone, power, reflexes, coordination) β†’ sensory testing β†’ higher cortical functions β†’ formal gait assessment. This order is endorsed by the Royal Australasian College of Physicians (RACP) neurology training curriculum.

Neurological History

The neurological history is the most powerful localising tool in clinical neurology. In many cases, the history alone β€” before a single examination manoeuvre β€” will identify the likely anatomical level of the lesion and narrow the differential diagnosis substantially. Allocate adequate time; do not rush.

Presenting Complaint Domains

🧠
Headache
First history domain
Key questions SOCRATES: Site, Onset (sudden = thunderclap β†’ SAH until proven otherwise), Character, Radiation, Associated symptoms (nausea, photophobia, visual aura, neck stiffness), Timing (duration, frequency), Exacerbating/relieving factors, Severity
Red flags Thunderclap onset, new headache >50 years, progressive worsening, headache with systemic illness/fever, headache with papilloedema, headache with focal neurological signs, headache with altered consciousness
πŸ’ͺ
Weakness
Second history domain
Key questions Distribution (one limb = monoparesis, same-side arm + leg = hemiparesis, both legs = paraparesis), onset (acute stroke, subacute inflammatory/demyelinating, chronic degenerative), fatigability (MG, ALS), progression pattern
Localisation UMN pattern (extensors of arm, flexors of leg) vs LMN pattern (specific myotome or nerve territory); proximal = myopathy/neuromuscular junction; distal = neuropathy
⚑
Seizures
Third history domain
Key questions Aura (focal onset suggests structural lesion), description of event (witness account is essential), duration, postictal state (Todd's paralysis), tongue biting (lateral = seizure; tip = syncope), incontinence, number of episodes, precipitants (sleep deprivation, alcohol, flashing lights)
Important distinction First unprovoked seizure requires MRI brain with epilepsy protocol + EEG within 24–48 hours; status epilepticus (>5 min or cluster without recovery) is a medical emergency (dial 000)
πŸ”„
Dizziness & Vertigo
Fourth history domain
Key questions True vertigo (room spinning) vs presyncope vs disequilibrium vs light-headedness; associated hearing loss/tinnitus (peripheral vestibular); associated diplopia/ataxia/dysarthria (central β€” posterior fossa)
Red flags Vertigo with any new neurological sign (diplopia, dysarthria, ataxia, Horner's) = posterior circulation stroke until proven otherwise
πŸ—£οΈ
Speech Disturbance
Fifth history domain
Key distinction Dysarthria (slurred speech = cerebellar, bulbar, or extrapyramidal) vs dysphasia/aphasia (language disturbance = cortical lesion); expressive (non-fluent, Broca's) vs receptive (fluent but nonsensical, Wernicke's)
πŸ‘οΈ
Visual Disturbance
Sixth history domain
Key questions Monocular (optic nerve/retinal) vs binocular (chiasmal or retrochiasmal); visual field defect pattern (homonymous hemianopia, bitemporal, quadrantanopia); diplopia (monocular = refractive; binocular = CN III/IV/VI or neuromuscular junction)
🚽
Sphincter Dysfunction
Seventh history domain
Key questions Urinary retention or incontinence, faecal incontinence, constipation; associated with back pain and sensory level β†’ cauda equina syndrome (surgical emergency) or myelopathy
Red flag Saddle (perianal) anaesthesia + urinary retention + bilateral sciatica = cauda equina syndrome β†’ same-day MRI and neurosurgical referral
🚢
Gait & Memory
Eighth & ninth domains
Gait Falls? Progressive unsteadiness? Worsening over time? Wheelchair use? Walking aid?
Memory/cognition Progressive vs static? Short-term vs long-term? Functional impairment (driving, finances, medication management)? Personality change (frontal lobe)?

Past Medical, Drug, Family & Social History

  • Past medical history: Previous stroke/TIA, epilepsy, head injury (with loss of consciousness), neurosurgery, meningitis/encephalitis, autoimmune conditions, malignancy (brain metastases), diabetes (neuropathy), hypertension (hypertensive encephalopathy).
  • Medications: Anticoagulants/antiplatelets (haemorrhage risk), antipsychotics (movement disorders, NMS), aminoglycosides (vestibulotoxicity), phenytoin (cerebellar atrophy), opioids (myoclonus), lithium (tremor, toxicity).
  • Family history: Epilepsy, migraine, Huntington disease, Charcot-Marie-Tooth, muscular dystrophies, hereditary neuropathies, familial Alzheimer disease.
  • Social history: Alcohol (Wernicke-Korsakoff, cerebellar degeneration, peripheral neuropathy), recreational drugs (stroke, seizures), occupation (driving assessment requirements β€” Austroads guidelines), travel (neurocysticercosis, cerebral malaria, TB meningitis).
⚠️
Red-flag summary β€” refer urgently (same-day) if any of: Thunderclap headache, new unilateral weakness/speech disturbance (stroke code β€” call 000), progressive bilateral leg weakness with sensory level (cord compression), papilloedema with headache (raised intracranial pressure), saddle anaesthesia with sphincter dysfunction (cauda equina), first seizure with focal signs, rapidly progressive cognitive decline over weeks (CJD, autoimmune encephalitis).

Cranial Nerve Examination (CN I – CN XII)

The cranial nerve examination is performed in numerical order from CN I (olfactory) through CN XII (hypoglossal). Each nerve is tested systematically with both qualitative and quantitative assessment where applicable.

