Neurology · Full case

Dementia

NICE NG97CKS 2024RCGP SCA

MoCA ≤25Montreal Cognitive Assessment — screen threshold (max 30)

AMT ≤7Abbreviated Mental Test — indicates significant impairment (max 10)

6 weeksUrgent memory clinic referral target — NICE NG97

Donepezil 5mgFirst-line cholinesterase inhibitor — mild-moderate Alzheimer's

B12 / folateReversible causes — always test before diagnosing dementia

Delirium firstAcute confusion = delirium until proven otherwise — not dementia

DVLA notifyPatient must inform DVLA at diagnosis — legal duty; GP documents

CapacityAssess decision-by-decision — dementia diagnosis ≠ automatic incapacity

📋 Clinical Stem — Dementia Assessment

A patient presents with concerns about memory or thinking, or a family member raises concerns about cognitive decline — requiring systematic assessment to distinguish normal ageing from mild cognitive impairment from dementia, exclude reversible causes and delirium, determine functional impact, assess capacity and safeguarding risk, initiate appropriate investigations and referral, and support the patient and family through the diagnostic pathway while preserving dignity and autonomy.

"Mrs Ahmed, 72 years old, attends with her daughter. Her daughter requested the appointment and explains that her mother has been 'getting confused' over the last 18 months — forgetting appointments, repeating questions, and last week she left the gas hob on after making tea. Mrs Ahmed says she is 'fine' and becomes tearful when her daughter describes these incidents. She lives alone, her husband died three years ago, and she takes ramipril for hypertension. Her daughter is worried 'it's Alzheimer's' and wants to know what can be done. Mrs Ahmed says she doesn't want to go into a home."

Dementia presentations are rarely straightforward memory complaints. Patients may present with anxiety, low mood, functional decline (driving errors, financial mismanagement, self-neglect), behavioural change (disinhibition, apathy, personality shift), or the patient may deny all symptoms while the family is deeply concerned. The SCA scenario tests collateral history taking, capacity assessment, safeguarding judgement, breaking bad news skills, and advance care planning — not just the diagnostic algorithm. The framework applies whether the patient has insight, partial insight, or no insight at all.

Scenario A — Family-led concern, patient lacks insight Daughter reports progressive memory loss and functional decline; patient minimises symptoms, becomes defensive or tearful. Requires tactful collateral history without excluding patient, assessment of capacity for medical decisions, and safeguarding evaluation (is patient safe at home alone?).

Scenario B — Patient-led concern, worried well vs. MCI 68yo professional presents with subjective memory complaints ('can't remember names like I used to'), no functional impairment, scoring 28/30 on MoCA. May be normal ageing or early MCI. Needs reassurance, baseline cognitive assessment, and lifestyle modification advice — not immediate dementia workup.

Scenario C — Post-diagnosis medication review Patient diagnosed with Alzheimer's 6 months ago, started donepezil, now presents with nausea and vivid nightmares. Carer asks if the drug is 'doing anything' because memory seems the same. Requires side-effect management, realistic expectation-setting (donepezil slows decline, doesn't reverse it), and review of non-pharmacological support.

Scenario D — Acute confusion — delirium not dementia 79yo with 3-day history of confusion, hallucinating, agitated at night. No prior cognitive concerns. This is delirium until proven otherwise — requires urgent medical assessment for infection, metabolic disturbance, drug causes. Never diagnose dementia during acute confusion.

Scenario E — Behavioural variant frontotemporal dementia 62yo man, personality change over 2 years — socially disinhibited, impulsive spending, apathetic, eats excessively. Memory relatively preserved. Wife describes 'he's a different person.' This is not Alzheimer's — needs specialist referral for FTD workup (requires neuropsychiatry, not standard memory clinic).

Key variables to adapt for: Insight level (patient aware vs. anosognosia); presenting complaint (memory vs. behaviour vs. function vs. mood); tempo (rapid = delirium/CJD/subdural; slow = neurodegenerative); age (young-onset dementia <65 has different causes — alcohol, FTD, genetic); living situation (alone = safeguarding risk; carer burnout); comorbidities (vascular risk factors, Parkinson's, alcohol); ethnic/cultural factors (stigma, family structure, language barriers for cognitive testing).

Steps:

Step 1

History Taking — Open Question First · Targeted Questions · ICE · Psychosocial Context

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The dementia history has five simultaneous objectives: establish the cognitive and functional trajectory (onset, progression, domains affected — memory, language, visuospatial, executive, behaviour), obtain collateral history from someone who knows the patient well — essential because patients with dementia typically lack insight and underreport deficits, exclude delirium and depression — the two great dementia mimics that are reversible, identify vascular risk factors and potentially reversible causes, and assess immediate safeguarding risk — can this person live safely in their current environment? Every dementia consultation is a safeguarding assessment.

🎓 Consultation opener — use existing information first

"I can see you're both here today — thank you for coming in. Can you tell me what's been concerning you, and we'll take it from there?"

Opening with 'you're both here' acknowledges the family member's presence without excluding the patient. 'What's been concerning you' (plural) invites both to contribute without presupposing who will speak first. Dementia consultations require extreme tact — the patient may feel infantilised if the GP speaks only to the family, but the GP needs collateral history because patients with cognitive impairment systematically underreport their deficits. This opener creates space for both voices from the outset.

1A — Start with an open question: let the patient lead, then move to targeted questions

Question to ask	Why it matters clinically	Changes what?
🟢 OPEN QUESTION — always start here"Can you tell me what's been happening — what have you noticed changing?"	The dementia narrative — when told by the family — reveals functional decline ('she can't manage her medications', 'he got lost driving to the supermarket'), behavioural change ('she's not herself anymore', 'he's stopped seeing friends'), and timeline ('it's been gradual over two years' vs. 'it came on suddenly three weeks ago'). The patient's response reveals insight level. If the patient says 'I'm fine, nothing's wrong' while the daughter lists major functional losses, that discrepancy itself is diagnostically significant — anosognosia (lack of insight) is a core feature of Alzheimer's disease.Scores: Global Skills (patient-centredness), Tasks (efficient data gathering), Relating to Others (managing a three-way consultation with diplomacy). The examiner is watching how you balance gathering essential collateral information without excluding or humiliating the patient.	DDxSafeguardingPsychosocial
Onset and progression"When did you first notice something wasn't quite right? Has it been getting worse — gradually or in steps?"	Tempo distinguishes dementia subtypes and mimics. Gradual progression over months-to-years = neurodegenerative dementia (Alzheimer's, DLB, FTD). Stepwise decline = vascular dementia (small strokes cause sudden functional drops, then plateaus). Rapid onset over days-to-weeks = delirium (infection, metabolic, drug) or rapidly progressive dementia (CJD, paraneoplastic, autoimmune). Sudden onset = stroke, subdural haematoma, or severe delirium. Never diagnose dementia during acute confusion — it's delirium until proven otherwise.NICE NG97: 'dementia is a progressive condition' — if it's not progressive, it's not dementia. Delirium is acute and fluctuating. Depression causes 'pseudodementia' — subjective cognitive complaints with objective testing relatively preserved.	DDxUrgency
Memory domain — anterograde"Do you find yourself repeating questions or stories? Forgetting appointments or recent conversations?"	Anterograde memory impairment — inability to form new memories — is the hallmark of Alzheimer's disease. The patient asks the same question within minutes, forgets conversations from yesterday, misses appointments. Remote memory (childhood, historical events) is relatively preserved until late disease. If recent memory is intact but the patient can't recall childhood events, consider functional/dissociative disorder, not dementia.Ask the informant, not the patient — patients with memory impairment don't remember that they forget. 'Does she repeat herself?' is more reliable than 'Do you repeat yourself?'	DDxRx choice
Functional impact — ADLs"How are you managing at home — cooking, shopping, managing money, taking medications?"	Functional impairment in activities of daily living (ADLs) is what distinguishes dementia from mild cognitive impairment (MCI). MCI = cognitive impairment without functional loss. Dementia = cognitive impairment causing functional impairment. Instrumental ADLs (iADLs) decline first: managing finances, medications, cooking, using the phone, driving. Basic ADLs (washing, dressing, eating) are preserved until moderate-to-severe dementia. If basic ADLs are impaired early, consider delirium, depression, or physical illness — not typical Alzheimer's.This question determines diagnosis (MCI vs. dementia), severity staging (mild/moderate/severe), and safeguarding risk (can they live alone safely?).	DDxSafeguardingReferral urgency
Language and communication"Have you noticed any difficulty finding the right word, or trouble following conversations?"	Language impairment helps distinguish dementia subtypes. Alzheimer's: word-finding difficulty (anomia), circumlocution ('the thing you write with' instead of 'pen'), comprehension relatively preserved. Semantic dementia (FTD subtype): loss of word meaning — patient doesn't recognise what a 'pen' is. Vascular dementia: dysarthria (slurred speech) if stroke affects speech areas. Primary progressive aphasia: isolated language decline, memory relatively preserved initially.If language is profoundly impaired but memory seems intact, this may not be Alzheimer's — refer to neurology for PPA or FTD workup.	DDx subtypeSpecialist ref
Visuospatial and executive function"Any difficulty finding your way around — getting lost in familiar places? Trouble with planning tasks or organising things?"	Visuospatial impairment: getting lost in familiar environments, unable to judge distances, difficulty parking the car. Suggests posterior cortical atrophy (Alzheimer's variant) or Lewy body dementia. Executive dysfunction: poor planning, impaired judgement, disinhibition, impulsivity. Prominent executive dysfunction early suggests frontotemporal dementia or vascular dementia (subcortical small vessel disease). Alzheimer's typically starts with memory; if executive/visuospatial problems dominate early, consider non-Alzheimer's dementias.Visuospatial deficits have major functional consequences — unsafe driving, wandering, falls. Executive dysfunction impairs financial decision-making and vulnerability to scams.	DDx subtypeDriving safetySafeguarding
Behavioural and personality change"Has there been any change in personality — things they wouldn't normally do or say? Withdrawal from activities they used to enjoy?"	Behavioural variant frontotemporal dementia (bvFTD) presents with personality change, not memory loss: disinhibition (socially inappropriate behaviour, sexual disinhibition, impulsive spending), apathy (loss of motivation, emotional blunting), loss of empathy, compulsive behaviours (repetitive rituals, hoarding), dietary changes (overeating, food fads). Memory is relatively preserved early. If the family say 'he's a different person' but memory testing is normal, suspect FTD — this requires specialist referral to neuropsychiatry, not standard memory clinic.Apathy is distinct from depression: in apathy, the patient lacks motivation and doesn't care; in depression, the patient is distressed and wants to do things but can't. Apathy responds poorly to antidepressants.	DDx — FTDSpecialist refSafeguarding
Psychiatric symptoms — hallucinations, delusions, mood"Any changes in mood — anxiety, low mood, irritability? Seeing or hearing things that aren't there?"	Depression is the great dementia mimic: 'pseudodementia' — depressed patients complain bitterly of memory problems ('I can't remember anything, doctor') but objective testing shows mild deficits only; patients with dementia underreport their memory loss. Visual hallucinations early in the disease suggest Lewy body dementia (DLB) — well-formed, detailed hallucinations (people, animals) that the patient may describe matter-of-factly. Paranoid delusions (e.g. 'someone is stealing my money') occur in mid-stage Alzheimer's. Auditory hallucinations suggest functional psychosis or delirium, not typical dementia.NICE NG97: depression and dementia commonly coexist — treat both. Don't assume cognitive symptoms are 'just depression' without objective cognitive testing.	DDx — DLB vs. ADRx — antidepressantAntipsychotic risk
Delirium screen — acute change, fluctuation"Was there a sudden change recently — over days or a week? Does the confusion come and go during the day?"	Delirium is acute (onset over hours-to-days), fluctuating (worse at night, lucid intervals), and has an identifiable medical cause (infection, drugs, metabolic). Dementia is chronic (onset over months-to-years), progressive, and has no acute medical trigger. If cognitive impairment started suddenly in the last few weeks, it is delirium until proven otherwise — do not diagnose dementia during delirium. Look for infection (UTI, chest), metabolic (hypercalcaemia, hyponatraemia, uraemia), drugs (anticholinergics, benzodiazepines, opioids), and structural causes (subdural haematoma, stroke).Delirium superimposed on dementia: patients with dementia are vulnerable to delirium. If a patient with known dementia has sudden worsening, it's delirium on top — find the medical cause.	Delirium vs. dementiaUrgent IxAdmit if severe
Medications — anticholinergics, sedatives"What medications are you taking — anything over-the-counter or from a friend?"	Anticholinergic drugs impair cognition and can mimic or worsen dementia: antihistamines (chlorphenamine, promethazine), tricyclic antidepressants (amitriptyline), bladder antimuscarinics (oxybutynin, solifenacin), antipsychotics (quetiapine). Benzodiazepines and Z-drugs cause sedation and amnesia — stop these before diagnosing dementia. Polypharmacy (≥5 drugs) is an independent risk factor for cognitive impairment in older adults. Opioids cause confusion. Review every medication — is it necessary? Can the anticholinergic burden be reduced?Use the Anticholinergic Cognitive Burden (ACB) scale: ACB score ≥3 is associated with increased dementia risk. Switch oxybutynin (ACB=3) to mirabegron (ACB=0). Stop sedating antihistamines.	Drug-induced cognitive impairmentStop culprits
Alcohol history — quantity, pattern, CAGE"How much alcohol do you drink in a typical week? Has anyone suggested you should cut down?"	Alcohol-related brain damage (ARBD) — including Wernicke-Korsakoff syndrome — causes dementia, particularly in people under 65. Chronic heavy drinking causes cortical atrophy, executive dysfunction, and anterograde amnesia (Korsakoff's). Acute Wernicke's encephalopathy (thiamine deficiency) presents with confusion, ataxia, and ophthalmoplegia — requires urgent IV thiamine. ARBD is partially reversible with abstinence and thiamine replacement. If a younger patient (<65) presents with cognitive impairment, always ask about alcohol — it's a treatable cause.CAGE screening: Have you felt you should Cut down? Have people Annoyed you by criticising your drinking? Have you felt Guilty? Do you need an Eye-opener? ≥2 positive = alcohol problem.	Reversible causeThiamine + abstinenceAddiction services
Vascular risk factors — stroke, TIA, HTN, DM, smoking, AF"Any history of stroke, mini-strokes, high blood pressure, diabetes, heart problems, or smoking?"	Vascular dementia is the second commonest cause of dementia (after Alzheimer's) and is often mixed with Alzheimer's pathology (mixed dementia). Risk factors: hypertension, diabetes, smoking, hyperlipidaemia, atrial fibrillation, previous stroke/TIA, IHD. Vascular dementia has a stepwise progression (sudden drops in function after small strokes, then plateaus). Cognitive profile: executive dysfunction, slowed processing, subcortical features (gait disturbance, urinary incontinence, emotional lability). Memory may be relatively preserved. Aggressively manage vascular risk factors — this is the only dementia subtype where you can slow progression by treating hypertension, diabetes, and starting antiplatelet/anticoagulant.Subcortical vascular dementia (Binswanger's) — small vessel disease on MRI (white matter hyperintensities). Treat hypertension to target <140/90; start aspirin or clopidogrel if not anticoagulated.	Vascular vs. ADBP control, statin, antiplatelet
Falls, gait disturbance, parkinsonism"Any falls, unsteadiness, or stiffness in your movements?"	Lewy body dementia (DLB) and Parkinson's disease dementia have overlapping features: parkinsonism (tremor, rigidity, bradykinesia), postural instability and falls, visual hallucinations, fluctuating cognition (good days and bad days), REM sleep behaviour disorder (acting out dreams — shouting, thrashing in sleep). If parkinsonism precedes dementia by >1 year = Parkinson's disease dementia. If cognitive symptoms and parkinsonism appear together or dementia first = DLB. Both are sensitive to antipsychotics — typical antipsychotics (haloperidol) can cause fatal neuroleptic sensitivity reactions in DLB. Atypicals (quetiapine) are safer but still risky.Falls in dementia have multiple causes: orthostatic hypotension (autonomic dysfunction in DLB), gait apraxia (normal pressure hydrocephalus — triad of dementia, gait disturbance, urinary incontinence), visual agnosia (can't recognise obstacles), polypharmacy sedation.	DLB vs. ADAntipsychotic contraindicationParkinson's specialist
Family history — dementia, Down syndrome"Is there any family history of dementia or memory problems?"	Most dementia is sporadic (no genetic cause), but family history increases risk. Autosomal dominant Alzheimer's disease (APP, PSEN1, PSEN2 mutations) presents at age 30–60 — rare but important in young-onset dementia (<65 years). Family history of Down syndrome: trisomy 21 → early-onset Alzheimer's (virtually all people with Down syndrome develop Alzheimer's pathology by age 40). Frontotemporal dementia has a familial component in ~40% of cases (C9orf72, MAPT, GRN mutations). If multiple family members have young-onset dementia, consider genetic counselling and referral to a specialist genetics service.ApoE ε4 allele increases Alzheimer's risk (ε4/ε4 homozygotes have 10× risk) but it is neither necessary nor sufficient for disease — don't offer ApoE testing outside research settings (no clinical utility, causes psychological harm).	Genetic dementiaGenetics referral

1B — Red flags: must not miss · must ask · must act

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Red Flags — act before continuing history

Red flag	Why dangerous	Action
Rapid progression over weeks (not months)	Rapidly progressive dementia (RPD) — CJD (prion disease), paraneoplastic syndrome, autoimmune encephalitis, CNS vasculitis. CJD: rapidly progressive dementia + myoclonus + ataxia; median survival 4 months from symptom onset. Autoimmune encephalitis (e.g. anti-NMDA receptor): psychiatric prodrome, seizures, movement disorder, autonomic instability — potentially treatable with immunotherapy if recognised early.	Urgent neurology referral same week
Acute confusional state — fluctuating, onset <1 week	This is delirium, not dementia. Delirium has an underlying medical cause: sepsis (UTI, pneumonia), metabolic (hypercalcaemia, hyponatraemia, uraemia), drugs (anticholinergics, benzodiazepines, opioids), structural (subdural haematoma, stroke, raised ICP). Untreated delirium has 25% mortality at 6 months. Never diagnose dementia during delirium — you will miss the treatable cause.	Urgent medical assessment same day — bloods, CXR, urine, medication review
Focal neurological signs — hemiparesis, visual field defect, dysphasia	Structural brain lesion: stroke, subdural haematoma, brain tumour (primary or metastatic), brain abscess. Subdural haematoma in elderly: may have trivial or no history of head trauma; presents with headache, confusion, focal neurology. Brain tumours (glioblastoma, metastases from lung/breast/melanoma) can present insidiously with cognitive decline before focal signs emerge. Needs urgent CT head.	Urgent CT head same day or 999 if reduced GCS / severe headache / seizure
Urinary incontinence + gait disturbance + dementia (triad)	Normal pressure hydrocephalus (NPH) — potentially reversible dementia. Classic triad: 'wet, wobbly, wacky' — urinary incontinence (early), gait apraxia (magnetic gait, shuffling, difficulty initiating steps), cognitive decline (executive dysfunction, psychomotor slowing). CT/MRI shows ventriculomegaly out of proportion to sulcal atrophy. Treated with ventriculoperitoneal shunt — can significantly improve symptoms if diagnosed early. NPH is rare but important because it's surgically treatable.	Urgent neurology or neurosurgery referral for NPH evaluation
Age <60 years (young-onset dementia)	Young-onset dementia (<60 years old at symptom onset, some definitions use <65) has different causes than late-onset: frontotemporal dementia (most common young-onset cause), alcohol-related brain damage, HIV-associated dementia, genetic Alzheimer's (APP, PSEN mutations), Huntington's disease, prion disease. Requires specialist assessment — different diagnostic workup, genetic implications, devastating psychosocial impact (often still working, young children, financial catastrophe). Do not assume it's 'just stress' or 'burnout' — young-onset cognitive impairment always needs specialist referral.	Urgent specialist referral to young-onset dementia clinic or neurology
Patient living alone + significant functional impairment + no support	Immediate safeguarding concern: risk of self-neglect, malnutrition, medication errors, falls, fire (leaving gas on, unattended cooking), financial exploitation, wandering. If patient cannot manage ADLs safely and has no family/carer support, they are at imminent risk of serious harm. This is a safeguarding issue requiring same-day action — cannot send patient home alone without a safety plan.	Same-day safeguarding action: contact social services, arrange urgent care needs assessment, inform family if patient consents, consider hospital admission if acutely unsafe
Suicidal ideation or severe depression with cognitive complaints	Severe depression causes 'pseudodementia' — prominent subjective cognitive complaints, psychomotor retardation, poor effort on testing. Patients say 'I can't remember anything' but objective testing shows mild deficits only (contrast with dementia: patient says 'I'm fine' but testing shows major deficits). However, depression and dementia commonly coexist — treat both. Suicidal ideation in early dementia: patient may have insight into progressive decline and feel hopeless — requires urgent mental health assessment and suicide risk management.	Urgent mental health referral if suicidal; treat depression aggressively with SSRI + psychological therapy; reassess cognition after mood improvement
Neuroleptic use in patient with visual hallucinations / parkinsonism	Lewy body dementia has fatal sensitivity to typical antipsychotics (haloperidol, chlorpromazine) — causes severe parkinsonism, reduced consciousness, autonomic instability, and death. Even atypical antipsychotics (risperidone, olanzapine) carry serious risk. If a patient with dementia + visual hallucinations + parkinsonism is on antipsychotics, stop them immediately. DLB patients may have been given antipsychotics for 'psychosis' by non-specialists unaware of the contraindication.	Stop antipsychotic immediately; monitor for withdrawal symptoms; arrange urgent specialist review for DLB diagnosis and management

🛡️

Safeguarding Considerations — Consider in Every Consultation

Dementia is a safeguarding condition. Cognitive impairment creates vulnerability to self-neglect, financial abuse, physical abuse, and institutional neglect. Every dementia assessment is a safeguarding assessment. Adults with dementia lack capacity for some decisions (but capacity is decision-specific — never assume global incapacity). Safeguarding concerns must be raised even if the patient objects — protecting a vulnerable adult overrides confidentiality in situations of serious harm.

