Dementia

Common Types of Dementia

Alzheimer’s Disease (~40%)
- Most common cause
- May coexist with vascular pathology (“mixed dementia”)
Vascular Dementia (~20%)
- Often follows strokes or chronic small vessel disease
Dementia with Lewy Bodies (~20%)
- Key features:
  - Progressive cognitive decline
  - Fluctuating cognition
  - Visual and/or auditory hallucinations
  - Parkinsonism
  - Marked sensitivity to antipsychotics
  - Recurrent unexplained falls
  - Transient loss of consciousness
Other (~20%)
- Frontotemporal Dementia
  - Prominent behavioural changes
  - Disinhibition
  - Executive dysfunction
- Subcortical Dementias
  - e.g. Parkinson’s disease, Huntington’s disease
- Alcohol-related or Toxic Dementia
  - Alcohol, heavy metals (lead, mercury)
- Normal Pressure Hydrocephalus
  - Triad: gait disturbance, urinary incontinence, dementia
- Infectious Causes
  - HIV-associated neurocognitive disorder
  - Neurosyphilis
  - Prion disease (e.g. Creutzfeldt–Jakob disease)
- Metabolic, Endocrine, and Nutritional Deficiencies
  - Hypothyroidism
  - Hypocalcaemia
  - B12, folate, thiamine deficiency
- Structural Lesions
  - Space-occupying lesions (e.g. tumour, subdural haematoma)

Differential Diagnoses of Dementia

1. Primary Neurodegenerative Disorders

Alzheimer’s disease
Dementia with Lewy bodies
Frontotemporal dementia (Pick’s disease)
Huntington’s disease

2. Vascular Causes

Multi-infarct dementia
Strategic infarcts
Chronic small vessel disease

3. Metabolic and Genetic Conditions

Hypothyroidism
Hypocalcaemia
Mitochondrial cytopathies
Wilson’s disease
Leukodystrophies

4. Infectious

HIV-associated neurocognitive disorder
Neurosyphilis
Prion disease (e.g. Creutzfeldt–Jakob)

5. Normal Pressure Hydrocephalus

Classic triad: gait disturbance, dementia, urinary incontinence

6. Toxic Causes

Alcohol-related cognitive impairment
Heavy metal exposure: lead, mercury

7. Nutritional Deficiencies

Thiamine (Wernicke-Korsakoff syndrome)
Vitamin B12
Folate

8. Psychiatric Disorders

Pseudodementia (typically due to major depressive disorder)
Severe depression with cognitive impairment

9. Traumatic Brain Injury

Chronic traumatic encephalopathy (e.g. “punch-drunk” syndrome in boxers)

10. Intracranial Lesions

Subdural haematoma
Brain tumours (especially frontal or temporal lobe)

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 adversity^A
– 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 activity^A
– Chronic kidney disease^A

Later life Stroke^A
– History of head trauma^A
– Epilepsy
– Delirium
– History of depression/chronic grief
– Social isolation/loneliness
– Physical inactivity
– Anticholinergic medications^A
– Polypharmacy^A
– Vision problems^A

^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

Assessments to be made in dementia(carer/family input preferable)

Clinical History

Cognitive Symptoms

Memory impairment
- Early: short-term forgetfulness
- Later: long-term memory loss
Executive dysfunction
- Difficulty planning, organising, learning, problem-solving
- Poor judgment, impaired reasoning, reduced insight
Language difficulties (Aphasia)
- Word-finding issues, repetition, incomplete sentences
- Difficulty understanding or expressing language
Motor planning impairment (Apraxia)
- Difficulty executing learned tasks (e.g. dressing, using a phone, driving)
Perceptual impairment (Agnosia)
- Failure to recognise familiar people, objects, or places

Behavioural Changes (including “Behavioural and Psychological Symptoms of Dementia” BPSD)

Behavioural and psychological symptoms are common in people with dementia and can emerge from both neurodegenerative progression and acute behavioural syndromes. Distinguishing between persistent behavioural changes due to disease progression and the syndrome of Behavioural and Psychological Symptoms of Dementia (BPSD) is critical for appropriate management.

A. Behavioural and Psychiatric Changes with Worsening Dementia

These changes reflect the gradual and persistent alterations in personality, behaviour, and mood that occur as a direct consequence of neurodegeneration.

Pathophysiology and Features:

Result from atrophy and dysfunction of brain regions (e.g. frontal or temporal lobes).
Often represent the baseline behavioural phenotype of a given dementia subtype.
Changes may be:
- Due to neurodegeneration (e.g. apathy in frontotemporal dementia).
- Exacerbated by communication barriers, frustration, or confusion (e.g. irritability, social withdrawal).
Typically progressive and non-episodic.

