GERIATRICS

Dementia

overview

  • Dementia is a syndrome, not a single disease
  • About 9% of Australians aged ≥65 years have dementia.
  • It involves cognitive impairment severe enough to impair independent daily functioning
  • Alzheimer disease is the most common cause of dementia.

Main principles of care

Guidelines emphasise:

  • Timely diagnosis
  • Supporting people to live well with dementia
  • Delaying functional decline
  • Person-centred care
  • Non-pharmacological approaches first
  • Family and carer support/training

Diagnosis principles

  • Cognitive symptoms should NOT be dismissed as “normal ageing.”
  • Early exploration of symptoms is recommended.

Referral recommendations

Patients with suspected dementia should be referred to:

  • Memory clinics
  • Geriatricians
  • Neurologists
  • Psychiatrist

Key history points

  • Onset of symptoms
  • Rate of progression
  • Cognitive domains affected:
    • Memory
    • Language
    • Executive function
    • Orientation
    • Visuospatial function
    • Attention / concentration
  • Functional impact:
    • ADLs
    • IADLs
    • Medication management
    • Finances
    • Meal preparation
    • Transport
    • Driving
  • Behavioural or psychological symptoms:
    • Agitation
    • Wandering
    • Hallucinations
    • Disinhibition
    • Sleep disturbance
    • Paranoia
  • Mood symptoms, especially depression and anxiety
  • Sleep quality
  • Alcohol or substance use
  • Recent medication changes
  • Anticholinergic or sedative medication burden
  • Falls or gait disturbance
  • Driving safety
  • Financial vulnerability
  • Home safety
  • Carer stress / supports

Collateral history

  • Obtain collateral history from:
    • Family
    • Carer
    • RACF staff
    • Nursing staff
    • Allied health
  • Important because patients may:
    • Minimise symptoms
    • Lack insight
    • Under-report functional decline

Cognitive assessment

  • Use an appropriate validated cognitive screening tool:
    • GPCOG
    • MMSE
    • MoCA
    • Mini-Cog
    • RUDAS
    • KICA, especially for Aboriginal and Torres Strait Islander patients where appropriate
  • Choose tool based on:
    • Language
    • Cultural background
    • Education level
    • Clinical context
    • Sensory impairment

Functional assessment

  • Assess ADLs:
    • Washing
    • Dressing
    • Toileting
    • Feeding
    • Mobility
    • Continence
  • Assess IADLs:
    • Medication management
    • Finances
    • Shopping
    • Cooking
    • Cleaning
    • Telephone use
    • Transport
    • Driving

Mood / delirium screening

Screen for depression

  • Screen for anxiety
  • Screen for delirium, especially if:
    • Acute onset
    • Fluctuating cognition
    • Reduced attention
    • Recent illness
    • Recent medication change
    • Infection risk

Physical examination

  • Neurological examination
  • Gait and balance assessment
  • Cardiovascular examination
  • Nutritional assessment
  • Vision assessment
  • Hearing assessment
  • Falls risk assessment

Initial investigations

  • Medication review
  • FBC
  • UEC / eGFR
  • LFT
  • Calcium
  • Glucose / HbA1c
  • TSH
  • Vitamin B12 / folate
  • Lipids

Additional investigations if clinically indicated

  • ESR / CRP
  • MSU
  • HIV serology
  • Syphilis serology
  • Sleep study
  • Other targeted tests depending on history and examination

Brain imaging

  • Consider CT brain or MRI brain to:
    • Exclude structural pathology
    • Assess vascular burden
    • Assess atrophy pattern
    • Assess for normal pressure hydrocephalus
    • Investigate atypical features
  • Imaging is particularly important if:
    • Young onset
    • Atypical presentation
    • Rapid progression
    • Focal neurological signs
    • Gait disturbance
    • Recent head trauma
    • Anticoagulant use

Management priorities

  • Treat reversible causes
  • Optimise vascular risk factors:
    • BP
    • Diabetes
    • Lipids
    • Smoking
    • Weight
    • Exercise
  • Rationalise medications:
    • Reduce anticholinergic burden
    • Reduce sedatives where possible
    • Review opioids, benzodiazepines, antipsychotics and hypnotics
  • Correct hearing and vision impairment
  • Encourage regular exercise
  • Establish structured routine
  • Encourage meaningful activity
  • Promote social engagement
  • Optimise nutrition and hydration
  • Falls prevention
  • Carer support and education

Safety issues to discuss

  • Driving safety
  • Medication supervision
  • Wandering risk
  • Falls risk
  • Home safety
  • Cooking safety
  • Financial vulnerability
  • Risk of exploitation
  • Need for increased supervision or supports

Future planning

  • Discuss while capacity is retained:
    • Advance care planning
    • Enduring Power of Attorney
    • Substitute decision-maker
    • Future accommodation preferences
    • Goals of care
    • Escalation preferences

Referral indications

  • Consider referral to:
    • Memory clinic
    • Geriatrician
    • Neurologist
    • Old-age psychiatrist
    • Neuropsychologist
  • Refer particularly if:
    • Diagnosis uncertain
    • Young-onset symptoms
    • Atypical presentation
    • Rapid progression
    • Hallucinations
    • Parkinsonism
    • Prominent behavioural symptoms
    • Complex capacity concerns
    • Complex driving concerns
    • Need for formal neuropsychological assessment

Behavioural and psychological symptoms

  • Before attributing symptoms to dementia, assess for:
    • Pain
    • Delirium
    • Constipation
    • Infection
    • Medication adverse effects
    • Environmental triggers
    • Unmet needs
    • Hunger / thirst
    • Sleep disturbance
    • Sensory impairment

Behaviour management approach

  • Use ABC behavioural analysis:
    • A — Antecedent: what happened before?
    • B — Behaviour: what exactly occurred?
    • C — Consequence: what happened after?
  • Use non-pharmacological strategies first:
    • Reassurance
    • Redirection
    • Routine
    • Calm environment
    • Meaningful activities
    • Pain management
    • Sleep optimisation
    • Carer education

Pharmacological treatment

  • Reserve medication for:
    • Severe distress
    • Risk of harm to patient
    • Risk of harm to others
    • Failure of non-pharmacological strategies
  • Before prescribing:
    • Obtain consent or proxy consent where appropriate
    • Document indication clearly
    • Discuss risks and benefits
    • Set review date
    • Have deprescribing plan
  • Antipsychotics:
    • Generally avoid unless clearly indicated
    • Use lowest effective dose
    • Review regularly
    • Attempt deprescribing when stable
    • Use particular caution in:
      • Lewy body dementia
      • Parkinson disease dementia
    • Reason: risk of neuroleptic sensitivity and worsening parkinsonism / cognition.


Common dementia subtypes

  • Alzheimer disease (AD)
  • Vascular dementia (VaD)
  • Dementia with Lewy bodies (DLB)
  • Parkinson disease dementia (PDD)
  • Frontotemporal dementia (FTD)
  • Mixed dementia

Less common causes:

  • Creutzfeldt-Jakob disease – Rapidly progressive dementia, myoclonus, ataxia, visual symptoms, akinetic mutism late
  • Huntington disease – Chorea, psychiatric symptoms, executive dysfunction, family history
  • Wernicke-Korsakoff syndrome – Chorea, psychiatric symptoms, executive dysfunction, family history
  • Normal pressure hydrocephalus – Chorea, psychiatric symptoms, executive dysfunction, family history

DSM-5 dementia criteria

Major neurocognitive disorder requires:

  • Significant cognitive decline
  • Impairment in:
    • Memory
    • Language
    • Learning
    • Other cognitive domains
  • Loss of independence in daily activities:
    • Finances
    • Medication management
    • Complex tasks

Dementia subtypes

Dementia subtypeCourse / timingKey clinical featuresAssociated featuresRisk factorsImaging / biomarkersImportant notes
Alzheimer diseaseInsidious onset. Gradual progression.Early: memory loss, impaired learning.
Later: language deficits, visuospatial impairment.
Depression or apathy early

Behavioural changes later

Poor judgement

Dysphagia and gait disturbance late
Age
APOE-e4
family history
Down syndrome
smoking
hypertension
low activity
traumatic brain injury
MRI/CT: hippocampal and temporoparietal atrophy.