CN I β€” Olfactory Nerve

  • Test each nostril separately with a familiar non-irritant odour (e.g., coffee, vanilla) while occluding the opposite nostril.
  • Loss of smell (anosmia) may indicate frontal lobe pathology (meningioma, traumatic shearing of olfactory fibres from anterior skull-base fracture), nasal mucosal disease, or early Parkinson disease / Lewy body dementia.
  • Document as: "CN I β€” intact bilaterally / anosmia right / hyposmia left."

CN II β€” Optic Nerve

  • Visual acuity: Snellen chart at 6 metres (with distance correction). Document each eye separately: "R 6/6, L 6/9." If patient cannot read the chart, test finger counting β†’ hand movements β†’ light perception.
  • Visual fields: Confrontation testing β€” sit 1 metre opposite, test each eye individually. Ask patient to fix on your nose. Move fingers or a red pin in each quadrant. Map any scotoma or field defect (homonymous hemianopia, bitemporal hemianopia, quadrantanopia).
  • Pupillary reactions: Test direct and consensual responses using a penlight. Then perform the relative afferent pupillary defect (RAPD / Marcus Gunn pupil) test using the swinging-torch test. A RAPD indicates optic nerve pathology (optic neuritis, ischaemic optic neuropathy).
  • Fundoscopy: Examine in a darkened room. Assess optic disc margins (blurred = papilloedema or papillitis), cup-to-disc ratio, retinal vessels (AV nipping in hypertension), macula, and look for haemorrhages, exudates, or cotton-wool spots. Normal cup-to-disc ratio is <0.5.
🚨
Papilloedema (swollen optic discs bilaterally) indicates raised intracranial pressure. This is a medical emergency. Causes include space-occupying lesion, cerebral venous sinus thrombosis, idiopathic intracranial hypertension, and malignant hypertension. Arrange urgent CT brain and refer to ophthalmology/neurology the same day.

CN III, IV, VI β€” Oculomotor, Trochlear, Abducens

  • Inspect: Ptosis (CN III palsy, Horner syndrome, myasthenia gravis), pupil size and symmetry, position of rest (outward and down = CN III palsy; hypertropia = CN IV palsy).
  • Eye movements: Ask patient to follow your finger/pen in an "H" pattern. Test all six cardinal directions of gaze. Note any diplopia and in which direction it is worst.
  • Pupil assessment: CN III carries parasympathetic fibres for pupillary constriction. A CN III palsy with a dilated pupil (blown pupil) is a compressive lesion (posterior communicating artery aneurysm β€” emergency) until proven otherwise. A CN III palsy with a normal pupil is likely ischaemic (diabetes, hypertension).
  • Internuclear ophthalmoplegia (INO): Failure of adduction on the affected side with nystagmus of the abducting eye β€” suggests medial longitudinal fasciculus lesion (multiple sclerosis in young patients, stroke in older patients).

CN V β€” Trigeminal Nerve

  • Sensory: Test light touch and pin-prick in all three divisions β€” V1 (ophthalmic β€” forehead), V2 (maxillary β€” cheek), V3 (mandibular β€” jaw). Compare sides.
  • Motor (muscles of mastication): Ask patient to clench jaw β€” palpate masseter and temporalis bulk. Ask patient to open mouth against resistance β€” lateral pterygoid; deviation of jaw to the weak side indicates ipsilateral CN V motor weakness.
  • Reflexes: Corneal reflex (afferent CN V1, efferent CN VII) β€” lightly touch cornea with cotton wisp from the side. Jaw jerk (afferent and efferent CN V3) β€” place finger on chin, tap with reflex hammer; brisk jaw jerk indicates bilateral UMN lesion above the pons.

CN VII β€” Facial Nerve

  • Inspect: Facial asymmetry at rest. Ask patient to raise eyebrows, close eyes tightly ("don't let me open them"), puff out cheeks, show teeth, smile.
  • UMN vs LMN distinction:
Feature UMN (Central) Lesion LMN (Peripheral) Lesion
Forehead sparing Yes β€” forehead receives bilateral UMN input No β€” entire ipsilateral face affected
Common causes Stroke, tumour Bell palsy, Ramsay Hunt (VZV), parotid tumour, sarcoidosis
Other signs Often with hemiparesis, dysarthria Hyperacusis (nerve to stapedius), loss of taste (chorda tympani), ear pain

CN VIII β€” Vestibulocochlear Nerve

  • Hearing: Finger rub test (each ear) β†’ Rinne test (tuning fork on mastoid then near ear canal β€” air conduction > bone conduction = normal = positive Rinne) β†’ Weber test (tuning fork on vertex β€” lateralises to affected ear in conductive loss; lateralises to unaffected ear in sensorineural loss).
  • Vestibular: Dix-Hallpike manoeuvre if vertigo suspected (tests for benign paroxysmal positional vertigo β€” BPPV). Head impulse test for vestibulo-ocular reflex (peripheral vs central vertigo). Test for nystagmus β€” peripheral (horizontal, unidirectional, suppressed by fixation) vs central (vertical, bidirectional, not suppressed by fixation).