Common Features by Stage:

Early dementia:
- Apathy
- Depression
- Anxiety
Moderate dementia:
- Irritability
- Agitation
- Wandering
- Delusions
Late dementia:
- Aggression
- Hallucinations
- Disinhibition
- Vocalisations

These features may not always require active intervention unless they escalate, cause distress, or compromise care.

B. Behavioural and Psychological Symptoms of Dementia (BPSD)

BPSD is a clinical syndrome comprising a broad range of non-cognitive symptoms that commonly occur in dementia. It is a defined clinical entity and is often the focus of management due to its impact on quality of life, caregiver burden, and risk of institutionalisation.

Aetiology:

BPSD arises from a complex interplay of:

Neurodegenerative changes
Environmental stressors
- hospitalisation
- unfamiliar settings
Unmet physical or emotional needs
- frustration
- pain
- toileting
- loneliness
Interpersonal dynamics (e.g. caregiver approach)
Medical comorbidities (e.g. infection, pain, delirium)

Clinical Domains and Examples:

1. Psychiatric Symptoms

Depression
Low mood, anhedonia
Anxiety, emotional lability
Poor sleep or appetite, weight loss
Delusions (commonly paranoid: theft, persecution)
Hallucinations (often visual > auditory)

2. Cognitive/Delirium-like Features (especially in Lewy body dementia)

Disorientation
Fluctuating attention
Altered sleep-wake cycle

3. Sleep Disturbances

Day/night reversal (may gradually emerge but becomes BPSD if disruptive)
Insomnia
Fragmented sleep
Daytime drowsiness

4. Behavioural Disturbances

Personality change (may straddle BPSD and progression)
Disinhibition (general or sexual)
Impulsivity
Wandering
Agitation, pacing, shouting
Verbal or physical aggression
Resistance to care
Apathy or withdrawal
Repetitive behaviours
Disruption of routine activities
Sundowning
Inappropriate behaviour

Clinical Distinction and Management Implications

Feature	Changes with Progression	BPSD
Nature	Chronic, persistent	Episodic, reactive
Examples	Apathy, loss of empathy, language decline	Delusions, hallucinations, aggression, anxiety
Trigger	Neurodegeneration	Multifactorial (neurobiology + environment + unmet needs)
Timeline	Gradual, predictable staging	Fluctuating, acute-onset or triggered
Impact	May be tolerated	Often distressing or disruptive
Management	Supportive long-term planning Often no intervention unless distressing	Active management needed Structured behavioural and/or pharmacological intervention

BPSD is a clinical management construct—used when symptoms result in distress, disruption, or require active treatment.
Pharmacological treatment (e.g. risperidone, SSRIs) may be indicated for severe BPSD, guided by Australian Therapeutic Guidelines: Psychotropic.

Key Teaching Point

Not all behavioural symptoms in dementia are BPSD. Behavioural changes may reflect the underlying disease progression. However, when symptoms escalate, become disruptive, or respond to environmental or medical triggers, they should be classified and managed as BPSD.

2. Functional Assessment

Activities of Daily Living (ADLs)

Bathing, dressing, toileting, feeding, continence, transfers
Tools: Barthel Index

Instrumental Activities of Daily Living (IADLs)

Managing finances, medication, meal prep, shopping, housekeeping, transport, telephone use

Other considerations:

Falls risk, safety (e.g. stove use, appliances, driving)
Self-neglect: poor hygiene, malnutrition

3. Medical and Risk Factor Review

Medical comorbidities: neurological, psychiatric, cardiovascular, recent surgery
Contributors to cognitive decline:
- Pain, infection, incontinence, hearing or vision impairment
Substance use: alcohol intake
Medication review: especially recent changes, anticholinergics, sedatives
Family history of dementia or neurodegenerative disease
Psychosocial factors: recent stressors, legal/financial issues, life events

4. Social Context

Carer availability and burden
Home environment: accessibility, safety, hygiene
Support network: family, friends, services
Socioeconomic factors

5. Physical Examination

Evaluate for treatable contributors to cognitive decline:
- Delirium, infection (e.g. UTI), heart failure
- Vision and hearing impairments
- Nutritional status

6. Cognitive Screening Tools

GPCOG (General Practitioner Assessment of Cognition)

Sensitivity: 85% | Specificity: 86%
Two components:
- Patient section (9 questions)
  - Score 9 = no impairment
  - Score 5–8 = needs informant interview
  - Score ≤4 = cognitive impairment
- Informant section (6 questions)
  - Score 4–6 = likely intact
  - Score ≤3 = likely impaired

MMSE (Mini-Mental State Examination)