FDG-PET: parietal/temporal hypometabolism.

CSF: amyloid beta may assist diagnosis.
Most common dementia subtype.
Vascular dementiaRelated to cerebrovascular disease.

May show stepwise decline.
Temporal relationship with stroke/TIA.
Executive dysfunction is common.
Mood/personality changes.
Parkinsonian gait or bradykinesia possible.
Hypertension
dyslipidaemia
diabetes
smoking, atrial fibrillation.
MRI/CT: infarcts, white matter disease, generalised atrophy.Pure vascular dementia is uncommon

approximately 12%.

Mixed Alzheimer/vascular pathology is common.
Dementia with Lewy bodiesGradual progression.Core features:
– fluctuating cognition
– parkinsonism
– visual hallucinations
– REM sleep behaviour disorder.
Severe neuroleptic sensitivity
falls
syncope
autonomic dysfunction
delirium episodes.
Older age
often associated with synuclein pathology.
FDG-PET: posterior hypometabolism

DaT scan: abnormal dopamine transporter uptake.
Be cautious with antipsychotics due to neuroleptic sensitivity.
Parkinson disease dementiaDementia develops more than 1 year after established Parkinson motor symptoms.– Bradyphrenia
– inattention
– executive dysfunction
– visuospatial deficits
Hallucinations, anxiety/depression, REM sleep disorder, daytime somnolence.Established Parkinson disease.DaT scan: abnormal.

FDG-PET: posterior hypometabolism.
Distinguished from DLB by timing:
Parkinson motor symptoms precede dementia by more than 1 year.
Frontotemporal dementiaInsidious onset. Gradual progression.
Often presents earlier than AD,
commonly age 56–65 years.
Behavioural variant:
– disinhibition
– apathy
– loss of empathy
– compulsive behaviour
– hyperorality
– dietary changes.

Primary progressive aphasia:
– word-finding difficulty
– speech/language impairment- grammar/comprehension deficits.
May overlap with progressive supranuclear palsy
corticobasal degeneration
or
motor neuron disease.
Family history/genetic forms more common than in AD;
younger age of onset.
MRI/CT: frontal and/or temporal lobe atrophy. FDG-PET: frontal/temporal hypometabolism.Memory may be relatively preserved early, especially in behavioural variant FTD

Differential diagnoses of dementia

CategoryExamplesKey distinguishing features
Primary neurodegenerativeAlzheimer disease
DLB
FTD
Parkinson disease dementia
Huntington disease
Progressive decline
subtype-specific pattern
VascularMulti-infarct dementia
strategic infarct
chronic small vessel disease
Stroke/TIA history
vascular risks
focal neurology
executive dysfunction
DeliriumInfection
dehydration
hypoxia
pain
constipation
medication toxicity
Acute onset
fluctuating course
impaired attention
altered consciousness
PsychiatricDepression/pseudodementia
severe anxiety
psychosis
Mood symptoms prominent
cognitive effort may fluctuate
may coexist with dementia
Medication/substanceBenzodiazepines
opioids
anticholinergics
sedatives
alcohol
illicit substances
Temporal link to medications/substances
may improve with rationalisation
Metabolic/endocrineHypothyroidism
calcium abnormality
renal/hepatic impairment
hypoglycaemia/hyperglycaemia
Systemic symptoms
abnormal blood tests
NutritionalB12
folate
thiamine deficiency
Neuropathy
ataxia
macrocytosis
malnutrition
alcohol risk
InfectiousHIV
neurosyphilis
prion disease
rapid progression
neurological signs
Structural intracranialSubdural haematoma
tumour
normal pressure hydrocephalus
Head trauma
anticoagulation
focal neurology
headache
gait/incontinence
TraumaticChronic traumatic encephalopathy
repeated head injury
History of repeated concussion/head trauma
Genetic/metabolic rare causesWilson disease
mitochondrial cytopathies
leukodystrophies
Younger onset
family history
movement disorder
multisystem features

“4 Ds” not to miss

DMeaningClinical clue
DementiaChronic progressive cognitive and functional declineMonths to years, progressive impairment
DeliriumAcute fluctuating disturbance in attention/awarenessHours to days, fluctuating, medically unwell
DepressionMood disorder causing cognitive symptomsLow mood, anhedonia, poor sleep/appetite, low motivation
DrugsMedication/substance-related cognitive impairmentRecent medication change, sedatives, anticholinergics, opioids, alcohol

Modifiable protective and risk factors for dementia

Protective factors for dementia: Strengthening, building cognitive reserve
Early life
– Healthy pregnancy
– Secure home environment
– Good diet
– Good hearing and language acquisition
– Strong development and engagement in education and learning
Middle and later life Social and cultural connection
– Healthy lifestyle
– Good diet and healthy weight
– Smoking cessation
– Regular physical activity
– Safe alcohol consumption
– Education and employment
– Cognitive stimulation
Risk factors for dementia: Damaging, reducing or limiting cognitive reserve
Childhood and adolescence Childhood trauma and early life adversityA
– Middle ear disease and hearing impairment
– Low level of education
– Smoking
Middle life Hearing impairment A
– Hypertension A
– Other cardiovascular risk factors including atrial fibrillation, dyslipidaemia
– Smoking
– Diabetes
– Obesity
– Psychosocial stressors
– Excessive alcohol intake
– Traumatic brain injury
– Air pollution
– Low physical activityA
– Chronic kidney diseaseA
Later life StrokeA
– History of head traumaA
– Epilepsy
– Delirium
– History of depression/chronic grief
– Social isolation/loneliness
– Physical inactivity
– Anticholinergic medicationsA
– PolypharmacyA
– Vision problemsA
AThese factors have been derived from cohort studies in the Kimberley, Far North Queensland and urban and regional New South Wales.3–5
other:
Apo E4 Allele: Confers 8% risk if two Alleles

Differentiate normal ageing, MCI, dementia, delirium and depression

Normal ageing

Features may include:

  • Occasional forgetfulness
  • Slower recall
  • Misplacing items occasionally
  • Remembering later
  • No progressive functional decline
  • Independent with ADLs and IADLs

Normal ageing should not cause major impairment in:

  • Medication management
  • Finances
  • Cooking
  • Driving
  • Personal care
  • Safety awareness

Mild Cognitive Impairment

MCI suggests:

  • Modest cognitive decline
  • Symptoms greater than expected for age
  • Patient may rely more on notes, reminders, family prompts, or phone alerts
  • Independence is largely preserved
  • Complex activities can still be performed, though may require more effort or compensatory strategies

MCI may:

  • Progress to dementia
  • Remain stable
  • Improve if reversible factors are treated
  • Review patients with MCI after 6–18 months, or sooner if there is progression.

Dementia / Major Neurocognitive Disorder

Dementia is more likely when there is:

  • Significant acquired decline in cognition
  • Decline in one or more domains:
    • Memory
    • Language
    • Learning
    • Attention
    • Executive function
    • Visuospatial ability
    • Judgement
  • Functional impact affecting independence
  • Need for help with complex daily tasks such as:
    • Paying bills
    • Managing medications
    • Shopping
    • Cooking
    • Transport
    • Appointments
    • Safe driving

Delirium

Consider delirium if symptoms are:

  • Acute or subacute
  • Fluctuating over hours to days
  • Associated with impaired attention
  • Worse at night
  • Associated with infection, dehydration, pain, constipation, medication change, urinary retention, hypoxia, metabolic disturbance, or recent hospitalisation

Features:

  • Inattention
  • Altered level of consciousness
  • Disorganised thinking
  • Perceptual disturbance
  • Sleep-wake disturbance
  • Hyperactive, hypoactive, or mixed presentation

Delirium is a medical emergency and should be actively excluded before diagnosing dementia.

Depression-related cognitive impairment

Consider depression if:

  • Low mood
  • Anhedonia
  • Sleep/appetite disturbance
  • Psychomotor slowing
  • Poor motivation
  • Excessive guilt or hopelessness
  • Subjective memory complaints
  • “I don’t know” answers on testing
  • Symptoms coincide with mood decline

Depression can mimic or worsen cognitive impairment and is a reversible or treatable contributor. Mood assessment is important because depression and other mood disorders can cause memory problems and symptoms overlapping with dementia



History-taking

Patient history

Onset and time course

Ask:

  • When did symptoms start?
  • Was onset sudden or gradual?
  • Has it been progressive, stepwise, fluctuating, or stable?
  • Any acute deterioration?
  • Any recent infection, fall, head injury, hospitalisation, medication change, or bereavement?

