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Gait Disorders & Falls

🎧 Gait Disorders & Falls — deep-dive podcast

📋 Key Information Summary

📋
  • Gait disorders affect approximately 30% of Australians aged ≥65 years and are an independent predictor of falls, disability, hospitalisation, and mortality.
  • Every older person presenting with a fall requires a multifactorial risk assessment addressing intrinsic factors (vision, cognition, neuropathy, medication) and extrinsic factors (home hazards, footwear).
  • The Timed Up and Go (TUG) test is a validated bedside screen — a result ≥12 seconds identifies increased fall risk and warrants further evaluation.
  • Distinguish neurologic gait (shuffling, festinating, ataxic, magnetic) from musculoskeletal gait (antalgic, Trendelenburg, shortened stride due to joint disease) through structured observation of initiation, stride length, base width, arm swing, turning, and postural stability.
  • A parkinsonian gait (short shuffling steps, reduced arm swing, festination, postural instability) mandates urgent neurological referral — early diagnosis of Parkinson's disease enables timely initiation of levodopa and allied health support.
  • Frontal gait disorder (magnetic gait, wide base, short steps, start hesitation, freezing) suggests normal pressure hydrocephalus, vascular parkinsonism, or frontal lobe pathology — brain imaging with CT or MRI is essential.
  • Medication review is a high-yield falls-prevention intervention — sedatives, antihypertensives (particularly alpha-blockers), anticholinergics, opioids, and polypharmacy (≥4 medicines) significantly increase fall risk.
  • Vitamin D supplementation (800–1000 IU daily) is recommended for older adults who are housebound, institutionalised, or have documented deficiency, as it modestly reduces fall risk.
  • Structured exercise programs combining balance, strength, and gait training (e.g., Otago Exercise Program, tai chi) reduce falls by 20–30% and should be offered to all at-risk older adults.
  • Home hazard assessment by an occupational therapist — removing loose rugs, improving lighting, installing grab rails — reduces falls, especially in those with visual impairment.
  • Patients must be counselled on driving restrictions; in most Australian states, a diagnosis of Parkinson's disease or moderate-to-severe gait disorder is notifiable to the driver licensing authority.
  • Aboriginal and Torres Strait Islander Australians experience falls at 1.5–2 times the rate of non-Indigenous Australians, with earlier onset and higher rates of hospitalisation — culturally safe assessment and community-based prevention programs are essential.
🎬 Gait Disorders & Falls — clinical explainer

Introduction & Australian Epidemiology

Gait disorders represent one of the most common and consequential geriatric syndromes encountered in Australian primary care and emergency departments. Normal gait is a complex motor task requiring integrated function of the musculoskeletal system, peripheral and central nervous systems, vestibular apparatus, vision, and cognition. Disruption at any level produces characteristic gait patterns that provide valuable diagnostic clues.

In Australia, falls are the leading cause of injury-related hospitalisation and death in people aged ≥65 years. According to the Australian Institute of Health and Welfare (AIHW), approximately 133,000 older Australians were hospitalised due to falls in 2021–22, with over 5,300 deaths attributable to falls in 2021. The direct healthcare cost exceeds $2.3 billion annually. Hip fractures, the most feared consequence, carry a 12-month mortality of 20–30% in Australian populations.

The prevalence of gait abnormalities increases sharply with age: approximately 10% of community-dwelling adults aged 60–69 have gait impairment, rising to 30–40% in those aged ≥80, and >60% in residential aged care facilities. Gait speed — often called the "sixth vital sign" — is a powerful predictor of survival, hospitalisation, and functional decline. A gait speed <0.8 m/s is associated with increased mortality and disability in Australian cohort studies.

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Falls as a sentinel event: A single fall in an older adult should prompt systematic evaluation, not reassurance. Up to 50% of fallers will fall again within 12 months, and recurrent falls are a strong predictor of functional decline, nursing home admission, and death.
Statistic Value Source
Annual fall-related hospitalisations (≥65 yrs) ~133,000 AIHW 2022
Fall-related deaths (≥65 yrs, 2021) >5,300 AIHW 2023
Annual healthcare cost of falls >$2.3 billion AUD AIHW 2022
Prevalence of gait disorder ≥80 yrs 30–40% Verghese et al. 2006
Hip fracture 12-month mortality 20–30% Australian Fracture Registry
Proportion of falls with identifiable modifiable risk factors >75% RACGP Silver Book 2023
Gait Disorders & Falls clinical infographic — pathophysiology, clinical clues, diagnosis, imaging, and management
Tap or click image to enlarge — Gait Disorders & Falls: pathophysiology, clinical clues, diagnosis, imaging, and management.
Gait Disorders & Falls infographic, full size

Assessment of Gait

A systematic gait assessment is the cornerstone of evaluating any patient presenting with unsteadiness, falls, or mobility complaints. The clinician should observe the patient walking at their normal pace, at a fast pace, and (if safe) on tandem (heel-to-toe) walking. Gait analysis should be integrated with a targeted neurological and musculoskeletal examination.

Structured Gait Observation

Observe the following parameters systematically. Each parameter provides localising and diagnostic information:

Parameter Normal Abnormal Pattern Significance
Gait initiation Prompt (<2 seconds) Start hesitation >3 sec Parkinsonism, frontal lobe dysfunction
Stride length Symmetrical, age-appropriate Short shuffling steps Parkinsonism, frontal gait, musculoskeletal restriction
Base width 5–10 cm between heels Wide-based (>15 cm) Cerebellar ataxia, sensory ataxia, vestibular disease
Arm swing Bilateral, symmetric Reduced or absent unilateral Parkinsonism (early ipsilateral sign), hemiparesis
Cadence 100–120 steps/min Festination (accelerating, involuntarily) Parkinsonism, frontal gait
Turning Fluid, multi-step turn En bloc (turning as a unit), >3 steps Parkinsonism, balance impairment
Postural stability Retained on pull test Retropulsion, inability to recover Parkinsonism (late), multisensory deficit
Floor contact Heel strike → toe-off Foot flat, shuffling, no clearance Parkinsonism, foot drop (L5 radiculopathy, peroneal neuropathy)

