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 subtype | Course / timing | Key clinical features | Associated features | Risk factors | Imaging / biomarkers | Important notes |
|---|---|---|---|---|---|---|
| Alzheimer disease | Insidious 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 dementia | Related 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 bodies | Gradual 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 dementia | Dementia 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 dementia | Insidious 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
| Category | Examples | Key distinguishing features |
|---|---|---|
| Primary neurodegenerative | Alzheimer disease DLB FTD Parkinson disease dementia Huntington disease | Progressive decline subtype-specific pattern |
| Vascular | Multi-infarct dementia strategic infarct chronic small vessel disease | Stroke/TIA history vascular risks focal neurology executive dysfunction |
| Delirium | Infection dehydration hypoxia pain constipation medication toxicity | Acute onset fluctuating course impaired attention altered consciousness |
| Psychiatric | Depression/pseudodementia severe anxiety psychosis | Mood symptoms prominent cognitive effort may fluctuate may coexist with dementia |
| Medication/substance | Benzodiazepines opioids anticholinergics sedatives alcohol illicit substances | Temporal link to medications/substances may improve with rationalisation |
| Metabolic/endocrine | Hypothyroidism calcium abnormality renal/hepatic impairment hypoglycaemia/hyperglycaemia | Systemic symptoms abnormal blood tests |
| Nutritional | B12 folate thiamine deficiency | Neuropathy ataxia macrocytosis malnutrition alcohol risk |
| Infectious | HIV neurosyphilis prion disease | rapid progression neurological signs |
| Structural intracranial | Subdural haematoma tumour normal pressure hydrocephalus | Head trauma anticoagulation focal neurology headache gait/incontinence |
| Traumatic | Chronic traumatic encephalopathy repeated head injury | History of repeated concussion/head trauma |
| Genetic/metabolic rare causes | Wilson disease mitochondrial cytopathies leukodystrophies | Younger onset family history movement disorder multisystem features |
“4 Ds” not to miss
| D | Meaning | Clinical clue |
|---|---|---|
| Dementia | Chronic progressive cognitive and functional decline | Months to years, progressive impairment |
| Delirium | Acute fluctuating disturbance in attention/awareness | Hours to days, fluctuating, medically unwell |
| Depression | Mood disorder causing cognitive symptoms | Low mood, anhedonia, poor sleep/appetite, low motivation |
| Drugs | Medication/substance-related cognitive impairment | Recent 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 |
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.
| Domain | Conditions to ask about | Why it matters |
|---|---|---|
| Neurological | Stroke/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 risk | Hypertension, diabetes, dyslipidaemia, atrial fibrillation, ischaemic heart disease, peripheral vascular disease | Major risk factors for vascular cognitive impairment and mixed dementia |
| Psychiatric | Depression anxiety bipolar disorder psychosis previous psychiatric admissions | Depression/anxiety can mimic or worsen cognitive symptoms — “pseudodementia” |
| Respiratory / sleep | Obstructive sleep apnoea COPD chronic hypoxia | Fatigue, poor attention, impaired concentration |
| Endocrine / metabolic | Thyroid disease B12 deficiency diabetes renal disease liver disease | Potentially reversible contributors |
| Recent illness / surgery | Recent 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
| Pattern | Think about |
|---|---|
| Cognitive decline + gait disturbance + urinary incontinence | Normal pressure hydrocephalus |
| Cognitive decline + tremor/stiffness/slowness | Parkinson disease dementia / Lewy body dementia |
| Cognitive decline + falls + vascular risk factors | Vascular dementia / mixed dementia |
| Cognitive decline + weight loss + weakness + reduced activity | Frailty, malignancy, depression, systemic disease |
Behavioural changes and BPSD
Behavioural symptoms are common in dementia. The key clinical task is to distinguish:
- Gradual behavioural/personality change from dementia progression,
- 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 / pattern | Behavioural clues |
|---|---|
| Alzheimer disease | Apathy, anxiety, irritability later |
| Frontotemporal dementia | Disinhibition, loss of empathy, apathy, compulsive behaviour, dietary change |
| Dementia with Lewy bodies | Visual hallucinations, fluctuating cognition, REM sleep behaviour disorder, sensitivity to antipsychotics |
| Vascular dementia | Executive 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 group | Examples | Cognitive concern |
|---|---|---|
| Benzodiazepines | Diazepam, temazepam, oxazepam, alprazolam | Sedation, falls, delirium, memory impairment |
| Sleeping tablets | Zopiclone, zolpidem, sedating antihistamines | Sedation, impaired alertness, falls |