CN IX & X β€” Glossopharyngeal & Vagus Nerves

  • Speech quality: Hoarseness (recurrent laryngeal nerve / CN X), nasal speech (palatal weakness), wet/gurgling voice (secretion pooling).
  • Palatal movement: Ask patient to say "Ahhh" β€” observe soft palate. Uvula deviates away from the side of the lesion (CN X palsy). In bilateral vagal palsy, palate does not elevate at all.
  • Gag reflex: Afferent CN IX, efferent CN X β€” touch posterior pharyngeal wall (each side). Absent gag may indicate LMN bulbar pathology. Note: a unilateral absent gag is common and may be a normal variant.
  • Swallowing: Offer a sip of water β€” coughing or nasal regurgitation suggests dysphagia. If concerned, do NOT proceed to full oral intake; refer for formal swallow assessment (speech pathology).

CN XI β€” Accessory Nerve

  • Sternocleidomastoid (SCM): Ask patient to turn head against resistance β€” tests contralateral SCM (CN XI). Weakness = head turns away from the weak side.
  • Trapezius: Ask patient to shrug shoulders against resistance. Observe for scapular winging and compare bulk of upper trapezius bilaterally.

CN XII β€” Hypoglossal Nerve

  • Inspect tongue at rest: Fasciculations (LMN lesion β€” motor neurone disease), wasting (LMN), deviation (tongue deviates towards the side of an LMN lesion).
  • Tongue protrusion: Ask patient to stick tongue out β€” deviation towards the weak side (LMN) or away from the weak side if there is a contralateral UMN lesion (the "wrong" side pattern because the hypoglossal nucleus is supplied by the contralateral corticobulbar tract for protrusion).
  • Tongue movements: Rapid side-to-side movements. Slow, clumsy movements suggest UMN (pseudobulbar) involvement.
πŸ“
Documentation mnemonic: Record each nerve as: CN I β€” intact; CN II β€” VA R 6/6 L 6/9, fields full to confrontation, fundi: discs pink and flat bilaterally; CN III, IV, VI β€” EOM intact, pupils 3 mm β†’ 2 mm equal and reactive; CN V β€” sensation intact V1-V3, masseters bulk and power normal; CN VII β€” face symmetric; CN VIII β€” hearing intact, no nystagmus; CN IX, X β€” palate elevates symmetrically, gag intact; CN XI β€” SCM and trapezius 5/5; CN XII β€” tongue midline, no fasciculations.

Motor System Examination

The motor system is examined in a systematic sequence: inspection β†’ tone β†’ power β†’ reflexes β†’ plantar responses. Test each component in the upper limbs, then the lower limbs. Always compare sides.

Inspection

  • Bulk: Look for muscle wasting (LMN lesion, disuse, myopathy) and fasciculations (LMN β€” particularly motor neurone disease). Compare muscle groups bilaterally β€” deltoids, thenar/hypothenar eminences, quadriceps, calves.
  • Involuntary movements: Tremor (resting = parkinsonian; postural/action = essential tremor, anxiety, thyrotoxicosis), chorea (Huntington disease, Sydenham chorea), athetosis, dystonia, myoclonus, tics.

Tone

  • Upper limbs: With patient relaxed, passively rotate the wrist, flex/extend the elbow. Assess for spasticity (velocity-dependent increase β€” "clasp-knife" β€” UMN), rigidity (constant increase, "lead-pipe" or "cogwheel" β€” extrapyramidal), or hypotonia (LMN, cerebellar).
  • Lower limbs: Lift the knee from the bed (supine) and let it drop β€” the normal heel glides smoothly down. Roll the leg inward and outward. Test ankle clonus if spasticity is suspected β€” briskly dorsiflex the ankle. Sustained clonus (>3 beats) is pathological.

Power β€” MRC Grading

Grade Description Documentation
0 No contraction 0/5
1 Flicker/trace of contraction 1/5
2 Active movement with gravity eliminated 2/5
3 Active movement against gravity 3/5
4 Active movement against gravity and some resistance 4/5
5 Normal power 5/5

Key Muscle Testing β€” Upper Limbs

C5
Shoulder abduction
Deltoid β€” resist downward pressure on abducted arms
C6
Elbow flexion / Wrist extension
Biceps, brachioradialis, extensor carpi radialis
C7
Elbow extension / Wrist flexion
Triceps, flexor carpi radialis
C8
Finger flexion
Flexor digitorum profundus β€” resist at DIP joints
T1
Finger abduction
Interossei β€” resist squeezing fingers apart

Key Muscle Testing β€” Lower Limbs

L1-L2
Hip flexion
Iliopsoas β€” resist leg raising from flexed position
L3-L4
Knee extension
Quadriceps β€” resist leg straightening; L4 also tests ankle dorsiflexion (tibialis anterior)
L5
Great toe dorsiflexion / Hip abduction
Extensor hallucis longus, gluteus medius
S1
Ankle plantarflexion / Eversion
Gastrocnemius/soleus, peronei β€” resist standing on toes
S2
Knee flexion
Hamstrings

Deep Tendon Reflexes (DTRs)

Ensure relaxation, use a consistent brisk tap, and compare sides. Grade on a 0–4+ scale.

Reflex Root Level Technique
Biceps C5, C6 Tap your thumb placed over biceps tendon at the antecubital fossa
Brachioradialis C5, C6 Tap the radius just above the wrist
Triceps C7, C8 Tap the triceps tendon just above the olecranon
Knee (patellar) L3, L4 Tap the patellar tendon with leg hanging relaxed over edge of bed
Ankle (Achilles) S1, S2 Dorsiflex the foot slightly and tap the Achilles tendon

Grading: 0 = absent; 1+ = diminished; 2+ = normal; 3+ = brisk (may be normal in a brisk person); 4+ = clonus.

