Dementia
Exam Tips
- For diagnosis, remember: decline in at least two cognitive domains plus functional impairment, not explained by delirium or major psychiatric illness.
- Lewy body clue triad: fluctuating cognition, recurrent well-formed visual hallucinations, and spontaneous parkinsonism; marked antipsychotic sensitivity is high yield.
- Differentiate dementia from delirium in OSCEs by time course and attention: delirium is acute/fluctuating with impaired attention and altered arousal.
- In viva questions, always mention reversible-screen bloods and structural brain imaging before final subtype labelling.
- State first-line non-pharmacological management for BPSD, then cautious, time-limited antipsychotic use only for severe risk/distress.
- Drug safety marks: check pulse/ECG considerations before cholinesterase inhibitors and monitor for bradycardia, syncope, GI side effects, and weight loss.
Definition
Dementia is a chronic, progressive clinical syndrome causing decline in at least two cognitive domains (for example memory, language, visuospatial or executive function) severe enough to impair everyday independence. The decline is beyond expected ageing and must not be better explained by delirium or another major psychiatric disorder. In UK practice, diagnosis is clinical and subtype-based (for example Alzheimer’s disease, vascular dementia, Lewy body dementia, frontotemporal dementia) because prognosis and treatment differ.
Pathophysiology
Most dementia is neurodegenerative or vascular. Alzheimer’s disease is driven by amyloid-beta accumulation, tau-related neurofibrillary pathology, synaptic loss, cortical/hippocampal atrophy, and a marked cholinergic deficit with neuroinflammation; mixed Alzheimer’s plus vascular pathology is common. Vascular dementia results from cumulative cerebrovascular injury (large infarcts, lacunes, small-vessel ischaemic change, cerebral amyloid angiopathy) causing disconnection of frontal-subcortical and cortical networks. Dementia with Lewy bodies and Parkinson’s disease dementia are alpha-synucleinopathies with cortical/subcortical Lewy bodies, producing fluctuating cognition, hallucinations, and parkinsonism. Frontotemporal dementia involves frontal/temporal lobar degeneration (often tau or TDP-43 related), typically causing early behavioural or language-predominant syndromes. See Figure: coronal MRI hippocampal atrophy pattern in Alzheimer’s disease; See Figure: diffuse white-matter ischaemic change/lacunes in vascular cognitive impairment.
Risk Factors
- Increasing age (strongest risk factor)
- Mild cognitive impairment
- Family history/genetic risk (APP, PSEN1, PSEN2 in some young-onset cases; ApoE4 susceptibility for late-onset Alzheimer’s disease)
- Down’s syndrome and learning disability
- Cardiovascular risk burden (hypertension, diabetes, obesity, smoking, physical inactivity)
- Previous stroke/cerebrovascular disease
- Parkinson’s disease
- Depression
- Hearing impairment
- Low educational attainment and low cognitive/social engagement
Clinical Features
Symptoms
- Progressive memory impairment (especially new learning/short-term memory in Alzheimer’s disease)
- Word-finding difficulty, language breakdown, or reduced fluency
- Executive dysfunction (planning, organisation, finances, medication errors)
- Visuospatial problems (getting lost, misjudging distances)
- Personality or behavioural change, apathy, irritability, disinhibition
- Fluctuating attention/cognition and recurrent visual hallucinations (suggest Lewy body disease)
- Sleep disturbance (including possible REM sleep behaviour disorder in Lewy body disease)
- Functional decline in ADLs/IADLs (shopping, cooking, hygiene, toileting)
Signs
- Objective cognitive impairment on bedside or formal testing
- Impaired orientation, delayed recall, language, praxis, or executive tasks
- Neurological focal signs or gait disturbance (supports vascular contribution/other structural causes)
- Parkinsonism (bradykinesia, rigidity, reduced arm swing) in Lewy body spectrum disorders
- Frontal release signs or marked behavioural syndrome in frontotemporal dementia
- Weight loss, frailty, poor mobility, falls risk in later disease
- Evidence from collateral history of progressive functional loss and behavioural/psychological symptoms