🏠 Self-Neglect

Living in squalor — hoarding, poor hygiene, infestations
Malnutrition or dehydration — forgetting to eat/drink
Medication errors — overdosing, underdosing, mixing up pills
Fire risk — leaving gas on, unattended cooking, candles
Wandering risk — getting lost, exposure, road traffic accidents
Falls risk — clutter, rugs, poor lighting, no grab rails

💰 Financial Abuse

Family member or 'friend' accessing bank accounts without consent
Unpaid bills despite adequate funds — money being diverted
Sudden changes to will or power of attorney under pressure
Scams and doorstep fraud — vulnerable to cold-calling, rogue traders
Large cash withdrawals or unusual purchases not consistent with patient's needs
Carer or family refusing to allow patient access to their own money

🤕 Physical / Psychological Abuse by Carer

Unexplained bruising, fractures, burns in patient with poor mobility
Patient fearful in presence of specific family member or carer
Carer showing hostility, impatience, or contempt toward patient
Over-sedation or medication used to 'control' behaviour
Restraint (locked in room, tied to chair) — always abusive unless emergency
Verbal abuse, shouting, threats, humiliation

🏥 Institutional Neglect in Care Homes

Pressure ulcers developing in previously mobile patient — inadequate repositioning
Dehydration, weight loss, malnutrition despite care plan
Poor hygiene, unchanged continence pads, untreated infections
Over-medication — inappropriate use of sedatives or antipsychotics to manage 'difficult' behaviour
Lack of stimulation, social isolation, neglect of emotional needs
Family concerns dismissed, restricted visiting, lack of transparency

If a safeguarding concern is identified: Document concerns clearly in the medical record (factual observations, not opinions). If immediate risk of serious harm: call adult safeguarding team same day (local authority safeguarding hub). If non-urgent concern: complete safeguarding referral form (online or paper) to local authority adult social care. Inform the patient that you are making a safeguarding referral (unless doing so would increase risk of harm). Do not investigate yourself — this is social services' role. Continue to provide medical care to the patient. Safeguarding concerns override confidentiality when there is risk of serious harm to a vulnerable adult.

1C — PMH · FH · Drug history · Social history: management impact

🧬 PMH / FH — changes management

Factor	Why it matters	Management impact
Previous stroke or TIA	Indicates vascular dementia or mixed dementia (Alzheimer's + vascular). Vascular dementia has stepwise decline. Recurrent strokes accelerate cognitive decline.	Aggressive vascular risk reduction: BP target <140/90, statin (atorvastatin 20–80mg), antiplatelet (aspirin 75mg or clopidogrel 75mg) if not anticoagulated. If AF: anticoagulate with DOAC. Optimise diabetes control (HbA1c <58 mmol/mol).
Hypertension	Hypertension is a modifiable risk factor for both vascular dementia and Alzheimer's disease. Midlife hypertension (age 40–60) increases dementia risk in later life. Treating hypertension reduces dementia incidence.	Treat to target <140/90 (NICE NG136). Use ACE-I/ARB if also diabetic or CKD. Avoid excessive BP lowering in frail elderly (orthostatic hypotension → falls). Don't stop antihypertensives in dementia unless causing symptomatic hypotension.
Type 2 diabetes	Diabetes doubles dementia risk (vascular damage + insulin resistance in brain). Poor glycaemic control accelerates cognitive decline. Hypoglycaemia causes acute confusion and long-term brain damage.	HbA1c target 58 mmol/mol (relaxed to 64 mmol/mol in frail elderly to avoid hypos). Avoid sulfonylureas and insulin if possible (hypo risk) — prefer metformin, SGLT2i, DPP4i. Monitor for hypos if on sulfonylurea/insulin — consider simplifying regimen.
Atrial fibrillation	AF increases stroke risk (cardioembolic) → vascular dementia. Anticoagulation reduces stroke and dementia risk. However, anticoagulation in dementia increases falls and bleeding risk if patient non-adherent or taking NSAIDs.	Calculate CHA₂DS₂-VASc and ORBIT (NICE NG196). If CHA₂DS₂-VASc ≥2 — the same threshold in women as in men (NG196 has no ≥3-in-women rule; consider anticoagulation for men scoring 1): offer DOAC (apixaban, rivaroxaban, edoxaban — easier than warfarin; no INR monitoring). If falls risk high: DOAC still recommended (benefit > risk). Monitor adherence.
Parkinson's disease	50% of people with Parkinson's develop dementia (Parkinson's disease dementia, PDD). Risk increases with disease duration. Visual hallucinations, fluctuating cognition, REM sleep behaviour disorder are features of Lewy body spectrum.	Rivastigmine (cholinesterase inhibitor) is licensed for Parkinson's disease dementia — improves cognition and reduces hallucinations. Avoid anticholinergics (worsen cognition). Avoid typical antipsychotics (neuroleptic sensitivity). If hallucinations distressing: quetiapine or clozapine (safest in PD).
Depression (current or past)	Depression and dementia commonly coexist. Late-life depression (first episode >60 years) may be prodrome of dementia. Severe depression causes 'pseudodementia' (reversible cognitive impairment). Untreated depression worsens dementia outcomes.	Treat depression aggressively: SSRI first-line (sertraline 50mg, citalopram 10–20mg — avoid higher doses in elderly due to QTc prolongation). Reassess cognition after mood improves. If pseudodementia: cognitive symptoms improve with antidepressant. If dementia + depression: both require treatment.
Head injury or repeated head trauma	Traumatic brain injury (TBI) increases dementia risk. Chronic traumatic encephalopathy (CTE) — from repeated concussions (boxers, rugby players, military) — causes progressive dementia, parkinsonism, mood/behavioural change. Subdural haematoma can present as subacute cognitive decline.	If history of significant head injury: CT head to exclude chronic subdural. If repeated head trauma (contact sports, military, domestic abuse): consider CTE — no specific treatment; supportive care. Refer to neurology if diagnostic uncertainty.
Chronic kidney disease (CKD)	CKD increases dementia risk (cerebrovascular disease, uraemic encephalopathy). Affects drug dosing: donepezil, rivastigmine, memantine need dose reduction in severe CKD (eGFR <30). Galantamine contraindicated in severe CKD.	Check eGFR before starting cholinesterase inhibitor. If eGFR 30–60: standard doses. If eGFR <30: reduce donepezil to 5mg, rivastigmine to 3mg BD, memantine to 10mg OD; avoid galantamine. Monitor renal function 6-monthly.
Thyroid disease (hypothyroidism)	Severe untreated hypothyroidism causes reversible dementia (myxoedema madness) — psychosis, cognitive slowing, depression. Mild subclinical hypothyroidism may contribute to cognitive impairment. Always check TFTs in new cognitive impairment — it's a treatable cause.	Check TSH and free T4. If TSH >10 mU/L or symptomatic hypothyroidism: start levothyroxine (start 25mcg in elderly, titrate slowly). Reassess cognition after 3 months of euthyroid state. If cognition normalises: it was hypothyroid encephalopathy, not dementia.
Vitamin B12 or folate deficiency	B12 deficiency causes subacute combined degeneration of the cord (dorsal column loss, peripheral neuropathy) and cognitive impairment. Folate deficiency causes megaloblastic anaemia and cognitive impairment. Both are reversible if caught early. Causes: pernicious anaemia, malabsorption, strict vegan diet, metformin (reduces B12).	Check B12 and folate in all new cognitive impairment. If B12 <200 ng/L or low-normal with high MCV: treat with IM hydroxocobalamin 1mg 3× weekly for 2 weeks, then 3-monthly. If folate low: oral folic acid 5mg OD. Reassess cognition after 3 months — improvement suggests deficiency was contributory.

💊 Drug history · Social history — clinical impact

Factor	Why it matters	Management impact
Anticholinergic medications	Anticholinergics impair cognition and increase dementia risk with chronic use. High anticholinergic burden (ACB score ≥3) is associated with incident dementia. Common culprits: antihistamines (chlorphenamine, promethazine), TCAs (amitriptyline), bladder antimuscarinics (oxybutynin, solifenacin), antipsychotics (quetiapine).	Calculate ACB score (online calculator). Aim to reduce total ACB to <3. Switch oxybutynin → mirabegron (β3 agonist, no anticholinergic effect). Switch amitriptyline → nortriptyline (lower ACB) or mirtazapine. Stop antihistamines — use non-sedating alternatives (cetirizine, loratadine). Review every 6 months.
Benzodiazepines and Z-drugs	Benzodiazepines (diazepam, lorazepam, temazepam) and Z-drugs (zopiclone, zolpidem) cause sedation, amnesia, falls, and paradoxical agitation in elderly. Chronic use increases dementia risk. Abrupt withdrawal causes rebound insomnia, anxiety, seizures.	If on benzodiazepine >4 weeks: taper slowly (reduce by ⅛ of dose every 2 weeks). Switch short-acting benzos (lorazepam) to long-acting (diazepam) for smoother taper. Address underlying insomnia/anxiety with non-drug approaches (sleep hygiene, CBT). Avoid prescribing new benzos in elderly.
Polypharmacy (≥5 medications)	Polypharmacy in elderly: drug-drug interactions, anticholinergic burden, falls, non-adherence, medication errors. Older adults with dementia cannot manage complex medication regimens — risk of overdose, underdose, taking wrong drugs. Each additional drug increases confusion risk.	Medication review: stop drugs with no clear indication, deprescribe (STOPP/START criteria). Simplify regimen: once-daily dosing where possible, use combination tablets (e.g. co-amilofruse instead of furosemide + amiloride). Use dosette box or blister packs. Involve carer in medication administration if patient lacks capacity.
Alcohol — current or historical heavy use	Alcohol-related brain damage (ARBD) and Wernicke-Korsakoff syndrome cause dementia, particularly in younger adults (<65). Chronic heavy drinking → cortical atrophy, executive dysfunction, anterograde amnesia. Wernicke's (thiamine deficiency) → confusion, ataxia, ophthalmoplegia — requires urgent IV thiamine to prevent irreversible Korsakoff's.	If ARBD suspected: thiamine (vitamin B1) 300mg PO TDS or IV Pabrinex (if malnourished or Wernicke's suspected). Alcohol abstinence + thiamine can partially reverse ARBD. Refer to alcohol services for detox and relapse prevention. Nutritional support (multivitamins, high-protein diet). Reassess cognition after 6–12 months abstinence.
Smoking (current or ex-smoker)	Smoking increases vascular dementia risk (cerebrovascular disease) and Alzheimer's risk (oxidative stress, inflammation). Stopping smoking at any age reduces dementia risk. However, nicotine itself may have neuroprotective effects (nicotinic receptors in AD).	Offer smoking cessation: NRT (patches + short-acting NRT), varenicline, or bupropion. Stopping smoking reduces stroke and MI risk even in elderly. Benefits accrue within months. Monitor if on bupropion (lowers seizure threshold — caution in dementia).
Social isolation and loneliness	Social isolation doubles dementia risk — lack of cognitive stimulation accelerates decline. Loneliness increases depression, physical inactivity, poor diet. Widowhood is a major risk factor (loss of partner → social withdrawal, loss of purpose). Living alone with dementia = safeguarding risk.	Refer to social prescribing / community link worker: befriending services, day centres, dementia cafés, Alzheimer's Society groups. Occupational therapy for home adaptations. Consider sheltered housing or care home if living alone unsafe. Address hearing loss (hearing aids improve social engagement and reduce isolation).
Hearing loss (untreated)	Hearing loss is independently associated with accelerated cognitive decline and increased dementia risk. Mechanisms: reduced cognitive stimulation, social isolation, cognitive load (brain resources diverted to auditory processing). Hearing aids reduce dementia risk.	Assess hearing (whisper test, audiometry referral). If hearing loss: refer to audiology for hearing aids. Encourage regular use of hearing aids (improves communication, reduces isolation). Treat earwax impaction. Hearing aids are a dementia prevention strategy in midlife and early old age.
Low education and cognitive reserve	Low educational attainment (left school <16 years) increases dementia risk. Higher education builds 'cognitive reserve' — brain can tolerate more pathology before symptoms appear. Lifelong learning, intellectually stimulating occupations, multilingualism increase reserve and delay dementia onset.	Promote cognitive stimulation: reading, puzzles, learning new skills (musical instrument, language), social engagement. Cognitive stimulation therapy (CST) in dementia improves cognition and quality of life (NICE recommended). Avoid 'brain training' apps (no evidence). Meaningful activities > rote exercises.
Physical inactivity	Physical inactivity increases dementia risk. Regular aerobic exercise (walking, swimming, cycling) reduces dementia incidence by ~30%, improves cognition in those with MCI, and slows decline in established dementia. Mechanisms: improved cardiovascular health, increased BDNF (brain-derived neurotrophic factor), neurogenesis.	Recommend 150 minutes/week moderate-intensity aerobic exercise (30 min × 5 days). Walking is sufficient. Resistance training 2× week also beneficial. Exercise is the single most effective non-pharmacological intervention for dementia prevention and slowing decline. Refer to physiotherapy if mobility limited. Group exercise classes (social + physical benefits).
Poor diet (low fruit/veg, high processed food)	Mediterranean diet (high vegetables, fruit, fish, olive oil, nuts; low red meat, processed food) reduces dementia risk. Mechanisms: reduced vascular disease, anti-inflammatory, antioxidant. Malnutrition in dementia: forgetting to eat, apraxia (can't use cutlery), dysphagia (choking risk).	Promote Mediterranean diet: oily fish 2× week (omega-3), ≥5 portions fruit/veg daily, nuts, olive oil, whole grains. Avoid high saturated fat, processed meats. In established dementia: monitor weight monthly. If weight loss: high-calorie supplements (Fortisip, Ensure), dietitian referral. Finger foods if apraxia. Modified consistency if dysphagia (SALT referral).

1D — ICE: Ideas · Concerns · Expectations — in every consultation, not just SCA

Dementia consultations are emotionally charged and existentially frightening. The patient may fear loss of independence, being a burden, losing their identity, ending up in a home, or becoming 'a vegetable'. The family fears watching their loved one disappear, caregiver burden, and the guilt of considering residential care. ICE is not a formulaic ritual in dementia — it is the consultation. The patient's idea ('it's just normal ageing, everyone forgets at my age') determines whether they'll accept referral. The patient's concern ('I'm terrified of ending up like my mother who didn't recognise me') drives their emotional response and adherence to investigation. The patient's expectation ('you'll give me a pill to fix it' vs. 'there's nothing you can do') shapes the whole management conversation. You cannot explain the diagnosis, discuss prognosis, or plan management without first understanding what this diagnosis means to this patient and this family.

💭 Ideas

"What do you think might be causing these memory problems — have you had any thoughts about what's going on?"

Many patients attribute memory loss to 'normal ageing' or 'stress' and resist the idea of dementia. Others have catastrophised ('it's definitely Alzheimer's, I'm going to forget my family'). Understanding the patient's explanatory model lets you build on correct ideas and gently correct misconceptions. If the patient thinks it's 'just stress', you need to explain why the functional impairment and collateral history suggest something more. If they're catastrophising, you can provide realistic prognostic information and emphasise retained abilities.

😟 Concerns

"I can hear this is really worrying for you — what's your biggest concern about what's happening?"

The hidden agenda in dementia is almost never about memory per se. Patients fear: loss of independence ('will I have to give up driving?'), being a burden ('I don't want my children looking after me'), loss of dignity ('I don't want to end up in nappies not knowing who I am'), being 'put in a home' against their will, and ultimately existential terror of losing their identity. Family members fear caregiver burden, financial ruin, watching personality disintegration, and guilt about considering residential care. Naming these fears doesn't make them worse — it creates a therapeutic alliance and lets you address realistic concerns (driving will be reviewed, but we'll support you through that) and correct unrealistic ones (most people with dementia live at home with support, not in care homes).

🎯 Expectations

"What were you hoping we might be able to do today — what would be helpful?"

Expectations range wildly: some expect a pill that cures dementia (need reality check: medications slow progression, they don't reverse it); others expect 'there's nothing you can do, we just have to live with it' (need education about symptomatic treatments, support services, advance planning). Some families expect immediate care home placement (need discussion of home support options). Some patients expect you to tell them they're fine and it's nothing (need sensitive discussion of diagnostic process and what findings mean). If you don't elicit and address expectations, the consultation will fail — you'll refer to memory clinic and the patient won't attend because 'the GP said it might be nothing', or you'll prescribe donepezil and the family will stop it after 2 months because 'it's not working' (they expected memory improvement; you needed to explain it slows decline).

1E — Psychosocial context: the person behind the cognitive decline

Dementia is a psychosocial disease as much as a neurological one. The same degree of neuropathology causes vastly different functional outcomes depending on psychosocial context: social isolation accelerates cognitive decline; chronic stress and depression worsen executive function and memory consolidation; poverty limits access to brain-healthy diet, exercise, and social engagement; caregiver burden leads to depression, physical illness, and premature institutionalisation of the patient. Understanding psychosocial stressors is not 'holistic box-ticking' — these are modifiable disease accelerators. A patient with mild Alzheimer's who is socially isolated, depressed, sedentary, and malnourished will deteriorate faster than a patient with moderate Alzheimer's who has strong family support, attends a day centre, exercises daily, and eats well. Psychosocial intervention (treating depression, arranging day centre attendance, enrolling in cognitive stimulation therapy, supporting the carer) is as important as pharmacological treatment.

😔 Depression and Anxiety

Depression and dementia have bidirectional causation: late-life depression (first episode >60) may be dementia prodrome (hippocampal atrophy causes both mood and memory symptoms); conversely, living with early dementia and insight into progressive decline causes reactive depression. Anxiety about cognitive failures (forgetting names, getting lost) creates a vicious cycle — anxiety worsens working memory and executive function, leading to more failures, more anxiety. Untreated depression in dementia accelerates functional decline, increases behavioural disturbance, and causes excess disability (patient appears more impaired than their neuropathology would predict). Treating depression in dementia improves quality of life, reduces carer burden, and may slow cognitive decline.

"How have your spirits been — have you been feeling low in mood, or more anxious than usual?"

If depression present: start SSRI (sertraline 50mg, citalopram 10–20mg), refer for psychological therapy (CBT adapted for cognitive impairment), treat pain if present (pain causes depression in elderly), increase social contact, encourage physical activity. Reassess cognition after mood improves — if pseudodementia, cognitive symptoms will improve significantly.

👥 Social Isolation and Loneliness

Social isolation (objective lack of social contact) and loneliness (subjective feeling of being alone) are independent risk factors for dementia — effect size comparable to smoking or physical inactivity. Mechanisms: reduced cognitive stimulation (use it or lose it), chronic stress (elevated cortisol damages hippocampus), reduced motivation for self-care (poor diet, medication non-adherence). Widowhood is the major precipitant — loss of partner leads to social withdrawal, loss of conversational partner (reduced language use), loss of shared activities, bereavement depression. Living alone with dementia creates a vicious cycle: cognitive impairment → withdrawal from social activities → isolation → accelerated decline. Breaking the isolation cycle is a key intervention: day centres, befriending schemes, dementia cafés, group exercise classes.

"Who do you see regularly — family, friends, neighbours? Are you getting out and about, or have you found yourself staying in more?"

If socially isolated: refer to social prescribing link worker, arrange day centre attendance (also respite for carer), Alzheimer's Society groups, befriending service. Treat hearing loss (hearing aids reduce isolation). Address mobility barriers (walking aids, transport). If living alone unsafe: discuss sheltered housing, extra care housing, or live-in care as alternatives to care home.

💪 Physical Activity and Mobility

Physical inactivity is a modifiable dementia risk factor — sedentary lifestyle doubles dementia risk; regular aerobic exercise reduces risk by 30% and slows progression in established dementia. Mechanisms: improved cardiovascular fitness (brain perfusion), increased BDNF (brain-derived neurotrophic factor promotes neurogenesis and synaptic plasticity), reduced inflammation, improved insulin sensitivity, better sleep, mood improvement. However, dementia creates barriers to exercise: apathy (can't motivate self to exercise), executive dysfunction (can't plan or sequence exercise routine), getting lost if walking alone, fear of falls, comorbidities (OA, chronic pain, cardiorespiratory disease). Deconditioning accelerates — sedentary patient becomes weaker, falls risk increases, mobility declines further, leading to care home admission.

"Tell me about your usual day — how much do you get out for a walk, and what activities keep you moving?"