Plantar Responses

  • Stroke the lateral border of the sole from heel to the base of the little toe, then curve medially across the metatarsal heads, using a blunt object (orange stick or key β€” not a sharp object, as pain causes withdrawal).
  • Normal (flexor): Toes flex downward.
  • Abnormal (extensor β€” Babinski sign): Great toe dorsiflexes (extends) and smaller toes fan out. This indicates a UMN lesion (corticospinal tract disruption).
  • If no response, try stroking the shin or dorsum of the foot. Document: "Plantars downgoing bilaterally" or "Right extensor, left flexor."

UMN vs LMN Patterns β€” Distinguishing Features

Upper Motor Neurone (UMN)
Central / Corticospinal
  • Increased tone (spasticity β€” clasp-knife)
  • Hyperreflexia (with clonus)
  • Extensor plantar response (Babinski +)
  • Weakness in extensor pattern (arm extensors weaker than flexors)
  • Minimal wasting early (disuse atrophy later)
  • No fasciculations
Lesion: Cortex, internal capsule, brainstem, corticospinal tract
Lower Motor Neurone (LMN)
Peripheral / Anterior Horn / Nerve Root
  • Decreased tone (flaccidity)
  • Hyporeflexia or areflexia
  • Flexor (normal) or absent plantar response
  • Weakness in myotomal/nerve distribution
  • Muscle wasting (early and prominent)
  • Fasciculations present
Lesion: Anterior horn cell, nerve root, plexus, peripheral nerve

Cerebellar Signs

  • Dysdiadochokinesia: Inability to perform rapid alternating movements (e.g., rapid pronation–supination of hand on thigh). Test both sides and compare.
  • Finger-nose-finger test: Ask patient to alternately touch their nose and your finger (held 30–40 cm away). Cerebellar lesion produces intention tremor β€” tremor worsens as finger approaches target. Also look for past-pointing.
  • Heel-shin test: Patient places one heel on the opposite knee and slides it down the shin. Ataxia of heel-shin movement = ipsilateral cerebellar hemispheric lesion.
  • Truncal ataxia: Unsteadiness when sitting or standing with a wide-based gait β€” midline cerebellar (vermis) lesion.
  • Rebound phenomenon: Patient flexes elbow against your resistance, which you suddenly release β€” patient's forearm overshoots (loss of check reflex).
  • Nystagmus: Coarse, horizontal nystagmus with the fast component towards the side of a cerebellar hemispheric lesion.
  • Speech: Scanning/staccato dysarthria (cerebellar speech).

Sensory System, Higher Cortical Functions & Gait

Sensory System Examination

Sensory testing relies on patient cooperation and is inherently subjective. Always test with the patient's eyes closed. Compare sides and proximal vs distal. Test in a dermatomal pattern to detect a sensory level (suggesting myelopathy).

Modalities Tested

Dorsal Column
Light touch
Cotton wisp β€” touch each dermatome and compare sides. Large-fibre (AΞ²) pathway.
Spinothalamic
Pin-prick
Neurotip or disposable needle β€” test dermatomes C4 β†’ T1 β†’ T10 β†’ L1 β†’ S1 on each side. Ascending then descending to map any sensory level.
Dorsal Column
Vibration
128 Hz tuning fork on bony prominences β€” start distally (great toe, medial malleolus, interphalangeal joints) and work proximally if impaired. Ask patient to indicate when vibration stops.
Dorsal Column
Proprioception (Joint Position Sense)
Hold sides of great toe (or thumb) and move up/down β€” ask patient to identify direction. Start with small movements. Proprioceptive loss in the feet = dorsal column or large-fibre peripheral neuropathy (e.g., B12 deficiency, diabetic neuropathy).
Cortical
Cortical (Discriminative) Sensation
Two-point discrimination, stereognosis (identify object by touch), graphesthesia (identify number written on palm). Impaired in contralateral parietal lobe lesion.

Romberg Test

  • Ask patient to stand with feet together and eyes open β€” ensure steady. Then ask patient to close eyes for 30 seconds while you stand close to catch them.
  • Positive Romberg (falls with eyes closed): Sensory ataxia β€” loss of proprioceptive/vestibular input. Patient relies on vision to compensate; removing visual input reveals ataxia. Causes: B12 deficiency, tabes dorsalis, large-fibre neuropathy.
  • Negative Romberg but unsteady with eyes open: Cerebellar ataxia β€” cerebellum does not rely on vision, so removing it does not worsen balance (may actually be slightly better because visual vertigo is removed).

Sensory Patterns β€” Localising Value

Pattern Description Suggests
Glove-and-stocking Bilateral, symmetrical, distal > proximal Peripheral neuropathy (diabetes, alcohol, B12)
Dermatomal Follows a single or adjacent dermatomes Radiculopathy, herpes zoster
Sensory level Everything below a certain spinal level Myelopathy (transverse myelitis, cord compression, syringomyelia)
Hemisensory Entire contralateral body Thalamic stroke, cortical lesion
Dissociated (pin-prick loss, vibration preserved or vice versa) Separate tracts affected Syringomyelia (cape-like pin-prick loss, vibration intact), Brown-SΓ©quard

Higher Cortical Functions

Screening of higher cortical functions should be performed in any patient with suspected cognitive decline, speech difficulty, or focal cortical signs. Formal cognitive testing tools (MoCA, MMSE) complement the bedside assessment but do not replace it.