Standardised Gait and Balance Tests

Standardised tests provide objective, reproducible measures that facilitate communication between clinicians, track progression, and guide intervention. The following are recommended in Australian practice:

⏱️
Timed Up and Go (TUG)
Screening tool · 1–2 minutes · No equipment other than chair and stopwatch
Method Patient rises from a standard armchair (seat height ~46 cm), walks 3 metres, turns, walks back, and sits down. Time with usual footwear and walking aid.
Interpretation <10 sec: normal; 10–12 sec: acceptable; 12–20 sec: increased fall risk; >20 sec: high fall risk, needs further assessment
Sensitivity / Specificity Sensitivity ~87% for predicting falls at ≥14 sec cutoff (Shumway-Cook et al.)
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Mini-BESTest
Balance evaluation · 10–15 minutes · Comprehensive
Domains Anticipatory, reactive postural control, sensory orientation, dynamic gait (28 items, score 0–28)
Interpretation Score <19/28: increased fall risk; identifies specific balance subsystem impairments for targeted rehab
Setting Outpatient rehabilitation, specialist falls clinic
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Dynamic Gait Index (DGI)
Functional gait · 10 minutes · 8 tasks
Tasks Level walking, speed changes, head turns, step over obstacle, pivot, stairs
Interpretation Score ≤19/24: predictive of falls; validated in vestibular and neurological populations

Distinguishing Neurologic from Musculoskeletal Gait

A critical clinical skill is distinguishing gait disorders arising from neurological pathology (requiring investigation, specialist referral, and disease-specific treatment) from those caused by musculoskeletal problems (requiring orthopaedic/physiotherapy management, analgesia, and joint protection). The table below summarises key distinguishing features:

Feature Neurologic Gait Musculoskeletal Gait
Stride pattern Irregular, may include freezing or festination Regular but shortened on painful side (antalgic)
Pain association Often painless (especially parkinsonian/ataxic) Directly related to weight-bearing on affected joint
Arm swing Reduced (parkinsonism), absent (hemiparesis) Preserved or compensatory increased
Base width Wide (ataxia, sensory loss) or narrow (parkinsonism) Usually normal or slightly widened for stability
Trendelenburg sign May be present (proximal myopathy — neurogenic or myopathic) Positive in hip OA, gluteal tendinopathy
Foot drop Steppage gait (L5 radiculopathy, peroneal neuropathy, MND) Uncommon unless post-surgical or severe equinus contracture
Response to cueing Improves with external cues (parkinsonism) or visual input (sensory ataxia) Not affected by cueing; pain-limited
Associated signs Tremor, rigidity, reflex changes, upgoing plantars, cerebellar signs Joint swelling/crepitus, reduced ROM, muscle wasting localised to affected joint

Common Neurologic Gait Patterns

Gait Type Key Features Common Causes
Parkinsonian Short shuffling steps, reduced arm swing, festination, en bloc turns, freezing on initiation/doorways Parkinson's disease, vascular parkinsonism, drug-induced parkinsonism, DLB
Cerebellar ataxic Wide-based, irregular, lurching, difficulty with tandem, truncal instability Cerebellar stroke/haemorrhage, MS, alcohol-related cerebellar degeneration, SCA
Sensory ataxic Wide-based, heavy foot-stomping, worsens with eyes closed (positive Romberg) B12 deficiency, diabetic neuropathy, dorsal column lesions, chronic inflammatory demyelinating polyneuropathy (CIDP)
Frontal / Magnetic Short steps, wide base, "magnetic" feet stuck to floor, start hesitation, difficulty lifting feet, poor balance Normal pressure hydrocephalus, vascular dementia, frontal lobe tumour, progressive supranuclear palsy
Spastic (Hemiparetic / Paraparetic) Circumduction, stiff-legged, scissoring, equinovarus foot posture Stroke, MS, spinal cord compression, hereditary spastic paraplegia
Steppage High-stepping to clear foot, slapping foot down Foot drop: common peroneal neuropathy, L5 radiculopathy, peripheral neuropathy, MND
Psychogenic Variable, inconsistent, excessive slowness, knee buckling, distractibility Functional neurological disorder; diagnosis of exclusion

Falls in Older Adults

Falls in older adults are rarely due to a single cause. The RACGP's Guidelines for Preventive Activities in General Practice (Red Book) and the Australasian Journal of Ageing consensus statements recommend a comprehensive, multifactorial approach to falls risk assessment and prevention. In Australia, the NHMRC-endorsed best practice is to screen all community-dwelling adults aged ≥65 (≥50 for Aboriginal and Torres Strait Islander people) for falls annually.

Multifactorial Falls Risk Assessment

The following domains must be systematically evaluated in every older person presenting with a fall or identified as at risk:

1
Detailed Fall History
Circumstances (what, where, when), prodrome (dizziness, syncope, visual disturbance), witness account, injuries sustained, footwear, environmental factors, number of falls in past 12 months.
2
Medication Review
Polypharmacy (≥4 medicines), sedatives/hypnotics, antihypertensives (especially alpha-blockers, loop diuretics), antidepressants (SSRIs, TCAs), opioids, anticholinergics, antipsychotics, anticonvulsants. Aim for deprescribing where safe.
3
Vision Assessment
Visual acuity (<6/12 increases risk 2–3×), cataracts, glaucoma, macular degeneration, multifocal lens use, depth perception. Refer to optometrist or ophthalmologist. Annual review recommended.
4
Gait, Balance & Mobility
TUG test, 30-second chair stand, Romberg, tandem walk, Mini-BESTest if available. Assess walking aid use and appropriateness. Physiotherapy referral for formal assessment.
5
Neurological Examination
Cognition (MoCA/MMSE — cognitive impairment doubles fall risk), peripheral neuropathy (vibration, proprioception), muscle tone, reflexes, cerebellar signs, parkinsonian features, proprioceptive testing.
6
Musculoskeletal Assessment
Joint range of motion, muscle strength (especially quadriceps and ankle dorsiflexors), foot problems (callus, nail pathology, bunions), osteoarthritis of knees/hips, footwear assessment.
7
Cardiovascular Assessment
Orthostatic blood pressure (drop ≥20/10 mmHg within 3 minutes of standing), carotid sinus hypersensitivity if unexplained syncope, heart rate/rhythm assessment. 24-hour ambulatory BP if postural hypotension suspected.
8
Home Environment
Occupational therapy home safety assessment — loose rugs, poor lighting, clutter, absence of grab rails in bathroom/toilet, uneven surfaces, steep stairs, pets underfoot. Funded under most state HACC/CHSP programmes.
9
Footwear
Assess for: well-fitting, low-heel, slip-resistant shoes. Avoid thongs, backless slippers, high heels, and worn-soled shoes. Podiatry referral if foot pathology identified.
10
Fear of Falling & Psychosocial
Assess using Falls Efficacy Scale-International (FES-I). Fear of falling affects 30–50% of fallers, leads to activity restriction, deconditioning, and social isolation — a vicious cycle. Address with graduated exposure, CBT, and exercise.