Total score: 30
- 19–24 = Mild dementia
- 10–18 = Moderate dementia
- <10 = Severe dementia
Limitations:
- Insensitive to early changes and executive function
- Education and age may affect performance

Clock Drawing Test

Assesses executive and visuospatial functions
Pros: quick, not education-dependent
Cons: does not assess memory/language

RUDAS (Rowland Universal Dementia Assessment Scale)

Designed for culturally and linguistically diverse populations

KICA (Kimberley Indigenous Cognitive Assessment)

Validated for older Indigenous Australians

Neuropsychiatric Inventory (NPI)

Cornell Scale for Depression in Dementia

BEHAVE-AD

7. Risk Prediction Tools

UK Biobank Dementia Risk Score (UKBDRS)

Factors include age, education, parental history, deprivation index, diabetes, stroke, depression, hypertension, hypercholesterolaemia, sex, and living situation

8. Reversible Causes of Cognitive Impairment to Exclude

Hypothyroidism
B12/folate/thiamine deficiency
Depression (“pseudodementia”)
Medications (especially anticholinergic burden)
Infection (e.g. UTI, pneumonia)
Subdural haematoma
Normal pressure hydrocephalus
Alcohol-related brain injury
Electrolyte disturbances (e.g. calcium)
Sleep disorders (e.g. OSA)

Investigation Rationale and comments

Management

📝 Legal and Advance Care Planning

Assess capacity to complete:
- Enduring Power of Attorney (financial decisions)
- Enduring Guardianship (health and lifestyle decisions)
- Advance Care Directives
- Will and testament
Address legal matters early while the patient still has decision-making capacity

📄 Advance Care Planning

Discuss goals of care
Document patient wishes regarding future health interventions
Engage substitute decision-makers

💊 Medication Management

Rationalise medications (avoid anticholinergics, CNS depressants)
Consider Webster packing for medication compliance
Regular medication reviews:
- Check for adverse effects, interactions
- Ensure continued indication
Monitor for and manage comorbidities (e.g. diabetes, hypertension, cardiovascular disease)

🩺 Diagnostic and Specialist Input

Refer to dementia specialist service for diagnosis confirmation (if uncertain)
Consider neuropsychological assessment
Assess and manage cognitive and behavioural symptoms

🚗 Driving and Safety

Assess driving safety:
- Cognitive assessment
- Occupational therapist driving review if required
- Notify authorities if unfit to drive
Home safety:
- Occupational therapist assessment
- Modify environment as needed (e.g. lighting, railings, locks)
- Use of orienting cues
Provide a calm, safe, structured environment with appropriate stimulation

👥 Psychosocial and Support Services

Refer to:
- Dementia Australia (education, resources, support)
- Alzheimer’s Australia (now under Dementia Australia)
- Social worker for care coordination and carer support
- ACAT for assessment of support needs (e.g. respite, home help, residential care)
- Allied health (OT, physiotherapy, dietitian, speech therapy)
Support for caregivers:
- Carer training programs
- Respite services
- Counselling and education
- Carer’s allowance/pension (Centrelink)

📚 Education

Provide education to patient, family, and caregivers:
- Dementia process and progression
- Behavioural and cognitive symptoms
- Management strategies
- Use materials from Dementia Australia
Encourage positive lifestyle strategies:
- Social connection
- Cognitive stimulation/training
- Physical activity
- Healthy diet

🧠 Mental Health and Behavioural Management

Screen for and treat:
- Depression
- Anxiety
- Delirium
- Pain and unmet needs
Consider nonpharmacological interventions as first-line
Refer to psychologists or psychiatrists as needed

🔄 Ongoing Monitoring

Regular review of:
- Cognitive function
- Behavioural changes
- Physical health
- Functional capacity
- Medication adherence
Monitor carer health and burden; offer support and counselling

Non-pharmacological treatments

🧠 Psychological Interventions

Cognitive Behavioural Therapy (CBT)
- Useful for early-stage dementia.
- Aids in adjustment to diagnosis, future planning, and managing depression.
Reminiscence Therapy
- Encourages recalling past experiences using stimuli such as photographs, music, or familiar objects.
- Enhances emotional wellbeing and cognitive function.
Counselling and Support
- Support for patients, families, and caregivers.
- Helps with coping, grief, and understanding disease progression.
Dementia Support Groups
- Peer support for patients and carers.
- Facilitates shared experiences and emotional support.