1
Orientation
Person (name, date of birth), place (hospital name, city, state), time (day, date, month, year, season). Disorientation to time is the earliest sign of delirium or dementia.
2
Attention & Concentration
Serial 7s (100 β†’ 93 β†’ 86 β†’ …) or WORLD backwards. Digit span (normal 7 Β± 2). Impaired attention = delirium, diffuse encephalopathy, or frontal lobe dysfunction.
3
Memory
Registration: Name 3 objects, ask patient to repeat them. Recall: Ask again at 5 minutes. Normal recall = 3/3. Impaired short-term memory with intact long-term memory = hippocampal/diencephalic lesion (early Alzheimer disease, Korsakoff syndrome).
4
Language Assessment
Fluency: Spontaneous speech β€” is it fluent (normal rate, melody) or non-fluent (effortful, telegraphic)? Comprehension: Follow one-step and multi-step commands. Repetition: "No ifs, ands, or buts." Naming: Point to objects (watch, pen, strap). Reading & writing.
5
Aphasia Classification
Broca's (expressive/non-fluent): Telegraphic speech, impaired repetition, relatively preserved comprehension. Wernicke's (receptive/fluent): Fluent but meaningless, impaired repetition and comprehension. Global: All domains impaired. Conduction: Fluent, good comprehension, impaired repetition.
6
Visuospatial & Frontal Lobe
Visuospatial: Clock-drawing test (numbers, spacing, hands). Copy interlocking pentagons. Frontal lobe: Luria hand sequences (fist-edge-palm), go/no-go test (tap once when examiner taps twice), abstract reasoning (proverb interpretation).

Gait Assessment

Gait is the final component of the neurological examination and integrates motor, sensory, cerebellar, and extrapyramidal function. Observe the patient walking, turning, and performing specific gait manoeuvres.

Gait Type Characteristics Cause
Hemiplegic Circumduction of affected leg, stiff extended arm, foot scuffs Stroke, UMN lesion
Parkinsonian Shuffling, short steps (marche Γ  petits pas), reduced arm swing, festination (accelerating), en bloc turning, stooped posture Parkinson disease, drug-induced parkinsonism
Ataxic (cerebellar) Wide-based, staggering, irregular, unable to tandem walk Cerebellar lesion, alcohol intoxication
Sensory ataxic Wide-based, heavy stomping, worsens with eyes closed (positive Romberg) B12 deficiency, large-fibre neuropathy
Steppage High stepping to clear dropped foot, slapping foot down Common peroneal nerve palsy, L5 radiculopathy, peripheral neuropathy
Waddling Trendelenburg sign β€” trunk sways side to side due to hip abductor weakness Muscular dystrophy, proximal myopathy, hip dysplasia
Antalgic Limping, shortened stance phase on painful side Hip/knee pathology (not neurological)

Additional Gait Manoeuvres

  • Tandem gait (heel-to-toe): Walk in a straight line placing heel directly in front of toes. Unsteadiness suggests cerebellar or proprioceptive dysfunction.
  • Toe walking: Tests S1 (gastrocnemius/soleus) β€” bilateral inability suggests myopathy or bilateral S1 radiculopathy/neuropathy.
  • Heel walking: Tests L5 (tibialis anterior β€” dorsiflexion) β€” bilateral inability suggests bilateral L5 pathology or peripheral neuropathy.
  • Hop on each foot: Integrates coordination and power β€” cerebellar patients cannot hop on the ipsilateral foot.
  • Pull test (postural stability): Stand behind patient, pull shoulders briskly backwards. Normal response is a corrective step. Parkinson disease patients may take many small steps backwards (retropulsion) or fail to correct.
⚠️
Falls risk: In the Australian context, falls are a leading cause of injury-related hospitalisation and death in people aged β‰₯65 years (AIHW). Any patient with an abnormal gait, positive Romberg, or cerebellar signs should be assessed for falls risk using validated tools (e.g., Timed Up and Go, Falls Risk for Older People β€” Community setting). Consider allied-health physiotherapy referral and home-hazard assessment.

Special Populations

πŸ‘Ά

Paediatric Neurological Examination

Children require an age-appropriate examination approach. Engagement and play-based assessment are essential for accurate findings.
Developmental milestones
Always assess age-appropriate gross motor, fine motor, language, and social milestones. Use the Rourke Baby Record or ASQ-3 for standardised assessment. Motor milestones (sitting 6 months, walking 12 months, running 18 months) guide assessment of motor delay.
Head circumference
Plot on WHO growth chart at every visit. Crossing centiles upward suggests hydrocephalus or megalencephaly; crossing downward suggests microcephaly (congenital infection, genetic syndrome). Fontanelle assessment β€” a bulging fontanelle suggests raised ICP (meningitis, hydrocephalus).
Tone in infants
Assess passive tone by traction response (pull to sit), vertical suspension (ventral and ventral suspension), horizontal suspension. Hypotonia in infancy may indicate cerebral palsy, spinal muscular atrophy, Prader-Willi syndrome, or metabolic myopathy. Hypertonia in infancy (scissoring of legs, fisting) suggests spastic cerebral palsy.
Primitive reflexes
Moro, grasp, rooting, ATNR β€” should disappear by 4–6 months. Persistence beyond expected age suggests UMN pathology (cerebral palsy). Asymmetric ATNR may indicate hemiplegia.
Reflexes in children
DTRs are brisker in normal children β€” 3+ may be normal. Plantar response is normally extensor (upgoing) until 12 months of age β€” an upgoing plantar beyond 12 months is pathological.
πŸ‘΄

