Almost all of the diagnostic work is done here. Cognitive testing confirms and characterises what the history has already suggested — it rarely rescues a history that was never taken properly. Budget most of the consultation for this step.

Take a collateral history, separately where you can

An informant who knows the patient well is not optional — anosognosia is common, and in bvFTD and svPPA the patient's own account can be the least reliable part of the assessment. Interviewing patient and informant apart lets each speak freely; it also lets you compare accounts, which is itself diagnostic information.

• What changed, and when did you first notice? Push for a specific anchoring event — a birthday, a holiday, a hospital admission — rather than accepting "a couple of years".
• What can they no longer do that they could do before? Function is more informative than symptom lists, and it feeds directly into step 4.
• Has it been steady, stepwise, fluctuating, or fast? The shape of the decline narrows the differential more than any single symptom.
• Whose idea was this appointment? A patient dragged in by family, versus one who came worried on their own, points in different directions.

The shape of the decline

Probe every domain, not just memory

Leading with memory questions biases the whole history towards Alzheimer's. Walk the six DSM-5-TR domains deliberately — SAMPLES on the Flowchart tab — asking for a concrete example of each.

• Learning and memory — repeating questions, misplacing items, forgetting recent conversations or appointments. Ask whether reminders and cues help: benefit from cueing suggests a retrieval problem rather than a storage one.
• Executive function — managing bills and the chequebook, following a recipe, planning a trip, coping when the routine changes, new poor judgement or scam vulnerability.
• Complex attention — losing the thread in conversation, unable to do two things at once, needing quiet to function.
• Language — word-finding pauses, circumlocution, substituting "thing", losing the meaning of words (svPPA), effortful halting speech with grammatical errors (nfvPPA).
• Perceptual-motor — getting lost in familiar places, difficulty parking or judging gaps, trouble dressing, misreading or bumping into objects (consider posterior cortical atrophy).
• Social cognition — loss of empathy or warmth, tactlessness, apathy mistaken for depression, new rigid routines, dietary change or sweet craving, disinhibition. Often the earliest change in bvFTD, and the one families report as "personality", not "memory".

Neuropsychiatric and sleep history

• Visual hallucinations — well-formed, of people or animals, early in the course, points strongly to DLB. Distinguish from Charles Bonnet in visual loss.
• REM sleep behaviour disorder — acting out dreams, shouting, falling out of bed, often years before cognitive change. Ask the bed partner; it can precede DLB or PD by a decade.
• Depression, anxiety, apathy — carefully separate apathy (reduced initiation with intact mood) from depression, and consider whether mood is the cause of the cognitive picture rather than a consequence (step 6).
• Delusions — theft, infidelity, misidentification, phantom boarder.
• Sleep-disordered breathing — snoring, witnessed apnoeas, daytime somnolence; treatable and frequently missed.

Systems review that changes the differential

• Gait and falls — early gait disturbance with urinary incontinence raises NPH; falls within the first year with parkinsonism raise PSP or DLB.
• Continence — early urinary incontinence is atypical for AD and worth pursuing.
• Autonomic — postural dizziness, syncope, constipation, erectile dysfunction (DLB, MSA).
• Hearing and vision — uncorrected sensory loss both mimics and accelerates cognitive decline, and is one of the largest modifiable risk factors.
• Head injury, seizures, stroke or TIA, cardiac and vascular history.

Medications, substances and risk background

• Full medication reconciliation, including over-the-counter and complementary agents. Total anticholinergic burden, benzodiazepines, opioids, sedating antihistamines and antiemetics — note the start date against the timeline of decline.
• Alcohol quantified honestly, plus nutritional risk (thiamine).
• Vascular risk — hypertension, diabetes, AF, smoking, lipids, sleep apnoea.
• Family history — ages at onset, and specifically any early-onset dementia, motor neurone disease, Huntington's, or a psychiatric-then-neurological pattern in a parent.
• Education, literacy, occupation, first language and cultural background — you need these before you can interpret a single cognitive score in step 3.

Social, safety and legal

• Living situation, who else is at home, and who is doing what for whom.
• Carer identity, health and strain — the carer's capacity determines much of what is possible in step 10.
• Driving, cooking and appliance safety, wandering, firearms access, and management of money — including anyone with access to accounts. See Fitness to drive.
• Existing enduring power of attorney, advance health directive, or will — establish what already exists now, because capacity to make new ones is finite.