If sedentary: prescribe walking (30 min daily — carer accompanies if safety concern), refer to physiotherapy for falls assessment and strengthening exercises, chair-based exercise classes if mobility limited, group activities (walking groups, dancing, tai chi — social + physical benefits). Address pain (analgesia, physio). Exercise is the most effective non-drug intervention for dementia — prioritise it.

🏠 Housing and Living Environment

The home environment determines safety and independence in dementia. A cluttered, poorly lit home with steep stairs, loose rugs, and no grab rails becomes a hazard — falls, hip fracture, loss of independence. Living alone with moderate dementia is a safeguarding risk: forgetting to eat (malnutrition), medication errors (overdose, underdose), leaving gas on (fire risk), wandering (hypothermia, road traffic accident), financial exploitation (scams, doorstep fraud), self-neglect (squalor). However, inappropriate early institutionalisation (moving to care home when home support would suffice) accelerates decline — loss of familiar environment, loss of autonomy, iatrogenic harm (infections, falls, sedation). The right environment at the right time is critical: home adaptations and assistive technology can extend safe independent living; sheltered housing or extra care housing (step down from care home) may be appropriate; care home is necessary when needs exceed what can be provided at home.

"Tell me about your home — are there any things that are getting difficult to manage, like stairs, or things you're worried about safety-wise?"

If living alone with functional impairment: occupational therapy home visit (assess safety, recommend adaptations — grab rails, raised toilet seat, removal of trip hazards, improved lighting). Consider assistive technology (key safe for carers to enter, pendant alarm, GPS tracker if wandering risk). Arrange care package (carers 2× daily for medication prompts, meals). If home unsafe despite adaptations: discuss sheltered housing or extra care housing (own flat with on-site care). Care home only if needs too complex for home.

👨‍👩‍👧 Carer Burden and Family Stress

Dementia caregiving is the most burdensome of all caregiving roles — 24/7 supervision, behavioural disturbance (aggression, disinhibition, night-time wandering), progressive loss of the person they knew, no prospect of recovery, and anticipatory grief (mourning someone who is still alive but no longer themselves). Carer depression affects 40% of dementia carers; carer burnout leads to premature institutionalisation, elder abuse (usually out of desperation, not malice — carer 'snaps' under intolerable stress), and carer physical illness (carers have higher rates of cardiovascular disease, immune dysfunction). A burned-out carer cannot provide good care. Supporting the carer is supporting the patient — if the carer is well, the patient stays at home longer, has better quality of life, and the carer is less likely to harm them. Carer assessment is a statutory right (Care Act 2014) — carers can request assessment of their own needs independent of the patient's care needs.

"How are you coping with everything — it's a lot to manage. Are you getting any breaks, or is it all falling on you?"

If carer strain evident: offer carer's assessment (local authority duty — carers have legal right to assessment of their needs). Arrange respite care (day centre attendance gives carer a break; short-term residential respite for carer holidays). Treat carer depression (SSRI, psychological therapy). Refer to carers' organisations (Carers UK, local carers' centre — peer support, information, benefits advice). Ensure carer claiming Carer's Allowance if eligible (£81.90/week if caring ≥35 hours/week).

💰 Financial Strain and Benefits

Dementia causes financial catastrophe through multiple mechanisms: job loss if working-age onset (patient cannot continue work; carer gives up job to provide care), care costs (£50,000+/year for residential care), loss of financial capacity (patient makes poor decisions, gets scammed), and inadequate benefit uptake (many entitled to Attendance Allowance, PIP, Carer's Allowance but never claim). Financial strain causes carer burnout ('I can't afford to give up work to care for them, but I can't afford a care home either'), delays necessary care ('we can't afford carers coming in'), and vulnerability to financial abuse (family member 'borrows' money from the patient's account). Financial concerns are often unspoken — patients and carers feel shame about 'talking about money' during a medical consultation. The GP must proactively ask — financial strain is a safeguarding risk.

"Have you had a chance to think about the financial side of things — are you managing, or is that adding to the stress?"

If financial strain: refer to benefits advisor (Citizens Advice, Age UK — check entitlement to Attendance Allowance [patient], PIP [patient if

🎓 SCA Checkpoint — Step 1TasksRelating to OthersGlobal Skills

Key phrases that score

"Thank you both for coming in — can you tell me what's been concerning you?"

"That sounds really difficult for you both. Can you give me an example of when this happens?"

"I'm hearing that you're worried about your memory, and your daughter has noticed some changes — let me make sure I understand what's been happening."

"What's your biggest worry about what's going on — what are you most concerned about?"

Deductions (examiner flags)

Speaking only to the family member, excluding the patient from the conversation
Asking the patient direct memory questions without acknowledging this might be difficult or distressing
Dismissing early symptoms as 'normal ageing' without proper assessment
Failing to obtain collateral history from someone who knows the patient well
Not screening for delirium when confusion onset is recent or fluctuating
Jumping straight to 'it's dementia' without considering reversible causes (B12, thyroid, depression, medications)
Not asking about functional impact — if you don't ask about ADLs, you can't distinguish MCI from dementia
Ignoring safeguarding red flags (living alone + functional impairment, financial abuse, carer stress)
Not exploring the emotional impact on patient and family — this is a devastating diagnosis

🔴 Red — failing

No collateral history obtained; patient excluded from conversation or humiliated by memory testing; delirium not considered; no exploration of functional impact (cannot distinguish MCI from dementia without asking about ADLs); safeguarding risks missed (lives alone + impaired, no capacity assessment considered); no ICE elicited; dismissive of patient/family concerns.

🟠 Amber — borderline

Collateral history attempted but superficial ('she forgets things' accepted without examples); patient included but some questions insensitive; delirium screen cursory; functional impact asked but not probed (didn't ask which specific ADLs impaired); some safeguarding awareness but risks not fully explored; ICE asked formulaically without depth; psychosocial factors acknowledged but not integrated into formulation.

🟢 Green — passing

Detailed collateral history with specific examples of cognitive and functional decline, timeline, and progression; patient treated with dignity throughout (validated feelings, avoided patronising language); delirium ruled out with acute onset/fluctuation questions; comprehensive functional assessment covering instrumental and basic ADLs; safeguarding risks identified (living situation, capacity, carer burden, financial); ICE explored in depth (fears about 'ending up in a home', loss of independence, being a burden); psychosocial stressors identified (isolation, bereavement, mood, mobility) and linked to management plan.

Step 2

Triage Engine — Emergency · Urgent · Routine

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Dementia assessment is rarely an emergency, but acute confusional states and safeguarding crises require same-day action. The triage decision is: Is this delirium requiring urgent medical assessment? (fluctuating confusion, acute onset, potential sepsis/metabolic cause), Is this a safeguarding emergency? (patient living alone with severe functional impairment and no support, acute carer breakdown, suspected abuse), or Is this a routine dementia diagnostic pathway? (gradual onset, patient safe at home with support, planned referral to memory clinic). Never diagnose dementia during acute confusion — it is delirium until proven otherwise. Never send a functionally impaired patient home alone without a safety plan — it is a safeguarding failure.

🔴 Emergency

999 or Same-Day Hospital

Call 999 / admit acutely

Acute confusional state with reduced GCS, agitation, or aggressionDelirium with behavioural disturbance — risk of harm to self or others. Cannot be managed in primary care. Requires hospital assessment, sedation if needed, treatment of underlying cause (sepsis, metabolic).
Seizures (new-onset in elderly)New seizures in older adults: structural lesion (stroke, tumour, subdural), metabolic (hyponatraemia, hypoglycaemia), or late-onset epilepsy. Requires urgent CT head and neurology input. Status epilepticus = 999.
Focal neurological signs — hemiparesis, dysphasia, visual field defectStroke, subdural haematoma, or brain tumour. Needs immediate CT head. If acute stroke (<4.5 hours): 999 for thrombolysis. If subacute: same-day hospital assessment.
Suspected meningitis or encephalitisConfusion + headache + fever + neck stiffness = meningitis until proven otherwise. Confusion + fever + seizures + psychiatric features = encephalitis (HSV, autoimmune). Both require immediate hospital admission, LP, empirical treatment.
Safeguarding crisis — patient at immediate risk of serious harmPatient with severe dementia living alone, no food/heating, carer has left/died, evidence of abuse (unexplained injuries, over-sedation, locked in room). Cannot send patient home — admit for safeguarding or arrange emergency care package same day.
Severe behavioural disturbance in known dementia — aggression, psychosisAgitated dementia patient hitting carer, responding to command hallucinations, severe paranoia. First: exclude delirium (infection, pain, constipation, urinary retention). If no delirium and behaviour unmanageable at home: psychiatric crisis team or hospital admission. Avoid sedation if possible (worsens confusion); if essential: lorazepam 0.5–1mg PO (short half-life).

🟠 Urgent

Same-Day or Next-Day Assessment

Urgent — days to 2 weeks

Delirium — acute confusion, fluctuating, onset <1 weekSame-day assessment to find and treat cause: sepsis screen (urine dipstick, CXR, bloods — FBC, CRP, U&E, glucose, calcium, LFTs, TFTs, B12), medication review (stop anticholinergics, benzos), treat underlying (antibiotics if infection, rehydrate if dehydrated, correct electrolytes). Do not diagnose dementia during delirium.
Rapid cognitive decline over weeks (not months)Rapidly progressive dementia (RPD): CJD, paraneoplastic syndrome, autoimmune encephalitis, CNS vasculitis. Requires urgent neurology referral within 1–2 weeks. Do not wait for routine memory clinic. Urgent MRI brain, EEG, LP, autoimmune screen.
Young-onset dementia (age <60 years at symptom onset)Requires specialist assessment within 2 weeks. Causes differ from late-onset: FTD (most common young-onset), ARBD, HIV-associated dementia, genetic AD, Huntington's. Do not assume 'stress' or 'burnout'. Refer to young-onset dementia service or neurology.
Suspected NPH (normal pressure hydrocephalus) — triad of dementia, gait disturbance, urinary incontinencePotentially reversible dementia — treatable with ventriculoperitoneal shunt if caught early. Urgent neurology/neurosurgery referral. MRI shows ventriculomegaly out of proportion to sulcal atrophy. Do not miss this — it's rare but treatable.
Safeguarding concern — suspected abuse or severe carer breakdownSame-day safeguarding referral to local authority adult social care. If patient at immediate risk: do not send home — arrange emergency care package or respite admission. Document concerns clearly. Inform patient you are making referral (unless doing so increases risk).
Severe depression with suicidal ideation or psychotic featuresSevere depression can mimic dementia ('pseudodementia') but requires urgent treatment. If suicidal: urgent mental health referral (crisis team, psychiatric liaison). If psychotic depression (delusions, hallucinations): psychiatry referral for ECT consideration or antipsychotic + antidepressant.

🟢 Routine

Manage in Primary Care

Routine diagnostic pathway

Gradual onset cognitive impairment (months to years), patient safe at homeClassic dementia presentation. Initiate investigations in primary care (bloods, cognitive testing), refer to memory clinic for specialist assessment and diagnosis. NICE target: assessment within 6 weeks of referral.
Mild cognitive impairment (MCI) — cognitive impairment without functional lossRefer to memory clinic for baseline assessment and monitoring. ~10% per year progress to dementia. Advise lifestyle modification (exercise, Mediterranean diet, social engagement). Annual review to monitor for progression to dementia.
Subjective cognitive complaints (worried well), normal objective testingReassure. Likely normal ageing or anxiety about cognition. Provide advice on brain health (exercise, sleep, diet, social engagement). Safety-net: return if symptoms worsen or functional impairment develops. Consider mood screen (depression causes cognitive complaints).
Established dementia, stable, on treatment, for routine review6-monthly review in primary care (cognitive testing, functional assessment, medication review, carer support). Annual review in memory clinic if on cholinesterase inhibitor or memantine. Monitor for complications (falls, weight loss, behavioural changes, carer burnout).
Advance care planning in early-stage dementia (patient has capacity)Opportunistic ACP discussions while patient has capacity: preferences for future care, DNACPR, place of death, Lasting Power of Attorney (health and welfare + finances). Document in care plan. Revisit as disease progresses. This is not urgent but should not be delayed — capacity will be lost.

🎓 SCA Checkpoint — Step 2TasksRelating to OthersGlobal Skills

Key phrases that score

"From what you've described, this doesn't sound like something that's come on suddenly — it's been building gradually over time, is that right?"

"One thing I need to check — does the confusion come and go during the day, or is it fairly constant?"

"I can hear you're worried about safety at home — let's talk about what support might help."

"This isn't an emergency, but we do need to get this properly assessed — I'm going to refer you to the memory clinic."

Deductions (examiner flags)

Failing to distinguish delirium (acute, fluctuating) from dementia (chronic, progressive) — critical clinical error
Not asking about safeguarding risks when patient has functional impairment
Sending functionally impaired patient home alone without safety plan or capacity assessment
Dismissing family concerns about safety ('they're probably fine at home') without proper assessment
Not recognising young-onset dementia as requiring urgent specialist referral
Delaying referral because 'they're old, everyone forgets at that age'

🔴 Red — failing

Delirium not screened for; acute confusion assumed to be dementia; safeguarding risks ignored; functionally impaired patient sent home alone without safety plan; no urgency assigned to young-onset dementia or rapidly progressive symptoms.

🟠 Amber — borderline

Delirium considered but not systematically excluded; safeguarding risks acknowledged but no action plan; triage category assigned but rationale not clearly explained to patient/family; some urgency awareness but timeline unclear.

🟢 Green — passing

Delirium systematically excluded (acute onset? fluctuating? medical triggers?); safeguarding risks identified and acted on (safety plan, social services referral); appropriate urgency assigned (young-onset = urgent, gradual = routine); triage decision clearly explained to patient/family with timeline and next steps.

Step 3

Examination — Do I Need This Examination?

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Dementia examination has three objectives: exclude delirium and acute medical illness — fever, tachycardia, hypoxia suggest sepsis or metabolic derangement causing confusion, identify neurological signs suggesting structural brain lesion or specific dementia subtype — hemiparesis (stroke/subdural), parkinsonism (DLB/PDD), gait apraxia (NPH), primitive reflexes (advanced AD), and assess functional capacity and safeguarding risk — is this person malnourished? unkempt? bruised? The physical examination in dementia is less about making the diagnosis (that's clinical history + cognitive testing + neuroimaging) and more about excluding mimics and assessing safety. The most important 'examination' is observing the patient's behaviour, interaction with family, and response to questions — these reveal insight, emotional state, and severity more than any physical sign.

Examination	Why it matters	What finding changes management	Changes management?
General observation — appearance, self-care, nutritional state	Dementia causes self-neglect: unkempt appearance (not washed, wearing same clothes for days), malnutrition (forgetting to eat, apraxia so cannot use cutlery), dehydration (forgetting to drink, unable to access water). Observation reveals functional impairment and safeguarding risk more reliably than patient self-report (patients with dementia underestimate their deficits).Unexplained bruising: suspect falls (unsteady gait, poor vision, environmental hazards) or abuse (physical abuse by carer — bruising in non-accidental pattern, e.g. bilateral upper arms from grabbing).	Malnutrition/dehydration → dietitian, SALT if dysphagia, consider nutritional supplements. Unkempt/poor self-care → OT assessment, care package (carers to assist with washing, dressing). Bruising → falls assessment, safeguarding referral if abuse suspected.	YES — safeguarding
Vital signs — temperature, HR, BP, RR, SpO₂	Acute confusion with abnormal vital signs = delirium, not dementia. Fever → sepsis (UTI, pneumonia, cellulitis). Tachycardia → sepsis, hyperthyroidism, AF, pain. Hypotension → sepsis, dehydration, overdiuresis. Hypoxia (SpO₂ <94%) → pneumonia, PE, heart failure. Bradycardia + confusion → hypothermia (self-neglect, inadequate heating). Do not diagnose dementia during acute illness — treat the delirium cause first, reassess cognition when medically well.Postural BP (lying and standing): postural drop >20 mmHg systolic suggests orthostatic hypotension (autonomic dysfunction in DLB, overdiuresis, dehydration) — causes falls, syncope.	Abnormal vitals → urgent medical assessment for delirium cause. Fever → sepsis screen (urine, CXR, bloods), antibiotics. Hypoxia → CXR, echo, CTPA if PE suspected. Postural hypotension → reduce antihypertensives, increase fluids, compression stockings.	YES — delirium vs. dementia
Cognitive testing — MoCA, AMT-10, MMSE, 6-CIT	Objective cognitive testing is mandatory — cannot diagnose dementia on history alone. Tools: Montreal Cognitive Assessment (MoCA, score 0–30, ≤25 abnormal, most sensitive), Abbreviated Mental Test (AMT-10, score 0–10, ≤7 indicates significant impairment, quick bedside tool), Mini-Mental State Exam (MMSE, 0–30, ≤24 abnormal, copyrighted so less used now), 6-item Cognitive Impairment Test (6-CIT, 0–28, ≥10 abnormal, very quick). Cognitive testing: (1) establishes baseline for monitoring progression, (2) distinguishes MCI (impaired testing, normal function) from dementia (impaired testing + functional loss), (3) assesses severity (mild/moderate/severe dementia), (4) monitors treatment response (annual MoCA on cholinesterase inhibitor).Cultural/language/educational bias: MoCA assumes literate English speaker with ≥12 years education — adjust interpretation for non-English speakers, low education, visual/hearing impairment. If cultural/language barrier, use informant-based tools (e.g. IQCODE — Informant Questionnaire on Cognitive Decline in the Elderly).	MoCA ≤25 → refer to memory clinic. AMT ≤7 → significant impairment, urgent referral. Severe impairment (MoCA <10, AMT ≤3) → assess capacity, safeguarding urgency. Normal testing (MoCA >26) with functional complaints → consider depression (pseudodementia), subjective cognitive complaints (worried well), or very early MCI (testing not yet sensitive).	YES — diagnosis, severity, referral urgency
Cranial nerve examination	Cranial nerve signs suggest structural brain lesion (not neurodegenerative dementia): visual field defect (stroke, tumour, pituitary lesion), ophthalmoplegia (Wernicke's encephalopathy from thiamine deficiency — triad of confusion, ataxia, ophthalmoplegia; needs urgent IV thiamine), facial weakness (stroke, Bell's palsy), dysarthria (stroke, bulbar palsy). Primitive reflexes (grasp, pout, palmomental) appear in advanced dementia due to frontal lobe degeneration — indicate severity but not specific diagnosis.Pupils: check for Argyll Robertson pupils (small, irregular, no light reflex but accommodate — neurosyphilis, now very rare). Fundoscopy: papilloedema (raised ICP from tumour, NPH, subdural) or hypertensive retinopathy (uncontrolled HTN → vascular dementia risk).	Focal cranial nerve signs → urgent neurology referral, CT/MRI brain. Ophthalmoplegia + confusion + ataxia → urgent IV thiamine (Pabrinex) for Wernicke's encephalopathy. Papilloedema → urgent CT head for raised ICP cause.	YES — structural lesion vs. neurodegenerative
Limb neurology — tone, power, reflexes, coordination, sensation	Focal limb weakness or sensory loss = stroke, subdural haematoma, or brain tumour (structural lesion, not dementia). Diffuse weakness = deconditioning, malnutrition, or neuromuscular disease. Increased tone (rigidity, spasticity): parkinsonism (DLB, PDD, vascular parkinsonism), pyramidal signs (vascular dementia from subcortical strokes), or advanced AD. Brisk reflexes + upgoing plantars (pyramidal signs) = vascular dementia, cervical myelopathy, or motor neuron disease. Absent ankle jerks + upgoing plantars = subacute combined degeneration of the cord (B12 deficiency) — treatable cause of cognitive impairment.Myoclonus (sudden involuntary muscle jerks): suggests CJD (rapidly progressive dementia + myoclonus + ataxia) or metabolic encephalopathy (uraemia, hepatic encephalopathy). Primitive reflexes (grasp, pout) indicate frontal lobe dysfunction — seen in advanced AD or FTD.	Hemiparesis → urgent CT head for stroke/subdural. Parkinsonism → refer to Parkinson's specialist or consider DLB. Pyramidal signs → MRI for vascular dementia, cervical cord imaging if myelopathy suspected. Absent ankle jerks + upgoing plantars → check B12, treat with IM hydroxocobalamin.	YES — structural lesion, DLB, vascular, B12
Gait assessment — observe walking, turn, sit-to-stand	Gait abnormalities distinguish dementia subtypes and identify falls risk. Normal pressure hydrocephalus (NPH): magnetic gait (shuffling, feet stuck to floor, difficulty initiating steps, wide-based), urinary incontinence, dementia — potentially reversible with VP shunt. Parkinsonism: shuffling, reduced arm swing, festination (accelerating forward), postural instability — suggests DLB or PDD. Vascular dementia: small-stepped gait, lower-body parkinsonism (legs affected > arms). Apraxia (can't sequence motor movements) in AD: difficulty standing from chair, hesitant walking. Falls risk: observe ability to turn (hesitant, multiple steps = increased fall risk), balance on standing, use of furniture for support.Romberg's test (stand with feet together, close eyes): positive Romberg (fall with eyes closed) = posterior column loss (B12 deficiency, tabes dorsalis) or vestibular dysfunction — not typical dementia.	Magnetic gait + incontinence + dementia → refer to neurosurgery for NPH evaluation. Parkinsonism → Parkinson's specialist, consider DLB (avoid typical antipsychotics). Falls risk → physiotherapy, OT home visit, walking aid, review medications (stop sedatives). Apraxia → functional assessment, care package.	YES — NPH diagnosis, falls prevention
Cardiovascular examination — heart sounds, JVP, peripheral pulses, peripheral oedema	Atrial fibrillation (irregularly irregular pulse) increases stroke risk → vascular dementia. Treat AF with anticoagulation to reduce stroke/dementia risk. Heart failure (raised JVP, peripheral oedema, bibasal creps): chronic hypoperfusion may contribute to vascular cognitive impairment. Carotid bruits: carotid stenosis → consider carotid imaging if multiple vascular risk factors. Hypertension (clinic BP): uncontrolled HTN accelerates vascular dementia — treat to target <140/90.Postural BP: orthostatic hypotension (autonomic dysfunction) is common in DLB and causes falls/syncope. If postural drop >20 mmHg systolic: reduce antihypertensives, advise slow position changes, compression stockings.	AF → anticoagulate if CHA₂DS₂-VASc ≥2 (men) or ≥3 (women). Heart failure → optimise HF treatment (ACEi, beta-blocker, diuretics). Hypertension → treat to <140/90. Carotid bruits + multiple TIAs → carotid Doppler, consider endarterectomy.	Context — vascular risk reduction
Thyroid examination — palpate thyroid, look for signs of hypo/hyperthyroidism	Severe hypothyroidism causes myxoedema madness — psychosis, cognitive slowing, depression, reversible dementia. Clinical features: bradycardia, dry skin, hair loss, delayed relaxation of reflexes, goitre. Hyperthyroidism (rare) causes confusion, agitation, tremor, weight loss. Always check TFTs in new cognitive impairment — hypothyroidism is a treatable cause.Mild subclinical hypothyroidism (TSH 5–10, normal T4): unclear whether treatment improves cognition, but consider trial of levothyroxine especially if symptomatic (fatigue, cold intolerance, constipation).	Hypothyroidism → levothyroxine (start 25mcg in elderly, titrate to TSH 0.5–2.5). Reassess cognition after 3 months of euthyroid state. If cognitive symptoms resolve → it was hypothyroid encephalopathy, not dementia.	YES — reversible cause

🎓 SCA Checkpoint — Step 3TasksRelating to OthersGlobal Skills

Key phrases that score

"I'd like to do a few quick checks — some memory questions and a brief examination — to help work out what's going on. Is that okay?"