| Anticholinergics | Oxybutynin, amitriptyline, promethazine, some antihistamines | Confusion, constipation, urinary retention, delirium |
| Opioids | Oxycodone, morphine, tapentadol, fentanyl | Sedation, delirium, constipation, falls |
| Antidepressants | TCAs, mirtazapine, SSRIs/SNRIs | Sedation, hyponatraemia, anticholinergic burden, interactions |
| Antipsychotics | Quetiapine, risperidone, olanzapine | Sedation, extrapyramidal effects, falls, anticholinergic effects |
| Antiepileptics / neuropathic pain agents | Pregabalin, gabapentin, valproate, levetiracetam | Sedation, dizziness, mood/cognitive effects |
| Alcohol | Regular or heavy intake | Cognitive 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
| Tool | Main purpose | Key scoring / interpretation | Strengths | Limitations / cautions |
|---|---|---|---|---|
| GPCOG General Practitioner Assessment of Cognition | Primary care cognitive screening tool | Patient 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 Examination | General cognitive screening and monitoring | Scored 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 Test | Brief screen of executive function, planning and visuospatial ability | No 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 Scale | Cognitive screening, especially for culturally and linguistically diverse patients | Scored 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 Assessment | Culturally appropriate cognitive assessment for Aboriginal and Torres Strait Islander people, especially rural/remote contexts | KICA-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 Assessment | Cognitive screen with stronger coverage of executive function and mild cognitive impairment | Scored 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
| Tool | What it assesses | How to use clinically |
|---|---|---|
| NPI / NPI-Q / NPI-NH Neuropsychiatric Inventory | Behavioural 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 Dementia | Depression 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-AD | Behavioural 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
| Tool | Purpose | Key point |
|---|---|---|
| UKBDRS UK Biobank Dementia Risk Score | Estimates 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
| Investigation | Purpose |
|---|---|
| FBC | Exclude anaemia, infection, haematological disease |
| EUC / renal function | Exclude metabolic disturbance, renal failure, dehydration |
| Glucose / HbA1c | Detect hypo/hyperglycaemia, diabetes |
| Calcium | Exclude hypercalcaemia/hyperparathyroidism |
| LFTs | Exclude hepatic dysfunction |
| TFTs | Exclude hypothyroidism or thyrotoxicosis |
| Vitamin B12 and folate | Detect nutritional deficiency |
| Lipids | Assess vascular risk factors |
| Cognitive screening (GPCOG, MMSE, MoCA, RUDAS) | Assess cognitive domains |
Inflammatory / Infective Tests
| Investigation | When to consider |
|---|---|
| ESR / CRP | Suspected inflammatory, autoimmune, infective or malignant process |
| MSU / urine MCS | If delirium or urinary symptoms present |
| HIV / syphilis serology | Young 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 finding | May be normal ageing | More concerning for pathology |
|---|---|---|
| Mild cortical volume loss | Common with ageing | Moderate/severe or disproportionate atrophy |
| Mild medial temporal atrophy | Can occur with age | Marked MTA, especially if young or symptomatic |
| Scattered punctate white matter lesions | Common in older adults | Confluent lesions, lacunes, microbleeds, strategic infarcts |
| Mild ventricular enlargement | Can occur with atrophy | Disproportionate ventriculomegaly, gait disturbance, urinary symptoms — consider NPH |
| Mild small vessel disease | Common with age/vascular risk | Extensive 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.
| Grade | Description |
|---|---|
| 0 | No cortical atrophy |
| 1 | Mild cortical atrophy |
| 2 | Moderate cortical atrophy |
| 3 | Severe 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.
| Grade | Description |
|---|---|
| 0 | No atrophy |
| 1 | Only widening of choroid fissure |
| 2 | Widening of choroid fissure and temporal horn; mild hippocampal volume loss |
| 3 | Moderate hippocampal volume loss |
| 4 | Severe 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.
| Grade | Description |
|---|---|
| 0 | No white matter lesions |
| 1 | Punctate white matter lesions |
| 2 | Early confluent white matter lesions |
| 3 | Large 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
| Investigation | Comments |
|---|---|
| CSF examination | Specialist referral only useful in – rapidly progressive dementia – CNS infection – CJD – NPH – Alzheimer biomarkers |
| Fasting homocysteine | if 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 PET | Difficult diagnostic cases; limited availability |
| Neuropsychological assessment | Provides 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 testing | Early-onset dementia with strong family history |
| ApoE genotyping | Not 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:
- Understand information
- Retain information
- Use/weigh information
- 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.