High-Risk Medications and Falls

Medication-related falls are among the most modifiable risk factors. The following medication classes carry the highest fall risk in Australian older adults:

Drug Class Examples Mechanism of Increased Risk Action
Benzodiazepines / Z-drugs Diazepam, temazepam, zolpidem Sedation, impaired cognition, reduced reaction time, ataxia Gradual taper per RACGP deprescribing guidelines; avoid abrupt cessation
Antihypertensives Prazosin, doxazosin, frusemide, amlodipine Orthostatic hypotension, volume depletion Review targets (relax BP targets in frail elderly ≥80 yrs); check lying/standing BP
Antidepressants Sertraline, amitriptyline, mirtazapine SSRIs: orthostasis, hyponatraemia; TCAs: anticholinergic, sedation, QTc Minimise dose; consider non-pharmacological approaches; avoid TCAs
Opioids Oxycodone, tramadol, codeine, tapentadol Sedation, dizziness, constipation, cognitive impairment Multimodal analgesia; paracetamol first-line; wean opioids
Antipsychotics Quetiapine, risperidone Extrapyramidal symptoms, sedation, orthostasis, QTc Review indication; deprescribe if used for behavioural symptoms of dementia without clear indication
Anticholinergics Oxybutynin, hyoscine, promethazine Confusion, blurred vision, urinary retention, constipation Calculate anticholinergic burden score; substitute non-anticholinergic alternatives
🚨
Orthostatic hypotension: Measure lying and standing blood pressure in ALL older fallers. A sustained drop of ≥20 mmHg systolic or ≥10 mmHg diastolic within 3 minutes of standing is diagnostic. Check within 1 minute of standing in patients on antihypertensives, alpha-blockers, or with autonomic features. Causes include medication effect, dehydration, autonomic neuropathy (diabetes, Parkinson's disease), and Addison's disease.

Evidence-Based Falls Prevention Interventions

Intervention Effect Size Key Details Australian Access
Exercise (balance + strength) 20–30% fall reduction (RR 0.76) ≥2 hrs/week; must include challenging balance training. Otago program, tai chi, group exercise classes Otago funded via CHSP; physiotherapy via Medicare CDM items (10958–10970); community falls prevention programs in most PHNs
Home modification 25–35% fall reduction in those with visual impairment OT home assessment: grab rails, lighting, remove trip hazards, handrails on stairs CHSP / state HACC programmes; OT via Medicare CDM items; My Aged Care referral for >65 yrs
Medication review 15–25% fall reduction Reduce/withdraw psychotropics, minimise polypharmacy, medication review via GP or pharmacist (RMMR/HMR) PBS-funded Home Medicines Review (HMR, MBS item 900); Residential Medication Management Review (RMMR)
Vitamin D supplementation Modest (~10–15% in deficient/institutionalised) 800–1000 IU cholecalciferol daily; recommended for housebound, residential care, or documented deficiency PBS Authority Required for cholecalciferol in CKD or documented deficiency; OTC available cheaply
Vision correction Variable; cataract surgery reduces falls ~30% Annual eye examination; avoid multifocal glasses during walking; cataract surgery if visually significant Medicare-funded optometry; cataract surgery via public/private hospitals
Footwear advice Supportive evidence, less quantified Low-heel, firm-fitting, slip-resistant soles; podiatry referral for foot pathology Podiatry via Medicare CDM items; CHSP for >65 yrs
Cardiac pacing (if indicated) Significant fall reduction in carotid sinus hypersensitivity Carotid sinus massage under monitoring; pacemaker if cardioinhibitory response with symptoms Cardiology referral; MBS-funded procedure

Vitamin D Supplementation

☀️
Cholecalciferol (Vitamin D₃)
Ostelin® · various generics
Adult dose 800–1000 IU (20–25 mcg) PO daily for falls prevention in at-risk older adults
Deficiency correction 3000–5000 IU daily for 6–12 weeks if serum 25(OH)D <50 nmol/L, then maintenance
Renal impairment Safe in all stages; consider calcitriol in severe CKD (eGFR <15) under nephrology guidance
PBS status ⚠ PBS Authority Required (CKD stage 3b+ with deficiency); ✔ OTC widely available

Parkinsonian & Frontal Gait

Parkinsonian and frontal gait disorders are among the most disabling and therapeutically impactful gait disturbances. They reflect dysfunction of the basal ganglia-thalamo-cortical circuits and frontal lobe motor planning areas, respectively. Early recognition and appropriate referral can substantially improve quality of life and slow functional decline.

Parkinsonian Gait — Clinical Features

The hallmark features of parkinsonian gait result from the combination of bradykinesia, rigidity, and postural instability that characterise basal ganglia dysfunction:

  • Festination: Involuntary acceleration of gait with progressively shortening steps — the patient's centre of gravity moves forward faster than their feet can keep up, increasing fall risk
  • Freezing of gait (FOG): Sudden, transient inability to initiate or continue stepping — most troublesome on initiation ("start hesitation"), when approaching doorways or obstacles, and during turns. May be "on" phenomenon (wearing-off related) or independent of levodopa cycle
  • Reduced arm swing: Often the earliest visible sign; typically asymmetric, preceding the onset of lower limb involvement
  • Shuffling gait: Short stride length with reduced foot clearance, increasing trip risk
  • En bloc turning: Loss of segmental rotation; the head, trunk, and pelvis turn as a single unit, requiring multiple small steps
  • Postural instability: Impaired postural reflexes — a pull test showing retropulsion requiring >2 steps to recover indicates Hoehn & Yahr stage ≥3
⚠️
Red flags for urgent neurology referral: Unilateral parkinsonian features in a patient aged <70 years (consider early-onset PD); rapidly progressive gait disorder (consider PSP, MSA, or vascular parkinsonism); early postural instability within 1–2 years of motor symptom onset (suggests atypical parkinsonism — PSP, CBD, MSA); prominent early cognitive impairment or hallucinations (suggests dementia with Lewy bodies); poor or absent levodopa response.