🧠 Behavioural Interventions

Behavioural Management Therapy
- Targets challenging behaviours (e.g. agitation, wandering, repetitive questioning).
- Employs structured approaches to modify behavioural responses.
Structured Routine and Activities
- Provides consistency and predictability.
- Engaging in activities aligned with the patient’s interests promotes engagement and purpose.
Montessori-Based Activities
- Promotes independence and meaningful engagement.
- Examples:
  - Sorting and Matching: objects or pictures based on colour, shape, or size.
  - Simple Puzzles: with large, familiar images.
  - Sensory Bins: using tactile and olfactory stimuli.
  - Art and Craft: focused on creative expression.
  - Memory Games: matching cards and word games with graded difficulty.

🏡 Environmental Interventions

Frequent Orientation Reinforcement
- Use of large clocks, calendars, and orientation cues.
- Staff should wear name badges and regularly reintroduce themselves.
Environmental Modifications
- Maintain a familiar, calm, and non-stressful environment.
Clear Signage
- Use large, simple labels with images for rooms and common areas.
Colour Contrasts
- Enhance visual navigation by using contrasting colours (e.g. doors vs. walls).
Good Lighting
- Maximise natural light, avoid shadows and harsh lighting.
Uncluttered Spaces
- Reduce visual overload; keep essential items only.
Familiar Objects
- Display personal items (photos, belongings) to provide comfort and recognition.
Adaptive Furniture
- Use comfortable, accessible furniture.
- Avoid sharp edges; chairs should be of appropriate height.
Safety Measures
- Install handrails, grab bars, and remove trip hazards.
Quiet Spaces
- Provide low-stimulation areas for rest or when agitated.
Memory Aids
- Label drawers and cupboards to support independence.
Clocks and Calendars
- Use large, visible displays to help with orientation to time and date.
Adaptable Spaces
- Modify spaces as needs evolve (e.g. flexible dining or resting areas).
Technology Integration
- Use tools like GPS trackers, smart home systems for safety and monitoring (especially useful for patients prone to wandering).

🎵 Alternative and Sensory Therapies

Massage and Aromatherapy
- Can reduce anxiety and promote relaxation.
Music and Dance Therapy
- Helps stimulate memory and mood, particularly in later stages.
Animal-Assisted Therapy
- Offers emotional support and encourages interaction.
Multi-Sensory Stimulation
- Combines light, sound, touch, and smell to enhance cognitive and emotional wellbeing.

📞 Dementia Support Services

Dementia Australia National Dementia Helpline
📞 1800 100 500
Dementia Behaviour Management Advisory Service (DBMAS)
24-hour specialised support for moderate to severe behaviours.
📞 1800 699 799
Carers Australia
Support and advocacy for carers.
My Aged Care
Gateway to Commonwealth-funded aged care services.

Pharmacological treatments

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.

Cholinesterase 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)

Pharmacological practices to address BPSDs

💊 Key Principle: Non-pharmacological interventions are first-line.
💊Pharmacological therapy is reserved for severe, distressing, or dangerous symptoms, where symptoms pose a risk to the person or others, and only when non-drug strategies have failed.
💊Avoid polypharmacy.
💊Always combine with nonpharmacological strategies.
💊Reassess efficacy regularly—do not keep trialling if ineffective.

Ethical Considerations

1. Autonomy

Patients with dementia may have impaired decision-making capacity, especially in moderate to advanced stages.
Where possible, clinicians should:
- Engage patients in shared decision-making.
- Engage a substitute decision-maker (SDM) guided by the patient’s known values and preferences.
- Respect advance care directives if present.

2. Respect for Persons

Acknowledge the inherent dignity of individuals with dementia, regardless of cognitive decline.
Avoid dehumanising behaviours (e.g., over-sedation, coercion).
Ensure communication is respectful, even when capacity is impaired.

3. Beneficence

Aim to relieve suffering, reduce distress, and improve quality of life.
Pharmacological treatments may be appropriate if:
- BPSD is severe (e.g., aggression, psychosis, severe agitation).
- Nonpharmacological strategies are ineffective.
- Safety of the patient or others is at risk.

4. Nonmaleficence

Psychotropics carry significant risks:
- Antipsychotics: ↑ risk of stroke and mortality → black box warning by the FDA (supported by TGA).
- Benzodiazepines: Falls, sedation, worsening cognition.
Treatment should minimise harm:
- Start low, go slow.
- Regularly reassess need and deprescribe where possible.

5. Justice

Equitable access to effective treatment regardless of socioeconomic status, location, or cognitive capacity.
Consider disparities in residential aged care access to geriatric and psychiatric services.
Avoid ageism or diagnostic overshadowing (e.g., dismissing symptoms as ‘just dementia’).

6. Fidelity and Veracity

Clinicians must:
- Act in the patient’s best interest.
- Be honest with families about risks, goals, and limitations of therapy.