In typical Alzheimer's disease the neurological examination is largely normal early on — which is exactly why it matters. Examination is mostly a search for the findings that say this is not typical AD, and for the treatable contributors.

General

• Lying and standing blood pressure — postural drop supports DLB/MSA, and is a falls and delirium risk in its own right.
• Weight and nutrition — unintentional loss is common in advancing dementia and is a prognostic marker; dietary change and sweet preference suggest bvFTD.
• Hearing and vision, with the aids and glasses actually in use — test cognition only after correcting what you can. Cerumen impaction is worth excluding before you conclude anything.
• Cardiovascular — irregular pulse (AF), carotid bruits, heart failure signs.
• Signs of alcohol excess, chronic liver disease, thyroid disease.

Neurological signs and what they point to

A screening score is a measurement, not a diagnosis. Two patients can score 22 on the MoCA for entirely different reasons; which items they lost is worth more than the number they finished with.

Before you administer anything

• Glasses and hearing aids on, quiet room, adequate light, no informant prompting from the corner.
• Not in acute delirium, not acutely unwell, not in pain, not sedated — and note if any of these apply.
• Test in the patient's first language wherever possible, with a professional interpreter rather than a family member. Translating a memory test on the fly invalidates it.
• Record education, literacy, occupation and premorbid ability — you cannot interpret the result without them.

Choosing the instrument

Cut-offs are indicative screening thresholds, not diagnostic in isolation — interpret alongside age, education, language, sensory function, and premorbid ability.

Reading the profile

• Delayed recall that does not improve with cueing or recognition — a storage (hippocampal) deficit, characteristic of typical AD.
• Recall that jumps with cueing — a retrieval deficit; think subcortical, vascular, frontal-executive, depression or medication effect.
• Trails B, letter fluency, abstraction and serial subtraction disproportionately affected — executive/frontal-subcortical pattern.
• Naming and single-word comprehension lost with fluent, empty speech — semantic.
• Cube, clock and intersecting pentagons disproportionately affected — visuospatial; consider DLB or posterior cortical atrophy.
• Effortful, agrammatic speech with speech apraxia — nfvPPA.
• A near-normal score with a family reporting profound change — take the family seriously. Screening instruments are weakest at exactly the two ends where you most need them: high premorbid ability, and bvFTD, where MMSE and MoCA can both be normal.

When to go further

• Formal neuropsychological assessment — young onset, high premorbid ability with normal screening but convincing history, ambiguous mild NCD, suspected mimic (particularly depression), medicolegal or capacity questions, or when subtype differentiation will change management.
• Speech pathology assessment — suspected primary progressive aphasia, where the variant classification often turns on language features a screening tool does not sample.
• Repeat testing — when the diagnosis is uncertain, a documented change over 6–12 months is often more informative than another cross-sectional test today. Use the same instrument, and mind practice effects.

Pattern-recognition tools

Four bedside references, each one opening in place: the screening instruments and how to read their profiles, a heat-map of which features carry weight in which condition, and criteria-oriented checklists for the individual subtypes. Compiled by Rhymie Yusoff from the sources on the Education page.

DSM-5-TR Criterion B turns entirely on function: does the cognitive deficit interfere with independence in everyday activities? If yes, it is major NCD; if the person compensates but is still independent, it is mild. This is a clinical judgement about a specific person's real life — no test score makes it for you.

Instrumental ADLs go first

Complex, cognitively demanding tasks fail before basic self-care does. Ask about each one concretely, and ask the informant, not just the patient.

• Finances — paying bills on time, banking, unusual purchases, susceptibility to scams, unopened mail. Often the very first IADL to go, and the highest-consequence.
• Medications — missed or doubled doses, whether a blister pack has become necessary, whether someone else now manages them.
• Transport — driving incidents, getting lost, giving up night driving, stopping altogether.
• Shopping and cooking — repeat purchases, spoiled food in the fridge, meals simplified or skipped, appliances left on.
• Telephone and technology — managing calls, messages, and any device they previously used confidently.
• Housework and home maintenance — a decline in standards that the person has not noticed.

Then basic ADLs

• Bathing, dressing, grooming, toileting, transfers, feeding, continence — typically preserved until moderate disease, so early loss here should prompt a search for a physical cause or a non-AD diagnosis.

