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.
Study aid only. These notes are written with the help of AI. Not for guiding clinical decisions.