Interpretation:

  • Gradual progressive decline → Alzheimer disease, Lewy body dementia, Parkinson disease dementia, frontotemporal dementia
  • Stepwise decline → vascular dementia
  • Fluctuating cognition → delirium or Lewy body dementia
  • Rapid progression → urgent specialist assessment; consider delirium, malignancy, autoimmune, prion disease, infection, subdural, medication/toxic causes

Cognitive domains

Ask specifically about:

Memory

  • Forgetting recent conversations
  • Repeating questions
  • Misplacing items
  • Forgetting appointments
  • Difficulty learning new information
  • Getting lost in familiar places

Language

  • Word-finding difficulty
  • Losing train of thought
  • Difficulty following conversations
  • Reduced vocabulary
  • Comprehension problems

Executive function

  • Planning problems
  • Difficulty organising tasks
  • Poor problem solving
  • Difficulty using appliances
  • Trouble managing medications or finances
  • Reduced ability to multitask

Attention and concentration

  • Easily distracted
  • Difficulty following TV, reading, conversations
  • Fluctuating alertness

Visuospatial function

  • Getting lost
  • Difficulty parking
  • Trouble judging distances
  • Problems dressing
  • Difficulty reading maps or using familiar routes

Judgement and insight

  • Poor financial decisions
  • Scams
  • Unsafe driving
  • Leaving stove on
  • Reduced awareness of deficits

Medical history

1. Relevant medical comorbidities

Ask about conditions that may cause, mimic, worsen, or increase the risk of cognitive decline.

DomainConditions to ask aboutWhy it matters
NeurologicalStroke/TIA
Parkinson disease
epilepsy/seizures
head injury
CNS infection
brain tumour
Vascular dementia
Parkinson disease dementia
seizure-related confusion
post-traumatic cognitive impairment
Cardiovascular / vascular riskHypertension, diabetes, dyslipidaemia, atrial fibrillation, ischaemic heart disease, peripheral vascular diseaseMajor risk factors for vascular cognitive impairment and mixed dementia
PsychiatricDepression
anxiety
bipolar disorder
psychosis
previous psychiatric admissions
Depression/anxiety can mimic or worsen cognitive symptoms — “pseudodementia”
Respiratory / sleepObstructive sleep apnoea
COPD
chronic hypoxia
Fatigue, poor attention, impaired concentration
Endocrine / metabolicThyroid disease
B12 deficiency
diabetes
renal disease
liver disease
Potentially reversible contributors
Recent illness / surgeryRecent hospital admissio
anaesthetic
surgery
infection
fall
delirium episode
May suggest delirium or cognitive step-down after acute illness

Look for reversible contributors

Screen for factors that may worsen cognition or mimic dementia.

Screen for:

  • Pain
  • Infection
  • Constipation/urinary retention
  • Hearing or vision impairment
  • Sleep disturbance
  • Dehydration/malnutrition
  • Alcohol/substance use
  • Recent stressors or bereavement

Questions:

  • “Any fevers, cough, dysuria?”
  • “Any pain affecting sleep or concentration?”
  • “Any hearing or vision problems?”
  • “How is your sleep?”

Delirium Screen — Must Exclude

Look for acute/subacute change:

  • Acute deterioration
  • Fluctuating confusion
  • Fever/infection
  • Dysuria/cough
  • Dehydration
  • Recent admission/surgery
  • Medication changes

Key point:
Acute + fluctuating confusion = delirium until proven otherwise.

Falls / Gait / Frailty

Ask about:

  • Falls
  • Slower walking
  • Tremor/stiffness
  • Shuffling gait
  • Incontinence
  • Weight loss/frailty
PatternThink about
Cognitive decline + gait disturbance + urinary incontinenceNormal pressure hydrocephalus
Cognitive decline + tremor/stiffness/slownessParkinson disease dementia / Lewy body dementia
Cognitive decline + falls + vascular risk factorsVascular dementia / mixed dementia
Cognitive decline + weight loss + weakness + reduced activityFrailty, malignancy, depression, systemic disease

Behavioural changes and BPSD

Behavioural symptoms are common in dementia. The key clinical task is to distinguish:

  1. Gradual behavioural/personality change from dementia progression,
  2. Behavioural and Psychological Symptoms of Dementia — BPSD, where symptoms are distressing, disruptive, triggered, or require active management. (see management section)

These are usually gradual, persistent changes caused by neurodegeneration.

They may reflect the dementia subtype. For example:

Dementia subtype / patternBehavioural clues
Alzheimer diseaseApathy, anxiety, irritability later
Frontotemporal dementiaDisinhibition, loss of empathy, apathy, compulsive behaviour, dietary change
Dementia with Lewy bodiesVisual hallucinations, fluctuating cognition, REM sleep behaviour disorder, sensitivity to antipsychotics
Vascular dementiaExecutive dysfunction, emotional lability, apathy, gait disturbance

Medication review

Medication history is essential because many medicines can cause confusion, sedation, falls, delirium, or worsen cognition.

Medication groupExamplesCognitive concern
BenzodiazepinesDiazepam, temazepam, oxazepam, alprazolamSedation, falls, delirium, memory impairment
Sleeping tabletsZopiclone, zolpidem, sedating antihistaminesSedation, impaired alertness, falls
AnticholinergicsOxybutynin, amitriptyline, promethazine, some antihistaminesConfusion, constipation, urinary retention, delirium
OpioidsOxycodone, morphine, tapentadol, fentanylSedation, delirium, constipation, falls
AntidepressantsTCAs, mirtazapine, SSRIs/SNRIsSedation, hyponatraemia, anticholinergic burden, interactions
AntipsychoticsQuetiapine, risperidone, olanzapineSedation, extrapyramidal effects, falls, anticholinergic effects
Antiepileptics / neuropathic pain agentsPregabalin, gabapentin, valproate, levetiracetamSedation, dizziness, mood/cognitive effects
AlcoholRegular or heavy intakeCognitive impairment, falls, liver disease, Wernicke-Korsakoff risk

Mood screen — depression / “pseudodementia”

Screen for depression/anxiety (“pseudodementia”):

  • Low mood
  • Loss of enjoyment
  • Poor sleep
  • Appetite change
  • Low energy
  • Hopelessness

Question:

  • “Have you been feeling down or losing interest in things?”

Safety Assessment

Ask about:

  • Driving
  • Falls
  • Medication errors
  • Leaving stove on
  • Wandering
  • Living alone
  • Financial vulnerability
  • Aggression/disinhibition

Social & Support History

  • Who lives with them?
  • Carers/family support?
  • My Aged Care/home services?
  • transport
  • ADLs/IADLs?
  • Advance care planning/EPOA?

Collateral History — Essential

Ask family/carers about:

  • Timeline (acute vs gradual vs fluctuating)
  • Functional decline
  • Personality change
  • Wandering/aggression
  • Hallucinations/paranoia
  • Safety concerns
  • Carer stress


Cognitive Screening Tools

ToolMain purposeKey scoring / interpretationStrengthsLimitations / cautions
GPCOG General Practitioner Assessment of CognitionPrimary care cognitive screening toolPatient section scored out of
9. 9 = cognitive impairment unlikely.
5–8 = do informant section.
0–4 = cognitive impairment likely.

Informant section scored out of 6;
≤3 suggests impairment.
Original validation: sensitivity about 85%, specificity about 86%.
Designed for general practice.
Quick. Includes collateral history via informant section.
Includes clock drawing.
Screening tool only.
Abnormal result requires full clinical assessment, collateral history, medication review, delirium/depression exclusion, pathology ± imaging.
SMMSE / MMSE Standardised Mini-Mental State ExaminationGeneral cognitive screening and monitoringScored out of 30. Traditional severity guide:
21–24 mild
10–20 moderate
<10 severe
but cut-offs vary by age, education, language and setting.
Widely known

useful for serial monitoring if same version used.
Less sensitive for early dementia, mild cognitive impairment, and executive dysfunction.