Geriatric Neurological Examination

Older adults may have age-related confounders that complicate neurological interpretation.
Cognitive screening
Perform cognitive screening (MoCA or MMSE) in all patients β‰₯65 with any complaint of memory difficulty, family concern, or functional decline. The Montreal Cognitive Assessment (MoCA) is more sensitive than MMSE for mild cognitive impairment (MCI). Australian norms are available β€” adjust for education level.
Age-related changes
Ankle reflexes may be diminished normally with ageing (assess with reinforcement β€” Jendrassik manoeuvre). Vibration sense at the great toe may be reduced mildly. Mild distal sensory loss in a glove-and-stocking pattern may be present without pathological cause. Pupils become smaller and less reactive (senile miosis).
Delirium screening
Use the Confusion Assessment Method (CAM) to distinguish delirium (acute, fluctuating, inattention, altered consciousness) from dementia (chronic, progressive, relatively preserved consciousness). Delirium is a medical emergency requiring investigation of precipitant (infection, medication, metabolic, pain).
Medication review
Polypharmacy is common. Anticholinergic medications, benzodiazepines, opioids, antipsychotics, and anticonvulsants may cause cognitive impairment, sedation, falls, and movement disorders. Perform a Home Medicines Review (HMR, MBS item 900) where possible.
Falls
One in three Australians aged β‰₯65 falls each year. Neurological causes include peripheral neuropathy (diabetic, B12 deficiency), cerebellar ataxia, Parkinson disease, stroke, and vertigo. Multi-factorial falls risk assessment (including lying/standing blood pressure, visual acuity, footwear, home hazards) is recommended by the Royal Australian College of General Practitioners (RACGP) Red Book.
🀰

Pregnancy

Pregnancy alters neurological examination findings and diagnostic pathways.
Reflexes
DTRs may be brisker in pregnancy β€” this can be physiological. However, brisk reflexes with clonus in the context of pre-eclampsia/eclampsia indicate magnesium deficiency (treat with IV magnesium sulfate per ANZCOR guidelines). Always check blood pressure and proteinuria in any pregnant woman with brisk reflexes.
Carpal tunnel syndrome
Very common in pregnancy due to fluid retention. Phalen's test and Tinel's sign at the wrist. Usually resolves postpartum. Night splints first line; corticosteroid injection if severe (methylprednisolone is PBS-listed).
Headache
New-onset headache in pregnancy β€” consider pre-eclampsia (BP, proteinuria, LFTs, platelets), cerebral venous sinus thrombosis (MRI/MRV), reversible cerebral vasoconstriction syndrome, and idiopathic intracranial hypertension. Avoid CT if possible (MRI preferred); if CT required, abdominal shielding is essential.
Epilepsy in pregnancy
Uncontrolled seizures pose greater risk to the fetus than antiepileptic medication. Lamotrigine and levetiracetam are considered lower teratogenic risk (RANZCOG, RACP guidelines). Sodium valproate is teratogenic and contraindicated in pregnancy (fetal valproate syndrome β€” TGA boxed warning). Ensure 5 mg/day folic acid for women with epilepsy planning pregnancy.
🫘

Renal Impairment

Uraemia causes a toxic neuropathy (distal, symmetrical, sensorimotor) and may cause asterixis, encephalopathy, and seizures. Assess for these findings in patients with eGFR <15 mL/min/1.73 mΒ² or on dialysis.
Restless legs syndrome
Very common in end-stage kidney disease (ESKD) β€” up to 30% prevalence. Assess with detailed history. Iron studies (target ferritin >200 Β΅g/L, transferrin saturation >20%). Gabapentin (renally adjusted) or pramipexole are treatment options β€” discuss with nephrologist.
Dialysis-associated
Dialysis disequilibrium syndrome (headache, confusion, seizures β€” during or after first dialysis), dialysis dementia (aluminium toxicity β€” now rare with modern water treatment), subdural haemorrhage (anticoagulation during haemodialysis).
🫁

Hepatic Impairment

Hepatic encephalopathy is a key differential for any patient with liver disease and altered mental status or new neurological signs.
Assessment
Grade hepatic encephalopathy clinically (West Haven criteria β€” Grade I: subtle changes, sleep disturbance; Grade II: lethargy, disorientation; Grade III: confusion, marked disorientation; Grade IV: coma). Asterixis (flapping tremor) is characteristic β€” ask patient to hold arms outstretched with wrists extended and eyes closed. Flapping = positive.
Peripheral neuropathy
Alcoholic liver disease: alcohol causes direct peripheral neuropathy (distal, sensory predominant). Also consider thiamine deficiency (Wernicke encephalopathy β€” treat immediately with IV thiamine per Australian Alcohol Guidelines).
πŸ›‘οΈ