Instruments worth using

Before you attribute a functional loss to cognition

• Is it physical? Arthritis, weakness, breathlessness, pain and frailty all cause functional loss without cognitive impairment.
• Is it sensory? Uncorrected hearing or vision loss disables independently.
• Is it motivational or mood-related? Apathy and depression reduce performance without reducing capability.
• Is it environmental or lifelong? Someone whose spouse always did the banking has not lost a skill they never exercised — ask what changed, not just what they cannot do.

Turning the assessment into a plan

• Refer for My Aged Care assessment for home supports and, where appropriate, a comprehensive assessment for higher-level care — the wait times mean starting early is part of the treatment.
• Occupational therapy home assessment for safety, equipment and simplification of high-risk tasks.
• Name explicitly which functions are now unsafe to perform unsupervised, and document it — particularly driving, cooking, medication management and finances.
• Re-measure function at review; functional trajectory is the most meaningful progression marker you have, and more useful than a repeated screening score.

Neither severity nor aetiology can be finalised until delirium has been excluded or has resolved. A cognitive score obtained during a delirium tells you about the delirium, not about the underlying brain — and a diagnosis of dementia made on that score will follow the patient for the rest of their life.

Screen everyone at first contact

What separates delirium from dementia at the bedside

Delirium superimposed on dementia

• Dementia is the single largest risk factor for delirium, and the two coexist constantly — finding one never excludes the other.
• The diagnostic question is not "which is it?" but "what is the baseline, and what is new?" Establishing the premorbid baseline from an informant, using something like the IQCODE, is what makes the distinction possible.
• Where a delirium is present, treat it, then re-assess cognition once it has resolved — commonly weeks to months later, not at discharge.
• An episode of delirium is itself a marker of substantially increased risk of subsequent dementia diagnosis; arrange follow-up cognitive review even when the patient returns to apparent baseline.

Look for the precipitant

The PITCHED checklist in step 10 works just as well as a delirium precipitant screen as it does for behavioural symptoms — pain, infection, thirst, constipation, hunger, environment and drugs account for a large share of what precipitates delirium in this population. Add hypoxia, retention, electrolyte disturbance, and any recent medication change.

The decline should not be better explained by another mental disorder or by a reversible cause. Truly reversible dementias are uncommon, but partially reversible contributors sit on top of a neurodegenerative process very often — and treating them is frequently the largest single improvement you can offer.

The standard screen

• Bloods: FBC, EUC, LFTs, calcium, glucose or HbA1c, TSH, vitamin B12 and folate.
• Consider by indication: ESR/CRP, syphilis and HIV serology, vitamin D, coeliac serology, copper/caeruloplasmin in young onset, drug levels, and a toxicology screen where substance use is plausible.
• Structural neuroimaging — step 8.
• Sleep study where sleep-disordered breathing is suspected.

Mimics to screen for

• Depression / pseudodementia
  Often subacute onset, prominent "I don't know" answers, effort-dependent testing, mood symptoms preceding cognitive complaints — improves with treatment of the mood disorder. Late-life depression can also be a prodrome of dementia, so treat the mood and re-test rather than choosing between the two.
• Other psychiatric disorders
  Anxiety, psychotic disorders, and severe distress can all impair attention and processing speed on bedside testing.
• Substance or medication effects
  Anticholinergics, benzodiazepines, opioids, alcohol, sedating antihistamines and antiepileptics. Check the temporal relationship against the decline, calculate the anticholinergic burden, and run a structured deprescribing trial before accepting the diagnosis.
• Uncorrected sensory impairment
  Hearing or visual loss can masquerade as cognitive impairment on bedside testing, and independently accelerates decline. Correct it, then re-test.
• Delirium not yet resolved
  Revisit step 5 if the picture is fluctuating or acute.
• Endocrine and metabolic
  Hypothyroidism, hypercalcaemia, hyponatraemia, hypoglycaemia and B12 deficiency — all on the standard screen, all worth correcting even when they are clearly not the whole story.
• Normal pressure hydrocephalus
  Gait disturbance first, then urinary incontinence, then cognition. Ventriculomegaly out of proportion to sulcal atrophy with a tight high convexity (DESH) on imaging — refer for tap test and neurosurgical opinion.
• Chronic subdural haematoma
  Often no recalled head injury, particularly on anticoagulants. Fluctuating conscious state or focal signs; found on the scan you ordered in step 8.
• Obstructive sleep apnoea
  Impairs attention, memory consolidation and executive function; treatment produces measurable cognitive gains.
• Alcohol-related brain injury and thiamine deficiency
  Consider Wernicke encephalopathy in any malnourished or alcohol-dependent patient with confusion, ataxia or eye movement abnormality — treat with parenteral thiamine first and confirm later.
• Chronic pain and its treatment
  Both the pain and the opioid can be doing the damage; each is modifiable.