Legal Considerations (Australia)

1. Consent and Capacity

Informed consent must be obtained from:
- The patient, if they have decision-making capacity.
- A substitute decision-maker (e.g., enduring guardian, next of kin) if the patient lacks capacity.
Decision-makers must act in line with the patient’s known values and best interests.

2. Advance Care Planning

Advance care directives should be reviewed and respected.
Include documented preferences for or against psychotropic medication use in behavioural crises.

3. Use of Restrictive Practices

Chemical restraint (e.g., use of antipsychotics to control behaviour) is legally regulated:
- Permitted only when absolutely necessary to prevent harm.
- Requires documentation, review, and oversight.
- Must be the least restrictive and proportionate intervention.
- Regulated under the Quality of Care Principles 2014 (Cth) in residential aged care.

4. Reporting Obligations

Elder abuse or neglect concerns (e.g., medication overuse or under-treatment) may trigger:
- Mandatory reporting (varies by state/territory).
- Referral to Aged Care Quality and Safety Commission or Public Guardian.

Antipsychotics

First-line for AD, mixed AD/vascular dementia (etg)
Avoid routine use due to:
- Increased risk of stroke, cardiovascular events, mortality, sedation, falls, delirium, and worsening cognitive decline
Can be trialled:
- For severe aggression, psychosis, persistent distressing hallucinations, or dangerous behaviours
- 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; max 12 weeks use
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
SSRIs (e.g. citalopram)	Agitation, depression	Start low (e.g. 10 mg/day)	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.

Risperidone

Indication

PBS-approved for BPSD:
- Up to 12 weeks use for persistent psychosis, agitation, or aggression in patients with moderate to severe Alzheimer’s, unresponsive to non-pharmacological strategies
- Off-label in other dementias

Dosing Strategy

Start at 0.25 mg twice daily
Titrate by 0.25 mg every 48 hours as needed
Usual effective dose: 0.5 mg twice daily
Max: 1 mg twice daily

Evidence

Risperidone has the strongest evidence base for BPSD, particularly aggression and psychosis
Consider state-based legal requirements for consent (informed/proxy) before initiating antipsychotics

Side Effects

Type	Specific Effects
CNS	Sedation, insomnia, dizziness, somnolence
Metabolic	Weight gain, hyperprolactinaemia
Cardiovascular	Orthostatic hypotension, bradycardia
Extrapyramidal	Parkinsonism, akathisia, tardive dyskinesia
GI	Constipation, sialorrhoea

⚠ Caution: May worsen Parkinsonism, increase fall risk, and precipitate neuroleptic malignant syndrome in vulnerable patients.

Antidepressants

Depression may manifest atypically (apathy, withdrawal, anhedonia), and may not always respond to antidepressants.
Use Cornell Scale for assessment.
Optimise non-drug management first (psychological therapy preferred).
Limited evidence for antidepressants in dementia (Cochrane review).
Consider antidepressant only if:
- No response to nonpharmacological strategies after 4–6 weeks.
- Previous positive response.
- Moderate–severe major depression.
SSRIs have the best evidence for agitation, especially citalopram, though use must be cautious:
- Citalopram:
  - 10 mg PO daily (>65 years); max 20 mg
  - may reduce agitation but associated with QT prolongation, hyponatraemia, and worsening cognition at higher doses (>20 mg in older adults).
- Escitalopram
  - 5 mg PO daily (>65 years); max 10 mg
- Sertraline
  - 50 mg PO daily; max 200 mg
Avoid TCAs (e.g. amitriptyline, doxepin):
- Due to strong anticholinergic effects, which worsen cognition, sedation, falls risk.

Benzodiazepines

Not recommended for long-term use due to:
- Sedation, falls, delirium, dependence, respiratory depression, worsening cognition
If needed for short-term severe agitation or anxiety, can trial:
- Oxazepam (short-acting, no active metabolites):
  - 7.5–15 mg PO, up to 4 times daily
  - Avoid > 2 weeks continuous use
Avoid lorazepam or long-acting benzos like diazepam in the elderly

Nonpharmacological practices to address BPSDs

AGGRESSION

Keep Calm: Allow time, space, and maintain composure.
Who is unsafe and why?
- Identify risk of harm and necessary interventions.
Exclude delirium, pain, discomfort, infection.
Triggers:
- Threat perception?
- Fear linked to past trauma or abuse?
Psychosocial/environmental interventions:
- Personalised sensory/touch strategies.
Assessment tools:
- RAGE, CMAI, OVERT, NPI-C aggression subscale, PAS Pittsburgh Agitation Scale

AGITATION

Check for pain/discomfort: Constipation, infection, temperature/clothing issues.
Exclude delirium
Check stimulation level: Too much or too little?
Understand the person:
- Historical stress responses?
- Previous activities?
Environmental changes: Recent changes in staff or routine?
Interventions:
- Sensory/touch activities (music, massage, pets)
Assessment tools:
- CMAI, PAS, NPI (Agitation/Aberrant Motor Behaviour)
Review medication: Check for akathisia, side effects