| Domain | Intervention | Examples / Practical Strategies | Purpose / Benefits |
|---|---|---|---|
| General principle | Non-pharmacological management first-line | Use before medications where possible – especially for BPSD | Reduces behavioural symptoms, distress, agitation, sleep disruption, and carer burden |
| Frequent orientation reinforcement | Orientation cues and repeated reassurance | Large clocks calendars orientation boards repeated introductions by staff/carers | Supports orientation, reduces confusion, improves sense of safety |
| Staff communication strategies | Visible name badges regular re-introduction simple and clear communication | Builds familiarity, reduces anxiety, improves engagement | |
| Calm, familiar environment | Maintain predictable surroundings | Predictable routines familiar rooms low-stress environment | Reduces agitation, confusion, and distress |
| Reduce environmental triggers | Minimise noise overstimulation frequent room changes | Helps prevent behavioural escalation and sundowning | |
| Clear signage | Visual navigation supports | Large labels pictures/icons simple wording | Improves navigation, independence, and confidence |
| Orientation aids | Signs for bedroom bathroom dining room activity areas | Reduces wandering, confusion, and dependence | |
| Colour contrasts | Use contrast for key objects | Contrasting colours for doors toilet seats handrails furniture | Improves visual recognition, safety, and mobility |
| Falls prevention support | Clearly visible edges rails seating bathroom fixtures | Reduces falls risk and improves environmental awareness | |
| Good lighting | Optimise lighting | Natural daylight even lighting night lights where appropriate | Supports sleep–wake cycle, reduces confusion and falls |
| Avoid problematic lighting | Avoid shadows glare harsh fluorescent lighting | Reduces misperceptions, agitation, and visual confusion | |
| Uncluttered spaces | Simplify layout | Reduce excess furniture visual clutter complex room layouts | Improves mobility and reduces falls/confusion |
| Safe walking areas | Clear pathways remove obstacles | Promotes independence and safer mobility | |
| Familiar objects | Personalised environment | Family photographs personal items familiar music/artwork | Supports identity, comfort, memory, and emotional security |
| Reminiscence support | Meaningful objects familiar scents music photos | May reduce distress and improve connection | |
| Adaptive furniture and safety | Safe and accessible furniture | Stable comfortable accessible chairs/beds/tables | Supports independence, transfers, and comfort |
| Environmental safety measures | Handrails grab rails non-slip flooring removal of trip hazards | Falls prevention and safer mobility | |
| Quiet / low-stimulation areas | Calming spaces | Quiet room low lighting reduced noise minimal activity | Useful for agitation, sundowning, anxiety, and sensory overload |
| Memory aids | Practical cognitive supports | Labelled drawers reminder notes medication prompts daily planners | Supports independence, routine, and task completion |
| Adaptable spaces | Modify environment as needs change | Adapt for mobility decline supervision needs continence needs behavioural changes | Maintains safety and function as dementia progresses |
| Technology integration | Assistive technology | GPS trackers medication reminders smart home monitoring fall alarms | Enhances safety and monitoring |
| Ethical balance | Balance safety privacy autonomy and dignity | Avoids overly restrictive or intrusive care |
Alternative and Sensory Therapies
| Therapy | Examples | Potential Benefits |
|---|---|---|
| Massage and aromatherapy | Gentle massage, calming scents such as lavender where appropriate | May reduce anxiety, promote relaxation, and improve sleep |
| Music therapy | Personalised familiar music, singing, rhythm activities | Improves mood, engagement, memory stimulation, and social interaction |
| Dance / movement therapy | Gentle dancing, seated movement, rhythm-based activity | Promotes engagement, mobility, enjoyment, and social participation |
| Animal-assisted therapy | Visits from trained therapy animals, supervised pet interaction | May improve emotional wellbeing, reduce loneliness, and encourage interaction |
| Multi-sensory stimulation | Light, sound, touch, smell-based activities | May 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
| Drug | Formulation | Dosage Range |
|---|---|---|
| Donepezil (Aricept) | Oral tablets | 5–10 mg daily |
| Galantamine (Galantyl) | Extended-release capsules | 8–24 mg daily |
| Rivastigmine (Exelon) | Transdermal patch | 4.6–9.6 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)
| Drug | PBS Status |
|---|---|
| Donepezil, Galantamine, Rivastigmine | Mild to moderate Alzheimer’s disease (specialist confirmed) |
| Memantine | Moderate to severe Alzheimer’s disease (specialist confirmed) |
| Risperidone | BPSD 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:
| Contributor | Examples |
|---|---|
| Neurodegeneration | Frontal/temporal dysfunction, impaired impulse control |
| Environmental triggers | Hospitalisation, unfamiliar settings, noise, overstimulation, change in routine |
| Unmet physical needs | Pain, hunger, thirst, toileting, constipation, urinary retention |
| Unmet emotional needs | Loneliness, fear, boredom, frustration |
| Communication barriers | Unable to express pain, discomfort, fear, or confusion |
| Care approach | Rushed care, unfamiliar carers, lack of explanation, personal care distress |
| Medical illness | Infection, delirium, dehydration, hypoxia, medication toxicity |
Clinical domains of BPSD
| Domain | Features to ask about |
|---|---|
| Mood symptoms | Depression, low mood, anxiety, emotional lability, tearfulness |
| Psychotic symptoms | Delusions, paranoia, theft accusations, persecution ideas, hallucinations — often visual |
| Sleep disturbance | Insomnia, fragmented sleep, day/night reversal, daytime drowsiness |
| Agitation | Restlessness, pacing, shouting, irritability, sundowning |
| Aggression | Verbal aggression, physical aggression, threats, striking out |
| Resistance to care | Refusing showering, medications, meals, personal care |
| Disinhibition | Socially inappropriate behaviour, sexual disinhibition, impulsivity |
| Wandering | Exit-seeking, getting lost, repetitive walking |
| Apathy / withdrawal | Reduced motivation, reduced engagement, social withdrawal |
| Repetitive behaviours | Repeated questions, checking, calling out, hoarding |
| Personality change | Loss of empathy, irritability, suspiciousness, changed social behaviour |
Distinguishing progression from BPSD
| Feature | Dementia progression | BPSD |
|---|---|---|
| Nature | Chronic, persistent | Episodic, reactive, fluctuating |
| Timeline | Gradual, predictable staging | Acute-onset, fluctuating, triggered, or escalating |
| Examples | Apathy, loss of empathy, language decline, gradual social withdrawal | Delusions, hallucinations, aggression, anxiety, agitation, resistance to care |
| Trigger | Neurodegeneration | Multifactorial: neurobiology + environment + unmet needs + medical illness |
| Impact | May be tolerated or managed supportively | Often distressing, disruptive, unsafe, or burdensome |
| Management | Education, support, routine, long-term planning | Active 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:
| Symptom | Medication may be considered? |
|---|---|
| Mild wandering | Usually no |
| Mild calling out | Usually no |
| Apathy alone | Usually no |
| Insomnia alone | Avoid sedatives where possible |
| Severe aggression with risk of harm | Yes, after assessment |
| Distressing hallucinations/delusions | Yes, after assessment |
| Severe anxiety/depression | Consider SSRI or targeted treatment |
| Acute fluctuating agitation | Exclude 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
- Increased risk of
- 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:
| Drug | Indication | Dose Range | Notes |
|---|---|---|---|
| Risperidone | Aggression 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 |
| Olanzapine | Psychosis 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 |
| Quetiapine | used 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 |
| Oxazepam | Short-term severe anxiety/agitation | 7.5–15 mg up to QID | Short-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
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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:
- Off-road cognitive/perceptual assessment
- 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
- Provide preventive advice on dementia risk factors https://www.racgp.org.au/clinical-resources/clinical-guidelines/key-racgp-guidelines/view-all-racgp-guidelines/preventive-activities-in-general-practice/mental-health/dementia
🧬 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 Type | Recommendations |
|---|---|
| Physical activity | Recommend in adults (normal/MCI) to reduce cognitive decline |
| Smoking cessation | Offer to tobacco users to reduce cognitive decline risk |
| Diet | Mediterranean-style or healthy balanced diet; avoid vitamin/supplement use for prevention |
| Alcohol use | Offer interventions to reduce hazardous use in adults with/without MCI |
| Cognitive training | May be offered in older adults with normal cognition or MCI |
| Social activity | Insufficient evidence for dementia prevention; still support social inclusion |
| Weight management | Manage midlife overweight/obesity to reduce dementia risk |
| Hypertension | Manage in adults; may reduce dementia risk |
| Diabetes | Manage via medication/lifestyle to reduce dementia risk |
| Dyslipidaemia | Manage at midlife to reduce dementia risk |
| Depression | Treat depression (medication/psychological), but insufficient evidence for dementia prevention |
| Hearing loss | Insufficient evidence for hearing aids as dementia prevention, but recommend screening and hearing aid provision for management |