Affected by education, literacy, language and culture.

RACGP lists SMMSE as an option, but it should not be used alone to diagnose dementia.
Clock Drawing TestBrief screen of executive function, planning and visuospatial abilityNo single universal scoring system.

Often used as part of GPCOG or Mini-Cog.
Very quick.
Helpful for executive/visuospatial impairment.
Not a comprehensive cognitive test.

Does not adequately assess memory, language, orientation or functional impact. Should not be used alone.
RUDAS Rowland Universal Dementia Assessment ScaleCognitive screening, especially for culturally and linguistically diverse patientsScored out of 30.

Commonly used cut-off around ≤22 for possible major neurocognitive disorder;

some studies use ≤23 or other thresholds depending on setting.
Designed to minimise effects of language, culture and education compared with MMSE.

Good option when English is not first language or education level affects testing.
Still a screening tool. Interpret cautiously if physical disability, sensory impairment, interpreter issues or acute illness affect performance.
KICA Kimberley Indigenous Cognitive AssessmentCulturally appropriate cognitive assessment for Aboriginal and Torres Strait Islander people, especially rural/remote contextsKICA-Cog scored out of 39.

Some sources use ≤33/39 as possible dementia requiring further assessment;

original validation reported strong sensitivity/specificity using cut-offs around 31/32, with later work supporting higher cut-offs in some populations.
Developed and validated for older Indigenous Australians;
incorporates culturally appropriate items and informant components.
Use the correct version and local guidance.

Not a generic test for all populations.
Requires culturally safe administration and collateral history.
MoCA Montreal Cognitive AssessmentCognitive screen with stronger coverage of executive function and mild cognitive impairmentScored out of 30.

Traditional cut-off <26 suggests impairment, but specificity can be low in older or lower-education populations.
More sensitive than MMSE for MCI/executive dysfunction.Can over-call impairment if education/language/culture not considered. Licensing/training requirements may apply. Not always the first GP tool.

Behaviour, mood and BPSD tools — not cognitive screening tools

ToolWhat it assessesHow to use clinically
NPI / NPI-Q / NPI-NH Neuropsychiatric InventoryBehavioural and psychological symptoms of dementia: delusions
hallucinations
agitation
depressio
anxiety
apathy
disinhibition
irritability
aberrant motor behaviour
sleep and appetite symptoms.
Useful for documenting BPSD severity, carer distress, RACF behavioural monitoring, and response to non-pharmacological or medication interventions.

NPI scoring commonly uses frequency × severity, with caregiver distress also recorded.
Cornell Scale for Depression in DementiaDepression symptoms in people with dementia, using patient and informant input.Scores
<6 generally suggest no significant depressive symptoms;

>10 suggests probable major depression;

>18 suggests definite major depression.

Useful because depression can mimic or worsen cognitive impairment.
BEHAVE-ADBehavioural pathology in Alzheimer disease, including delusions, hallucinations, activity disturbance, aggression, diurnal rhythm disturbance, affective disturbance and anxiety/phobias.Useful in specialist/research/RACF contexts for BPSD severity and treatment response. Less commonly used in routine Australian GP practice than NPI-type tools.

Risk prediction tools — not diagnostic tools

ToolPurposeKey point
UKBDRS UK Biobank Dementia Risk ScoreEstimates future dementia risk, not current cognitive impairment.Includes age, education, parental dementia, deprivation, diabetes, stroke, depression, hypertension, hypercholesterolaemia, sex and living situation. It was developed in UK cohorts and should be used cautiously outside validated populations. It does not diagnose dementia and does not replace clinical assessment.

Investigations

Routine Baseline Investigations

InvestigationPurpose
FBCExclude anaemia, infection, haematological disease
EUC / renal functionExclude metabolic disturbance, renal failure, dehydration
Glucose / HbA1cDetect hypo/hyperglycaemia, diabetes
CalciumExclude hypercalcaemia/hyperparathyroidism
LFTsExclude hepatic dysfunction
TFTsExclude hypothyroidism or thyrotoxicosis
Vitamin B12 and folateDetect nutritional deficiency
LipidsAssess vascular risk factors
Cognitive screening (GPCOG, MMSE, MoCA, RUDAS)Assess cognitive domains

Inflammatory / Infective Tests

InvestigationWhen to consider
ESR / CRPSuspected inflammatory, autoimmune, infective or malignant process
MSU / urine MCSIf delirium or urinary symptoms present
HIV / syphilis serologyYoung onset, atypical presentation, risk factors

Imaging

CT Brain

Common first-line imaging in many GP settings.

Consider if:
  • onset age <60,
  • rapid progression,
  • focal neurological signs,
  • seizures,
  • recent head trauma,
  • anticoagulant use,
  • gait disturbance,
  • atypical presentation,
  • diagnostic uncertainty.
Helps exclude:
  • tumour,
  • subdural haematoma,
  • hydrocephalus,
  • stroke,
  • significant cerebrovascular disease.

MRI Brain

More sensitive than CT for:

  • hippocampal atrophy,
  • vascular disease,
  • white matter disease,
  • frontotemporal changes,
  • atypical dementias.
Consider when:
  • subtype unclear,
  • young-onset dementia,
  • rapid decline,
  • focal neurological signs,
  • atypical symptoms.

score in MRI

MRI findingMay be normal ageingMore concerning for pathology
Mild cortical volume lossCommon with ageingModerate/severe or disproportionate atrophy
Mild medial temporal atrophyCan occur with ageMarked MTA, especially if young or symptomatic
Scattered punctate white matter lesionsCommon in older adultsConfluent lesions, lacunes, microbleeds, strategic infarcts
Mild ventricular enlargementCan occur with atrophyDisproportionate ventriculomegaly, gait disturbance, urinary symptoms — consider NPH
Mild small vessel diseaseCommon with age/vascular riskExtensive Fazekas 2–3 burden with executive dysfunction or gait decline
1. GCA Scale — Global Cortical Atrophy

Assesses overall cortical atrophy, usually based on sulcal widening and gyral volume loss.

GradeDescription
0No cortical atrophy
1Mild cortical atrophy
2Moderate cortical atrophy
3Severe cortical atrophy

Interpretation:

  • Mild GCA may be seen with normal ageing.
  • Moderate to severe GCA may support neurodegenerative disease if consistent with clinical symptoms.
  • Asymmetrical or regional atrophy may suggest specific dementia patterns, for example frontotemporal dementia.
2. MTA Scale — Medial Temporal Lobe Atrophy

Assesses hippocampal and medial temporal lobe atrophy.

GradeDescription
0No atrophy
1Only widening of choroid fissure
2Widening of choroid fissure and temporal horn; mild hippocampal volume loss
3Moderate hippocampal volume loss
4Severe hippocampal volume loss

Interpretation:

  • MTA is particularly relevant in suspected Alzheimer disease.
  • Higher MTA scores are more concerning in younger patients.
  • In older patients, some medial temporal atrophy can occur with ageing, so interpretation should be age-adjusted.
  • Bilateral MTA supports Alzheimer-type pathology, but is not diagnostic alone.
3. Fazekas Scale — White Matter Lesions

Grades white matter hyperintensities due to chronic small vessel ischaemic change.

GradeDescription
0No white matter lesions
1Punctate white matter lesions
2Early confluent white matter lesions
3Large confluent white matter lesions

Interpretation:

  • Fazekas 1 is common with ageing and vascular risk factors.
  • Fazekas 2–3 suggests more significant small vessel disease.
  • Higher scores may support vascular cognitive impairment or mixed dementia, especially with hypertension, diabetes, dyslipidaemia, smoking, stroke/TIA history or gait disturbance.

ECG

Consider especially before prescribing:

  • donepezil,
  • rivastigmine,
  • galantamine.

Reason:

  • acetylcholinesterase inhibitors may worsen:
    • bradycardia,
    • conduction disease,
    • syncope risk.

EEG

Not routine.

Consider only if:

  • seizures suspected,
  • episodic confusion,
  • delirium,
  • Creutzfeldt–Jakob disease,
  • encephalitis,
  • atypical fluctuating states.