Immunocompromised

Immunocompromised patients (HIV/AIDS, transplant recipients, chemotherapy, biologics) are at risk of opportunistic CNS infections and treatment-related neurotoxicity.
HIV-associated
HIV-associated neurocognitive disorder (HAND) β€” subcortical pattern (psychomotor slowing, impaired concentration, gait disorder). Opportunistic infections: cerebral toxoplasmosis, cryptococcal meningitis, progressive multifocal leukoencephalopathy (PML β€” JC virus), CMV encephalitis. Consider CNS lymphoma (EBV-associated).
Transplant/chemotherapy
Tacrolimus/cyclosporine neurotoxicity (posterior reversible encephalopathy syndrome β€” PRES β€” headache, seizures, visual disturbance, hypertension). Methotrexate leukoencephalopathy. Immune reconstitution inflammatory syndrome (IRIS) in HIV patients starting ART.
Key examination point
Have a low threshold for neuroimaging (MRI with contrast preferred) in any immunocompromised patient with new neurological symptoms. Lumbar puncture (with appropriate CSF studies including India ink, cryptococcal antigen, viral PCR, cytology) may be indicated β€” check platelets and coagulation first.

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Health Considerations
Disproportionate burden
Aboriginal and Torres Strait Islander Australians experience a significantly higher burden of neurological disease compared to non-Indigenous Australians. Cerebrovascular disease (stroke and TIA) is 1.7 times more prevalent, epilepsy is 2–3 times more common, and traumatic brain injury rates are substantially higher β€” particularly in remote communities. The AIHW reports that diseases of the nervous system are among the top 10 leading causes of disease burden for Aboriginal and Torres Strait Islander peoples.
Stroke risk factors
Higher prevalence of modifiable stroke risk factors including hypertension, type 2 diabetes (3–4 times more common), smoking (3 times more common), chronic kidney disease, rheumatic heart disease, and atrial fibrillation. The Stroke Foundation recommends targeted stroke awareness campaigns in Aboriginal and Torres Strait Islander communities, including recognition of FAST (Face, Arms, Speech, Time) signs and the importance of calling 000 immediately.
Epilepsy and seizures
Epilepsy is significantly more prevalent, with higher rates of uncontrolled seizures. Causes include higher rates of traumatic brain injury, neurocysticercosis in some regions, perinatal hypoxic injury, and CNS infections. Access to neurology services and EEG is limited in remote areas. Telehealth epilepsy clinics and Royal Flying Doctor Service outreach are vital for management continuity. PBS authority prescriptions for antiepileptic medications are available through remote area Aboriginal Health Workers and registered nurse prescribers in some jurisdictions.
Remote access barriers
Specialist neurological assessment (neurology, neurosurgery) is concentrated in major metropolitan and regional centres. Remote-living Aboriginal and Torres Strait Islander patients may face delays of weeks to months for specialist review. Neuroimaging (CT and especially MRI) is available only in regional hospitals at minimum. Telehealth and fly-in-fly-out (FIFO) neurologist services are expanding but remain inconsistent across jurisdictions. The Royal Flying Doctor Service provides emergency aeromedical retrieval for time-critical neurological emergencies (stroke, status epilepticus, spinal cord compression).
Cultural considerations
Neurological examination requires building rapport and trust. Always explain what you are going to do before each part of the examination and gain consent. Some examination components (eye examination with fundoscopy, touching the face for CN V/VII testing) may be culturally sensitive β€” discuss with the patient and, where possible, involve an Aboriginal and/or Torres Strait Islander health worker or liaison officer. Acknowledge that concepts of neurological illness (e.g., "fits," "funny turns," "bad spirits") may differ and use culturally appropriate language. Where English is a second language (many communities use Kriol, Yumplatok, or other first languages), ensure interpreter services are engaged (available through AUSLAN and Indigenous language interpreter services).
Rheumatic fever and neurological sequelae
Acute rheumatic fever (ARF) and rheumatic heart disease (RHD) remain significantly more common in Aboriginal and Torres Strait Islander peoples, particularly in the Northern Territory, Queensland, and Western Australia. Sydenham chorea (a major manifestation of ARF) presents as involuntary choreiform movements and should be considered in any Aboriginal or Torres Strait Islander child or young adult with new-onset involuntary movements. Refer to the RHDAustralia clinical guidelines (2020 edition) for ARF/RHD diagnosis and management.
Neurocognitive effects of otitis media
Chronic suppurative otitis media (CSOM) is extremely prevalent in remote Aboriginal communities (up to 30% of children in some communities). Conductive hearing loss from CSOM affects language development, educational attainment, and social engagement β€” with downstream effects on cognitive assessment and communication during neurological examination. Always assess hearing as part of the neurological examination in Aboriginal and Torres Strait Islander patients and consider whether hearing impairment may confound cognitive testing results.
B12 and nutritional neuropathy
Vitamin B12 deficiency (causing subacute combined degeneration of the cord β€” dorsal column and corticospinal tract involvement) and other nutritional deficiencies may be more common in remote communities with limited access to fresh food (food insecurity is a major determinant of health). Assess B12, folate, and thiamine levels in any Aboriginal and Torres Strait Islander patient with peripheral neuropathy or myelopathy findings.

Quick Reference β€” Neurological Examination Checklist

Use this checklist to ensure all components of the neurological examination have been performed and documented.