ANXIETY

Understand the person:
- History of anxiety or trauma?
- Triggers and preferences?
Triggers:
- Situational or timing-related?
Routine:
- Structured, familiar schedule
Minimise overstimulation
Psychosocial/environmental interventions:
- Music, routine, pet therapy, calming sensory input
Differentiate depression, anxiety, apathy
Assessment tools:
- RAID, IQAD

APATHY

Understand the person:
- Interests, hobbies, preferences
Tailor activities:
- Multi-sensory, music, pets, etc.
Engage one-on-one: 10 mins per shift
Monitor engagement level
Assessment tools:
- AES, Apathy Inventory, NPI-C Apathy subscale
Consider depression or delirium
Review medication

DEPRESSION

Assess:
- Suicide or self-harm risk
Differentiate from delirium, sleep disturbance, etc.
Psychiatric history:
- Major depression?
- Grief or adjustment?
Exercise:
- Gentle, enjoyable physical activity
Psychosocial/environmental interventions:
- Reminiscence, music, pets
Review medication
Assessment tools:
- CSDD, GDS

DISINHIBITION (SOCIAL/SEXUAL)

Observe triggers and early cues
Is behaviour distressing/harming others?
Assess for need for privacy
Inappropriate urination/behaviour: Consider neurocognitive impairment
Assessment tools:
- NPI-C Disinhibition subscale
Psychosocial/environmental interventions:
- Modified clothing, redirection, positive contact
Avoid shaming or punishment
Keep responses neutral, consistent, safe

PSYCHOTIC SYMPTOMS (Delusions and Hallucinations)

Assess for psychiatric history:
- Schizophrenia or other major mental disorders?
Assess for immediate risk:
- Harm to self/others, suicidal ideation
Exclude:
- Delirium (see Delirium card)
- Pain, discomfort, infection
Clarify misperceptions:
- Claims like theft may be misinterpretations
Optimise sensory input:
- Appropriate lighting, clean glasses, hearing aids
Assessment tools:
- NPI: Delusions and Hallucinations subscale
- BEHAVE-AD: Suitable for acute, community, and residential aged care
Psychosocial/environmental interventions:
- Music, outings, exercise, pets or robotic animals
Review:
- Medication (dosage, interactions)
- Consider psychiatric referral

SLEEP DISTURBANCE

Treat underlying causes:
- Manage pain, depression, anxiety, sleep apnoea
- Exclude delirium (see Delirium card)
Review medication:
- Dosage, interactions, sedating effects, underlying conditions
Exercise and daylight exposure:
- Encourage daily walking or gardening
Sleep hygiene:
- Routines based on history/preferences
- Use warm drinks, soothing scents (e.g. lavender), hand massage, soft music, bedtime rituals
Reduce environmental disruption:
- Limit noise/light at night
- Consider relocating to quieter area
Toileting needs at night?
Assessment tools:
- Sleep-log
- NPI / NPI-C Sleep Disorders subscale

WANDERING

Level of Risk:
- Getting lost, falls, sleep disturbance, exits, unsafe spaces
Check environment:
- Too noisy/stimulating? Too quiet?
- Adjust surroundings accordingly
Tailored engagement:
- Small or large group activities
- Multi-sensory (music, outdoors, pets)
Therapeutic touch:
- Massage to reduce need to walk or restlessness
Environmental interventions:
- Disguise exits, install boundary cues/signs
- Provide cues for toilet/bed
ID and contact info:
- Ensure patient wears up-to-date ID
Assessment tools:
- Revised Algase Wandering Scale (RAWS)
  - Long-term care and community versions available

Driving with dementia

Overview

Driving is a complex task requiring intact cognition, perception, attention, motor coordination, and executive function. Dementia can impair one or more of these domains, increasing the risk of unsafe driving. However, not all individuals with mild dementia are unsafe drivers, and decisions must be made case-by-case.

Austroads (via Assessing Fitness to Drive for Commercial and Private Vehicle Drivers, 2022) provides legal and clinical standards that guide decision-making in Australia.

Legal and Regulatory Context (Australia)

Dementia is a notifiable condition under Austroads AFTD guidelines.
Clinicians are obligated to notify patients of their legal duty to report any medical condition that may affect driving to their state or territory driver licensing authority.
Licensing authorities make the final decision, often based on medical input and/or occupational therapy driving assessments.
Patients with mild dementia may be permitted to drive, subject to conditional licensing and periodic review.