Most of dementia assessment is unhurried and outpatient. These are the features that should pull a patient out of that pathway — because the diagnosis is likely to be something other than a common neurodegenerative dementia, because the investigation set is different, or because the window for treatment is short.

Structural imaging is part of the standard workup for a new diagnosis of dementia, for two separate reasons: to exclude a lesion that changes management, and to support or refute the suspected subtype. It does not make the diagnosis — a normal scan does not exclude dementia, and atrophy on a scan does not create it.

Which modality

• MRI is preferred where it is available and tolerated — better grey/white differentiation, better assessment of the medial temporal lobes, and the only way to see microbleeds, restricted diffusion and small infarcts properly.
• CT is acceptable when MRI is contraindicated, unavailable, or not tolerated. It will still exclude a tumour, subdural or hydrocephalus, and gives a usable impression of atrophy and vascular burden.
• Where the clinical question is urgent (step 7), image on the urgent pathway rather than waiting for an outpatient MRI slot.

What to ask for on the request

• Coronal T1 perpendicular to the long axis of the hippocampus — the plane in which medial temporal atrophy is actually scored. Ask for it by name; you will not get it by default.
• FLAIR for white matter hyperintensity burden.
• T2*-weighted or SWI for microbleeds and superficial siderosis — essential if cerebral amyloid angiopathy is a consideration, and mandatory before any anti-amyloid therapy.
• DWI where rapid progression or prion disease is in the differential.
• State the clinical question on the request. "Cognitive decline" gets you a report about atrophy; "suspected svPPA — assess anterior temporal asymmetry" gets you an answer.

Read it yourself, with the rating scales

Four visual rating scales cover most of what a structural scan contributes in this population. All four, with real template sections and worked grades, are in the neuroradiology pane.

Patterns worth knowing

• Alzheimer's — medial temporal and posterior/parietal atrophy, usually symmetric.
• bvFTD — frontal and anterior temporal atrophy, often strikingly asymmetric.
• svPPA — asymmetric anterior temporal lobe atrophy, typically left-predominant, with a "knife-edge" appearance.
• Vascular — strategic infarcts, lacunes, confluent white matter change; the burden should plausibly explain the deficit.
• DLB — relatively preserved medial temporal lobes compared with AD of similar severity.
• PSP — midbrain atrophy, the hummingbird and morning-glory signs.
• CAA — lobar microbleeds and cortical superficial siderosis on SWI.

Beyond structural imaging

Everything above now assembles into a diagnosis with four parts: whether it is a neurocognitive disorder, whether it is major or mild, how severe it is, and what is causing it.

The four criteria, in summary

The Flowchart tab works through each criterion in full, including the SAMPLES domain list and the major-versus-mild distinction.

Severity — and staging with CDR

DSM-5-TR specifies severity for major NCD as mild, moderate or severe, defined by which activities need assistance: instrumental activities (mild), basic activities (moderate), or full dependence (severe). The Clinical Dementia Rating is a clinician-rated global stage that maps onto this and is more reproducible for tracking over time — use it to stage once the diagnosis is made, not to make it.

Aetiological subtype

• Specify the presumed cause — Alzheimer's disease, frontotemporal lobar degeneration, Lewy body disease, vascular disease, traumatic brain injury, substance/medication use, HIV infection, prion disease, Parkinson's disease, Huntington's disease, another medical condition, multiple aetiologies, or unspecified.
• Most subtypes carry a probable versus possible distinction, generally turning on whether there is genetic evidence or a sufficiently clear and characteristic clinical course. Say which you mean; "probable" and "possible" are not interchangeable in a letter that will follow the patient.
• Multiple aetiologies is the honest answer more often than it is given. Mixed Alzheimer and vascular pathology is the commonest finding at autopsy in this age group; a formulation that names both is usually closer to the truth than one that forces a single label.

Behavioural specifier

Record with or without behavioural disturbance, and name the specific symptoms — psychotic symptoms, mood disturbance, agitation, apathy, or other. This is not a formality: it determines much of step 10, and it is the part of the diagnosis carers most need written down.

Writing the formulation

A formulation written this way answers, in one paragraph, every question the next clinician will have — and makes explicit which parts are firm and which are provisional.