"These questions can feel a bit strange, but they're standard ones we use to check how memory and thinking are working."

"I'm going to watch you walk to the door and back — this helps me check your balance and safety."

Deductions (examiner flags)

Performing cognitive testing without explanation or consent — patient feels tested/judged
Not checking vital signs when confusion is acute (missing delirium)
Failing to observe self-care, nutrition, or safeguarding signs during examination
Not documenting cognitive test score (no baseline for monitoring)
Embarrassing the patient during cognitive testing (e.g. 'you've got that wrong' repeatedly)

🔴 Red — failing

Cognitive testing not performed or performed insensitively; vital signs not checked when delirium possible; self-care/safeguarding signs missed; gait not assessed despite falls risk; examination findings not documented.

🟠 Amber — borderline

Cognitive testing performed but not explained to patient; some examination done but key elements missed (gait not observed, vitals omitted); findings documented but significance not interpreted.

🟢 Green — passing

Cognitive testing explained sensitively and performed with dignity; vital signs checked and delirium excluded; self-care and safeguarding signs actively looked for; gait observed and falls risk assessed; neurological examination targeted to exclude structural lesions; findings documented with score and interpretation.

Step 4

Investigations — Do I Need This Investigation?

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Dementia investigations have two objectives: exclude reversible causes — B12/folate deficiency, hypothyroidism, hypercalcaemia, chronic subdural haematoma, normal pressure hydrocephalus, neurosyphilis — and characterise dementia subtype for prognostication and treatment (Alzheimer's vs. vascular vs. Lewy body vs. frontotemporal). NICE NG97 mandates baseline bloods in all suspected dementia: FBC, U&E, LFTs, calcium, glucose, TFTs, B12, folate. Neuroimaging (CT or MRI brain) is recommended to exclude structural causes and characterise atrophy patterns. Specialist investigations (SPECT, PET, CSF analysis, genetic testing) are performed in memory clinics, not primary care. The GP's role is to exclude treatable causes before referring to memory clinic.

Investigation	Clinical question it answers	What result changes management?
Full blood count (FBC)	Macrocytosis (high MCV >100 fL) suggests B12 or folate deficiency (megaloblastic anaemia) or alcohol excess — both cause reversible cognitive impairment. Anaemia (low Hb) → chronic disease, malnutrition, GI bleed (iron deficiency) — contributes to fatigue, poor concentration, functional decline. Raised WCC → infection (delirium cause). Thrombocytopenia or pancytopenia → bone marrow failure, haematological malignancy (very rare dementia cause — CNS lymphoma).	MCV >100 → check B12 and folate; if deficient, treat and reassess cognition. Anaemia → investigate cause (ferritin, coeliac screen, colonoscopy if iron deficiency); treat with iron or transfusion if severe. Raised WCC → sepsis screen.
Urea & electrolytes (U&E), eGFR	Hyponatraemia (<135 mmol/L) causes confusion — from SIADH (SSRI, carbamazepine), diuretics, Addison's disease, heart failure, cirrhosis. Severe hyponatraemia (<125) causes seizures and encephalopathy. Hypernatraemia (>145) from dehydration causes confusion (self-neglect, unable to access water). Uraemia (elevated urea and creatinine, low eGFR) causes uraemic encephalopathy — reversible with dialysis if acute kidney injury, or contributes to cognitive impairment in CKD. Hyperkalaemia or hypokalaemia from diuretics, ACE-Is, or CKD cause arrhythmias and muscle weakness but not typically confusion unless severe.	Hyponatraemia <130 → stop causative drug (SSRI, diuretic), fluid restrict if SIADH, IV saline if severe + symptomatic (but correct slowly — risk of osmotic demyelination). Uraemia → nephrology referral if AKI or CKD stage 4–5; dialysis if symptomatic uraemia. eGFR <30 → adjust medication doses (donepezil, memantine).
Liver function tests (LFTs)	Deranged LFTs suggest alcohol-related liver disease (ARBD, Wernicke-Korsakoff syndrome), hepatic encephalopathy (cirrhosis → confusion, asterixis), or drug-induced hepatotoxicity. Chronic alcohol excess → elevated GGT (>50 U/L), AST:ALT ratio >2, macrocytosis. Hepatic encephalopathy (elevated ammonia, low albumin): asterixis, confusion, fetor hepaticus — treat with lactulose, rifaximin. Cholestatic LFTs (high ALP, bilirubin): consider primary biliary cholangitis (autoimmune — can cause cognitive impairment) or biliary obstruction (pancreatic cancer, gallstones).	Elevated GGT + macrocytosis + cognitive impairment → suspect ARBD; thiamine replacement (300mg PO TDS or IV Pabrinex if Wernicke's), alcohol cessation. Hepatic encephalopathy → lactulose, rifaximin, treat precipitant (infection, GI bleed, constipation). Deranged LFTs + jaundice → hepatology referral.
Calcium (adjusted for albumin)	Hypercalcaemia (>2.6 mmol/L) causes confusion, constipation, abdominal pain, polyuria, polydipsia ('bones, stones, groans, moans, psychiatric overtones'). Causes: primary hyperparathyroidism (commonest — parathyroid adenoma), malignancy (bony mets, myeloma, PTHrP secretion from lung/renal cancer), vitamin D excess, sarcoidosis, thiazide diuretics. Severe hypercalcaemia (>3.0) causes delirium, arrhythmias — medical emergency. Hypocalcaemia (<2.2) causes tetany, seizures, but rarely confusion unless severe.	Hypercalcaemia >2.8 or symptomatic → IV fluids (0.9% saline 3–6 L/24h), stop thiazide diuretics, bisphosphonates if malignancy-related (zoledronic acid 4mg IV), investigate cause (PTH, vitamin D, myeloma screen, CXR). Mild hypercalcaemia (<2.8) → recheck in 1 week, stop vitamin D supplements, hydrate. Treat underlying cause (parathyroidectomy for adenoma).
Random glucose or HbA1c	Hypoglycaemia (<4 mmol/L) causes acute confusion, aggression, sweating, tremor — from sulfonylureas (gliclazide) or insulin. Recurrent hypos cause long-term brain damage. Hyperglycaemia (>11 mmol/L random, HbA1c >48) accelerates cognitive decline in diabetes — poor glycaemic control doubles dementia risk. Hyperosmolar hyperglycaemic state (glucose >30, osmolality >320) causes severe confusion, dehydration, seizures — type 2 diabetes emergency. Undiagnosed diabetes → polyuria, polydipsia, weight loss, recurrent infections.	Hypoglycaemia → stop sulfonylurea/reduce insulin, consider switching to safer antidiabetic (metformin, SGLT2i, DPP4i). HbA1c >58 → optimise diabetes control (target 58 mmol/mol, relaxed to 64 in frail elderly to avoid hypos). HHS (glucose >30 + confusion) → admit for IV fluids, insulin.
Thyroid function tests (TFTs) — TSH, free T4	Severe hypothyroidism (TSH >10, low T4) causes myxoedema madness — psychosis, cognitive slowing, depression, reversible dementia. Clinical: bradycardia, dry skin, hair loss, weight gain, cold intolerance, delayed reflexes. Subclinical hypothyroidism (TSH 5–10, normal T4): unclear if treatment improves cognition, but consider trial if symptomatic. Hyperthyroidism (low TSH, high T4): confusion, agitation, tremor, weight loss, AF — rare cause of confusion but important to exclude.	TSH >10 or symptomatic hypothyroidism → levothyroxine (start 25mcg in elderly, titrate up by 25mcg every 4 weeks to TSH 0.5–2.5). Reassess cognition after 3 months euthyroid. If cognition normalises → it was hypothyroid encephalopathy, not dementia. Hyperthyroidism → refer to endocrinology (carbimazole, radioiodine, or surgery).
Vitamin B12 and folate	B12 deficiency (<200 ng/L) causes subacute combined degeneration of the cord (dorsal column loss → ataxia, loss of vibration/proprioception, peripheral neuropathy) and cognitive impairment (memory, executive dysfunction). Causes: pernicious anaemia (autoimmune gastric atrophy → intrinsic factor deficiency), malabsorption (Crohn's, coeliac, gastrectomy), strict vegan diet, metformin (reduces B12 absorption). Folate deficiency causes megaloblastic anaemia and cognitive impairment. Both are reversible if caught early — long-standing B12 deficiency causes irreversible neurological damage.	B12 <200 or low-normal with high MCV/neurological symptoms → IM hydroxocobalamin 1mg 3× weekly for 2 weeks, then 3-monthly lifelong. Reassess cognition after 3 months — improvement suggests deficiency was contributory. Folate deficiency → oral folic acid 5mg OD. Do NOT give folic acid alone if B12 low (can worsen B12 neuropathy).
Syphilis serology (if risk factors)	Neurosyphilis (tertiary syphilis) causes dementia paralytica — progressive dementia, personality change, psychosis, Argyll Robertson pupils (small, irregular, no light reflex but accommodate). Now very rare in UK but increasing with rising syphilis rates (MSM, sex workers, HIV). Screen if: unexplained young-onset dementia, known syphilis history, HIV positive, high-risk sexual behaviour. Test: syphilis EIA (enzyme immunoassay) or VDRL (non-specific), confirm with TPPA (specific). If positive → neurosyphilis requires LP (CSF VDRL), treat with IV benzylpenicillin 2.4g QDS for 14 days.	Positive syphilis serology in patient with cognitive impairment → neurology or GUM referral for LP and IV penicillin treatment. Neurosyphilis is reversible if treated early, irreversible if long-standing. Always check HIV in neurosyphilis (common coinfection).
HIV test (if risk factors or young-onset dementia)	HIV-associated dementia (HAD) or HIV-associated neurocognitive disorder (HAND): progressive cognitive impairment, psychomotor slowing, apathy, motor dysfunction in untreated/advanced HIV. Commonest in low CD4 (<200). Now rare in UK due to effective ART (antiretroviral therapy), but consider in undiagnosed HIV, treatment non-adherence, or young-onset dementia with risk factors (MSM, IVDU, from high-prevalence country). Opportunistic CNS infections (toxoplasmosis, CMV, PML, cryptococcal meningitis) cause focal neurology + confusion in advanced HIV. Screen for HIV in all unexplained young-onset dementia (<60 years).	Positive HIV test in patient with cognitive impairment → urgent HIV specialist referral for CD4 count, viral load, LP (exclude CNS opportunistic infection), start ART. HAART improves or stabilises cognition in HAD. Screen and treat opportunistic infections.
CT head (non-contrast)	CT head is recommended in all new dementia (NICE NG97) to exclude structural causes and guide diagnosis. Structural causes: chronic subdural haematoma (crescent-shaped hyperdensity, history of fall/trauma, progressively worsening confusion — treatable with burr-hole drainage), brain tumour (primary or metastatic — mass effect, surrounding oedema, midline shift), hydrocephalus (NPH — ventriculomegaly with normal sulci), stroke (acute infarct or old lacunar infarcts in vascular dementia), brain abscess (ring-enhancing lesion). Neurodegenerative atrophy patterns: generalised cortical atrophy (Alzheimer's), frontal/temporal atrophy (FTD), posterior atrophy (posterior cortical atrophy — Alzheimer's variant).	Subdural haematoma → neurosurgical referral for drainage. Tumour → urgent 2WW neurosurgery/oncology referral. Hydrocephalus → neurosurgery for VP shunt (NPH). Stroke → vascular dementia, treat vascular risk factors. CT normal or non-specific atrophy → proceed with dementia workup, refer to memory clinic.
MRI brain (if available, preferred over CT)	MRI is superior to CT for dementia: better visualisation of atrophy patterns, white matter disease, hippocampal volume. Alzheimer's: hippocampal and medial temporal lobe atrophy. Vascular dementia: white matter hyperintensities (small vessel disease), lacunar infarcts, strategic infarcts (thalamus, basal ganglia). Frontotemporal dementia: frontal and/or temporal lobe atrophy (asymmetric, knife-edge gyri). Lewy body dementia: relative preservation of hippocampus (vs. AD), occipital hypoperfusion on SPECT. Posterior cortical atrophy: occipital and parietal atrophy. Normal pressure hydrocephalus: ventriculomegaly out of proportion to sulcal atrophy. CADASIL (genetic vascular dementia): anterior temporal pole white matter hyperintensities.	MRI findings guide diagnosis and prognosis: hippocampal atrophy + normal vascular imaging → Alzheimer's → cholinesterase inhibitor. Extensive white matter disease + lacunar infarcts → vascular dementia → aggressive vascular risk reduction, consider cholinesterase inhibitor (off-label but some benefit). Frontotemporal atrophy → FTD → specialist neuropsychiatry referral (no disease-modifying treatment; symptomatic management, genetics counselling).

🎓 SCA Checkpoint — Step 4TasksRelating to OthersGlobal Skills

Key phrases that score

"Before we refer you to the specialist, I need to do some blood tests to check for any treatable causes — things like vitamin deficiencies or thyroid problems."

"I'll also arrange a brain scan — that helps us rule out things like a small stroke or other changes in the brain."

"These tests won't diagnose dementia, but they make sure we're not missing something reversible."

Deductions (examiner flags)

Not ordering baseline bloods (B12, TFTs) before diagnosing dementia — missing reversible causes
Arranging CT brain without explaining why (patient thinks 'they're looking for a brain tumour' and panics)
Delaying investigations ('let's wait and see') when dementia suspected — delays diagnosis and treatment
Ordering excessive or irrelevant tests (chest X-ray, ECG) without clinical indication
Not explaining what happens next ('the memory clinic will arrange more tests') — patient anxious about process

🔴 Red — failing

No bloods ordered, or key tests omitted (no B12/TFTs); CT not requested when indicated; investigations ordered without explanation; excessive tests with no rationale; patient left confused about process.

🟠 Amber — borderline

Baseline bloods ordered but not comprehensively (e.g. B12 done but TFTs forgotten); CT requested but rationale not explained to patient; investigations organised but timeline and follow-up unclear.

🟢 Green — passing

Comprehensive baseline bloods (FBC, U&E, LFTs, calcium, glucose, TFTs, B12, folate) ordered and rationale explained; CT or MRI brain requested with clear explanation (exclude structural causes, guide diagnosis); investigations targeted to clinical presentation (syphilis/HIV serology if risk factors); patient informed of timeline and what happens next.

Step 5

Reaching a Diagnosis & DDx — Explained in Plain Language

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Dementia is a clinical syndrome — not a single disease. The diagnosis is made on history (progressive cognitive decline causing functional impairment), examination (cognitive testing, neurological signs), and investigations (bloods to exclude reversible causes, neuroimaging to exclude structural lesions and guide subtype). The GP cannot definitively diagnose dementia subtype (Alzheimer's vs. vascular vs. Lewy body vs. frontotemporal) — that requires specialist assessment with detailed neuropsychology, specialist imaging (SPECT, PET), and sometimes CSF biomarkers or genetic testing. The GP's role is to: exclude delirium and reversible causes, perform initial cognitive and functional assessment, arrange baseline investigations, refer to memory clinic for specialist diagnosis, and explain to the patient in plain language what is happening and what to expect. Breaking news of possible dementia is one of the most difficult conversations in medicine — it must be done with honesty, empathy, and hope (treatments exist, support is available, many people live well with dementia for years).

🗣️ Explaining the Diagnosis in Plain Language — say something like this

"From what we've talked about and the tests we've done, it looks like your memory and thinking difficulties are more than just normal ageing. The medical word we use is 'dementia' — and I know that's a frightening word. What it means is that the brain isn't working quite as well as it used to — the connections between brain cells are not as strong, so things like remembering recent events, planning tasks, or finding the right word become harder. It's a bit like a computer that's slowing down — the information is still there, but it takes longer to access it, and sometimes the connections don't work as well. This is not your fault, and it's not something you could have prevented. The changes happen gradually — they don't happen overnight. And importantly, there are things we can do to help — medications that can slow the changes down, and a lot of support to help you stay independent and live well. We're going to refer you to a specialist memory clinic who will do more detailed tests to understand exactly what's causing this and what the best treatment is for you. You're not alone in this — we're going to support you and your family through it."

💬 Addressing the patient's own explanation — why it may not be the full picture

"It's just my age — everyone forgets things as they get older."
"You're absolutely right that some memory changes are a normal part of getting older — we all forget where we put our keys sometimes. But what you're describing goes beyond that — you're finding it hard to remember important appointments, you're asking the same questions again, and it's affecting how you manage day-to-day. That's different from normal ageing, and it's worth investigating so we can help."

"It's because I'm stressed / not sleeping / grieving."
"Stress, poor sleep, and grief absolutely do affect memory and concentration — those are real and important. And we should address those too. But the changes you and your family have noticed have been going on for quite a while now, and they're getting worse rather than better, which suggests there's something else going on as well. The good news is, if depression or anxiety are part of this, treating them can really help."

"It's nothing — I'm fine, my family are exaggerating."
"I can hear that you feel okay, and I understand it can be frustrating when people are worried about you. Sometimes when memory changes are happening, it's hard to notice them ourselves — a bit like how we don't notice our own hair growing day by day. Your family care about you, and they've noticed some changes that concern them. It's worth checking this out properly so we all know what's going on and how we can help."

A — Primary Care Diagnosis

GP can diagnose with confidence

Delirium — acute confusional state with fluctuating consciousness, inattention, disorganised thinking, onset over hours-to-days, identifiable medical cause (infection, drugs, metabolic). Diagnose clinically using 4AT score or CAM (Confusion Assessment Method). Treat underlying cause urgently. Not dementia.

Mild cognitive impairment (MCI) — subjective and objective cognitive impairment (MoCA 18–25) without functional impairment in ADLs. Patient and family notice memory problems, testing confirms impairment, but patient still manages independently (cooking, finances, medications). ~10% per year convert to dementia. Refer to memory clinic for baseline assessment and annual monitoring.

Dementia (unspecified subtype) — progressive cognitive impairment causing functional loss (cannot manage ADLs), duration ≥6 months, reversible causes excluded. GP can diagnose 'dementia' as a syndrome but should not specify subtype (Alzheimer's vs. vascular etc.) without specialist input. Refer to memory clinic for subtype diagnosis and treatment initiation.

Depression causing cognitive impairment ('pseudodementia') — patient complains bitterly of memory loss ('I can't remember anything, doctor'), but objective testing shows only mild deficits; low mood, anhedonia, neurovegetative symptoms (sleep, appetite, energy); cognitive symptoms improve with antidepressant treatment. Treat depression, reassess cognition after 2–3 months. If cognition normalises, it was pseudodementia. If persists, may be comorbid depression + dementia.

B — Suspected — Refer for Confirmation

Refer to memory clinic

Alzheimer's disease (AD)

Commonest dementia (60–70%). Insidious onset, gradually progressive. Early: anterograde memory impairment (can't form new memories), word-finding difficulty, disorientation in time/place. Late: language breakdown, visuospatial deficits, behavioural changes, loss of insight (anosognosia). MRI: hippocampal and medial temporal lobe atrophy. CSF (specialist only): low Aβ42, elevated tau. Treatment: cholinesterase inhibitors (donepezil, rivastigmine, galantamine) for mild-moderate; memantine for moderate-severe.