Impact of Dementia on Driving Ability

Dementia may impair driving via:

Getting lost on familiar routes (visuospatial disorientation)
Poor concentration and attention (e.g. missing road signs)
Impaired judgement (e.g. unsafe overtaking, misjudging gaps)
Confusion under stress (e.g. pressing accelerator instead of brake)
Reduced insight and awareness of deficits
Slowed reaction time
Impaired visuomotor coordination

Clinical Assessment of Fitness to Drive

There is no single test that reliably predicts driving safety. Therefore, clinical judgement is essential.

Key Clinical Domains to Assess:

Driving History
- Recent accidents, near misses, police referrals
- Family or passenger concerns
Cognitive and Functional Domains
- Memory, attention, visuospatial function, executive function
- Praxis (ability to coordinate limbs with commands)
- Orientation and problem solving under pressure
Vision and Hearing
- Can they detect peripheral hazards, road signs, and sirens?
Reaction Time
- Can they brake or turn rapidly in response to hazards?
Insight and Judgment
- Do they acknowledge limitations or deny any impairment?
Behavioural Changes
- New-onset irritability, impulsivity, or aggression while driving
Functional Driving Tasks
- Lane discipline, obeying traffic signals, interpreting signs
- Ability to navigate unfamiliar detours or follow GPS/map

Cognitive Testing Caveats

Avoid over-reliance on MMSE:
- MMSE ≥24 does not guarantee safety
- MMSE <20 usually correlates with unsafe driving
Formal neuropsychological testing does not reliably predict driving performance.

Referral and Specialist Assessment

Occupational Therapy Driving Assessment (OTDA):
- Considered the “gold standard” for functional driving ability
- Limited by cost and availability
Refer to geriatrician or neurologist if uncertain or if dementia severity is unclear

Monitoring and Review

Six-monthly reviews are recommended for patients with mild dementia who continue to drive.
Re-assess:
- Dementia progression
- New medical events (e.g. stroke, delirium)
- Driving incidents

Counselling and Driving Retirement

Discuss driving early in the disease course.
Acknowledge the emotional and social impact of retiring from driving:
- Loss of autonomy
- Depression, isolation
- Increased risk of institutionalisation

Supportive Counselling Points:

Explore alternative transport (public, taxi, rideshare, community transport)
Consider trial periods without driving
Offer written information and involve family
Inform them of:
- Potential legal consequences (civil or criminal liability if unfit)
- Insurance risks (car or life insurance may be void)

Austroads Guidelines Summary (2022)

Severity of Dementia	Private Vehicle Licensing
Mild	May drive with conditions; 6-monthly review
Moderate or Severe	Unfit to drive
Unstable or progressive disease	Unfit until reviewed
OT driving assessment	Recommended if concern but borderline

Summary

Dementia may not automatically preclude driving, especially in early stages.
Regular review, thorough history, and domain-based clinical assessment are essential.
Use OT driving assessment where available.
Prioritise patient autonomy while ensuring public and individual safety.
Document all discussions and decisions clearly.

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

🧾 Practical Implementation Notes

Best time to act on risk factors: midlife
Useful tools: midlife health assessments, chronic disease care plans
Barriers to dementia diagnosis:
- Short consultations
- Diagnostic complexity
- Patient stigma, misunderstanding, or reluctance
Respect patient preference not to be told diagnosis, but communicate need for cognitive management
Promote secondary prevention if dementia diagnosed:
- Smoking cessation
- Hearing management
- Cardiovascular risk management
- Diet and exercise

TYPES

1. Alzheimer’s Disease

Epidemiology and Pathophysiology

Most common form of dementia, accounting for ~60–70% of cases.
Characterised by an insidious onset and progressive course.
Early symptom: short-term memory impairment.
As disease advances: language dysfunction (aphasia), dyspraxia, executive dysfunction, and personality/behavioural changes.

Neuropathology

Hallmark features:
- Extracellular beta-amyloid plaques
- Intracellular neurofibrillary tangles composed of hyperphosphorylated tau
Leads to neurodegeneration, particularly of cholinergic neurons in the basal forebrain → ↓ acetylcholine (ACh) concentration in the cerebral cortex and hippocampus.

2. Frontotemporal Dementia (FTD)

Typically younger onset (age 45–65)
Associated with focal frontal and temporal lobe atrophy
20–40% have familial inheritance patterns

Initial Features:

Personality change
Social disinhibition
Language dysfunction (progressive aphasia)
Loss of insight

Later:

Apathy, emotional blunting
Memory impairment occurs late

Includes Pick’s Disease as a histopathological variant.