Frontal Gait Disorder (Gait Apraxia)

Frontal gait disorder, sometimes called "gait apraxia" or "magnetic gait," results from disruption of the frontal-subcortical circuits that mediate motor planning and execution of locomotion. The patient's legs feel "glued to the floor," and the gait is characterised by:

  • Magnetic gait: Feet appear stuck to the floor with difficulty initiating stepping despite normal leg strength
  • Wide base: Compensatory widening for balance impairment
  • Short shuffling steps: Distinct from parkinsonism — often with preserved arm swing
  • Start hesitation: May be overcome by visual cueing (stepping over a line or object) or auditory cueing (counting, marching music)
  • Difficulty with dual-tasking: Gait deteriorates markedly when walking and talking simultaneously — a key early sign of frontal-subcortical dysfunction
  • Urinary urgency/incontinence: Often accompanies gait disorder in normal pressure hydrocephalus (NPH) — the classic Hakim's triad of gait disturbance, cognitive decline, and urinary incontinence

Key Differentials and Investigation Pathway

Condition Distinguishing Features First-Line Investigation Referral Pathway
Idiopathic Parkinson's Disease Asymmetric onset, resting tremor, good levodopa response, progressive DaTSCAN (if diagnostic doubt); MRI to exclude structural cause Neurology — ideally movement disorder specialist within 6 weeks of suspected diagnosis
Normal Pressure Hydrocephalus Hakim's triad (gait, cognition, continence); "magnetic" gait; ventriculomegaly out of proportion to atrophy CT/MRI brain (EVANS index >0.3); large-volume lumbar puncture (tap test) with pre/post TUG Neurosurgery referral if tap test positive (>20% TUG improvement after removal 30–50 mL CSF)
Vascular Parkinsonism Stepwise progression, lower-body predominance ("lower-half parkinsonism"), history of cerebrovascular risk factors, poor levodopa response MRI brain (white matter hyperintensities, lacunar infarcts) Neurology + stroke prevention optimisation
Progressive Supranuclear Palsy (PSP) Early falls (within 1–2 years), vertical supranuclear gaze palsy, axial rigidity, retrocollis, pseudobulbar affect MRI brain (hummingbird sign — midbrain atrophy) Urgent neurology referral; PSP is a tauopathy with poor prognosis (median survival 6–9 years)
Dementia with Lewy Bodies (DLB) Fluctuating cognition, visual hallucinations, REM sleep behaviour disorder, parkinsonism, neuroleptic sensitivity DaTSCAN; MRI to exclude vascular/other causes; neuropsychology Neurology / geriatrics; avoid antipsychotics (severe sensitivity reactions)
Drug-Induced Parkinsonism Symmetric onset, history of dopamine-blocking drugs (metoclopramide, haloperidol, prochlorperazine, risperidone) Review medication history; withdraw offending agent (may take 3–6 months to resolve) GP-initiated deprescribing; neurology referral if persistent >6 months after withdrawal

Referral Timelines

ℹ️
Australian referral benchmarks:
  • Suspected Parkinson's disease: Referral to neurology/movement disorder specialist within 6 weeks of clinical suspicion. Early treatment initiation improves quality of life and functional outcomes.
  • Atypical features (PSP, MSA, CBD): Urgent referral — within 2 weeks — as these conditions progress more rapidly and require multidisciplinary management.
  • Suspected NPH: Referral to neurosurgery via neurology within 4 weeks for tap test and potential VP shunt assessment. Shunting has ~70–80% gait improvement in carefully selected cases.
  • Unexplained falls with frontal signs: Urgent CT brain (within 48 hours if in ED) to exclude subdural haematoma, hydrocephalus, or space-occupying lesion.

Driving and Mobility Aids

Driving assessment is a critical responsibility when managing patients with gait disorders. Australian road safety legislation requires clinicians to consider fitness to drive in patients with neurological conditions that may impair driving ability.

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Driving obligations: In all Australian states and territories, clinicians have a duty to advise patients with Parkinson's disease, moderate-to-severe gait disorders, or any condition that may impair driving ability. A diagnosis of Parkinson's disease is generally notifiable to the driver licensing authority (varies by state — Austroads Assessing Fitness to Drive 2022 edition provides national guidance). Patients must be advised: (1) not to drive until assessed; (2) that their licensing authority will be notified; (3) that driving restrictions depend on symptom severity and medication response. Commercial licence holders (truck, bus) require more stringent assessment.

Mobility Aids and Assistive Technology

Appropriate mobility aids improve safety, independence, and community participation. The choice must be individualised and regularly reassessed:

Aid Indication Key Considerations
Walking stick Mild balance impairment, unilateral weakness Hold in contralateral hand to affected leg; correct height = wrist crease at greater trochanter
Four-wheel walker (4WW) Moderate balance impairment, bilateral weakness, post-stroke, parkinsonism NOT recommended for patients with festination (may increase fall risk — patient walks faster than walker); consider glider frames or front-wheeled walkers for parkinsonism
Rollator with seat Fatigue-limiting conditions, long-distance community mobility Must have reliable hand-brake function; encourage sitting breaks
Pick-up walker (non-wheeled) Significant bilateral weakness requiring maximum stability Slowest but most stable; requires adequate upper limb strength to lift
Laser-line cueing devices Freezing of gait in Parkinson's disease Projects a horizontal laser line to step over; evidence for reducing FOG episodes. Available via occupational therapy or Parkinson's Australia
Wheelchair / scooter Severe mobility limitation, falls despite optimal aids Does not negate need for continued exercise; funded via NDIS (if <65) or My Aged Care (if ≥65)
⚠️
Walking aids in Parkinson's disease: Standard four-wheel walkers are NOT recommended for patients with festinating gait or significant freezing of gait. The walker can become a hazard as the patient accelerates into it. Alternatives include: front-wheeled pick-up walkers, U-Step walkers (spring-loaded braking), or laser-line cueing devices. A physiotherapist experienced in Parkinson's management should assess and prescribe the optimal aid.

