Red flags
- Acute/subacute onset (days-weeks) -> delirium, encephalitis, autoimmune, not degenerative dementia
- Rapidly progressive dementia (decline over weeks-months) -> Creutzfeldt-Jakob disease, autoimmune encephalitis, treatable causes
- Memory loss with focal neurological signs, seizures, or headache -> structural/inflammatory cause
- Young age (<65) with memory complaint -> broader differential, higher yield for reversible causes
- Fluctuating course with visual hallucinations -> Lewy body dementia (also marks antipsychotic sensitivity)
- Head trauma, anticoagulation, and memory change -> chronic subdural hematoma
Differential by mechanism
By tempo (the key organising question)
- Acute/subacute (hours-weeks): delirium, encephalitis (infective/autoimmune), transient global amnesia, non-convulsive status, thiamine deficiency (Wernicke-Korsakoff)
- Chronic progressive (months-years): neurodegenerative dementia
Neurodegenerative causes (chronic)
- Alzheimer's disease - commonest; progressive episodic memory loss, later visuospatial/language involvement
- Vascular dementia - stepwise decline, vascular risk factors, executive dysfunction relatively prominent
- Lewy body dementia - fluctuating cognition, visual hallucinations, parkinsonism, REM sleep behaviour disorder
- Frontotemporal dementia - behavioural/personality change or language decline out of proportion to memory, younger onset
Reversible/treatable causes - always screen for these
- Depression (pseudodementia) - mood symptoms prominent, "don't know" answers vs confabulation
- B12/folate deficiency, hypothyroidism
- Normal pressure hydrocephalus (with gait apraxia, urinary incontinence)
- Medication effect (anticholinergics, benzodiazepines, opioids)
- Chronic subdural haematoma, brain tumour
- Obstructive sleep apnoea, alcohol-related cognitive impairment
Transient
- Transient global amnesia - sudden anterograde amnesia lasting hours, resolves completely, retained personal identity, no other neurological deficit
Focused history
- Tempo and trajectory - the single most important discriminator
- Collateral history essential - patient often unaware of the extent of deficit
- Specific domains affected - episodic memory, language, visuospatial, executive function, behaviour/personality
- Functional impact on IADLs (finances, medication management, driving) vs basic ADLs
- Mood symptoms, sleep (REM behaviour disorder, OSA symptoms), alcohol use
- Vascular risk factors, head trauma, anticoagulation
- Medication review, family history of dementia/early death
Focused examination
- Cognitive screening - MMSE or MoCA (MoCA more sensitive for mild/executive impairment); assess specific domains
- Delirium screen (4AT) if acute/fluctuating
- Parkinsonism, gait (magnetic/apraxic gait in NPH), focal neurological signs
- Mood assessment (geriatric depression scale)
- General medical exam - thyroid, cardiovascular, signs of alcohol use
Investigation strategy
- Screen every new presentation: FBE, UEC, calcium, glucose, TFT, B12/folate, LFT; syphilis/HIV serology in selected cases
- CT or MRI brain - all new presentations, to exclude structural cause (tumour, subdural, NPH pattern, significant vascular disease) and support pattern-based diagnosis (hippocampal atrophy in Alzheimer's)
- Formal neuropsychological testing if diagnosis unclear or for medicolegal/capacity purposes
- CSF studies (autoimmune/paraneoplastic panel, 14-3-3 protein) if rapidly progressive dementia suspected
- EEG if seizure/non-convulsive status or CJD suspected
- Amyloid PET/CSF amyloid-tau biomarkers - specialist-directed, increasingly relevant given anti-amyloid therapy eligibility (see Management)
Management
A. Sequence
1. Treat any acute driver first (delirium, encephalitis, metabolic)
2. Correct reversible contributors - B12/folate, thyroid, review deprescribing (anticholinergic/sedative burden), treat depression, manage OSA
3. Confirm and classify the dementia subtype once acute/reversible causes excluded
B. Alzheimer's disease
- Symptomatic: cholinesterase inhibitors (donepezil, rivastigmine, galantamine) for mild-moderate disease; memantine added/used in moderate-severe disease
- Disease-modifying: anti-amyloid monoclonal antibodies - donanemab TGA-approved (May 2025) and lecanemab TGA-approved (September 2025) for mild cognitive impairment/mild dementia due to Alzheimer's with confirmed amyloid pathology; neither is PBS-listed (PBAC declined donanemab in July 2025 over risk-benefit uncertainty) - out-of-pocket cost >$80,000/year, modest effect on decline, requires confirmed amyloid status and serial MRI monitoring for ARIA (amyloid-related imaging abnormalities)
- This is a fast-moving access area - check current PBAC/PBS status before advising a patient, since TGA approval alone does not mean funded access
C. Vascular dementia
- Aggressive vascular risk factor control (BP, lipids, diabetes, antiplatelet/anticoagulation as indicated) - the primary intervention, no specific disease-modifying drug
D. Lewy body dementia
- Avoid antipsychotics (severe neuroleptic sensitivity) - if unavoidable, lowest-dose quetiapine
- Cholinesterase inhibitors often particularly effective for cognitive/hallucination symptoms
E. Behavioural and functional support (all types)
- BPSD management as per Geriatric medicine note
- Advance care planning, driving assessment, capacity assessment where relevant
- Carer education and support, Dementia Australia referral
Traps
- Labelling acute/subacute confusion as "new dementia" without excluding delirium/encephalitis first
- Missing depression (pseudodementia) as a treatable cause of apparent cognitive decline
- Skipping the reversible-cause screen (B12, TFT, structural imaging) because the presentation "looks like" typical Alzheimer's
- Using antipsychotics in suspected Lewy body dementia
- Assuming anti-amyloid antibody therapy is currently accessible in Australia without checking current TGA/PBS status
Talk track
Tempo is the organising question - acute/subacute change is delirium or encephalitis until proven otherwise, chronic progressive change triggers a dementia work-up. Every new presentation gets a reversible-cause screen (bloods, structural imaging) before subtype classification, because depression, B12 deficiency, hypothyroidism, NPH, subdural haematoma and medication effect are all treatable mimics. Management then follows the subtype - vascular risk control for vascular dementia, avoid antipsychotics in Lewy body dementia, and for Alzheimer's the field is moving fast with anti-amyloid antibodies whose Australian access should be checked at the time, not assumed from training knowledge.
8 of 8 sections written · drafted 2026-09-13