General inspection
Consciousness (GCS), posture, abnormal movements, muscle wasting, fasciculations, scars, head circumference
Stance and gait
Normal gait, tandem gait, toe walking, heel walking, Romberg
CN I
Olfaction β€” each nostril, non-irritant
CN II
Visual acuity, fields (confrontation), pupil reactions (direct + consensual + RAPD), fundoscopy
CN III, IV, VI
Ptosis, pupil size, EOM full range, diplopia, INO
CN V
Sensation V1/V2/V3, masseter power, jaw jerk, corneal reflex
CN VII
Facial symmetry β€” forehead (UMN vs LMN), eyes, mouth
CN VIII
Hearing (finger rub, Rinne, Weber), nystagmus, Dix-Hallpike if vertigo
CN IX, X
Palate/uvula, gag reflex, voice quality, swallow
CN XI
SCM (turn head against resistance), trapezius (shrug)
CN XII
Tongue β€” wasting, fasciculations, deviation, protrusion, lateral movements
Upper limbs β€” tone
Wrist rotation, elbow flex/extend β€” spasticity, rigidity, hypotonia
Upper limbs β€” power
C5–T1 myotomes, MRC grading, compare sides
Upper limbs β€” reflexes
Biceps C5/6, brachioradialis C5/6, triceps C7/8
Upper limbs β€” coordination
Finger-nose-finger, dysdiadochokinesia
Lower limbs β€” tone
Knee drop, ankle clonus
Lower limbs β€” power
L1–S2 myotomes, MRC grading, compare sides
Lower limbs β€” reflexes
Knee L3/4, ankle S1/2, plantars (Babinski)
Lower limbs β€” coordination
Heel-shin test
Sensory
Light touch, pin-prick (map level), vibration, proprioception, Romberg
Higher functions
Orientation, attention, memory (register/recall), language (fluency/comprehension/repetition/naming), visuospatial, frontal lobe
Gait (formal)
Observe walking, turning, tandem, toe/heel walk, Romberg, pull test

πŸ“š References

  1. 1. Australian Institute of Health and Welfare (AIHW). Australia's Health 2022: Data Insights. Cat. no. AUS 240. Canberra: AIHW; 2022. Available from: https://www.aihw.gov.au/reports/australias-health/australias-health-2022
  2. 2. Royal Australian College of General Practitioners (RACGP). Guidelines for Preventive Activities in General Practice (Red Book). 9th edn. Melbourne: RACGP; 2018 (updated 2023).
  3. 3. Stroke Foundation (Australia). Clinical Guidelines for Stroke Management. Melbourne: Stroke Foundation; 2022. Available from: https://informme.org.au/en/Guidelines
  4. 4. Campbell WW, DeJong RN. DeJong's The Neurologic Examination. 8th edn. Philadelphia: Wolters Kluwer; 2020.
  5. 5. Fuller G. Neurological Examination Made Easy. 6th edn. Edinburgh: Elsevier; 2019.
  6. 6. Ropper AH, Samuels MA, Klein JP, Prasad S. Adams and Victor's Principles of Neurology. 12th edn. New York: McGraw-Hill; 2023.
  7. 7. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary Report 2023. Canberra: AIHW; 2023.
  8. 8. RHDAustralia (Rheumatic Heart Disease Australia). The 2020 Australian Guideline for Prevention, Diagnosis and Management of Acute Rheumatic Fever and Rheumatic Heart Disease. 3rd edn. Darwin: Menzies School of Health Research; 2020.
  9. 9. Australian Commission on Safety and Quality in Health Care (ACSQHC). National Safety and Quality Health Service Standards. 2nd edn. Sydney: ACSQHC; 2021.
  10. 10. Australasian Faculty of Rehabilitation Medicine (AFRM), Royal Australasian College of Physicians. Cognitive Impairment After Stroke β€” Rehabilitation and Recovery. Sydney: RACP; 2022.
  11. 11. Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG). Management of Epilepsy in Pregnancy. Clinical Guideline. Melbourne: RANZCOG; 2021 (C-Obs 53).
  12. 12. National Health and Medical Research Council (NHMRC). Evidence Review for Cognitively Impaired Conditions: Clinical Practice Guidelines for Dementia in Australia. Canberra: NHMRC; 2024.
  13. 13. Australian and New Zealand Society of Nephrology (ANZSN). Caring for Australasians with Renal Impairment (CARI) Guidelines: Neurological Complications of Chronic Kidney Disease. Sydney: ANZSN; 2023.
  14. 14. Menzies School of Health Research. EarInfoNet: Otitis Media Guidelines for Aboriginal and Torres Strait Islander Populations. 3rd edn. Darwin: Menzies; 2020.
  15. 15. Therapeutic Goods Administration (TGA). Sodium Valproate and Valproic Acid: Risk of Teratogenicity β€” Updated Prescribing Requirements. Canberra: Department of Health; 2024 (boxed warning).
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.

πŸ“š References

  1. 1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
  2. 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. 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. 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. 5. Smolen JS, LandewΓ© 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. 6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
  7. 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. 8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
  9. 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. 10. Pisetsky DS. Antinuclear antibody testing β€” misunderstood or misused? Clin Immunol. 2023;255:109717.
  11. 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. 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 TNFΞ± blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
  13. 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
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.

πŸ“š References

  1. 1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
  2. 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. 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. 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. 5. Smolen JS, LandewΓ© 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. 6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
  7. 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. 8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
  9. 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. 10. Pisetsky DS. Antinuclear antibody testing β€” misunderstood or misused? Clin Immunol. 2023;255:109717.
  11. 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. 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 TNFΞ± blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
  13. 13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).