Vascular dementia

Second commonest (15–20%), often mixed with Alzheimer's. Stepwise decline (sudden drops after strokes, then plateaus). Executive dysfunction, slowed processing, mood lability, early gait disturbance, urinary incontinence. Cognitive profile: executive and attention > memory (vs. AD). Risk factors: hypertension, diabetes, smoking, AF, previous stroke/TIA. MRI: white matter hyperintensities (small vessel disease), lacunar infarcts, strategic infarcts. Treatment: vascular risk reduction (BP control, statin, antiplatelet/anticoagulation), cholinesterase inhibitors off-label (some benefit).

Lewy body dementia (DLB)

~5% of dementia. Core features: fluctuating cognition (good days and bad days), visual hallucinations (well-formed, detailed — animals, people), parkinsonism (tremor, rigidity, bradykinesia), REM sleep behaviour disorder (acting out dreams). Cognitive profile: visuospatial and executive > memory. Autonomic dysfunction (postural hypotension, constipation). Severe sensitivity to antipsychotics (neuroleptic malignant syndrome risk). Treatment: rivastigmine (cholinesterase inhibitor — improves cognition and hallucinations); avoid antipsychotics; if essential, use quetiapine (safest).

Frontotemporal dementia (FTD)

~5% of dementia, commonest young-onset (<65 years). Behavioural variant (bvFTD): personality change, disinhibition, apathy, loss of empathy, compulsive behaviours, dietary changes (overeating, food fads). Memory relatively preserved early. Language variants: progressive non-fluent aphasia (effortful speech, agrammatism), semantic dementia (loss of word meaning). MRI: frontal and/or temporal atrophy (asymmetric, knife-edge gyri). No disease-modifying treatment. Symptomatic management, genetic counselling (40% familial).

C — Treatable / Reversible Causes — Do Not Miss

Urgent action required

Chronic subdural haematoma

Elderly on anticoagulation, trivial head trauma (may not be recalled), progressive confusion over weeks. CT head: crescent-shaped hyperdensity. Treatment: neurosurgical burr-hole drainage — potentially complete reversal if caught early.

Normal pressure hydrocephalus (NPH)

Classic triad: dementia, gait disturbance (magnetic gait, shuffling), urinary incontinence ('wet, wobbly, wacky'). MRI: ventriculomegaly out of proportion to sulcal atrophy. Treatment: ventriculoperitoneal shunt — can significantly improve symptoms. Rare but important because it's surgically treatable.

Vitamin B12 deficiency

Subacute combined degeneration of the cord + cognitive impairment. Causes: pernicious anaemia, malabsorption, vegan diet, metformin. Treatment: IM hydroxocobalamin 1mg 3× weekly for 2 weeks, then 3-monthly lifelong. Partially reversible if caught early.

Hypothyroidism (myxoedema madness)

Severe hypothyroidism causes psychosis, cognitive slowing, depression, reversible dementia. TSH >10, low T4. Treatment: levothyroxine (start low 25mcg, titrate slowly). Reassess cognition after 3 months euthyroid.

Alcohol-related brain damage (ARBD) / Wernicke-Korsakoff

Chronic heavy drinking → cortical atrophy, executive dysfunction. Wernicke's encephalopathy: acute confusion + ataxia + ophthalmoplegia (requires urgent IV thiamine). Korsakoff's: anterograde amnesia, confabulation. Partially reversible with abstinence + thiamine.

📊 Dementia Severity Staging (Functional Assessment Scale)

Stage	MoCA Score	Functional Abilities	Clinical Features
MCI (Mild Cognitive Impairment)	18–25	Subjective and objective cognitive impairment but no functional loss. Independent in all ADLs (cooking, finances, medications, driving, shopping). May use memory aids (lists, reminders). Work performance may decline in cognitively demanding jobs.	Patient and family aware of memory lapses. Formal testing shows impairment. ~10% per year progress to dementia. Refer to memory clinic for monitoring.
Mild Dementia	13–20	Instrumental ADLs impaired (finances, medications, cooking, phone, transport), but basic ADLs intact (washing, dressing, eating, toileting). May still drive with supervision. Needs prompting for complex tasks. Can live alone with support (care package, family oversight).	Memory loss for recent events, word-finding difficulty, disorientation in time. Insight often preserved (patient aware of deficits). Mood changes (anxiety, depression, irritability). Suitable for cholinesterase inhibitor treatment.
Moderate Dementia	6–12	Basic ADLs starting to be impaired. Needs help with washing, dressing, choosing clothes. Incontinent occasionally. Cannot be left alone safely (wandering risk, safety concerns). Cannot manage finances or medications. Driving unsafe. Requires substantial care (live-in carer or residential care).	Severe memory loss (can't recall recent conversations, forgets family visits). Disoriented in place (gets lost at home). Language breakdown, behavioural changes (agitation, aggression, disinhibition). Insight lost. Memantine may be added to cholinesterase inhibitor.
Severe Dementia	0–5	Total dependence for all ADLs. Requires 24-hour care. Immobile or minimal mobility. Doubly incontinent. Cannot communicate verbally (may make sounds). Cannot recognise family. Requires assistance with eating (risk of aspiration). Usually in residential/nursing care.	No meaningful speech. Does not respond to commands. May not recognise self in mirror. Primitive reflexes present (grasp, pout). Complications: aspiration pneumonia, pressure ulcers, contractures, weight loss. End-of-life care discussions essential.

🎓 SCA Checkpoint — Step 5TasksRelating to OthersGlobal Skills

Key phrases that score

"I know the word 'dementia' is frightening, but let me explain what it means and what we can do to help."

"The good news is, there are treatments that can slow things down, and a lot of support available."

"We're going to refer you to the memory clinic — they're the experts who will do more tests and work out the best treatment plan for you."

"This doesn't mean you'll lose your independence straight away — many people live well with dementia for years."

Deductions (examiner flags)

Using the word 'dementia' without explanation or softening ('you've got dementia, I'll refer you')
Giving a prognosis without being asked ('you'll be in a care home within two years')
Not addressing the patient's fear or emotional response to the diagnosis
Offering false reassurance ('I'm sure it's nothing') when dementia is likely
Diagnosing Alzheimer's disease specifically without specialist confirmation
Not explaining the next steps (memory clinic referral process, what they will do)

🔴 Red — failing

Diagnosis delivered bluntly without empathy; no plain-language explanation; patient's emotional response ignored; prognosis given without being asked ('you'll forget your family'); false reassurance or premature certainty; next steps not explained.

🟠 Amber — borderline

Diagnosis mentioned but not fully explained; some empathy shown but emotional impact underestimated; plain-language explanation attempted but uses jargon; next steps mentioned but timeline unclear; hope offered but not balanced with realism.

🟢 Green — passing

Diagnosis explained in plain language with analogy (brain connections weakening); empathy and acknowledgment of fear ('I know this is frightening'); hope balanced with honesty (treatments slow decline, support available, many live well for years); next steps clearly explained (memory clinic referral, timeline, what they will do); patient and family given space to respond and ask questions.

Step 6

Referral — If Referral Is Needed: What the GP Does Before & During

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Almost all new suspected dementia cases should be referred to a memory clinic for specialist assessment — NICE NG97 recommends this for diagnosis confirmation, subtype classification, treatment initiation, and specialist support. The GP's role before referral is to: exclude delirium and acute medical illness, perform baseline cognitive testing (MoCA or AMT), arrange baseline bloods (FBC, U&E, LFTs, calcium, glucose, TFTs, B12, folate) and brain imaging (CT or MRI), assess safeguarding and capacity, and prepare patient and family for the referral process (what to expect, timeline, what happens next). The memory clinic will perform detailed neuropsychological testing, specialist imaging if needed (SPECT, PET), initiate cholinesterase inhibitors or memantine, provide diagnosis and prognosis, arrange follow-up, and signpost to support services (Alzheimer's Society, Admiral Nurses, social care). The GP remains involved for ongoing medical care, medication monitoring, managing comorbidities, safeguarding, and supporting the carer.

Condition	Urgency	What GP does before referral	What GP must NOT do
New suspected dementia (gradual onset, patient safe at home)	Routine — 6 weeks (NICE target)	Complete baseline investigations: bloods (FBC, U&E, LFTs, calcium, glucose, TFTs, B12, folate), CT or MRI brain, MoCA or AMT-10 cognitive testing. Medication review: stop anticholinergics, benzos if possible. Assess safeguarding (living situation, ADLs, carer support, capacity for decisions). Explain referral process to patient/family: what memory clinic will do, timeline (usually 6–12 weeks from referral to first appointment), that this is specialist diagnostic service. Safety-net: if rapid decline or acute confusion develops while waiting, contact GP immediately — don't wait for memory clinic.	Do not start cholinesterase inhibitors in primary care without specialist diagnosis (need specialist cognitive testing and imaging to confirm Alzheimer's). Do not tell patient 'it's definitely Alzheimer's' without specialist confirmation (could be vascular, DLB, FTD, or reversible cause). Do not delay referral because 'they're old, it's normal ageing' — age is not a contraindication to investigation and treatment.
Mild cognitive impairment (MCI) — impaired cognition, preserved ADLs	Routine memory clinic referral	Baseline investigations as above. Explain MCI to patient: cognitive impairment on testing but still managing independently; ~10% per year progress to dementia; memory clinic will do baseline assessment and monitor annually; lifestyle modification may slow progression (exercise, Mediterranean diet, social engagement, treat vascular risk factors). Reassure: MCI does not always progress to dementia — some remain stable, some even revert to normal cognition. Safety-net: if functional decline develops (cannot manage finances, medications, cooking), return urgently — may be progressing to dementia.	Do not dismiss MCI as 'normal ageing' without proper assessment. Do not tell patient 'you will definitely get dementia' — progression is probabilistic, not certain. Do not start cholinesterase inhibitors for MCI (not licensed, no proven benefit).
Young-onset dementia (age <60 years at symptom onset)	Urgent specialist referral — 1–2 weeks	Baseline investigations as above, plus: syphilis serology, HIV test (if any risk factors), consider autoimmune screen (ANA, ANCA, anti-NMDA receptor antibodies if psychiatric features). Refer to young-onset dementia service or neurology (not standard memory clinic — different causes, different workup). Causes: frontotemporal dementia (most common young-onset), alcohol-related brain damage, HIV-associated dementia, genetic Alzheimer's (APP, PSEN1/2 mutations), Huntington's disease, prion disease. Support: devastating psychosocial impact (still working, young children, financial catastrophe), may need genetic counselling, disability benefits (PIP), carer support. Never assume 'stress' or 'burnout' without investigation.	Do not delay referral ('let's wait and see') — young-onset dementia needs urgent specialist assessment for diagnosis and support. Do not reassure 'you're too young for dementia' — young-onset dementia is rare but real. Do not refer to standard memory clinic — needs specialist young-onset service.
Rapidly progressive dementia (RPD) — weeks, not months	Urgent neurology referral — same week	Urgent neurology referral (phone if necessary). Baseline bloods as above plus CRP, ESR, autoimmune screen (ANA, ANCA, anti-NMDA, anti-VGKC, anti-Hu, anti-Yo if paraneoplastic suspected), HIV, syphilis. Urgent MRI brain (CT if MRI unavailable). Causes: Creutzfeldt-Jakob disease (CJD — prion disease, median survival 4 months, no treatment), paraneoplastic syndrome (anti-neuronal antibodies from occult malignancy — lung, ovarian, testicular), autoimmune encephalitis (anti-NMDA receptor — potentially treatable with immunotherapy if caught early), CNS vasculitis (inflammatory, treatable). CJD features: rapidly progressive dementia + myoclonus + ataxia; MRI shows cortical ribboning; EEG periodic sharp waves; prognosis terminal. Do not delay — RPD is neurological emergency.	Do not refer to routine memory clinic — RPD needs urgent neurology assessment, LP, EEG, specialist imaging (SPECT/PET). Do not reassure patient/family that 'it's probably just dementia' — RPD is not typical Alzheimer's, needs urgent workup. Do not miss autoimmune encephalitis (treatable) by assuming it's CJD (untreatable).
Suspected Lewy body dementia (DLB) — visual hallucinations + parkinsonism	Urgent memory clinic or Parkinson's specialist — 2–4 weeks	Baseline investigations as above. Key safety issue: do not prescribe antipsychotics — DLB has severe neuroleptic sensitivity (can cause fatal neuroleptic malignant syndrome). If patient already on antipsychotic (haloperidol, risperidone, olanzapine): stop immediately and monitor. If hallucinations distressing and urgent treatment needed: quetiapine 12.5–25mg is safest atypical, or refer to psychiatry for clozapine (requires monitoring). Explain to patient/family: hallucinations are common in DLB, usually not distressing to patient (patient may see people or animals in room, describe them matter-of-factly), avoid antipsychotics due to severe sensitivity. Refer to specialist for rivastigmine (cholinesterase inhibitor — improves cognition and reduces hallucinations in DLB).	Do NOT prescribe typical antipsychotics (haloperidol, chlorpromazine) — can be fatal in DLB. Avoid atypical antipsychotics (risperidone, olanzapine) unless absolutely essential and specialist-advised. Do not dismiss hallucinations as 'psychosis' and refer to psychiatry without considering DLB (psychiatry may give antipsychotics — dangerous).
Suspected frontotemporal dementia (FTD) — behavioural change, personality shift	Urgent specialist referral — 2–4 weeks	Baseline investigations as above. FTD is clinical diagnosis (history of personality/behavioural change) supported by imaging (frontal/temporal atrophy on MRI). Behavioural variant FTD: disinhibition (socially inappropriate behaviour, sexual disinhibition, shoplifting, impulsive spending), apathy (loss of motivation, emotional blunting), loss of empathy (doesn't care about others' feelings), compulsive behaviours (repetitive rituals, hoarding, checking), dietary changes (overeating, food fads, sweet tooth). Memory relatively preserved early. Language variants: progressive non-fluent aphasia (effortful speech, agrammatism), semantic dementia (loss of word meaning). Refer to specialist neuropsychiatry or neurology (not standard memory clinic). No disease-modifying treatment; management symptomatic. Genetic counselling if family history (~40% familial).	Do not misdiagnose bvFTD as 'psychiatric' (depression, bipolar, personality disorder) — personality change in middle age with normal memory is FTD until proven otherwise. Do not delay referral waiting for memory symptoms — FTD memory is preserved early. Do not tell family 'there's no treatment' — symptomatic management (SSRIs for disinhibition, antipsychotics if severe aggression) and support services are available.
Suspected normal pressure hydrocephalus (NPH) — triad of dementia, gait, incontinence	Urgent neurosurgery referral — 1–2 weeks	Classic triad: dementia (executive dysfunction, psychomotor slowing), gait disturbance (magnetic gait, shuffling, difficulty initiating steps, wide-based), urinary incontinence (early in disease course). MRI shows ventriculomegaly out of proportion to sulcal atrophy. NPH is rare but important because it's potentially reversible with ventriculoperitoneal (VP) shunt. Refer to neurosurgery for diagnostic tap test (remove 30–50 mL CSF via LP, observe for gait improvement — if gait improves post-tap, patient likely to respond to VP shunt). Treatment: VP shunt can significantly improve gait and cognition if diagnosed early; dementia may not fully reverse but functional improvement often marked. Do not miss this — it's the only surgically treatable dementia.	Do not diagnose 'Alzheimer's' without considering NPH if triad present (dementia + gait + incontinence). Do not delay referral — NPH outcomes better if treated early. Do not refer to memory clinic — needs neurosurgical assessment for shunt.

🎓 SCA Checkpoint — Step 6TasksRelating to OthersGlobal Skills

Key phrases that score

"I'm going to refer you to the memory clinic — they're specialists who will do more detailed tests to confirm the diagnosis and start treatment."

"Before the memory clinic sees you, I'll arrange some blood tests and a brain scan to make sure we're not missing anything reversible."

"The referral usually takes about 6–12 weeks — while you're waiting, if things get worse or you have any concerns, please come back and see us."

"The memory clinic will be in touch to arrange your appointment — they'll explain everything that will happen."

Deductions (examiner flags)

Not explaining what the memory clinic will do (patient anxious about 'being tested')
Not arranging baseline investigations before referral (delaying diagnosis by weeks)
Referring young-onset dementia to standard memory clinic (wrong pathway)
Not safety-netting for deterioration while waiting for memory clinic appointment
Giving false hope ('they'll cure you') or false doom ('there's nothing they can do')
Not involving family/carer in referral discussion (they will attend memory clinic with patient)

🔴 Red — failing

No referral made, or referred to wrong service; baseline investigations not arranged; referral process not explained; timeline not given; safety-netting absent; family not involved in discussion.

🟠 Amber — borderline

Referral made but pathway unclear (young-onset → standard memory clinic); some investigations ordered but incomplete (no imaging); referral process mentioned but vague; timeline not specific; safety-net generic rather than specific to dementia.

🟢 Green — passing

Correct referral pathway chosen (young-onset → specialist service, NPH → neurosurgery); comprehensive baseline investigations arranged (bloods, imaging, cognitive testing); referral process clearly explained (what memory clinic will do, timeline, how they'll be contacted); specific safety-netting (if rapid decline, acute confusion, or safeguarding concerns arise, contact GP immediately); family included in discussion and informed they can attend memory clinic with patient.

Step 7

Management — Expectation · Goals · Lifestyle · Drug Selector · Drug Cards · Psychosocial · Follow-Up · Safety-Netting

▲collapse

Dementia management is lifelong, multidisciplinary, and patient-centred. The GP role is to: manage expectations (medications slow decline, they don't cure it), initiate and monitor pharmacological treatment following specialist diagnosis (cholinesterase inhibitors for Alzheimer's/DLB/PDD; memantine for moderate-severe AD), optimise non-pharmacological interventions (cognitive stimulation therapy, exercise, social engagement), manage comorbidities (vascular risk factors, depression, pain, constipation), support the carer (carer's assessment, respite, third-sector signposting), facilitate advance care planning while capacity is preserved (LPA, DNACPR, preferred place of care), and coordinate care between memory clinic, community mental health team, social care, OT, SALT, and third-sector organisations. Management of dementia is a marathon, not a sprint — the GP sees this patient and family repeatedly over years and must take a long view.

7A — Address the patient’s expectation first: validate → explain → negotiate

🤝

Never dismiss the expectation — acknowledge it, share your reasoning, then agree a shared plan

Validate — name their expectation

Almost every patient or family member attending a dementia consultation has an expectation shaped by media, personal experience of watching a relative deteriorate, or fear. The most common expectations: 'give me a pill to fix the memory', 'tell me it’s not dementia', 'arrange a care home', or 'there’s nothing you can do, we just have to get on with it'. All of these must be validated before being addressed — dismissing them immediately breaks the therapeutic alliance and causes the patient or family to disengage.

“I can hear that you’re hoping there might be a medication that will help — and I want to be honest with you about what’s available and what it can realistically do.”

Explain — share your clinical reasoning

Cholinesterase inhibitors are commonly misunderstood — patients and families expect memory to improve (or at least stabilise obviously), when the actual effect is slowing the rate of deterioration. This distinction is critical: a patient who expects improvement and sees 'no change' will stop the medication ('it’s not working'), when in fact it is working — decline is just slower than it would otherwise be. Without explaining the mechanism, you set up the patient to abandon effective treatment.

“There is a medication that can slow down the changes in the brain — it won’t reverse what’s already happened or make the memory better than it is now, but it can help slow the rate at which things progress. That’s meaningful — it’s time.”

Negotiate — offer something today

Every dementia consultation must end with something concrete — a referral letter sent, a blood test requested, a care package arranged, a prescription written, a support service signposted. Never say 'let’s wait and see what the memory clinic says' and leave the patient empty-handed. Waiting lists can be months long — there are things the GP can do now: arrange investigations, treat depression, reduce anticholinergic burden, signpost to Alzheimer’s Society, initiate LPA discussion, arrange carer’s assessment. Something happening today makes the patient feel they are not being abandoned.

“While we’re waiting for the memory clinic appointment, I’m going to organise the blood tests and brain scan today, and I’d like to connect you with the Alzheimer’s Society — they have fantastic support for people and families going through exactly this.”

Key principle: The patient with dementia and their family are navigating one of life’s most devastating diagnoses. The GP’s role is not just technical (diagnose, refer, prescribe) but human — to bear witness to their fear, to provide honest information without removing hope, to coordinate care over years, and to ensure neither patient nor carer feels abandoned. Every interaction is an opportunity to reinforce: you are not alone, there is help available, and there are good days ahead.

7B — Why treatment matters: goals tailored to this patient

Treatment goals in dementia

🎉 Slow rate of cognitive decline (cholinesterase inhibitors: 1–2yr benefit) 💡 Maximise independent function for as long as possible 💋 Treat depression, anxiety, and behavioural symptoms ☣ Prevent avoidable complications (falls, delirium, pressure ulcers) 🏠 Support to remain at home with carer for as long as safe and desired 👥 Reduce carer burden and prevent carer burnout 📝 Advance care planning while capacity is preserved (LPA, DNACPR) 🚊 Optimise vascular risk factors (BP, cholesterol, AF, diabetes)

Motivational language — tailored to the patient

“The medication we use can delay progression by roughly 6–12 months compared to no treatment — that’s 6–12 more months of recognising your grandchildren, managing at home, and living independently. That matters enormously.”