Specialist / Advanced Investigations

InvestigationComments
CSF examinationSpecialist referral only
useful in
– rapidly progressive dementia
– CNS infection
– CJD
– NPH
– Alzheimer biomarkers
Fasting homocysteineif investigating B12/folate-related metabolic concerns. Elevated homocysteine is associated with vascular disease and cognitive decline, but routine testing rarely changes GP management.
FDG-PET / amyloid PET / tau PETDifficult diagnostic cases; limited availability
Neuropsychological assessmentProvides detailed assessment beyond screening tests such as GPCOG, MMSE, MoCA or RUDAS.
Useful for subtle cognitive impairment, high premorbid functioning, diagnostic uncertainty, differentiating dementia from psychiatric illness, capacity disputes, medico-legal issues, or monitoring progression.
Usually requires several hours and specialist referral.
Genetic testingEarly-onset dementia with strong family history
ApoE genotypingNot routinely recommended clinically

Management

Principles of Management

Management should be:

  • Regularly reviewed and adjusted over time
  • Person-centred
  • Function-focused
  • Safety-focused
  • Carer-inclusive
  • Culturally appropriate
  • Based on the patient’s values, goals, and preferences
  • Non-pharmacological first-line where possible

Treat Reversible or Contributing Factors

Assess and manage potentially reversible contributors:

  • Delirium
  • Depression/anxiety
  • Medication adverse effects
  • Anticholinergic burden
  • Alcohol/substance use
  • Sleep disorders (e.g. OSA)
  • Pain
  • Infection
  • Constipation
  • Hearing or vision impairment
  • Vitamin B12/folate deficiency
  • Thyroid dysfunction
  • Metabolic abnormalities

Optimise Vascular Risk Factors

Particularly important in vascular and mixed dementia.

Manage:

  • Hypertension
  • Diabetes
  • Dyslipidaemia
  • Smoking
  • Obesity
  • Sleep apnoea
  • Atrial fibrillation
  • Sedentary lifestyle

Encourage:

  • Physical activity
  • Mediterranean-style diet
  • Cognitive stimulation
  • Social engagement
  • Good sleep hygiene

💊 Medication Management

Rationalise Medications

Avoid or minimise:

  • Anticholinergics
  • Benzodiazepines
  • Sedatives/hypnotics
  • CNS depressants
  • Polypharmacy where possible

Goals:

  • Reduce falls
  • Reduce delirium risk
  • Improve cognition/function
  • Improve medication adherence

Consider:

  • Webster/blister packing
  • Supervised medication administration
  • Community pharmacy support

Regular Medication Reviews

Review for:

  • Adverse effects
  • Drug interactions
  • Ongoing indication
  • Adherence difficulties

Monitor and optimise comorbidities:

  • Diabetes
  • Hypertension
  • Cardiovascular disease
  • COPD
  • Chronic pain

🏠 Home Safety

Assess:

  • Falls risk
  • Wandering
  • Medication errors
  • Kitchen/fire safety
  • Financial vulnerability
  • Self-neglect

Consider:

  • Occupational therapist home assessment
  • Cognitive assessment
  • Driving review if required
  • Calm, safe, structured environment with appropriate stimulation

👥 Psychosocial and Support Services

Refer to:

  • Dementia Australia
  • Social worker
  • ACAT
  • Allied health:
    • OT
    • physiotherapy
    • dietitian
    • speech pathology

Supports may include:

  • Respite
  • Home care
  • Residential care assessment
  • Care coordination

📞 Dementia Support Services

Dementia Australia

National Dementia Helpline:
📞 1800 100 500

Provides:

  • Education
  • Counselling
  • Behavioural advice
  • Service navigation

Dementia Behaviour Management Advisory Service (DBMAS)

📞 1800 699 799

Provides specialised support for:

  • Moderate–severe BPSD
  • Crisis behavioural management
  • RACF behavioural support

Carers Australia

Provides:

  • Carer advocacy
  • Counselling
  • Education
  • Respite support

My Aged Care

Gateway to:

  • Home care packages
  • Respite
  • ACAT assessment
  • Residential care
  • Community supports

👨‍👩‍👧 Carer Support

Support for caregivers may include:

  • Carer training programs
  • Respite services
  • Counselling
  • Support groups
  • Education
  • Carer allowance/pension guidance

Regularly assess:

  • Burnout
  • Depression/anxiety
  • Physical health
  • Social isolation

📚 Education

Provide education to patient, family, and caregivers about:

  • Dementia progression
  • Behavioural symptoms
  • Communication strategies
  • Safety planning
  • Future planning

Encourage:

  • Social connection
  • Cognitive stimulation
  • Physical activity
  • Healthy diet
  • Structured routines

Use resources from:

  • Dementia Australia

📝 Legal and Advance Care Planning

Address early while capacity remains intact where possible.

Discuss:

  • Enduring Power of Attorney
  • Enduring Guardian arrangements
  • Advance Care Directive
  • Will and financial planning
  • Substitute decision-maker details
  • Goals of care

Preferences regarding:

  • Hospital transfer
  • CPR
  • Artificial feeding
  • Antibiotics
  • Palliative approach

Also discuss:

  • Consent to involve carers/family
  • Medication supervision if cognition declines

Capacity Principles

Capacity is:

  • Decision-specific
  • Time-specific
  • Functional
  • Not determined by diagnosis alone
  • Not determined solely by MMSE/MoCA score

Assess ability to:

  1. Understand information
  2. Retain information
  3. Use/weigh information
  4. Communicate a choice

Complex cases may require:

  • Neuropsychology
  • Psychiatry
  • Geriatric medicine
  • MDT assessment

Ongoing Monitoring

Regular review should include:

  • Cognitive function
  • Behavioural symptoms
  • Functional capacity
  • Physical health
  • Nutrition and weight
  • Medication adherence
  • Falls risk
  • Carer burden
  • Safety concerns
  • Capacity
  • Goals of care

Frequency depends on:

  • Severity
  • Rate of progression
  • Complexity
  • Support needs

Stable patients may be reviewed every 6–12 months, while complex or rapidly progressive cases may require much more frequent review

Non-Pharmacological Management of Dementia / Cognitive Impairment

Non-pharmacological interventions are first-line for behavioural symptoms, functional decline, anxiety/agitation, sleep disturbance, and carer distress.

DomainInterventionExamples / Practical StrategiesPurpose / Benefits
General principleNon-pharmacological management first-lineUse before medications where possible
– especially for BPSD
Reduces behavioural symptoms, distress, agitation, sleep disruption, and carer burden
Frequent orientation reinforcementOrientation cues and repeated reassuranceLarge clocks
calendars
orientation boards
repeated introductions by staff/carers
Supports orientation, reduces confusion, improves sense of safety
Staff communication strategiesVisible name badges
regular re-introduction
simple and clear communication
Builds familiarity, reduces anxiety, improves engagement
Calm, familiar environmentMaintain predictable surroundingsPredictable routines
familiar rooms
low-stress environment
Reduces agitation, confusion, and distress
Reduce environmental triggersMinimise noise
overstimulation
frequent room changes
Helps prevent behavioural escalation and sundowning
Clear signageVisual navigation supportsLarge labels
pictures/icons
simple wording
Improves navigation, independence, and confidence
Orientation aidsSigns for bedroom
bathroom
dining room
activity areas
Reduces wandering, confusion, and dependence
Colour contrastsUse contrast for key objectsContrasting colours for doors
toilet seats
handrails
furniture
Improves visual recognition, safety, and mobility
Falls prevention supportClearly visible edges
rails
seating
bathroom fixtures
Reduces falls risk and improves environmental awareness
Good lightingOptimise lightingNatural daylight
even lighting
night lights where appropriate
Supports sleep–wake cycle, reduces confusion and falls
Avoid problematic lightingAvoid shadows
glare
harsh fluorescent lighting
Reduces misperceptions, agitation, and visual confusion
Uncluttered spacesSimplify layoutReduce excess furniture
visual clutter
complex room layouts
Improves mobility and reduces falls/confusion
Safe walking areasClear pathways
remove obstacles
Promotes independence and safer mobility
Familiar objectsPersonalised environmentFamily photographs
personal items
familiar music/artwork
Supports identity, comfort, memory, and emotional security
Reminiscence supportMeaningful objects
familiar scents
music
photos
May reduce distress and improve connection
Adaptive furniture and safetySafe and accessible furnitureStable
comfortable
accessible chairs/beds/tables
Supports independence, transfers, and comfort
Environmental safety measuresHandrails
grab rails
non-slip flooring
removal of trip hazards
Falls prevention and safer mobility
Quiet / low-stimulation areasCalming spacesQuiet room
low lighting
reduced noise
minimal activity
Useful for agitation, sundowning, anxiety, and sensory overload
Memory aidsPractical cognitive supportsLabelled drawers
reminder notes
medication prompts
daily planners
Supports independence, routine, and task completion
Adaptable spacesModify environment as needs changeAdapt for mobility decline
supervision needs
continence needs
behavioural changes
Maintains safety and function as dementia progresses
Technology integrationAssistive technologyGPS trackers
medication reminders
smart home monitoring
fall alarms
Enhances safety and monitoring
Ethical balanceBalance safety
privacy
autonomy
and dignity
Avoids overly restrictive or intrusive care