3. Dementia with Lewy Bodies (DLB)

Dementia plus ≥2 of the following:
- Visual hallucinations
- Spontaneous parkinsonism
- Marked fluctuations in cognition/alertness (not explained by delirium)

Sensitivity to antipsychotics is common (can worsen parkinsonism).

4. Vascular Dementia

Related to cerebrovascular disease: infarcts, hypoperfusion, emboli
Often stepwise progression (e.g., after stroke)
May be multi-infarct or strategic infarct

Clinical Clues:

Focal neurological signs
Cardiovascular risk factors (HTN, AF, diabetes, PVD)
Imaging evidence of infarction/white matter disease

Management:

Antiplatelet therapy if prior stroke/TIA
AChEIs may help cognitive symptoms in progressive cases

5. Alcohol-Related Dementia / Korsakoff’s Syndrome

Cognitive deficits: new learning, executive dysfunction
Often frontal lobe dysfunction
Associated with thiamine deficiency

Consider Wernicke-Korsakoff syndrome if ataxia, ophthalmoplegia, confusion present.


FBC	X		Exclude anaemia and infection
ESR or CRP	X		Exclude inflammation, auto-immune disease, infection
Electrolytes	X		Exclude reversible metabolic causes of dementia: Delirium
Calcium	X		Hyperparathyroidism, other causes of hypercalcaemia
Glucose	X		Hypoglycaemia, hyperglycaemia
urea and creatinine	X		Kidney failure
LFT	X		Hepatic disease
Thyroid function	X		Exclude hypothyroidism or thyrotoxicosis
B12 & folate levels	X		Exclude vitamin and folate deficiency
CT scan of brain without contrast	X		Indications – age at dementia onset < 60- focal neurological signs- rapid progression of dementia- recent head trauma- use of anticoagulants- unusual symptoms or gait disturbance.Minimum neuroimaging to exclude presence of a tumour, intracranial space occupying lesion or haematoma. Structural imaging may not be needed in those presenting with moderate-to-severe dementia, if the diagnosis is already clear and other reversible causes have been excluded.
Fasting lipid study	X	X	Risk factor for cerebrovascular disease
Fasting homocysteine (HCy) levels		X	High levels are linked to heart disease, stroke and Alzheimer’s disease. HCy levels can be reduced by taking 1 mg of folic acid daily with additional oral vitamin B6 and B12.
Chest X-Ray (CXR)	X	X	Clinical presentation should determine whether CXR is needed to exclude lung disease or an occult tumour
ECG/EKG	X	X	An ECG should be considered if intending to prescribe acetylcholinesterase inhibitors
Mid-stream specimen of urine (MSU)	X	X	Exclude bacterial infection, a common comorbidity in older people
Serology for syphilis and HIV		X	Only in those with histories suggesting they are at risk
EEG			EEG should not be used as a routine investigation in people with dementia, but should be considered if a diagnosis of delirium or Creutzfeldt–Jakob disease is suspected, or in the assessment of associated seizure disorder in those with dementia.
MRI Scan*		X	Structural imaging or MRI can be used to exclude other cerebral pathologies and to help establish the dementia subtype diagnosis, unless clinical judgement indicates this is inappropriate or if it is contra-indicated (e.g. metal in body, claustrophobia). Structural imaging may not always be needed in those presenting with moderate-to-severe dementia if the diagnosis is already clear. HMPAO SPECT should not be used in people with mild cognitive impairment (MCI) either for the differen- tiation of dementia from MCI or for the differentiation of progressive from non-progressive MCI.
Cerebrospinal fluid (CSF) examination*		X	Specialist referral is required for CSF examination. It may be indicated if Creutzfeldt-Jakob disease is suspected or in rapidly progressive dementia. CSF testing may also be indicated for infectious causes (e.g. neurosyphilis), for confirmation of Alzheimer’s disease (increased levels of tau and phospho-tau and decreased levels of Aβ) or as part of a procedure to detect normal pressure hydrocephalus.
Positron emission tomography (PET)*		X	PET-FDG, i.e. routine glucose PET, or PET for amyloid or tau imaging can be performed upon specialist referral to diagnose neuronal injury or for difficult to diagnose cases. Note that amyloid and tau imaging are not readily available.²
Genetic testing*Familial dementiaApolipoprotein E genotyping		X	Genetic testing for familial dementia (e.g. autosomal dominant Alzheimer’s disease) can be performed upon specialist referral for early onset cases with very strong family histories.
Neuropsychological assessment*		X	Neuropsychological assessment extends beyond clinical cognitive testing¹ and requires specialist referral. Assessment is comprehensive, demanding and rigorous, usually requiring approx. 3 hours. It can be useful to diagnose the cause of dementia, especially to differentiate it from psychiatric conditions, to monitor progress and for medico-legal reasons.