Investigations
Management
Lifestyle Modifications
- Explain diagnosis early and provide carer-inclusive education, safety-netting, and written care plan
- Optimise vascular risk factors (BP, diabetes, lipids, smoking cessation, physical activity)
- Promote cognitive and social stimulation; support hearing/vision correction (for example hearing aids)
- Occupational therapy/home risk assessment for falls, wandering, cooking/medication safety
- Advance care planning, Lasting Power of Attorney discussions, and driving advice with DVLA notification where required
- Manage sleep, nutrition, hydration, continence, pain, and constipation to reduce behavioural escalation
Pharmacological Treatment
Acetylcholinesterase inhibitors
- Donepezil 5 mg at night for 1 month, then 10 mg at night if tolerated (usual max 10 mg daily)
- Rivastigmine oral 1.5 mg twice daily, increase every at least 2 weeks to 3 mg, 4.5 mg, then 6 mg twice daily (max 6 mg twice daily); patch 4.6 mg/24 h then 9.5 mg/24 h, may increase to 13.3 mg/24 h
- Galantamine 4 mg twice daily for 4 weeks then 8 mg twice daily; may increase to 12 mg twice daily (or MR 8 mg daily then 16 mg then 24 mg daily)
Used for mild-to-moderate Alzheimer’s disease; donepezil/rivastigmine also used in Lewy body/Parkinson’s disease dementia under specialist care. Safety: can cause bradycardia, syncope, heart block, GI upset, weight loss; caution in sick sinus syndrome, conduction disease, active peptic ulcer, and asthma/COPD; review pulse, weight, tolerability, and interactions (for example other rate-limiting drugs).
NMDA receptor antagonist
- Memantine 5 mg once daily, increase by 5 mg each week to 20 mg once daily (target)
Use in moderate Alzheimer’s disease when cholinesterase inhibitors are not tolerated/contraindicated, or in severe Alzheimer’s disease. Common adverse effects include dizziness, headache, constipation; reduce dose in renal impairment and monitor for confusion/agitation changes.
Behavioural and psychological symptoms of dementia (BPSD), only when severe risk persists after non-drug measures
- Risperidone 0.25-0.5 mg twice daily, titrate cautiously (often up to 1 mg twice daily), shortest duration possible (commonly up to 6 weeks)
Reserve for severe distress or immediate risk of harm after personalised non-pharmacological strategies fail. Major warnings: increased stroke and mortality risk in dementia, sedation, falls, extrapyramidal effects, QT prolongation; avoid routine long-term antipsychotic use and review frequently.
Complications
- Loss of independence in ADLs/IADLs and increasing care dependency
- Behavioural and psychological symptoms (agitation, psychosis, aggression, sleep disturbance, wandering)
- Falls, fractures, reduced mobility, and deconditioning
- Malnutrition, dehydration, dysphagia, aspiration pneumonia
- Delirium episodes with accelerated cognitive decline
- Incontinence, pressure injury, and recurrent hospital admissions
- Carer strain, burnout, safeguarding concerns, and earlier institutionalisation
- Higher mortality than age-matched people without dementia
Prognosis
Dementia is progressive and life-limiting, with variable trajectory by subtype, age, frailty, and comorbidity. A practical pattern is mild (about years 1-2), moderate (about years 2-5), then severe dependency thereafter, though progression rate differs widely. Median survival is often around 7-10 years when diagnosed in the late 60s/early 70s but may be closer to 3 years in people diagnosed in their 90s; delirium episodes are associated with faster decline.
Sources & References
🏥BMJ Best Practice(1)
đź’ŠBNF Drug References(2)
- Apomorphine hydrochloride[contraindications]
- Hydroxyzine hydrochloride[cautions]
âś…NICE Guidelines(1)
- Dementia[overview]
đź“–Textbook References(7)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1790)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 925, 926)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 997, 998)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 998)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 995)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1760)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1760, 1761)[context]