Alternative and Sensory Therapies

TherapyExamplesPotential Benefits
Massage and aromatherapyGentle massage, calming scents such as lavender where appropriateMay reduce anxiety, promote relaxation, and improve sleep
Music therapyPersonalised familiar music, singing, rhythm activitiesImproves mood, engagement, memory stimulation, and social interaction
Dance / movement therapyGentle dancing, seated movement, rhythm-based activityPromotes engagement, mobility, enjoyment, and social participation
Animal-assisted therapyVisits from trained therapy animals, supervised pet interactionMay improve emotional wellbeing, reduce loneliness, and encourage interaction
Multi-sensory stimulationLight, sound, touch, smell-based activitiesMay improve relaxation, emotional regulation, and engagement

Cognitive Enhancer Medications

General Principles

  • Avoid or minimise CNS-active medications that may worsen cognition (e.g. anticholinergics, sedatives).
  • Treat comorbid mood and sleep disorders cautiously and symptomatically:
    • Depression: Consider non-anticholinergic antidepressants (e.g. SSRIs like sertraline, escitalopram).
    • Anxiety/insomnia: Use short-acting benzodiazepines (e.g. oxazepam) only for short-term use, due to risks of confusion, falls, dependence.

Acetylcholinesterase Inhibitors (AChE-Is)

Mechanism of Action
  • Inhibit the enzyme that breaks down acetylcholine, enhancing cholinergic transmission in the brain.
  • Aimed at temporarily stabilising or improving cognition, behaviour, and function in Alzheimer’s disease (AD).
Indications
  • PBS-subsidised for mild to moderate Alzheimer’s disease (specialist-confirmed diagnosis required).
  • Not PBS-listed for other types of dementia (e.g. Lewy body, vascular), although clinical trials suggest potential benefit in some cases.
  • If ineffective or poorly tolerated, switching agents may be beneficial
Common Agents
DrugFormulationDosage Range
Donepezil (Aricept)Oral tablets5–10 mg daily
Galantamine (Galantyl)Extended-release capsules8–24 mg daily
Rivastigmine (Exelon)Transdermal patch4.6–9.6 mg/24 hours

Contraindications:

  • Gastrointestinal or ureteric obstruction
  • Active peptic ulcer disease
Expected Effects
  • Individual response varies:
    • Some patients experience mild cognitive or functional improvements.
    • Others may remain stable (delaying expected decline).
    • A proportion will derive no clinical benefit.
  • Improvements may occur in:
    • Memory and attention
    • Daily functioning
    • Behavioural and psychological symptoms (e.g. apathy, agitation)
Side Effects
  • Common: Nausea, vomiting, diarrhoea, anorexia, muscle cramps, dizziness, insomnia
  • Other: Bradycardia, hypotension, falls
Mitigation Strategies
  • Initiate at low dose and titrate slowly
  • Administer with food to reduce GI symptoms
  • Consider switching agents if one is not tolerated
Monitoring
  • Bradycardia (especially in those on beta-blockers or other rate-limiting medications)
  • GI bleeding (particularly with NSAIDs)
  • Weight loss or malnutrition
  • Clinical response via cognitive and functional tools (e.g. MMSE, ADLs)

Memantine (NMDA Receptor Antagonist)

Mechanism of Action
  • Modulates glutamatergic activity by blocking NMDA receptors — aims to protect neurons from excitotoxicity.
Indications
  • PBS-subsidised for moderately severe Alzheimer’s disease (MMSE 10–14), or intolerance/contraindications to AChEIs.
  • Specialist confirmation of diagnosis required
  • Off-label: Potential benefit in mild to moderate AD and vascular dementia (not PBS-listed)
Contraindications: History of seizures

Benefits

  • May improve:
    • Cognition
    • Function
    • Behavioural symptoms (e.g. aggression)
  • Often better tolerated than AChE inhibitors
Dosing
  • Oral formulation (e.g. Ebixa): typically titrated to 20 mg daily
  • Dose adjustment required in renal impairment
Side Effects
  • Generally well tolerated
  • Adverse effects: dizziness, constipation, confusion, hypertension
  • Rare: bradycardia, syncope
Monitoring
  • 30–50% of patients show modest benefit, a small proportion may have significant benefit.
  • Monitor for:
    • Improvements or stability in cognition, activities of daily living (ADLs), or behavioural symptoms.
  • No need for regular blood tests to monitor drug levels.
  • PBS requires ongoing clinical benefit to continue subsidised treatment.
Discontinuation Consideration:

Trial withdrawal (via gradual dose reduction) may be appropriate if:

  • No observed benefit after ≥12 months
  • Progressive deterioration
  • Severe/end-stage disease

Summary: PBS Access to Pharmacological Therapies in Dementia (Australia)

DrugPBS Status
Donepezil, Galantamine, RivastigmineMild to moderate Alzheimer’s disease (specialist confirmed)
MemantineModerate to severe Alzheimer’s disease (specialist confirmed)
RisperidoneBPSD in moderate to severe AD (up to 12 weeks only)

Behavioural and Psychological Symptoms of Dementia — BPSD

BPSD refers to non-cognitive symptoms of dementia that cause distress, disruption, safety concerns, carer burden, or require active management.

BPSD often arises from a combination of:

ContributorExamples
NeurodegenerationFrontal/temporal dysfunction, impaired impulse control
Environmental triggersHospitalisation, unfamiliar settings, noise, overstimulation, change in routine
Unmet physical needsPain, hunger, thirst, toileting, constipation, urinary retention
Unmet emotional needsLoneliness, fear, boredom, frustration
Communication barriersUnable to express pain, discomfort, fear, or confusion
Care approachRushed care, unfamiliar carers, lack of explanation, personal care distress
Medical illnessInfection, delirium, dehydration, hypoxia, medication toxicity

Clinical domains of BPSD

DomainFeatures to ask about
Mood symptomsDepression, low mood, anxiety, emotional lability, tearfulness
Psychotic symptomsDelusions, paranoia, theft accusations, persecution ideas, hallucinations — often visual
Sleep disturbanceInsomnia, fragmented sleep, day/night reversal, daytime drowsiness
AgitationRestlessness, pacing, shouting, irritability, sundowning
AggressionVerbal aggression, physical aggression, threats, striking out
Resistance to careRefusing showering, medications, meals, personal care
DisinhibitionSocially inappropriate behaviour, sexual disinhibition, impulsivity
WanderingExit-seeking, getting lost, repetitive walking
Apathy / withdrawalReduced motivation, reduced engagement, social withdrawal
Repetitive behavioursRepeated questions, checking, calling out, hoarding
Personality changeLoss of empathy, irritability, suspiciousness, changed social behaviour

Distinguishing progression from BPSD

FeatureDementia progressionBPSD
NatureChronic, persistentEpisodic, reactive, fluctuating
TimelineGradual, predictable stagingAcute-onset, fluctuating, triggered, or escalating
ExamplesApathy, loss of empathy, language decline, gradual social withdrawalDelusions, hallucinations, aggression, anxiety, agitation, resistance to care
TriggerNeurodegenerationMultifactorial: neurobiology + environment + unmet needs + medical illness
ImpactMay be tolerated or managed supportivelyOften distressing, disruptive, unsafe, or burdensome
ManagementEducation, support, routine, long-term planningActive assessment and management; treat triggers; behavioural strategies; medication only if severe/persistent/risky

Management

– Pharmacological For Behavioural and Psychological Symptoms of Dementia — BPSD, medication is not first-line.