Nothing on the pharmacological list below matters as much as the first three items on the non-pharmacological one. Plan the management as a package with a named review date, not as a prescription.

Disclosing the diagnosis

• Ask what they already suspect, and what they want to know, before you tell them. Most people want the diagnosis; a minority do not, and that preference deserves respect.
• Use the word. "Dementia" or "Alzheimer's disease", not "memory problems" — ambiguity denies people the chance to plan while they still can.
• Pair the diagnosis with what can be done: treatable contributors, supports, legal and financial planning, and the follow-up date. A diagnosis given without a plan is the version people remember badly.
• Offer a written summary and a second appointment. Very little of the first conversation is retained.

Non-pharmacological management — first, and continuing

• Treat every contributor found in step 6 — hearing and vision, sleep apnoea, depression, pain, deprescribing anticholinergics and sedatives.
• Vascular risk management — blood pressure, diabetes, lipids, AF, smoking. Relevant to every subtype, not only vascular dementia.
• Physical activity — the intervention with the best evidence across cognition, mood, falls and function. Prescribe it specifically.
• Cognitive stimulation therapy for mild–moderate disease; social engagement and structured routine.
• Occupational therapy for home safety, task simplification, and assistive technology.
• Carer education, training and support — carer strain predicts institutionalisation more strongly than the patient's cognitive score. Dementia Australia (National Dementia Helpline 1800 100 500), carer support groups, respite, and Carer Gateway.
• My Aged Care assessment for home supports; social work referral for financial and accommodation planning.
• Nutrition, dental and continence review; falls prevention; immunisation.

Medications

Dementia Medications Guide, compiled 18 Aug 2026 by Rhymie Yusoff, Consultant Geriatrician, from a clinical evidence summary (OpenEvidence) — cognitive-enhancing medications and BPSD medications, side by side.

BPSD — behavioural and psychological symptoms

Behaviour is communication. Before reaching for a drug, describe the behaviour precisely, look for what is driving it, and change that. Antipsychotics in this population carry an increased risk of stroke and death, and the number needed to harm is uncomfortably close to the number needed to treat.

PITCHED — the reversible drivers, checked every time

A Queensland-familiar checklist for the physical and environmental causes of changed behaviour in cognitive impairment. Work through it before, and alongside, anything pharmacological — it doubles as a delirium precipitant screen for step 5.

A structured approach to a behaviour

• Describe — what exactly happens, when, where, with whom, how often, and who is distressed by it. Ask the staff or carer to keep a short behaviour chart for a week.
• Investigate — work PITCHED; consider unmet need, boredom, fear, over- or under-stimulation, and the approach being used to deliver care.
• Create — a plan the people actually present can carry out, written down, with one or two changes at a time.
• Evaluate — at a defined date. If it did not work, change it rather than adding to it.
• Escalate to pharmacological treatment only where there is risk of harm or severe distress that has not responded — then start low, review within days to weeks, define a stopping point, and attempt withdrawal after 3 months of stability. Avoid antipsychotics entirely in suspected DLB or PDD.

Prescribing detail for each agent, including the Australian regulatory position, is in Part 2 — BPSD medications above.

Follow-up

Also review at each visit: current medication list and anticholinergic burden, continence, nutrition and weight, falls, pressure areas in later disease, immunisations, and whether the carer is coping.

Advance care planning

Start it early — while the person still has capacity to make the documents that matter. The window closes quietly, and families are left without authority at exactly the point they need it. Queensland instruments:

• Raise it at diagnosis, not at crisis. Frame it as ordinary planning that everyone should do, not as a conversation about dying.
• Document capacity for each instrument at the time it is made — capacity is decision-specific, and a dementia diagnosis alone never removes it. See Capacity assessment.
• Revisit at each stage transition, and make sure the documents are actually accessible — uploaded to My Health Record, copies with the substitute decision-maker, the GP and the residential facility.
• As the disease advances, shift the conversation to goals of care, hospital transfer preferences, and palliative care involvement. Advanced dementia is a terminal illness and deserves to be planned for as one.

Safety and risk, revisited at every review

• Driving — a legal reporting obligation as well as a clinical one in Queensland. See Fitness to drive.
• Finances — scam and elder-abuse vulnerability rises early; check who has account access and whether anything has changed.
• Home safety — cooking and appliances, smoking, wandering and getting lost, medication self-administration, firearms.
• Carer safety — ask directly about aggression, and about the carer's own health.