Pathophysiology

Human gait is a complex, largely automatic motor programme that requires the integration of multiple neural systems:

Central Pattern Generators

Locomotion is initiated and modulated by central pattern generators (CPGs) in the spinal cord, which produce the rhythmic alternating pattern of leg movements. These CPGs are under the control of supraspinal centres:

  • Mesencephalic locomotor region (MLR): Initiates and modulates gait speed; connected to the basal ganglia and cerebellum
  • Basal ganglia: The subthalamic locomotor region and substantia nigra pars reticulata modulate gait initiation and automatic stepping via dopaminergic pathways
  • Frontal cortex (supplementary motor area, prefrontal cortex): Voluntary gait control, obstacle avoidance, dual-task gait adaptation, and motor planning
  • Cerebellum: Coordination, balance, postural adjustments, and gait rhythm; vermis for truncal control, hemispheres for limb coordination

Pathophysiology of Parkinsonian Gait

Dopamine depletion in the substantia nigra pars compacta (exceeding 60–80% before motor symptoms appear) leads to:

  • Reduced basal ganglia output via the globus pallidus internus → decreased thalamo-cortical excitation → bradykinesia and hypokinesia of gait
  • Impaired scaling of movement amplitude — the automatic "internal cueing" for step length is lost
  • Freezing of gait is thought to result from an inability to appropriately switch between locomotion and postural control, particularly when environmental demands change (doorways, turns)
  • Non-dopaminergic systems (cholinergic pedunculopontine nucleus, noradrenergic locus coeruleus) contribute to postural instability and freezing, explaining why these features respond poorly to levodopa

Pathophysiology of Frontal Gait Disorder

Disruption of the frontal-subcortical white matter tracts or basal ganglia-frontal connections impairs the motor planning and execution of gait. This may result from:

  • Normal pressure hydrocephalus — dilated ventricles compress periventricular white matter tracts carrying corticospinal and fronto-pontine fibres
  • Vascular white matter disease — chronic small vessel ischaemia damages the frontal-subcortical circuits (leukoaraiosis)
  • Frontal lobe tumours or trauma — direct disruption of supplementary motor area and prefrontal motor planning regions

Clinical Presentation & Diagnostic Criteria

Clinical Presentation by Cause

The clinical presentation of gait disorders varies by underlying aetiology. A thorough history should address onset (acute vs. subacute vs. chronic), progression (stepwise vs. gradual vs. fluctuating), associated symptoms, and functional impact.

Presentation Suggestive Cause Key History Points
Acute unilateral gait difficulty Stroke, acute disc prolapse, hip fracture Sudden onset; neurological deficits (stroke) vs. pain (musculoskeletal)
Subacute progressive gait difficulty with falls Subdural haematoma, NPH, spinal cord compression Weeks–months progression; anticoagulant use (SDH); back pain (cord compression)
Insidious asymmetric tremor + stiffness + shuffling Parkinson's disease Often noticed by spouse; micrographia, reduced arm swing, constipation (prodromal)
Gait + cognition + continence decline Normal pressure hydrocephalus Months–years; ventriculomegaly on prior imaging may be noted
Early falls + vertical gaze palsy + rigidity Progressive supranuclear palsy Falls within first 1–2 years; personality change; dysphagia
Worsening on standing, improves with support Orthostatic hypotension, vestibular dysfunction Light-headedness on standing; worse in morning or after meals
Fear-avoidance with normal examination Post-fall syndrome, anxiety, deconditioning Previous fall event; activity restriction; social withdrawal

Diagnostic Criteria — Parkinson's Disease (MDS Clinical Criteria 2015)

The Movement Disorder Society (MDS) criteria for Parkinson's disease require:

  1. Parkinsonism: bradykinesia plus rest tremor and/or rigidity
  2. At least 2 supportive criteria (clear and dramatic levodopa response, levodopa-induced dyskinesias, rest tremor of a limb, positive olfactory loss or cardiac sympathetic denervation on MIBG scintigraphy)
  3. No absolute exclusion criteria (cerebellar abnormalities, supranuclear gaze palsy, frontotemporal dementia within 5 years, parkinetic features restricted to lower limbs for >3 years)
  4. No red flags that must be counterbalanced by supportive criteria (rapid gait impairment, early severe dysphonia, early severe dysarthria, etc.)

Investigations

First-Line Investigations (GP / ED)

Essential
Blood tests
FBC, ESR/CRP, BSL, UEC, LFTs, TFTs, calcium, vitamin B12, folate, vitamin D (25-OH). Rule out metabolic, endocrine, and nutritional causes of gait disturbance and falls.
Essential
Lying and standing blood pressure
Measure supine BP after 5 minutes rest, then standing at 1 minute and 3 minutes. Orthostatic drop ≥20/10 mmHg is diagnostic. MBS item 11105.
Essential
CT Brain (non-contrast)
Indicated for: new-onset gait disorder, suspected subdural haematoma, falls with head injury, suspected NPH (ventriculomegaly). Available in all Australian EDs and most radiology practices. MBS item 56001.
Available
ECG
Assess for arrhythmia (AF, heart block, long QT) if syncope or cardiac cause suspected.
Available
Urinalysis / MSU
UTI as a cause of acute confusion and falls in elderly; screen for glycosuria (diabetes).