First-line management is:

  • review unmet needs
  • identify and treat triggers: pain, infection, constipation, urinary retention, dehydration, hypoxia, delirium, medication adverse effects
  • environmental modification
  • routine, reassurance, validation, redirection
  • carer education
  • behaviour support plan

When medication may be appropriate

Medication may be considered when BPSD is:

  • severe
  • persistent
  • distressing to the person
  • dangerous to the person or others
  • causing major care failure
  • associated with psychosis, severe agitation or aggression
  • not responding to non-pharmacological strategies

Examples:

SymptomMedication may be considered?
Mild wanderingUsually no
Mild calling outUsually no
Apathy aloneUsually no
Insomnia aloneAvoid sedatives where possible
Severe aggression with risk of harmYes, after assessment
Distressing hallucinations/delusionsYes, after assessment
Severe anxiety/depressionConsider SSRI or targeted treatment
Acute fluctuating agitationExclude delirium first

Antipsychotics

  • Risperidone is the key PBS-listed antipsychotic for BPSD in Australia.
  • becomes a chemical restraint when it is used primarily to influence behaviour, rather than to treat a diagnosed mental or physical illness.
  • Avoid routine use due to:
    • Increased risk of
      • stroke
      • cardiovascular events
      • mortality
      • sedation
      • falls
      • delirium
      • worsening cognitive decline
  • Can be trialled for:
    • severe aggression
    • psychosis
    • persistent distressing hallucinations
    • dangerous behaviours
    • Immediate risk of harm
    • Failure of non-pharmacological interventions
    • Reversible causes addressed
  • Review within 4–12 weeks and aim to taper or stop if possible
Preferred Agents:
DrugIndicationDose RangeNotes
RisperidoneAggression
Psychosis (Alzheimer’s)
0.25–2 mg/day
Max: 2 mg/day (etg)
Only PBS-listed antipsychotic for BPSD in Australia
Review
– Within 2 weeks after initiation
– Then every 4–6 weeks
– Avoid >12 weeks where possible
– Taper 25–50% every 1–2 weeks if longer-term use or severe symptoms

Side effects:
– Sedation
– Dizziness
– Orthostatic hypotension
– Bradycardia
– Parkinsonism
– Akathisia
– Tardive dyskinesia
– Constipation
– Weight gain
– Hyperprolactinaemia
– Falls
– Neuroleptic malignant syndrome risk
OlanzapinePsychosis
Aggression
2.5–10 mg/day
Max: 10 mg/day (etg)
❌ Not PBS-listed for BPSD
– Off-label
– more sedating
– weight gain
– metabolic side effects
Quetiapineused in Lewy body dementia / Parkinson disease dementia (as per eTG)

Avoid antipsychotics if possible (↑sensitivity, worsened motor symptoms).
Start:
12.5–25 mg PO 1–2x daily

Titrate: +12.5–25 mg/day every ≥2 days

Max: 75 mg BD (ETG 2025)
❌ Not PBS-listed for BPSD

Preferred:
Rivastigmine or Donepezil
OxazepamShort-term severe anxiety/agitation

7.5–15 mg up to QIDShort-acting
max use < 2 weeks

Generally avoid long-term due to:
– Falls
– Sedation
– Delirium
– Dependence
– Respiratory depression
– Worsening cognition
SSRIs (e.g. citalopram)Depression
Anxiety
Agitation where non-drug measures insufficient
Citalopram 10 mg daily; max 20 mg in older adults

Escitalopram 5 mg daily; max 10 mg in older adults

Sertraline 50 mg daily; max 200 mg
Citalopram has best evidence (eTG)
Monitor for:
– hyponatraemia
– falls
– QT prolongation risk

Avoid :

  • Typical antipsychotics (e.g. haloperidol): high EPS and mortality
  • TCAs: anticholinergic effects worsen cognition
  • Long-term benzodiazepines: falls, sedation, dependence
Monitoring and Safety
  • All psychotropic medications must be:
    • Started low and titrated slowly
    • Reviewed regularly (ideally every 4–12 weeks)
    • Discontinued if ineffective
  • Obtain consent or proxy consent for psychotropics in aged care (especially in residential care)
Deprescribing Antipsychotics
  • Review within 2 weeks of initiation; stop if no benefit or adverse effects.
  • If benefit seen: continue with 4–6 weekly reviews.
  • Avoid use >12 weeks for BPSD.
  • If stopping after <12 weeks: abrupt cessation is fine (if symptoms not severe).
  • For longer-term use or severe symptoms:
    • Gradual taper: ↓25–50% every 1–2 weeks.
    • Monitor for withdrawal or symptom return.
    • Restart at minimum effective dose if needed; retry taper after 3 months.

Nonpharmacological practices to address BPSDs

Look for:

  • Pain
  • Delirium
  • Constipation
  • Urinary retention
  • Infection if symptomatic
  • Hunger/thirst
  • Fatigue
  • Fear
  • Trauma triggers
  • Overstimulation/understimulation
  • Sleep disturbance
  • Environmental change
  • Carer approach
  • Medication side effects
  • Akathisia
  • Sensory impairment

Use ABC analysis:

  • Antecedent: what occurred before?
  • Behaviour: what exactly happened?
  • Consequence: what happened after?

Australian guidelines recommend comprehensive behavioural assessment using ABC analysis and non-pharmacological interventions before medication.

Symptom-specific BPSD approach

Aggression

  • Keep calm; allow space and time
  • Identify who is unsafe and why
  • Exclude delirium, pain, infection, discomfort
  • Look for threat perception or trauma trigger
  • Use personalised sensory/touch strategies
  • Avoid confrontation

Agitation

  • Check pain, constipation, infection, clothing/temperature discomfort
  • Exclude delirium
  • Check stimulation level
  • Review environment, routine and staff changes
  • Use music, massage, pets, walking, calming sensory input
  • Review medications for akathisia or adverse effects

Anxiety

  • Explore past anxiety/trauma
  • Identify timing and situational triggers
  • Use structured familiar routine
  • Reduce overstimulation
  • Use calming sensory strategies
  • Differentiate anxiety from depression, apathy or delirium

Apathy

  • Identify interests and previous hobbies
  • Provide one-on-one engagement
  • Use tailored activities, music, pets, multisensory prompts
  • Consider depression or delirium
  • Review sedating medications

Depression

  • Assess suicide/self-harm risk
  • Differentiate depression from delirium and apathy
  • Explore grief/adjustment
  • Use gentle exercise, reminiscence, music, pets
  • Consider psychological therapy and SSRI if clinically indicated

Disinhibition

  • Identify triggers and early cues
  • Assess risk/distress to others
  • Provide privacy when appropriate
  • Use redirection and modified clothing
  • Avoid shaming or punishment
  • Keep staff responses neutral and consistent

Psychosis

  • Clarify hallucinations/delusions and risk
  • Exclude delirium, infection, pain, medication toxicity
  • Optimise lighting, glasses and hearing aids
  • Validate emotion without reinforcing delusion
  • Consider psychiatric/specialist referral if severe or unsafe

Sleep disturbance

  • Treat pain, depression, anxiety, OSA
  • Exclude delirium
  • Review medication timing and sedative effects
  • Daylight exposure and daytime activity
  • Bedtime routine, low noise/light, toileting plan
  • Use sleep log

Wandering

  • Assess risk of getting lost, falls, exits, unsafe spaces
  • Identify purpose: boredom, toilet, pain, anxiety, habit
  • Adjust environment
  • Provide safe walking areas
  • Use signage, boundary cues, ID bracelet/contact details
  • Consider GPS/safety technology if appropriate

Driving with dementia

General Principles

  • Dementia commonly impairs:
    • Memory
    • Attention
    • Visuospatial skills
    • Judgement
    • Executive function
    • Reaction time
    • Insight
    • Problem-solving ability
  • These impairments may significantly affect driving safety

Driving relies heavily on:

  • Attention
  • Executive function
  • Reaction time
  • Visuospatial skills
  • Insight
  • Problem-solving
  • Cognitive flexibility
  • Motor coordination

Deficits in these areas increase crash risk.