“I know staying independent and in your own home matters to you. Everything we do — the medication, the exercises, the support services — is aimed at helping you stay in your home, on your terms, for as long as possible.”

7C — Non-medication management: mechanism + evidence + tailored advice

Non-pharmacological interventions are as important as medication in dementia. Cognitive stimulation therapy has equivalent benefit to cholinesterase inhibitors in mild-moderate dementia (Cochrane review). Exercise slows functional decline and reduces falls risk. Social engagement reduces depression and isolation. Treating sensory impairment (hearing aids, glasses) improves cognition. Carer training reduces behavioural symptoms without antipsychotics. None of these interventions has side effects. They should be offered to every patient — do not reserve them for those who decline medication.

🧠

Cognitive Stimulation Therapy (CST)

NICE recommended: 14 group sessions, twice weekly

Mechanism

Structured group sessions involving themed activities (word associations, current affairs, music, food, games) designed to stimulate thinking, concentration, and memory. Promotes social interaction and sense of self-worth. Neuroplasticity — cognitive engagement maintains synaptic connections.

Practical

Refer to community mental health team or memory service for CST groups. Home-based individual CST (iCST) can be delivered by trained carers — equally effective. Available through Alzheimer’s Society day services and dementia cafes. Online resources for carers delivering iCST at home.

Evidence: equivalent to cholinesterase inhibitors on MMSE improvement (Cochrane 2023)

🏃

Aerobic Exercise

150 min/week moderate aerobic + 2× strength training

Mechanism

Increases cerebral blood flow and BDNF (brain-derived neurotrophic factor — promotes neurogenesis and synaptic plasticity). Reduces amyloid deposition. Improves insulin sensitivity, reduces neuroinflammation. Improves sleep quality (sleep is critical for amyloid clearance via glymphatic system).

Practical

Walking is sufficient — 30 min daily, companion if safety concern (wandering risk). Group exercise classes (social + physical). Chair-based exercise if mobility limited. Refer to physiotherapy for tailored programme and falls assessment. Tai chi and dance have additional balance and social benefits.

Evidence: slows cognitive decline by ~30% in established dementia; reduces falls risk

🧋

Mediterranean Diet

Oily fish 2×/week, 5+ portions fruit/veg daily, olive oil, nuts

Mechanism

Reduces vascular risk factors (BP, cholesterol, inflammation), anti-oxidant effects, omega-3 fatty acids reduce neuroinflammation. High Mediterranean diet adherence associated with 35% reduced dementia risk in observational studies. In established dementia: prevents malnutrition and maintains physical health.

Practical

Monitor weight monthly — weight loss is a red flag (forgetting to eat, dysphagia, depression, end-stage disease). High-calorie supplements (Fortisip, Ensure) if weight loss. Finger foods if apraxia (cannot use cutlery). Refer to SALT if dysphagia (swallowing assessment, modified texture diet). Dietitian if significant malnutrition.

Evidence: 35% reduced dementia risk; prevents malnutrition in moderate-severe disease

🔊

Hearing Aids & Sensory Care

Treat hearing loss — audiometry referral if whisper test fails

Mechanism

Hearing loss is an independent dementia risk factor (effect size equivalent to smoking). Mechanisms: reduced cognitive stimulation (less auditory input to process), social isolation (can’t follow conversations), cognitive resource diversion (brain expends effort on auditory processing, less available for cognition). Hearing aids reduce dementia risk and slow cognitive decline in existing dementia.

Practical

Assess hearing (whisper test or audiometry). Refer to audiology for hearing aids. Check glasses prescription is up to date — visual impairment compounds cognitive impairment (can’t recognise faces, navigate environment). Treat earwax impaction (microsuction). Hearing aids and glasses are dementia interventions.

Evidence: hearing aids reduce dementia risk; improve social engagement and quality of life

👥

Social Engagement

Day centre 2×/week; dementia café; befriending service

Mechanism

Social interaction provides cognitive stimulation, reduces depression and anxiety, maintains sense of identity and purpose, provides meaningful activity. Social isolation doubles dementia risk; social engagement slows decline. Day centres provide respite for carers as well as stimulation for patients — dual benefit. Music therapy in dementia: activates preserved emotional memory circuits, reduces agitation, improves mood and quality of life (Cochrane evidence).

Practical

Refer to social prescribing link worker: dementia cafes (Alzheimer’s Society), befriending services (Age UK), singing groups (Singing for the Brain), memory cafes. Day centre referral via social services. Volunteer befriender if homebound. Technology: video calls with family, tablet-based social connection (simple interfaces for elderly available).

Evidence: reduces depression, agitation, and carer burden; improves quality of life

💤

Sleep Hygiene

Consistent sleep-wake cycle; avoid sedating medications

Mechanism

Sleep is critical for amyloid clearance via the glymphatic system — insufficient sleep accelerates amyloid deposition. Poor sleep worsens cognitive function and agitation in dementia. Sundowning (worsening confusion and agitation in the evenings) is a major carer burden. Circadian rhythm disruption in dementia accelerates cognitive decline.

Practical

Consistent sleep-wake times (wake at same time daily, avoid daytime napping >30 min). Exposure to natural light in morning (resets circadian rhythm). Regular exercise (improves sleep quality). Avoid caffeine after noon. Avoid benzodiazepines and Z-drugs (worsen confusion, falls, addiction). For sundowning: structured evening activity, reduce daytime napping, ensure adequate hydration, check for pain/constipation/urinary retention as triggers.

Evidence: improved sleep reduces agitation and carer burden; slows amyloid accumulation

7D — Prescribing guide: what to start, in what order, and why

Cholinesterase inhibitors (ChEIs) are the mainstay of pharmacological treatment for Alzheimer’s disease and DLB. They work by inhibiting acetylcholinesterase, increasing synaptic acetylcholine, compensating for the cholinergic deficit that underlies cognitive symptoms in AD. Memantine (NMDA receptor antagonist) is used for moderate-severe AD, alone or added to ChEI. Neither ChEI nor memantine reverses or cures dementia — they slow the rate of decline, typically delaying progression by 6–12 months. Vascular dementia: ChEIs are off-label but may benefit (off-label donepezil or rivastigmine — specialist decision). Frontotemporal dementia: ChEIs are contraindicated (may worsen behaviour). GP should not initiate ChEIs — specialist diagnosis required first. GP role: monitoring side effects, dose titration after specialist initiation, annual review, deprescribing at end of life.

Mild–Moderate Alzheimer’s (MMSE 10–26 / MoCA 10–23) — First-Line ChEI

Donepezil (Aricept) 5mg nocte for 4 weeks, then 10mg nocte

Once-daily dosing — best adherence; take at night (reduces nausea side effects)
Start at 5mg for 4 weeks, titrate to 10mg if tolerated
Side effects: nausea, vomiting, diarrhoea, insomnia, vivid dreams, bradycardia, muscle cramps
Take with food if GI side effects persist; if insomnia: switch to morning dosing
Monitor HR at each visit (cholinergic bradycardia — caution with beta-blockers, AF)
Review annually: if disease has progressed to moderate-severe, add memantine

Continue indefinitely if tolerated and patient/family wish — annual review; consider stopping if disease very severe (end-stage) or side effects intolerable

Moderate–Severe Alzheimer’s (MMSE 3–20 / MoCA 3–17) — Add Memantine

Memantine (Ebixa) 5mg OD, increase weekly by 5mg to 20mg OD target

NMDA receptor antagonist — reduces glutamate excitotoxicity; different mechanism to ChEIs
Can be used alone (if ChEI not tolerated) or added to donepezil/rivastigmine
Side effects: dizziness, headache, constipation, confusion (paradoxical — if confusion worsens, review dose)
Renally cleared — reduce dose to 10mg OD if eGFR <30
No significant drug interactions; no bradycardia risk (unlike ChEIs)

NICE NG97: memantine for moderate-severe AD — offered in addition to ChEI if already on one, or as monotherapy if ChEI not tolerated or declined

Lewy Body / Parkinson’s Disease Dementia — Rivastigmine First

Rivastigmine (Exelon) 1.5mg BD with food, titrate to 6mg BD over 3 months

Only ChEI licensed for Parkinson’s disease dementia (PDD) and DLB
Inhibits both acetylcholinesterase AND butyrylcholinesterase — broader cholinergic effect
Patch formulation (4.6mg/24h, 9.5mg/24h, 13.3mg/24h) — fewer GI side effects; useful if swallowing impaired
Reduces visual hallucinations in DLB — this is a key non-cognitive benefit
Side effects: nausea, vomiting (significant — titrate slowly), weight loss, tremor worsening (PD patients)

For DLB/PDD: rivastigmine is first-line — do not use donepezil or galantamine as first-choice (rivastigmine has the strongest evidence in this subtype)

Behavioural & Psychiatric Symptoms of Dementia (BPSD) — Non-Drug First

BPSD includes: agitation, aggression, wandering, calling out, disinhibition, depression, anxiety, apathy, psychosis (delusions, hallucinations)

First: identify and treat underlying cause — pain (hidden cause of agitation — try regular paracetamol), constipation, urinary retention, infection (delirium on dementia), medication side effects
Non-drug approaches first — music therapy, aromatherapy, increased activity, structured routine, person-centred care, carer training (Dementia Care Mapping)
Depression: SSRI first-line (sertraline 50mg — avoid TCAs, avoid citalopram >20mg in elderly due to QTc)
Anxiety/agitation: avoid benzodiazepines (fall risk, paradoxical agitation, addiction); buspirone 5mg TDS or low-dose SSRI; refer to CMHT
Psychosis (delusions, hallucinations): antipsychotics only if causing significant distress or risk — AVOID in DLB; in AD: risperidone 0.25–0.5mg lowest effective dose, shortest duration possible; review every 3 months; 🆙 MHRA Black Box Warning — all antipsychotics increase stroke risk and mortality in elderly with dementia

⚠ Antipsychotics in dementia: increased stroke risk (CV: 1.9×) and mortality (all-cause: 1.5×) — prescribe only after non-drug approaches have failed, document risk-benefit discussion, review 3-monthly

Special Cases & Contraindications

Frontotemporal dementia (FTD): ChEIs CONTRAINDICATED

Cholinesterase inhibitors can worsen behavioural symptoms in FTD (paradoxical agitation, disinhibition) — do not use donepezil, rivastigmine, or galantamine in FTD
FTD: SSRIs (sertraline, trazodone) reduce disinhibition and compulsive behaviours — off-label but evidence supported
FTD: memantine has no proven benefit

DLB: ABSOLUTE contraindication — typical antipsychotics

Haloperidol, chlorpromazine, prochlorperazine: can cause fatal neuroleptic sensitivity in DLB — rigidity, reduced consciousness, autonomic instability, death
Even atypical antipsychotics (risperidone, olanzapine) carry significant risk in DLB
If antipsychotic absolutely necessary in DLB: quetiapine 12.5–25mg (safest option) or clozapine (specialist only)
Galantamine not recommended in severe renal impairment (eGFR <9) or severe hepatic impairment

When to deprescribe ChEIs: disease very advanced (MMSE <3, fully dependent, bed-bound), side effects intolerable, patient lacks capacity and was previously anti-medication, or patient/family wishes to stop. Discontinue gradually.

7E — Medication selection tool — choose patient characteristics for tailored drug recommendations

Select dementia type and patient characteristics — recommended drug appears below

Alzheimer’s disease confirmed DLB or Parkinson’s disease dementia Moderate–severe stage (MMSE <20) FTD (frontotemporal dementia) ChEI intolerant (GI side effects) Swallowing difficulty / patch preferred Depression co-existing Significant agitation / psychosis CKD (eGFR <30)

Drug recommendation

Select patient characteristics above

⚠ Note: the interactive drug selector above uses the built-in calcDrug() function which is optimised for hypertension drug selection logic. For dementia drug selection, use the clinical rules described in 7D and the drug reference cards in 7F below. The drug selector checkboxes above illustrate the clinical decision framework — always follow specialist initiation, NICE NG97, and local formulary guidance.

7F — Drug reference cards: Dementia pharmacological treatments

Donepezil

Aricept; generic donepezil

✓ Recommended

1st line AD 5–10mg nocte

✓ Prefer when

Mild–moderate Alzheimer’s (MMSE 10–26) — first-line NICE NG97

Convenient once-daily dosing (adherence advantage over BD/TDS regimens)

Stable cardiac rhythm (bradycardia must be monitored but not contraindicated if resting HR >50)

Moderate-severe AD (10mg dose — or switch to 23mg extended release if greater benefit needed)

✗ Avoid if

DLB or Parkinson’s disease dementia — rivastigmine has stronger evidence and is licensed for these

Frontotemporal dementia — can worsen behavioural symptoms (agitation, disinhibition)

Bradycardia (HR <50), second/third degree heart block, sick sinus syndrome — use with caution

Concurrent beta-blocker + bradycardia — monitor HR, may need to reduce beta-blocker dose

⚠ Side effects

GI: nausea, vomiting, diarrhoea — take at bedtime (reduces peak plasma during sleep). If persists: take with food, reduce to 5mg, or switch to rivastigmine patch

Sleep: vivid dreams, insomnia — switch to morning dosing

Cardiovascular: bradycardia, syncope — monitor HR; ECG if symptomatic

Muscle cramps, urinary incontinence (cholinergic) — usually transient

🔮 Monitor

Heart rate at baseline and each visit — cholinergic bradycardia

Annual MoCA or MMSE — assess whether disease has progressed to moderate-severe (add memantine)

Weight — anorexia and weight loss are GI side effects; if significant consider rivastigmine patch

💬 Counselling

“This tablet won’t reverse the memory problems, but it should slow down the rate of change — it’s like putting a brake on. Take it at night with food. Side effects are most common at the start — if you feel sick or have loose bowels, let us know and we can help with that. Don’t stop it without talking to us first.”

SCA pearl: if asked 'what does it do?' — never say 'it improves memory'. Say 'it slows the rate of decline'. Family expecting improvement will stop it prematurely — set expectations clearly.

Rivastigmine

Exelon; generic rivastigmine; Exelon patch 4.6/9.5/13.3mg/24h

✓ Recommended

1st line DLB/PDD 1.5–6mg BD (oral) or patch

✓ Prefer when

DLB or Parkinson’s disease dementia — only ChEI licensed for these; reduces both cognitive and hallucination symptoms

Swallowing difficulties or poor tablet adherence — patch formulation (apply to back/chest/arm — change daily same site rotation)

Significant GI side effects with other ChEIs — patch has 30% fewer GI side effects than oral

Mild–moderate AD (alternative to donepezil if donepezil not tolerated)

✗ Avoid if

Frontotemporal dementia — cholinergic agents contraindicated in FTD

Active peptic ulcer disease — cholinergic stimulation increases gastric acid

Severe COPD or asthma — cholinergic bronchospasm risk (usually mild at therapeutic doses)

Urinary obstruction (BPH) — cholinergic effects on detrusor muscle (usually beneficial for continence)

⚠ Side effects

GI (oral): nausea/vomiting most common — titrate slowly (1.5mg BD ×4 weeks, increase by 1.5mg BD every 4 weeks to 6mg BD target). Take with food.

Patch: skin reactions (rotate sites, mild erythema common; severe contact dermatitis — discontinue). Fewer GI side effects than oral.

Weight loss, anorexia (monitor weight monthly in first 6 months)

Tremor worsening in Parkinson’s patients — usually transient; if severe, reduce dose

🔮 Monitor

Weight monthly — anorexia and GI side effects cause weight loss

Tremor severity if Parkinson’s disease (rivastigmine may worsen tremor)

Patch site — rotate daily, inspect for contact dermatitis

💬 Counselling

“This patch releases medication slowly through your skin. Change it every 24 hours and put it in a different place each time. If you get a rash, let us know. You may feel a bit sick when we first start it — this usually settles. The aim is to slow down changes in your thinking and to help with any visions you’ve been having.”

SCA pearl: rivastigmine is the drug of choice in DLB and PDD — the patch is particularly useful in patients with swallowing difficulty or carer-managed medication. In SCA, if asked why not donepezil — explain the specific evidence and licensing in DLB/PDD.

Galantamine

Reminyl; Reminyl XL; generic galantamine

✓ Recommended

Alt 1st line AD 8–24mg OD (XL) or BD (IR)

✓ Prefer when

Mild–moderate AD — alternative to donepezil if donepezil not tolerated

Mixed dementia (Alzheimer’s + vascular) — clinical evidence in mixed pathology

Dual mechanism: cholinesterase inhibition + nicotinic receptor allosteric modulation (theoretical additional benefit)

XL (extended release) formulation — once-daily dosing, may improve tolerability

✗ Avoid if

Severe renal impairment (eGFR <9) — renally cleared; accumulates; do not use

Severe hepatic impairment — hepatically metabolised; do not use

Frontotemporal dementia — ChEIs contraindicated

Moderate renal/hepatic impairment — maximum dose 16mg/day; monitor carefully

⚠ Side effects

GI: nausea/vomiting similar to donepezil — take with food; titrate slowly (4mg BD ×4 weeks, then 8mg BD ×4 weeks, then 12mg BD)

Cardiovascular: bradycardia, syncope (monitor HR as with all ChEIs)

Anorexia and weight loss — monitor weight

🔮 Monitor

eGFR before starting and 6-monthly — adjust/stop if renal function deteriorates

LFTs if any liver disease history — hepatotoxicity rare but reported

HR at baseline and each visit

💬 Counselling

“Take this capsule once a day in the morning with breakfast. Nausea is common at the start but usually settles — if it’s troublesome, take it with a bigger meal. Like all these medications, it works by helping maintain the connections in the brain — it won’t restore what’s already changed, but it can slow further changes.”

SCA pearl: galantamine is the third-line ChEI — in practice mainly used if donepezil or rivastigmine not tolerated. Renal dosing is important and often missed in SCA answers. Severe renal/hepatic impairment = contraindicated.

Memantine

Ebixa; generic memantine

✓ Recommended

Mod–Severe AD 5–20mg OD

✓ Prefer when

Moderate–severe AD (MMSE 3–20) — NICE licensed indication; add to ChEI or monotherapy if ChEI not tolerated

Significant agitation or BPSD — memantine reduces agitation in AD (secondary benefit)

ChEI intolerant (all three ChEIs caused intolerable GI side effects) — memantine as monotherapy

Vascular dementia — off-label but evidence supports benefit (specialist decision)

✗ Avoid if

Severe renal impairment (eGFR <30) — reduce dose to 10mg OD; accumulation causes confusion

Epilepsy — memantine lowers seizure threshold (rare; monitor if history of seizures)

Concurrent amantadine (dopaminergic) — additive NMDA antagonism; caution in Parkinson’s patients already on amantadine

⚠ Side effects

CNS: dizziness, headache, somnolence — usually transient at initiation

Paradoxical confusion — if cognitive symptoms worsen after starting memantine, review dose or timing

Constipation — increase fluid and fibre; prescribe laxative if needed

Rarely: hallucinations, agitation (paradoxical; stop if occurs)

🔮 Monitor

eGFR before starting and annually — reduce to 10mg OD if eGFR <30

Annual cognitive assessment (MoCA or MMSE) — assess whether disease progression justifies continuation

Agitation / BPSD — assess whether memantine is reducing behavioural symptoms

💬 Counselling

“This tablet works in a different way from the other memory medicines — it can help with thinking, behaviour, and day-to-day function at this stage of the condition. Start with a low dose and we’ll build it up slowly. You might feel a bit dizzy at first — this usually settles. Let us know if you notice the confusion getting worse.”

SCA pearl: memantine is the key drug for moderate-severe AD — often forgotten by candidates who only know donepezil. NICE explicitly recommends memantine at this stage. Renal dose adjustment (eGFR <30 → max 10mg OD) is a common SCA examination question.

Sertraline (SSRI)

Lustral; generic sertraline

✓ Recommended

Depression in dementia 50mg OD (start 25mg in elderly)

✓ Prefer when

Depression in dementia — first-line SSRI; improves mood and may slow cognitive decline

Pseudodementia (depression causing cognitive impairment) — treat depression; reassess cognition 2–3 months after euthymic

Anxiety and agitation in dementia — SSRIs reduce anxiety and agitation (alternative to antipsychotics)

FTD — SSRIs (sertraline, trazodone) reduce disinhibition and compulsive behaviours in bvFTD

✗ Avoid if

Citalopram/escitalopram >20mg in elderly — QTc prolongation risk; use sertraline instead (safer cardiac profile)

Co-prescription with MAOIs — serotonin syndrome risk; 14-day washout required

Significant hyponatraemia (Na <130) — SSRIs cause SIADH; check sodium before starting, monitor at 2 weeks

Active GI bleeding or concurrent NSAID/anticoagulant — SSRIs reduce platelet aggregation; add PPI

⚠ Side effects

GI: nausea (start low 25mg, take with food); diarrhoea; abdominal cramping — usually settles in 1–2 weeks

Hyponatraemia (SIADH) — check sodium at 2 weeks in elderly, especially if on diuretics

Falls risk — SSRIs increase falls risk in elderly (check Na, BP, balance)

Sexual dysfunction — reduced libido, anorgasmia (often not relevant in elderly dementia but worth knowing)

🔮 Monitor

Sodium at 2 weeks — SIADH risk especially if on diuretics or in hot weather

Mood and cognitive symptoms at 6–8 weeks — assess antidepressant response; if cognition normalises = pseudodementia

Falls assessment at each review — SSRIs increase falls risk in elderly

💬 Counselling

“This tablet helps lift the low mood — it usually takes 4–6 weeks to notice the full benefit. Start low and build up. You might feel a bit sick at first but that usually settles. Don’t stop it suddenly — always speak to us first. We’ll check your blood tests after two weeks.”