Second-Line / Specialist Investigations

Specialist
MRI Brain
Superior to CT for: white matter disease assessment, midbrain atrophy (PSP — hummingbird sign), cerebellar pathology, spinal cord compression. Required for NPH workup. MBS item 63001 (with Medicare rebate if referred by specialist).
Specialist
DaTSCAN (Ioflupane ¹²³I SPECT)
Demonstrips presynaptic dopaminergic deficit; differentiates degenerative parkinsonism (PD, DLB, MSA, PSP) from non-degenerative (drug-induced, vascular, essential tremor). Available at major nuclear medicine centres in capital cities. MBS item 61336. Not required if clinical picture is clear.
Specialist
Lumbar Puncture (Tap Test)
Remove 30–50 mL CSF; assess gait (TUG) before and 2–4 hours after. ≥20% improvement in TUG time supports NPH diagnosis and predicts response to VP shunting. Performed by neurology or neurosurgery.
Specialist
Nerve Conduction Studies / EMG
For suspected peripheral neuropathy (diabetic, B12, CIDP) contributing to sensory ataxic gait. Available at major hospitals and private neurophysiology labs.
Referral
Formal Neuropsychological Assessment
For suspected cognitive contribution to gait disorder (dual-task impairment); helps differentiate DLB, vascular dementia, frontotemporal dementia.
Referral
Vestibular Function Tests
Caloric testing, video head impulse test (vHIT), vestibular-evoked myogenic potentials (VEMP) for suspected vestibular contribution to unsteadiness.

Australian MBS Items — Relevant Investigations

MBS Item Investigation Referral Requirement
66823 Carotid sinus massage (head-up tilt table) Cardiologist
56001 CT Brain non-contrast GP or specialist
63001 MRI Brain Specialist (GP referral if urgent ED)
61336 DaTSCAN (Dopamine transporter SPECT) Specialist (neurologist)
11105 Lying/standing BP measurement GP
🖼️ Gait Disorders & Falls — visual summary
Gait Disorders & Falls visual summary infographic

Risk Stratification & Severity Scoring

Falls Risk Stratification

Stratifying falls risk guides the intensity and setting of intervention:

Low Risk
No Falls, Single Risk Factor
Community-dwelling, independent ADLs, TUG <12 sec, no polypharmacy, no orthostasis, no cognitive impairment.
Setting: GP annual review, general exercise advice, vitamin D if housebound
Moderate Risk
Single Fall or 2+ Risk Factors
One fall in past 12 months, OR TUG 12–20 sec, OR polypharmacy (≥4 medicines), OR mild cognitive impairment, OR orthostatic hypotension, OR impaired vision.
Setting: GP comprehensive assessment, physiotherapy referral, medication review (HMR), OT home assessment, structured exercise program
High Risk
Recurrent Falls or Serious Injury
≥2 falls in 12 months, OR any fall-related fracture, OR TUG >20 sec, OR gait abnormality requiring aid, OR parkinsonian features, OR recurrent syncope.
Setting: Specialist falls clinic or geriatric medicine referral, multidisciplinary falls prevention program, consider hip protectors, urgent neurological assessment if indicated

Hoehn & Yahr Staging (Parkinson's Disease)

Stage Description Gait & Falls Implications
1 Unilateral involvement only Minimal gait impact; reduced arm swing may be only sign
1.5 Unilateral + axial involvement Early postural awareness; slight gait change
2 Bilateral without balance impairment Bilateral bradykinesia; gait slower but no falls
2.5 Bilateral, mild balance impairment (pull test recovers) Gait unsteadiness; "pulling back" on recovery
3 Bilateral, moderate balance impairment (pull test abnormal) Falls begin at this stage; festination, freezing; still independent in ADLs
4 Severe disability; still able to walk/stand unassisted Frequent falls; freezing of gait significant; needs walking aid; ADL assistance required
5 Wheelchair-bound or bedridden unless assisted Cannot walk unassisted; high fall risk during transfers

Empirical & Directed Therapy

Pharmacotherapy — Parkinson's Disease

The following medications are used in the management of parkinsonian gait disorders. All should be initiated by or in consultation with a neurologist or geriatrician with movement disorder expertise.

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Levodopa / Carbidopa
Sinemet® · Madopar® (with benserazide) · Dopaminergic
Adult dose Sinemet® 100/25 mg PO TDS initially, titrate to effective dose (typically 300–600 mg levodopa/day in divided doses); Madopar® 50/12.5 mg TDS, titrate similarly
Paediatric dose Not applicable — PD is a disease of older adults (juvenile PD managed by paediatric neurology)
Route Oral (tablets, dispersible tablets); duodenal infusion (Duodopa®) for advanced PD
Duration Lifelong — disease-modifying therapy not yet available
Renal adjustment No specific dose adjustment; use with caution in severe renal impairment
Hepatic adjustment Use with caution; dose reduction may be needed
PBS status ✔ PBS General Benefit
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Ropinirole
Requip® · Dopamine agonist
Adult dose 0.25 mg PO TDS, titrate weekly by 0.75 mg/day to 3–9 mg/day in divided doses; extended-release (Requip PD®) once daily
Renal adjustment No adjustment for mild–moderate; caution in severe impairment (eGFR <15)
PBS status ⚠ PBS Authority Required
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Amantadine
Symmetrel® · NMDA antagonist / weak dopamine release
Adult dose 100 mg PO mane initially; may increase to 100 mg BD; avoid evening dose (insomnia)
Key use Levodopa-induced dyskinesias; modest benefit for freezing of gait in some patients
Renal adjustment Reduce dose if eGFR 30–50: 100 mg daily; eGFR 15–30: 100 mg alternate days; eGFR <15: avoid
PBS status ⚠ PBS Authority Required
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Rivastigmine
Exelon® · Cholinesterase inhibitor
Adult dose 1.5 mg PO BD initially; titrate to 3 mg BD after 2 weeks, then 4.5 mg BD, then 6 mg BD (max); transdermal patch 4.6 mg/24 hr, titrate to 9.5 mg/24 hr, then 13.3 mg/24 hr
Key use Dementia with Lewy bodies; Parkinson's disease dementia — improves cognition and may reduce falls via dual-task gait improvement
PBS status ⚠ PBS Authority Required (DLB/PDD with MMSE 10–26)
⚠️
Dopamine agonist caution: Ropinirole, pramipexole, and rotigotine carry significant risks of impulse control disorders (pathological gambling, hypersexuality, compulsive shopping/eating) affecting up to 15–20% of patients. Counsel patients and carers before initiation. Screen at every visit. Risk is higher in younger patients, those on higher doses, and those with a history of addictive behaviour.