Driving variables

Dementia and Driving Risk

  • Drivers with dementia have a significantly increased crash risk compared with cognitively normal age-matched drivers.
  • Risk increases with disease progression/severity.
  • Loss of insight is common and may lead patients to underestimate impairment.
  • Many patients continue driving after diagnosis.
  • Some only stop after crashes or near misses occur.

Mild Dementia

Mild dementia does NOT automatically mean a patient must stop driving immediately.

  • Some patients with mild dementia may still drive safely.
  • Driving ability varies significantly between individuals.
  • Functional assessment and regular review are essential.

Austroads – Important Legal Principles

  • Dementia is a condition relevant to fitness to drive.
  • Patients have a legal obligation to notify the licensing authority if a condition may impair driving.
  • The licensing authority makes the final licensing decision.
  • Patients with dementia generally cannot hold an unconditional licence.
Conditional Licensing

May be considered in selected patients with mild dementia if:

  • Functional impairment is mild
  • Insight is preserved
  • Driving assessment is satisfactory
  • Regular review occurs

Possible conditions:

  • Periodic medical review
  • Occupational therapy driving assessment
  • Local area/radius restriction

Moderate–Severe Dementia

Generally incompatible with safe driving due to:

  • Significant cognitive impairment
  • Reduced insight
  • Impaired judgement/reaction time
  • Increased crash risk

Clinical Features Suggesting Unsafe Driving

History Red Flags

  • Recent crashes or near misses
  • Getting lost on familiar routes
  • Confusing pedals
  • Lane drifting
  • Failure to obey signs/lights
  • Poor judgement at intersections
  • Family/passenger concerns
  • Police concerns/reports
  • Aggressive or impulsive driving
  • Anxiety/confusion while driving

Functional Concerns

Assess:

  • Attention
  • Executive function
  • Visuospatial ability
  • Navigation
  • Problem-solving
  • Coordination
  • Praxis
  • Insight
  • Reaction time

Behavioural Indicators

  • Poor insight/denial
  • Hallucinations/delusions
  • Anxiety/panic when driving
  • Reduced confidence
  • Difficulty handling unexpected situations

Cognitive Testing – Helpful Cognitive Assessment Tools

Trail Making Test B (Trails B)

Often incorporated within the MoCA executive function tasks.

Assesses:

  • Processing speed
  • Attention
  • Executive function
  • Cognitive flexibility
  • Visuospatial functioning

These domains are critical for:

  • Intersections
  • Multi-tasking
  • Lane changes
  • Hazard response
  • Decision-making under pressure

Trail Making Test B — Interpretation

Probably Safe
  • < 2 minutes
  • < 2 errors
Uncertain
  • 2–3 minutes
  • Or 2 errors
Probably Unsafe
  • 3 minutes
  • Or ≥ 3 errors

Important caveat:

  • This is supportive information only.
  • Does NOT independently determine licence status.
Trail Making Test A
  • Often concerning if markedly slow, commonly >90 seconds in driving-screen contexts.
  • Screens processing speed and visual scanning.
  • Less useful than Trail B but helpful as part of a battery

Snellgrove Maze Test

Assesses:

  • Attention
  • Visuoconstructional ability
  • Executive planning
  • Foresight/problem-solving

Useful because driving requires:

  • Route planning
  • Hazard anticipation
  • Complex decision-making
  • Sustained attention

Poor performance may suggest:

  • Reduced ability to manage unexpected road situations
  • Impaired navigation/problem-solving

Clock Drawing Test

Very relevant to driving domains, but not sufficient alone. Abnormal clock drawing should increase concern, especially if combined with poor trail-making, poor insight, navigation errors or crashes.

Assesses multiple cognitive domains:

  • Visuospatial abilities
  • Executive function
  • Orientation/conceptualisation of time
  • Planning
  • Visual memory

Abnormal clock drawing may reflect:

  • Visuospatial impairment
  • Executive dysfunction
  • Planning difficulties

These impair:

  • Lane positioning
  • Navigation
  • Interpretation of road environments

Intersecting Pentagons / Cube Copying

Used in:

  • MMSE
  • MoCA

Assesses:

  • Attention
  • Visuospatial function
  • Constructional praxis

Poor performance may correlate with:

  • Difficulty judging distances
  • Poor spatial awareness
  • Reduced lane control
  • Parking difficulties

Gold Standard Assessment- Occupational Therapy On-Road Driving Assessment

sually includes:

  1. Off-road cognitive/perceptual assessment
  2. On-road practical driving assessment (if appropriate)

OT Driving Assessment Can Assess

  • Hazard perception
  • Reaction time
  • Lane maintenance
  • Navigation
  • Judgement
  • Insight
  • Real-world driving performance

Additional Benefits

May provide:

  • Vehicle modification advice
  • Driver rehabilitation
  • Safer driving strategies (if capacity retained)

Limitations

  • Cost
  • Access/wait times
  • Patient anxiety
  • Availability in rural areas

Management Approach

Begin Conversations Early

Driving discussions should occur:

  • Early after diagnosis
  • Before crises or accidents occur
  • While insight/capacity remains relatively preserved

Include Family and Care Partners

Important because:

  • Patients may minimise deficits
  • Insight may decline over time
  • Family often observe early problems

Discuss Alternatives to Driving

Examples:

  • Public transport
  • Community transport
  • Taxi subsidy schemes
  • Family support
  • Ride-share
  • Delivery services

Goal:

  • Preserve independence and social connection where possible.

Document Clearly

Document:

  • Advice provided
  • Risks discussed
  • Patient response
  • Family concerns
  • Reporting advice
  • Referrals made

Reporting Obligations in Australia

Queensland

  • No mandatory GP reporting requirement.
  • Patients are expected to self-report.
  • GPs may report if significant public safety risk exists.
  • Indemnity protections exist for reporting in good faith.

Transition From Driving

Loss of driving can:

  • Reduce independence
  • Increase depression risk
  • Increase social isolation
  • Accelerate RACF placement risk

Therefore transition planning is important.

Supportive Strategies

Discuss:

  • Family transport
  • Public transport
  • Taxi subsidy schemes
  • Community transport
  • Ride-share
  • Delivery services

Encourage gradual planning before crisis occurs.

Review Frequency

Patients with mild dementia who continue driving should usually undergo:

  • At least 6-monthly review
  • Earlier reassessment if deterioration occurs

Review:

  • Cognition
  • Function
  • Insight
  • Behaviour
  • Driving incidents
  • Carer concerns


Preventive Activities and Risk Reduction

🧬 Risk Factors (other than age)

  • Family history of Alzheimer’s
  • Repeated head trauma
  • Down syndrome
  • Elevated cardiovascular risk
  • Depression (past or present)
  • Low education
  • Smoking
  • Physical inactivity
  • Aboriginal or Torres Strait Islander background
  • Low social contact
  • Hearing loss

💡Risk Reduction Interventions

Intervention TypeRecommendations
Physical activityRecommend in adults (normal/MCI) to reduce cognitive decline
Smoking cessationOffer to tobacco users to reduce cognitive decline risk
DietMediterranean-style or healthy balanced diet; avoid vitamin/supplement use for prevention
Alcohol useOffer interventions to reduce hazardous use in adults with/without MCI
Cognitive trainingMay be offered in older adults with normal cognition or MCI
Social activityInsufficient evidence for dementia prevention; still support social inclusion
Weight managementManage midlife overweight/obesity to reduce dementia risk
HypertensionManage in adults; may reduce dementia risk
DiabetesManage via medication/lifestyle to reduce dementia risk
DyslipidaemiaManage at midlife to reduce dementia risk
DepressionTreat depression (medication/psychological), but insufficient evidence for dementia prevention
Hearing lossInsufficient evidence for hearing aids as dementia prevention, but recommend screening and hearing aid provision for management

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