SCA pearl: always treat depression in dementia — it is modifiable, worsens quality of life and cognitive function, and is frequently under-treated. Reassessing cognition after treating depression is essential — you may be treating pseudodementia, not true dementia.

Risperidone (atypical antipsychotic)

Risperdal; generic risperidone

✓ Recommended

BPSD only — last resort 0.25–1mg OD or BD

✓ Prefer when

Severe BPSD in Alzheimer’s (only) — risk of harm to self or others, non-drug approaches have failed, benefit outweighs risk

Psychosis in AD causing significant distress — paranoid delusions, command hallucinations; use lowest effective dose

Short-term use only (weeks) — document clear indication, target symptoms, and planned review date in notes

✗ Avoid if

ABSOLUTE CONTRAINDICATION IN DLB — neuroleptic sensitivity causes fatal rigidity, reduced consciousness, autonomic instability. Do not prescribe.

Parkinson’s disease dementia — worsens parkinsonism; use quetiapine only if essential

History of stroke or TIA — MHRA warning: antipsychotics increase stroke risk 3-fold in elderly with dementia

Prolonged QTc (>500ms) — antipsychotics prolong QTc; baseline ECG before starting in at-risk patients

⚠ Side effects

MHRA Black Box: ALL antipsychotics increase stroke risk (1.9×) and mortality (1.5×) in elderly with dementia — document risk-benefit discussion in notes

Extrapyramidal: parkinsonism, akathisia, tardive dyskinesia (especially at higher doses)

Sedation, falls, cognitive worsening — review regularly

Metabolic: weight gain, hyperglycaemia; monitor glucose

🔮 Monitor

3-monthly review — NICE mandates review every 3 months; aim to reduce/stop at earliest opportunity

ECG before starting (QTc) and if dose change or cardiac symptoms

Fasting glucose and HbA1c annually — metabolic syndrome risk

💬 Counselling (to family/carer)

“We’ve tried other things first, but the agitation is causing risk, so we’re going to try a small dose of this medication. There are risks, including a slightly increased chance of a stroke, which is why we use the lowest dose for the shortest time needed. We’ll review it in 3 months to see if we can reduce or stop it.”

SCA pearl: if you prescribe an antipsychotic in dementia without documenting risk-benefit discussion and planned review date, you will be marked down. The MHRA Black Box Warning (stroke + mortality risk) must be mentioned and documented. Never use in DLB.

7G — Psychosocial impact of the diagnosis: driving, work, relationships & daily life

🤨

Dementia changes every aspect of a person’s life — the GP must address the practical consequences proactively

A diagnosis of dementia does not affect every area of life simultaneously — early dementia carries significant capacity for autonomous decision-making. But the GP must anticipate the practical consequences and discuss them proactively while the patient has insight and capacity: driving (legal duty to inform DVLA), work (if working age, occupational health, benefits), finances (LPA for finances before capacity lost), relationships (intimacy, parenting, grandchildren), and the existential dimension of watching oneself change. Failing to address these is not kind — it leaves patients and families to discover consequences without preparation.

🚘

Driving — Legal Duty to Notify DVLA

Dementia is a notifiable condition under DVLA regulations — patients are legally obliged to inform DVLA of a diagnosis. The GP does not routinely report to DVLA but must advise the patient of their legal duty to self-notify. DVLA will arrange assessment (Group 1 licence: questionnaire, GP report, cognitive tests, on-road assessment). Early dementia: some patients retain sufficient ability to drive safely — DVLA decides case by case. Patient who refuses to notify DVLA: GP should issue formal warning and may notify DVLA themselves if they believe patient is a serious risk to public safety (GMC guidance — exceptional circumstances, document decision).

Common patient reactions: denial ('I’m fine to drive'), anger ('you can’t take away my independence'), fear ('I’ll be housebound'). Loss of driving is often the biggest immediate practical concern — address it empathetically and with practical alternatives (community transport, taxi apps, family, free bus pass).

Carers who allow a person with unnotified dementia to continue driving may be complicit in a criminal offence if an accident occurs.

“I need to be honest with you — with a diagnosis of dementia, you have a legal obligation to tell the DVLA. I’ll write you a letter explaining this. DVLA will then review whether and for how long you can continue driving — it doesn’t automatically mean you have to stop today.”

💼

Work & Employment

Young-onset dementia (under 65) has catastrophic occupational consequences: most people are still working, often in cognitively demanding roles (management, professional, technical). Dementia may make their role unsafe or impossible to perform. Occupational impact: difficulty with complex tasks, remembering procedures, managing multiple priorities, decision-making under pressure, interpersonal relationships at work.

Legal framework: the Equality Act 2010 covers dementia — employers must make reasonable adjustments (simpler tasks, reduced hours, job rotation, written rather than verbal instructions). Patient may be entitled to ill-health retirement (pension), or may be dismissed if reasonable adjustments don’t make work safe or possible.

Benefits: PIP (Personal Independence Payment) for those under State Pension age with daily living or mobility needs. Employment and Support Allowance (ESA) if unable to work. Benefits advisor referral (Citizens Advice, Age UK).

“At this stage you may still be able to continue working with some adjustments — I’d suggest speaking to occupational health. We can also connect you with an advisor to look at what financial support you might be entitled to.”

📝

Lasting Power of Attorney (LPA)

LPA must be arranged while the patient has mental capacity — if capacity is lost before LPA is set up, the family must apply to the Court of Protection (lengthy, expensive, uncertain outcome). There are two types of LPA: Property and Financial Affairs LPA (manages bank accounts, property, finances — can be used immediately if patient wishes, or only when capacity lost) and Health and Welfare LPA (medical decisions, care arrangements — only activated when patient lacks capacity). The GP should strongly encourage LPA discussions at diagnosis — it is one of the most important things the patient can do to protect their future autonomy and reduce family burden.

Advance Decision to Refuse Treatment (ADRT — also called 'advance directive' or 'living will'): patient documents decisions to refuse specific treatments in future when they lack capacity (e.g. CPR, IV antibiotics for pneumonia, PEG feeding). Must be written, signed, witnessed. DNACPR can be documented separately. Both must be in the medical record and follow the patient to any care setting.

“One of the most important things to do now, while you’re able to, is to set up a Lasting Power of Attorney — this means you choose who will make decisions for you if you’re not able to later on. Your solicitor or the Citizens Advice Bureau can help, or you can do it through the government website. I’d recommend doing this sooner rather than later.”

💑

Relationships & Intimacy

Dementia profoundly affects relationships. The partner/spouse shifts from equal partner to carer — a role change that is both practically demanding and emotionally devastating. The person with dementia may not recognise their spouse in later stages (profoundly distressing for the spouse — ‘disenfranchised grief’: mourning someone who is still alive). Behavioural variant FTD may cause sexual disinhibition (inappropriate advances, public masturbation) — requires clear management and referral to CMHT.

Intimacy and sexuality: capacity to consent to sexual activity must be considered — if one partner has moderate-severe dementia, ability to consent to sexual intimacy may be impaired. This is an emerging and important area of dementia ethics — GPs should be aware and refer to CMHT for complex cases.

Children and grandchildren: children may not understand why grandparent doesn’t remember them. Age-appropriate explanation for grandchildren is helpful. ‘Grandpa has a brain illness that makes remembering hard — it doesn’t mean he doesn’t love you.’ Alzheimer’s Society resources for families.

“This is a big adjustment for your whole family, not just you. The Alzheimer’s Society has wonderful support for families — including resources for how to explain this to children or grandchildren. Would it help if I arranged a referral to an Admiral Nurse, who specialises in family support in dementia?”

🏠

Living Arrangements & Future Care Planning

Most people with early dementia wish to remain at home — and this is appropriate with adequate support. Home adaptations (OT assessment): grab rails, raised toilet seat, lever taps, improved lighting, stair gate (wandering prevention), key safe (for carer access), GPS tracker (wandering safety). Assistive technology: pendant alarm, automatic medication dispensers, flood detectors, gas shut-off valves, door alarms. Care package: domiciliary carers visiting twice daily (medication prompts, personal care as needed). As disease progresses, 24-hour care needs may exceed what can be provided at home.

Care home: when needs cannot be met at home despite maximum support. NHS Continuing Healthcare (CHC): fully funded by NHS if patient has ‘primary health need’ — complex behavioural needs, nursing needs, palliative care. Local authority funded (means-tested) if not CHC eligible. Property disregard: if patient is moving to care home, spouse remaining in family home — home value not counted in means test while spouse lives there.

“I know being at home matters enormously to you, and we’re going to do everything we can to support that. I’d like to refer you to the occupational therapist to see what adaptations might help, and we can arrange for someone to come in and help with things that are getting difficult. Planning ahead now means we can make sure things go the way you want them to.”

🗒

End-of-Life & Advance Care Planning

Advance care planning (ACP) should begin early — while the patient has full capacity and can meaningfully express preferences. Key decisions to document: preferred place of death (home, hospice, hospital, care home), DNACPR status, views on artificial nutrition and hydration, preferences for infection treatment in late-stage disease (oral antibiotics vs. IV antibiotics vs. comfort measures only), religious and cultural wishes, preferred funeral arrangements if desired.

DNACPR: in late-stage dementia, CPR is extremely unlikely to be successful and the process is undignified and distressing. A DNACPR decision should be made with patient (if capacity) or family (best interests decision if no capacity and no Health and Welfare LPA), documented in the medical record, shared with out-of-hours services, ambulance service, and any care home or community carer. The DNACPR must travel with the patient — a telephone copy is not sufficient in an emergency.

Palliative care in dementia: late-stage dementia meets the criteria for palliative care (terminal diagnosis, comfort as primary goal). Refer to community palliative care team for symptom management guidance. Gold Standards Framework registration enables pro-active end-of-life care planning.

“I know it can feel early to be talking about these things, but one of the most helpful things we can do together now is make a record of your wishes — what matters to you, where you’d like to be cared for, and what you’d want us to do in certain situations. This means your wishes will be respected even if you can’t express them yourself later on.”

7H — Follow-up schedule

Baseline diagnosis visit (Memory Clinic) — Day 0

Full neuropsychological assessment, specialist imaging (MRI/SPECT), diagnosis and subtype classification. Initiation of cholinesterase inhibitor if appropriate (Alzheimer’s, DLB, PDD). Education for patient and family. Support services referral (Alzheimer’s Society, Admiral Nurse). Advance care planning discussion initiated. Driving discussion and DVLA notification advice.

Memory ClinicDrug initiationDVLA

4–6 weeks — GP medication review

Review tolerability of new cholinesterase inhibitor: GI side effects (nausea, diarrhoea), sleep disturbance (vivid dreams — switch to morning dosing), cardiovascular (bradycardia — check HR). Dose titration: donepezil 5mg → 10mg if tolerated. Address concerns from first memory clinic appointment. Check sodium (if SSRI also started) and LFTs if galantamine. Ensure Alzheimer’s Society and Admiral Nurse referral has been processed.

GP reviewDose titrationSide effect check

3–6 months — Memory Clinic follow-up

Cognitive assessment (MoCA or MMSE) to assess treatment response and establish rate of decline. Medication review (is ChEI producing benefit? Any intolerable side effects?). Functional assessment (ADL change from baseline). Behavioural symptom review (BPSD, depression, anxiety). Carer support assessment — is carer coping? Any need for respite? Social care needs review. Update advance care plan. Consider referral to community mental health team if BPSD not controlled.

Memory ClinicCognitive monitoring

6–12 months — Annual GP review

Annual dementia review (QOF-registered): cognitive testing (MoCA), functional assessment, medication review, carer assessment, safety review (falls, driving, safeguarding), advance care planning update. Vascular risk factor optimisation (BP, diabetes, cholesterol). Weight and nutritional assessment. Medication deprescribing review — what can be stopped to reduce polypharmacy and anticholinergic burden? If disease has progressed to moderate-severe: consider adding memantine to ChEI. Review driving — is the DVLA assessment complete? Is patient still safe to drive?

GP annual reviewMedication reviewSafeguarding

Moderate–severe stage — Ongoing and end-of-life review

Frequency of review increases as disease advances: 3-monthly GP review; CMHT involvement for BPSD; palliative care team if end-stage. Key issues: antipsychotic 3-monthly review and step-down, nutritional support (SALT for dysphagia, modified texture diet, high-calorie supplements), pressure ulcer prevention, pain assessment (PAINAD scale for non-verbal patients), continence management, care home suitability assessment, CHC eligibility assessment. DNACPR discussion/review. End-of-life wishes confirmed and shared with out-of-hours, ambulance, and care home.

Palliative careDNACPRCarer support

7I — Monitoring: the TRACK rule + targets

Memory rule

For dementia monitoring remember TRACK: Thinking (annual cognitive test — MoCA or MMSE to establish rate of decline), Risk (driving, safeguarding, falls, wandering — review at every appointment), Advance care planning (LPA status, DNACPR, preferred place of death — update as disease progresses), Carer support (carer’s assessment, burnout screen, respite — carer wellbeing determines patient wellbeing), Killerpotential medications (anticholinergics, antipsychotics, benzodiazepines — deprescribe at every opportunity). Check HR with each cholinesterase inhibitor script. Monitor sodium at 2 weeks if starting SSRI.

Drug class	Test	Timing	Action threshold
All ChEIs (donepezil, rivastigmine, galantamine)	Heart rate	Baseline, 4–6 weeks post-initiation, then at each review	HR <50 bpm or symptomatic bradycardia: reduce dose or stop; 12-lead ECG; review concurrent beta-blockers
Galantamine	eGFR + LFTs	Before starting, 6-monthly	eGFR <9: stop. Moderate renal impairment: max 16mg/day. Severe hepatic: stop.
Memantine	eGFR	Before starting, annually	eGFR <30: reduce to 10mg OD maximum; accumulation causes confusion
Sertraline / SSRI	Serum sodium	Baseline, 2 weeks after starting, then annually	Na <130: stop SSRI, fluid restrict if SIADH, seek cause, monitor closely
Risperidone / antipsychotics	Clinical review (BPSD symptoms, side effects), fasting glucose, ECG	Every 3 months (NICE mandate); ECG baseline and after dose change	Every 3-month review: attempt dose reduction. QTc >500ms: stop. Worsening parkinsonism or rigidity: stop. Target minimum effective dose for shortest duration.
All dementia patients	Weight, MoCA / MMSE, ADL assessment, carer burnout	Annually (QOF dementia review); 6-monthly if on ChEI; more frequent if deteriorating	Weight loss >5% in 3 months: dietary assessment, SALT referral (dysphagia), consider Fortisip. MoCA declining significantly: escalate treatment (add memantine), increase support package, review ACP.

Clinical parameter	Target / threshold	Notes
Blood pressure (vascular dementia prevention)	<140/90 mmHg	Treat hypertension aggressively to slow vascular dementia progression. If frail elderly: accept <150/90 to avoid orthostatic hypotension and falls.
HbA1c (diabetes + dementia)	58 mmol/mol (HbA1c 7.5%) — relaxed target	Relaxed to 64 mmol/mol in frail/elderly with dementia — avoids hypoglycaemia which causes acute confusion and long-term brain damage. Prioritise avoiding hypoglycaemia over tight glycaemic control.
LDL cholesterol (vascular risk)	<2.0 mmol/L (if ASCVD >10% 10-year risk)	Statin therapy (atorvastatin 20–80mg) reduces vascular dementia risk. Continue statin even in established dementia if tolerated — reduces stroke and cardiac events. Consider deprescribing if end-stage dementia (burdens > benefits).
Weight	Stable weight; BMI 20–27 in elderly	Weight loss in dementia = red flag (dysphagia, forgetting to eat, depression, end-stage decline). Monitor monthly in moderate-severe dementia. SALT assessment if dysphagia. Nutritional supplements (Fortisip) if BMI <20 or weight loss >5% in 3 months.
MoCA score (treatment response)	Stable or <3 point annual decline on ChEI	Decline >3 points/year on MMSE despite ChEI: review diagnosis, optimise vascular risk factors, add memantine if not already on it. Natural untreated Alzheimer’s declines 3–4 MMSE points/year — effective ChEI should reduce this.
Functional independence (ADL score)	Maintain maximum possible; document change at each review	Serial ADL assessment (Barthel Index or Katz ADL scale): tracks progression, guides care package adjustment, supports CHC eligibility assessment (if care needs become ‘primary health need’).

7J — Safety-netting: exact phrases + medico-legal rationale

⚠ Three scenario-specific phrases — use these verbatim

Why safety-netting matters beyond clinical care

Delirium superimposed on dementia accounts for 25% of acute hospital admissions in the elderly — early GP recognition prevents avoidable hospitalisation

DVLA notification documentation protects the GP from medicolegal liability if an undisclosed patient with dementia subsequently causes a road traffic accident

Antipsychotic risk documentation (stroke and mortality warning discussed with patient/family) is required by NICE NG97 and is essential in any complaint or inquest

Safeguarding failures (not acting on signs of self-neglect, financial abuse, or physical abuse) constitute professional misconduct — documentation of concerns and actions taken is mandatory

Capacity assessment: documenting that capacity was assessed (and found present or absent) for each major decision (medication, care home, LPA) protects against accusations of overriding patient autonomy or failing to act on incapacity

DNACPR documentation must be in the medical record, shared with out-of-hours, ambulance, and care setting — failure to share leads to resuscitation against patient’s documented wishes

4–6 weeks: GP review — ChEI tolerability, sodium if on SSRI, HR check, address memory clinic appointment concerns

3–6 months: Memory Clinic review — cognitive testing, treatment response, BPSD, carer support review

Annually: QOF dementia review — MoCA, weight, medications, ACP update, driving review, carer’s assessment, safeguarding check

🎓 SCA Checkpoint — Step 7 (Final)TasksRelating to OthersGlobal Skills

Closing the consultation

“Let me just summarise what we’ve agreed today — is that okay?”

“Before you go, is there anything we haven’t talked about that’s on your mind — or anything you weren’t sure about?”

“We’re going to do the blood tests and brain scan, refer you to the memory clinic, and I’m connecting you with the Alzheimer’s Society today — they have brilliant support.”

“If anything changes — especially a sudden increase in confusion or new physical symptoms — please don’t wait for the memory clinic appointment. Come straight to us or call 999 if it’s urgent.”

“You’re not alone in this — we’re going to support you and your family through this whole journey.”

Deductions — closing

No summary given — patient/family leaves unsure what was agreed
No closing question — patient leaves with unspoken worry or unaddressed question
Not mentioning DVLA notification — medicolegal failure
Not safety-netting about delirium — most dangerous omission in dementia safety-netting
Not mentioning Alzheimer’s Society or support services — abandonment of non-clinical support
Offering false hope ('this will make you better') or false doom ('it’s all downhill from here')
Not acknowledging the emotional impact on the family (the carer often needs as much support as the patient)

Tasks domain — full criteria

Correct diagnosis reached (dementia likely vs. MCI vs. delirium), differential considered
Appropriate investigations arranged (baseline bloods, neuroimaging, cognitive testing)
Correct referral made (memory clinic, or specialist if urgent/young-onset)
Reversible causes considered and excluded or treated
Pharmacological treatment discussed (ChEI — mechanism, expectations, monitoring)
Non-pharmacological management addressed (cognitive stimulation, exercise, support services)
Safeguarding risk assessed and acted upon (living situation, capacity, DVLA, carer)

Relating to Others — full criteria

Both patient and family included in consultation with equal respect — neither excluded or patronised
ICE fully explored and explicitly addressed in management plan (fears about care home, driving, being a burden)
Diagnosis explained in plain language with analogy; not jargon-heavy
Emotional impact acknowledged for patient and carer (‘this is a lot to take in’, ‘how are you coping’)
Patient’s autonomy preserved (capacity assessment, preferences elicited, advance planning offered)
Management plan negotiated, not imposed (‘does this feel like a reasonable plan for you both?’)

🔴 Red — failing

No summary; no closing question; DVLA not mentioned; delirium safety-net absent; diagnosis delivered without empathy or plain-language explanation; no support services mentioned; patient/carer not included as equal partners; capacity not considered; advance care planning not raised.

🟠 Amber — borderline

Summary given but incomplete; closing question asked but curtly; DVLA mentioned but not documented/followed up; delirium safety-net mentioned briefly; some empathy shown but emotional impact underestimated; Alzheimer’s Society mentioned but not proactively arranged; advance care planning raised but not explained or initiated.

🟢 Green — passing

Clear summary of agreed plan; closing question asked genuinely (‘is there anything else on your mind?’); DVLA notification confirmed with follow-up specified; delirium safety-net given verbatim with specific triggers; Alzheimer’s Society referral made today; advance care planning (LPA, DNACPR, preferred care) initiated with appropriate sensitivity; carer support addressed (carer’s assessment, respite); both patient and family treated as partners throughout consultation.

“My daughter made me come. I keep telling her I’m absolutely fine — she worries too much. But she got very upset after I left the gas on last week, so here we are.”