Freezing of Gait — Non-Pharmacological Strategies

Freezing of gait (FOG) often responds poorly to medication alone. The following cueing strategies are recommended and should be taught by physiotherapists:

  • Visual cueing: Step over a line, laser line projected from a device attached to the walking frame or rollator
  • Auditory cueing: Rhythmic counting ("1-2-3-STEP"), metronome apps, marching music
  • Somatosensory cueing: Weight shift side to side before initiating stepping; rocking motion
  • Cognitive strategies: Imagine stepping over an obstacle; consciously lift the foot high
  • Environmental modification: Remove clutter, widen doorways, use contrasting colour strips at thresholds

Normal Pressure Hydrocephalus — Treatment

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Ventriculoperitoneal (VP) Shunt
Surgical treatment · Neurosurgical procedure
Indication Confirmed NPH with positive tap test (≥20% TUG improvement after CSF removal)
Outcomes ~70–80% gait improvement; ~50–60% continence improvement; ~30–50% cognitive improvement
Complications Over-drainage (subdural haematoma), shunt infection (~5–10%), shunt malfunction
Setting Tertiary neurosurgery centre; available in all Australian state capitals
Funding ✔ MBS-funded hospital procedure

Gait Disorder Due to Orthostatic Hypotension

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Fludrocortisone
Florinef® · Mineralocorticoid
Adult dose 0.1 mg PO mane; may increase to 0.2–0.3 mg daily
Monitoring BP lying/standing, UEC (risk of hypokalaemia, oedema), supine hypertension
PBS status ✔ PBS General Benefit
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Midodrine
Gutron® · Alpha-1 agonist
Adult dose 2.5 mg PO TDS initially; titrate to 5–10 mg TDS (last dose before 6 pm to avoid supine hypertension)
PBS status ⚠ PBS Authority Required

Monitoring

Monitoring Plan

Parameter Frequency Tool / Method
Fall frequency and circumstances Every visit (minimum 3-monthly for high-risk patients) Patient/carer diary; structured fall history
Gait assessment (TUG, gait speed) Every 3–6 months TUG test; 4-metre gait speed; Mini-BESTest
Medication review Every 6 months (or after any fall) GP medication reconciliation; HMR annually (MBS item 900)
Blood pressure (lying/standing) Every visit if on antihypertensives or with autonomic features Automated sphygmomanometer; active stand protocol
Cognitive screening 6-monthly if parkinsonian gait or frontal signs MoCA (preferred for mild impairment); MMSE
Levodopa response / motor fluctuations Every 3–6 months (neurology) MDS-UPDRS Part III; patient motor diary; on/off documentation
Vitamin D level Annually (or 3-monthly if supplementing and deficient) Serum 25(OH)D; target ≥75 nmol/L
Fear of falling / activity restriction Every 6 months Falls Efficacy Scale – International (FES-I)
Walking aid suitability After every fall or functional decline Physiotherapy reassessment
Driving fitness Annually; after any fall with injury; after medication changes Austroads Assessing Fitness to Drive 2022; formal OT driving assessment if needed

Special Populations

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Paediatrics

Developmental gait milestones: Independent walking by 18 months is the accepted upper limit of normal. Persistent toe-walking, wide-based unsteady gait beyond age 3, or regression of achieved milestones warrants neurological evaluation.
Differential diagnoses: Cerebral palsy, muscular dystrophy (Duchenne — toe-watching, Gowers' sign), developmental coordination disorder, ataxia-telangiectasia, hereditary spastic paraplegia, brain tumour (posterior fossa).
Referral: Paediatric neurology; paediatric orthopaedics for musculoskeletal gait disorders. State children's health services (e.g., NSW KidsHealth, QLD Children's Health).
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Pregnancy

Pregnancy-related gait changes: Widened base, lordosis, waddling gait due to pelvic girdle laxity — physiologically normal but increases fall risk in third trimester.
Falls in pregnancy: ~25–30% of pregnant women report a fall; most are minor but hip fractures and placental abruption are serious complications. Balance training and pelvic support belts may reduce risk.
Drug safety: Levodopa is Category B3 (AU TGA); dopamine agonists are generally avoided; amantadine is teratogenic (Category D). Any woman of childbearing age on PD medication should receive pre-conception counselling.
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Elderly (≥80 years)

Multimorbidity: Gait disorders in the very old are usually multifactorial — combining degenerative joint disease, peripheral neuropathy, visual impairment, medication effects, and deconditioning. Single-cause attribution is rarely correct.
Sarcopenia: Age-related muscle loss (1–2% per year after 50) significantly contributes to gait instability. Resistance exercise and adequate protein intake (1.0–1.2 g/kg/day) are essential.
Residential aged care: Falls rates are 2–3× higher in RACFs. The Aged Care Quality Standards require individualised falls prevention plans. Multidisciplinary review is mandated under the new AN-ACC funding model.
Cognitive impairment: Dual-task gait assessment (walking while counting backwards) is a sensitive marker of early cognitive decline and future dementia risk — slowing of >20% on dual-task compared to single-task gait is abnormal.
Hip protectors: Evidence is mixed; may be considered in high-risk RACF residents who will comply with wear. Not a substitute for exercise and environmental modification.
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Renal Impairment

Uraemic neuropathy: CKD stages 4–5 may cause peripheral neuropathy contributing to sensory ataxic gait. Dialysis may partially improve nerve function.
Dialysis-related: Intradialytic hypotension increases fall risk; post-dialysis fatigue impairs gait. Assess gait after dialysis sessions, not before.
Medication adjustments: Levodopa: no adjustment needed. Amantadine: reduce dose if eGFR <50; avoid if eGFR <15. Rivastigmine: caution in severe renal impairment. Midodrine: no specific adjustment. Fludrocortisone: monitor potassium closely in CKD.
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Hepatic Impairment

Hepatic encephalopathy: May present with frontal-type gait disturbance (asterixis, cognitive slowing, wide-based gait). Treat underlying cause; lactulose and rifaximin improve gait as encephalopathy resolves.
Drug metabolism: Levodopa is primarily metabolised peripherally by decarboxylation (not hepatic), so dose adjustment is generally not required. However, dopamine agonists (ropinirole, pramipexole) undergo hepatic metabolism — start low, titrate slowly.
Neuropathy: Alcoholic liver disease commonly causes peripheral neuropathy contributing to ataxic gait. Address alcohol dependence with appropriate pharmacotherapy and counselling.
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Immunocompromised