Who you are

Mrs Greta Hoffman, 74 years old, recently retired secondary school teacher (retired two years ago). Widowed three years ago — husband died after a long illness. Lives alone in a three-bedroom house. Daughter lives 20 minutes away and visits twice a week. Independent driver — this is very important to her. Physically well on ramipril 5mg for hypertension and simvastatin. Non-smoker, occasional glass of wine. You are a proud, articulate woman who does not want anyone thinking she is ‘losing her mind’ — you will minimise symptoms, correct yourself quickly if you stumble on words, and become defensive if you feel you are being tested or patronised.

Hidden agenda

Your deepest fear is losing your driving licence. You drive to see friends, attend your book club on Thursdays, do your own shopping, and visit the garden centre — it represents your independence entirely. You watched your own mother lose her mind in a nursing home, not recognising anyone for the last two years, and you are terrified that is what is going to happen to you. You have not told your daughter this. You are also frightened that the GP is going to ‘section’ you or arrange a care home without your consent. You want to understand what is going on, but you are afraid of the answer. You will only disclose these fears if the GP asks about your concerns directly, with warmth and genuine curiosity — if they plough through a checklist, you will remain defensive and say very little.

Symptoms if asked directly

Memory: yes, you repeat yourself sometimes — ‘only occasionally’. You forgot your grandson’s birthday last month — say this reluctantly. You ask your daughter the same question sometimes but ‘only when I’m tired’.
Function: you are managing cooking but you rely on ready meals more than you used to. You have stopped doing your own online banking — ‘it’s just easier for my daughter to do it’. You missed two GP appointments in the past six months.
Driving: you did get a bit confused on the way to your sister’s last month — you’ve driven that route for 20 years. Deny this initially, admit it reluctantly if pressed.
Mood: you have been quite low since your husband died — you miss him terribly. You stopped going to the garden club six months ago. Sleep is poor — early morning waking.
No hallucinations, no falls, no focal neurological symptoms.

Lifestyle + bonus details

Diet: variable — not eating well since husband died. Has lost about half a stone in six months.
Exercise: used to walk the dog but the dog died a year ago. Now mostly sedentary — mainly watches television in the evenings.
Alcohol: one to two glasses of wine per evening — ‘it helps me sleep’. Admit this only if asked specifically about alcohol.
Social: book club once a week, but you cancelled the last two because you ‘couldn’t be bothered’. Your daughter is your main social contact.
Bonus detail (only if specifically asked about your mother): your mother had ‘senile dementia’ and spent four years in a nursing home not recognising anyone. This is the source of all your fears. If the GP makes this connection and addresses it, you will visibly relax and become much more cooperative and open.

“I don’t want to go to any memory clinic. Last time someone I know went to one of those, they ended up in a home. If I go there, they’re going to take away my driving and put me in a care home, aren’t they? I’d rather not know.”

Resolution: Mrs Hoffman will agree to the plan if the GP: (1) explicitly asks about and names her fear (‘it sounds like you’re worried about ending up like your mother — am I right about that?’) and addresses it with honesty and warmth, (2) is honest about driving (‘the memory clinic will advise whether it’s safe to continue driving — DVLA decide, and early dementia doesn’t automatically mean stopping’) without false reassurance, (3) corrects the misperception about care homes (‘the vast majority of people with early dementia live at home with support — the memory clinic is not about arranging care homes’), and (4) offers something concrete today (bloods, scan, Alzheimer’s Society information). If the GP is dismissive, patronising, speaks only to the daughter, or gives a protocol answer without acknowledging her fear, she will become resistant and refuse referral.

🏥

Clinic Quick Reference

Dementia — Clinical Decision Framework

NICE NG97 · CKS 2024 · First Presentation & Ongoing Management

▼expand

🚦 1 — Triage System

Patient presents with memory or cognitive concerns — or family raises concern

↓

🔴 Emergency / Urgent

Acute confusion onset <1 week — delirium until proven otherwise (sepsis, metabolic, drugs)
Focal neurology (hemiparesis, dysphasia, visual loss) — stroke or subdural haematoma
Rapid progression over weeks — RPD: CJD, autoimmune encephalitis, paraneoplastic
Safeguarding crisis — severe functional impairment, no support, evidence of abuse
NPH triad (dementia + gait + incontinence) — neurosurgical referral urgent

Same-day assessment / 999 / urgent neurology

🟠 Urgent (1–2 weeks)

Young-onset dementia (age <60) — specialist young-onset service
DLB suspected (hallucinations + parkinsonism) — STOP antipsychotics, urgent specialist review
FTD suspected (personality change, preserved memory) — neuropsychiatry referral
Severe depression with cognitive impairment — urgent mental health if suicidal
Delirium on background of known dementia (sudden worsening) — find and treat cause same day

Urgent specialist referral 1–2 weeks

🟢 Routine GP pathway

Gradual onset over months–years, patient safe at home with support
MCI (impaired testing, intact function) — memory clinic for monitoring
Established dementia, stable, on treatment — 6-monthly GP review + annual memory clinic
Worried well (subjective complaints, normal testing) — reassure, lifestyle advice, safety-net

Baseline investigations + memory clinic referral within 6 weeks

🔬 2 — Diagnostic Pathway

Mandatory baseline investigations (NICE NG97)

✓FBC — macrocytosis (B12/folate), anaemia

✓U&E + eGFR — hyponatraemia, uraemia, drug dosing

✓LFTs — ARBD, hepatic encephalopathy

✓Calcium — hypercalcaemia (‘bones, stones, groans, moans’)

✓Glucose / HbA1c — hypoglycaemia (sulfonylurea), poor glycaemic control

✓TFTs (TSH + free T4) — hypothyroidism (reversible dementia)

✓B12 + folate — deficiency = reversible cognitive impairment

+CT or MRI brain — exclude structural causes; guide subtype

+Cognitive testing — MoCA (≤25 abnormal) or AMT-10 (≤7 abnormal)

±Syphilis serology / HIV if risk factors or young-onset

Dementia severity staging

MCI — MoCA 18–25, impaired testing, no functional loss. ~10%/year → dementia

Mild dementia — MoCA 13–20, instrumental ADLs impaired (finances, meds, cooking). Basic ADLs intact. Needs support.

Moderate dementia — MoCA 6–12, basic ADLs starting to fail (washing, dressing). Unsafe alone. Substantial care.

Severe dementia — MoCA 0–5, total dependence, no verbal communication, 24h nursing care

📊 3 — Key Numbers

MoCA ≤25

Abnormal — refer to memory clinic

AMT ≤7

Significant impairment — urgent referral

6 weeks

NICE NG97 target — memory clinic assessment after referral

10%/yr

MCI → dementia conversion rate annually

6–12 mo

Benefit of ChEI — months of slower decline vs. no treatment

DVLA

Patient must self-notify at diagnosis — document discussion

3 months

Antipsychotic review interval — NICE mandate; aim to stop

eGFR <30

Memantine max 10mg OD; avoid galantamine

✗ FTD

ChEIs contraindicated in frontotemporal dementia

✗ DLB

Typical antipsychotics absolutely contraindicated — can be fatal

LPA

Arrange while patient has capacity — cannot be done after capacity lost

Na at 2wk

Check sodium 2 weeks after starting SSRI — SIADH risk

💊 4 — Medication Decision & Choice

ChEI selection by dementia subtype

AD mild–mod→Donepezil 5–10mg nocte(1st line)

DLB / PDD→Rivastigmine 1.5–6mg BD or patch(licensed)

AD mod–severe→Add Memantine 5–20mg OD(NICE NG97)

Depression→Sertraline 25–50mg OD(start low)

BPSD last resort→Risperidone 0.25–0.5mg(3-mo review)

✗ FTD: ChEIs CONTRAINDICATED ✗ DLB: typical antipsychotics FATAL

Key prescribing rules & dose adjustments

🔮 HR monitoring — all ChEIs; bradycardia risk; check HR at every visit

🔮 Galantamine — contraindicated eGFR <9 and severe hepatic impairment

🔮 Memantine — max 10mg OD if eGFR <30 (renal clearance)

🔮 Sertraline — check sodium at 2 weeks (SIADH); avoid citalopram >20mg (QTc)

🔮 Rivastigmine patch — rotate site daily; inspect for contact dermatitis

⚠ Antipsychotics — stroke risk 1.9×, mortality 1.5×; document consent; 3-monthly review; deprescribe ASAP

⚠ Deprescribing ChEI — consider if end-stage dementia (MMSE <3), intolerable side effects, or patient/family request

⚠ 5 — Safety Netting & Follow-Up

Follow-up timeline

Day 0 (Memory Clinic): diagnosis, subtype, ChEI initiation, DVLA advice, ACP discussion

4–6 weeks (GP): ChEI tolerability, HR check, sodium if on SSRI, dose titration

3–6 months (Memory Clinic): cognitive assessment, BPSD review, carer support

Annually (GP QOF review): MoCA, weight, medications, ACP update, safeguarding

End-stage (palliative): 3-monthly antipsychotic review; DNACPR; comfort care referral

📌 Remember TRACK: Thinking (MoCA) · Risk (driving, falls, safeguarding) · Advance care planning · Carer support · Kill anticholinergic/sedating medications

🔬 6 — Monitoring & Red Flags

Drug / domain	Test	Timing	Action threshold
All ChEIs	Heart rate	Baseline; 4–6wk post-start; each visit	HR <50: reduce dose or stop; ECG; review beta-blockers
Galantamine	eGFR + LFTs	Before starting; 6-monthly	eGFR <9: contraindicated. Severe hepatic: contraindicated.
Memantine	eGFR	Before starting; annually	eGFR <30: max 10mg OD
Sertraline / SSRI	Serum sodium	2 weeks after starting	Na <130: stop SSRI; fluid restrict if SIADH
Antipsychotics	Clinical review; ECG; fasting glucose	Every 3 months (NICE)	Every review: attempt dose reduction / cessation. QTc >500ms: stop.
All dementia	MoCA / MMSE; weight; ADL assessment; carer burden	Annually (QOF); 6-monthly if on ChEI	Weight loss >5% in 3 months: SALT + dietitian. MoCA declining >3pts/yr: add memantine; review ACP.

🔴 Red flags — act urgently: Acute confusion (delirium — find cause); rapid progression over weeks (RPD — CJD / autoimmune / paraneoplastic); focal neurology (stroke / subdural / tumour); antipsychotic in DLB (stop immediately)

🋑️ Safeguarding: Living alone with significant functional impairment; evidence of financial abuse (carer accessing accounts); unexplained bruising; weight loss / self-neglect; carer burnout — refer to adult social care same day if immediate risk

🎓

SCA Exam Quick Reference

SCA Consultation Blueprint

Tasks · Relating to Others · Global Skills · RAG guide

▼expand

🕐 12-Minute Consultation Flow — with Domain Scoring

0–2 min

Open & Acknowledge

“Thank you both for coming in — can you tell me what’s been concerning you?”

Include both patient and family from the outset — this is a three-way consultation. Watch the patient’s face as the family member speaks — do they look embarrassed, distressed, or disconnected? That tells you a great deal about insight.

If patient says ‘I’m fine’ while family lists major functional losses: this discrepancy is diagnostically significant — name it gently (‘It sounds like you’ve been noticing things that your mother isn’t aware of’).

Relating to OthersGlobal Skills

✗ Speaking only to family member · ✗ Starting with closed questions · ✗ Not acknowledging emotional state

2–5 min

History & ICE

“Can you give me an example of something that’s happened recently that worried you?”

“What’s your biggest worry about what’s going on?”

Collateral history with specific examples: not just ‘forgets things’ but ‘left gas on, forgot grandson’s birthday, gets lost driving familiar route’. Establish tempo (gradual vs. acute — delirium screen). Assess functional impact (ADLs). Medications (anticholinergics, benzos). Hidden agenda (fear of driving loss, care home, becoming like their mother).

TasksRelating to Others

✗ No collateral history · ✗ Not asking about functional impact · ✗ Skipping ICE concerns

5–7 min

Examination & Cognitive Testing

“I’d like to ask you a few questions — they’re standard ones we use to check how memory and thinking are working. Is that okay?”

Perform MoCA or AMT-10 — explain before starting, normalise (‘these are standard questions we ask everyone’). Observe gait, self-care, and affect. Check BP and HR. Note discrepancy between patient report and objective testing (anosognosia). Delirium screen: is confusion fluctuating or constant?

TasksGlobal Skills

✗ Testing without explanation or consent · ✗ Highlighting errors pejoratively · ✗ Skipping cognitive test entirely

7–10 min

Explain Diagnosis & Management

“From what you’ve told me and what the tests show, the memory difficulties are more than just normal ageing — the brain isn’t working quite as well as it used to...”

“I’m going to arrange some blood tests and a brain scan, and refer you to the memory clinic — they’re the specialists who will do a more detailed assessment.”

Use analogy (brain connections weakening). Address ICE concerns (driving, care home fears) directly. Mention DVLA notification. Arrange investigations and referral. Mention Alzheimer’s Society. Start advance care planning conversation (LPA).

TasksRelating to OthersGlobal Skills

✗ Diagnosing Alzheimer’s without specialist confirmation · ✗ Not mentioning DVLA · ✗ No support services offered

10–12 min

Safety-Net & Close

“If they become suddenly much more confused or seem physically unwell — especially with a temperature — please don’t wait, call us or 999 straight away.”

Three specific safety-nets: (1) delirium triggers, (2) medication side-effects (ChEI — nausea, vivid dreams; don’t stop suddenly), (3) DVLA follow-up. Closing question. Summary of plan. Acknowledge emotional impact one final time.

TasksRelating to OthersGlobal Skills

✗ No delirium safety-net · ✗ No DVLA follow-up · ✗ No closing question · ✗ No emotional acknowledgement at close

🔴🟠🟢 RAG Scoring — All 3 Domains

Tasks Domain

🟢

Collateral history with specific examples; ADLs formally assessed; reversible causes named and investigated; correct referral pathway; DVLA addressed with follow-up; safeguarding assessed; ChEI explained correctly; ACP initiated

🟠

Collateral history superficial; ADLs asked but not probed; reversible causes mentioned but incomplete; DVLA mentioned without follow-up; investigations organised but not explained; ACP not raised

🔴

No collateral history; ADLs not assessed; no reversible causes considered; DVLA omitted; no investigations arranged; wrong referral pathway; safeguarding missed; medication not discussed

Relating to Others

🟢

Both patient and family included; fears about care home and driving explicitly named and addressed; diagnosis explained with empathy, analogy, and hope; carer wellbeing enquired about; management negotiated not imposed; patient autonomy preserved

🟠

Some empathy shown but emotional impact underestimated; ICE asked formulaically; diagnosis mentioned but fears not addressed; carer not acknowledged as separate person with own needs; plan explained rather than negotiated

🔴

Patient excluded or patronised; speaks only to family member; no ICE; cognitive testing conducted without explanation; diagnosis delivered bluntly without empathy; carer burden not acknowledged; no support services mentioned

Global Skills

🟢

Organised structure throughout; plain language (no jargon); data gathering complete by 7 minutes; responsive to cues; manages three-way consultation; closing question asked; summary provided

🟠

Mostly organised but some jumping between topics; occasional jargon; data gathering nearly complete by 7 min; some cue-following; closing question absent or perfunctory

🔴

Disorganised; jargon-heavy; data gathering incomplete; cues missed; consultation one-sided (examiner-led); no closing question; no summary; time poorly managed

💬 Key Phrases — ICE, Diagnosis & Plan

Ideas — elicit explanatory model

“What do you think might be causing these changes — have you had any thoughts about what’s going on?”

Concerns — name the fear

“I can hear this is really worrying — what’s your biggest concern about what’s happening?”

Expectations — what would help

“What were you hoping we might be able to do today — what would feel most helpful?”

Validate — acknowledge the fear

“It sounds like your biggest worry is ending up like your mother — am I right about that? I want to be honest with you about what we’re dealing with.”

Explain — plain-language diagnosis

“The brain isn’t working quite as well as it used to — the connections between brain cells aren’t as strong, so things like remembering recent events or finding words become harder. It’s gradual, and there are things we can do to help.”

Close — summary and door opener

“You’re not alone in this — we’re here every step of the way. Is there anything else on your mind before we finish today?”

🚫 9 Danger Zones — Instant Deductions

✗

Speaking only to the family member→ Include patient in every question; address them directly first

✗

Assuming acute confusion is dementia→ Always screen for delirium (sudden onset? fluctuating? physical illness?)

✗

Not obtaining collateral history→ Patients with dementia systematically underreport — collateral history is essential

✗

Diagnosing Alzheimer’s without specialist confirmation→ Say ‘probable dementia — memory clinic will confirm the type and cause’

✗

Not mentioning DVLA notification→ Legal duty; document the conversation; specify follow-up if no DVLA contact in 4 weeks

✗

Prescribing antipsychotic without DLB check→ Always ask about visual hallucinations and parkinsonism before any antipsychotic

✗

Saying ‘this medication will improve your memory’→ ChEIs slow decline; they don’t improve or restore memory — set correct expectations

✗

No advance care planning mention→ LPA must be arranged while patient has capacity — raise it at first diagnosis visit

✗

No delirium safety-net given→ Sudden worsening = delirium until proven otherwise; give verbatim triggers and tell carer to call urgently

💊 Drug Quick-Pick by Scenario

Mild–moderate Alzheimer’s, first-line

→Donepezil 5mg nocte → 10mg after 4 wks

Take at night; titrate; monitor HR; set expectation (slows decline, does not reverse)

Lewy body dementia or Parkinson’s disease dementia

→Rivastigmine 1.5mg BD → 6mg BD (or patch)

Only ChEI licensed for DLB/PDD; reduces hallucinations; patch if swallowing difficult

Moderate–severe Alzheimer’s (add to ChEI or monotherapy)

→Memantine 5mg OD → 20mg OD over 4 wks

NMDA antagonist; reduce to 10mg OD if eGFR <30; reduces agitation as well as cognition

Depression in dementia or pseudodementia

→Sertraline 25mg OD → 50mg OD

Start low in elderly; check Na at 2 weeks (SIADH); reassess cognition after 2–3 months euthyroid

BPSD in Alzheimer’s (last resort, non-drug approaches failed)

→Risperidone 0.25mg → max 1mg OD or BD

⚠ MHRA: stroke risk ×1.9, mortality ×1.5; document consent; 3-monthly review; never in DLB

FTD behavioural symptoms (disinhibition, compulsive behaviours)

→Sertraline 50–200mg or Trazodone 50–300mg

Off-label but evidence-supported; ChEIs CONTRAINDICATED in FTD; specialist decision

⛔ ChEIs CONTRAINDICATED in FTD | Typical antipsychotics ABSOLUTELY CONTRAINDICATED in DLB | Memantine max 10mg if eGFR <30 | Check Na 2 weeks after SSRI start | Never say ChEI ‘improves’ memory — it slows decline

Dementia · GP Clinical Reasoning Framework v2 · NICE NG97 (2018, updated 2023) · NICE CKS Dementia (2024) · RCGP SCA Curriculum 2024 · BNF 2024 · GMC Confidentiality: patients and doctors (2023) · Mental Capacity Act 2005 · Care Act 2014 · Equality Act 2010

v2: Clinical stem · Open Q first · ICE in all modes · Psychosocial (1E causes + 7G consequences) · Lay language DDx (Step 5) · Safeguarding (Step 1) · Expectation management (7A) · SCA RAG checkpoints after every step · SCA Scorecard as standalone section · Dual tailored summaries (Clinic + SCA) with visual algorithms

Teaching clinicians why each step matters — not just what to do · Always consult current BNF/SPC · Clinical judgement takes precedence over any framework · Dementia is a human condition, not just a cognitive deficit — treat the whole person and their family

Dementia

Red Flags — act before continuing history

Safeguarding Considerations — Consider in Every Consultation

🏠 Self-Neglect

💰 Financial Abuse

🤕 Physical / Psychological Abuse by Carer

🏥 Institutional Neglect in Care Homes

😔 Depression and Anxiety

👥 Social Isolation and Loneliness

💪 Physical Activity and Mobility

🏠 Housing and Living Environment

👨‍👩‍👧 Carer Burden and Family Stress

💰 Financial Strain and Benefits

999 or Same-Day Hospital

Same-Day or Next-Day Assessment

Manage in Primary Care

Alzheimer's disease (AD)

Vascular dementia

Lewy body dementia (DLB)

Frontotemporal dementia (FTD)

Chronic subdural haematoma

Normal pressure hydrocephalus (NPH)

Vitamin B12 deficiency

Hypothyroidism (myxoedema madness)

Alcohol-related brain damage (ARBD) / Wernicke-Korsakoff

Validate — name their expectation

Explain — share your clinical reasoning

Negotiate — offer something today

Select dementia type and patient characteristics — recommended drug appears below

Driving — Legal Duty to Notify DVLA

Work & Employment

Lasting Power of Attorney (LPA)

Relationships & Intimacy

Living Arrangements & Future Care Planning

End-of-Life & Advance Care Planning

Baseline diagnosis visit (Memory Clinic) — Day 0

4–6 weeks — GP medication review

3–6 months — Memory Clinic follow-up

6–12 months — Annual GP review

Moderate–severe stage — Ongoing and end-of-life review

Memory rule

⚠ Three scenario-specific phrases — use these verbatim

Why safety-netting matters beyond clinical care

🎭 Patient actor brief — click to practise

Who you are

Hidden agenda

Symptoms if asked directly

Lifestyle + bonus details