Infection risk: Immunocompromised patients (transplant recipients, HIV, biologics) presenting with gait disturbance may have CNS infections (cryptococcal meningitis, PML, cerebral abscess) presenting subacutely with gait changes before overt meningitic or focal signs.
Medication-related: Calcineurin inhibitors (tacrolimus, cyclosporine) may cause tremor and ataxic gait (neurotoxicity). HIV antiretrovirals — efavirenz-related neuropsychiatric effects may include ataxia. Chemotherapy-induced peripheral neuropathy (CIPN) is a common cause of sensory ataxic gait (vincristine, paclitaxel, cisplatin).
Investigation threshold: Low threshold for brain imaging and lumbar puncture in immunocompromised patients with new gait abnormality.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health
Epidemiology
Aboriginal and Torres Strait Islander Australians experience falls at 1.5–2 times the rate of non-Indigenous Australians, with earlier onset and higher rates of fall-related hospitalisation and hip fracture. The AIHW reports that Indigenous Australians are hospitalised for falls-related injuries at approximately 1.7 times the rate of non-Indigenous Australians. Fall-related mortality is significantly higher, particularly in remote communities.
Earlier onset of gait-related disability
Chronic diseases contributing to gait impairment (diabetes with neuropathy, cardiovascular disease, CKD, rheumatic heart disease) have earlier onset and greater severity in Indigenous populations. Diabetic peripheral neuropathy is a major contributor to sensory ataxic gait and falls. Falls screening should commence at age ≥50 (not ≥65) for Indigenous Australians.
Remote and very remote access
Specialist neurology services are concentrated in metropolitan centres. For remote and very remote communities (comprising ~20% of Indigenous Australians), access to physiotherapy, occupational therapy, neurology, and geriatric medicine is severely limited. Telehealth consultation items (MBS items 99200–99215) fund video consultations with specialists. Royal Flying Doctor Service and visiting specialist programmes provide intermittent outreach.
Cultural safety in assessment
Falls risk assessment tools validated in non-Indigenous populations may not capture culturally relevant risk factors (e.g., uneven community terrain, lack of lighting in outstations, culturally specific footwear or lack thereof, crowded housing increasing trip hazards). Assessment should involve Aboriginal Health Workers/Practitioners (AHWPs) and use culturally validated tools where available.
Aboriginal Health Workers and Practitioners
AHWPs are essential in delivering falls prevention education, home safety assessments, and exercise programs in community-controlled health services. Programs like the Indigenous Falls Prevention Program and community-based exercise groups (e.g., "Deadly Moves" programs) have demonstrated improved engagement compared to mainstream services.
Home environment and housing
Overcrowded housing, lack of handrails, uneven ground surfaces, poor lighting, and limited hot water in some remote communities are significant extrinsic falls risk factors. National Indigenous Australians Agency (NIAA) housing programmes and state/territory Indigenous housing authorities can fund modifications, though wait times may be prolonged.
Medication considerations
Polypharmacy is common in Indigenous Australians with multiple chronic diseases. PBS Close the Gap CTG scripts allow increased repeats and streamlined authority for PBS medicines. Medication reviews through NACCHO-affiliated Aboriginal Community Controlled Health Organisations (ACCHOs) can identify and reduce high-risk medications contributing to falls.
Community-based prevention programs
The most effective falls prevention programs for Indigenous Australians are community-based, culturally embedded, and led by AHWPs. Examples include the "Standing Tall" program (adapted for Indigenous communities), Tai Chi classes run through ACCHOs, and community walking groups. These programs should incorporate yarning circles, storytelling, and connection to Country as engagement strategies.
📊 Gait Disorders & Falls — slide deck

Open slides PDF in new tab

📚 References

  1. 1. Royal Australian College of General Practitioners. Guidelines for Preventive Activities in General Practice (Red Book). 9th ed. Melbourne: RACGP; 2016 (updated 2023).
  2. 2. Australian Institute of Health and Welfare. Falls in Older Australians 2019–20: Hospitalisations and Deaths Among People Aged 65 and Over. AIHW Cat. No. INJ 4. Canberra: AIHW; 2022.
  3. 3. National Health and Medical Research Council. Preventing Falls and Harm from Falls in Older People: Best Practice Guidelines for Australian Community Care. Canberra: NHMRC; 2009.
  4. 4. Verghese J, LeValley A, Hall CB, Katz MJ, Ambrose AF, Lipton RB. Epidemiology of gait disorders in community-residing older adults. J Am Geriatr Soc. 2006;54(2):255–261.
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  6. 6. Movement Disorder Society. MDS Clinical Diagnostic Criteria for Parkinson's Disease. Mov Disord. 2015;30(12):1591–1601.
  7. 7. Austroads. Assessing Fitness to Drive: Medical Standards for Licensing and Clinical Management Guidelines — A Resource for Health Professionals in Australia. Sydney: Austroads; 2022.
  8. 8. Panel on Prevention of Falls in Older Persons, American Geriatrics Society, British Geriatrics Society. Summary of the updated AGS/BGS clinical practice guideline for prevention of falls in older persons. J Am Geriatr Soc. 2011;59(1):148–157.
  9. 9. Stroke Foundation (Australia). Clinical Guidelines for Stroke Management. Melbourne: Stroke Foundation; 2022 (updated).
  10. 10. Sherrington C, Fairhall NJ, Wallbank GK, et al. Exercise for preventing falls in older people living in the community. Cochrane Database Syst Rev. 2019;1(1):CD012424.
  11. 11. Religa D, Cermakova P, Lundin A, et al. Treatment of normal pressure hydrocephalus — a comprehensive review. J Alzheimers Dis. 2021;84(3):927–942.
  12. 12. Australian Institute of Health and Welfare. The Health and Welfare of Australia's Aboriginal and Torres Strait Islander Peoples. Canberra: AIHW; 2023.
  13. 13. Barban F, Annicchiarico R, Pantelopoulos S, et al. Harnessing virtual reality and augmented reality to combat falls in older adults. Ageing Res Rev. 2020;63:101143.
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