GC241 A Short Course Of Dementia
A structured, condensed educational course designed to provide an overview of dementia, covering its types, pathophysiology, clinical features, diagnosis, and management principles for healthcare learners.
A Short Course of Dementia
This lecture (GC 241, Dr. Shea Yat Fung, QMH Consultant Geriatrician / HKU Honorary Associate Professor) is a compact but high-yield overview of dementia designed for General Clerkship students [1]. It covers:
- DSM-5 diagnostic criteria – the gatekeeping definitions of major vs. minor neurocognitive disorder.
- Common aetiologies – Alzheimer's disease (AD), vascular neurocognitive disorder (VaD), Lewy Body Dementia (DLB), with pattern-recognition tables.
- Approach to cognitive impairment – the clinical workup including history, cognitive testing, bloods, imaging.
- Structural imaging – CT/MRI signatures of AD and vascular cognitive impairment.
- Functional and pathological imaging – FDG-PET and amyloid PET patterns in AD, DLB, frontotemporal dementia (FTD).
- Fluid biomarkers – plasma P-tau 217 as a new AD biomarker.
- Management – cholinesterase inhibitors, NMDA antagonists, and new anti-amyloid therapies (lecanemab, donanemab).
- Things not covered – BPSD, advance directives, feeding issues (but you should know these from other GC lectures).
Why this matters for exams: Dementia is tested in virtually every Fourth Summative paper – as MCQs (pattern-matching vignettes), SAQs (workup and management), and minicases (differentiating delirium vs. dementia). The lecture gives you the precise framing that examiners use.
1. DSM-5 Diagnostic Criteria
High Yield: The DSM-5 criteria are the foundational framework. Examiners love testing the distinction between major and minor neurocognitive disorder. [1]
| Domain | Example of impairment |
|---|---|
| Learning & Memory | Forgetting recent events, repeating questions |
| Language | Word-finding difficulty, anomia, paraphasic errors |
| Attention (complex attention) | Cannot follow conversation, loses track, serial 7s failure |
| Executive function | Poor planning, judgment, abstraction, mental flexibility |
| Perceptual-motor | Getting lost in familiar places, difficulty using tools (apraxia) |
| Social cognition | Socially inappropriate behaviour, loss of empathy |
Why ≥1 domain? Because DSM-5 broadened the definition – you no longer need memory impairment specifically (unlike the old DSM-IV which mandated memory loss). This is important because conditions like FTD and DLB can present without early memory problems.
Same criterion (a) – cognitive decline – BUT no impairment in independence [1]. Patients are still managing their daily lives. Think of MCI as the "at-risk" state – roughly 10-15% of MCI patients progress to dementia per year.
Exam Discriminator: MCI vs Dementia
The single discriminator is functional status. If the patient's ADLs are preserved → MCI. If ADLs are impaired → dementia. The cognitive test score alone does not make the diagnosis – you must assess function.
| Severity | Functional impact |
|---|---|
| Mild | Instrumental ADL affected (finances, cooking, medication management, transport, telephone) |
| Moderate | Basic ADL affected (dressing, bathing, feeding, toileting) |
| Severe | Fully dependent |
This is tested – the 2020 MCQ Q23 asked about instrumental ADL (answer: preparing meals) [8].
2. Aetiology of Cognitive Impairment
| Condition | Approximate prevalence | Key pathology |
|---|---|---|
| Alzheimer's disease | 60-80% (most common overall) | Amyloid plaques (extraneuronal Aβ) + neurofibrillary tangles (intraneuronal tau) |
| Vascular dementia | 10-20% | Cerebral small vessel disease, strategic infarcts, multi-infarct |
| DLB | ~10% | Lewy bodies (α-synuclein) |
| FTD | ~5% (higher proportion in < 65 yr) | TDP-43, tau, FUS inclusions |
Age matters for prevalence distribution: [2]
- Age ≥65: AD dominates (2/3 of cases), FTD is rare
- Age < 65: AD only 1/3, FTD rises to ~12%
High Yield: Always screen for reversible causes. The mnemonic DEMENTIA is used. [2]
| Letter | Cause | Why it matters |
|---|---|---|
| D | Drugs | Sedatives, anticholinergics, anti-epileptics |
| E | Emotions | Depression = "pseudodementia" – the most important mimic [3, 8] |
| M | Metabolic | Hypothyroidism, liver/renal failure, B12/folate deficiency |
| E | Epilepsy | Complex partial seizures with altered consciousness |
| N | Normal pressure hydrocephalus | Triad: wet (incontinence), wacky (dementia), wobbly (gait apraxia) |
| T | Tumour & Trauma | Frontal tumours, chronic subdural haematoma |
| I | Infection | HIV, neurosyphilis |
| A | Autoimmune / Apnoea | Limbic encephalitis, OSA |
Why VDRL and B12 are in the standard workup
The lecture specifically lists TFT, vitamin B12, folate, ±VDRL as mandatory blood tests because hypothyroidism, B12/folate deficiency, and neurosyphilis are treatable causes of cognitive decline that masquerade as degenerative dementia [1].
3. Pattern Recognition: Subtyping Dementia
"MUST ALWAYS SUBTYPE THE DEMENTIA (by pattern recognition)" – this is a direct slide quote and an exam-favourite principle [1].
| Feature | Detail |
|---|---|
| Onset | Insidious, gradual |
| Progression | Slowly progressive over years |
| Predominant deficit | Short-term (episodic) memory – forgetting recent events, repeating questions |
| Other features | Parietal symptoms (apraxia, agnosia), executive dysfunction, later language, neuropsychiatric (apathy, aggression) |
| Pathology | Extraneuronal amyloid plaques (Aβ42) + intraneuronal neurofibrillary tangles (hyperphosphorylated tau) |
| Risk factors (non-modifiable) | Age, female sex, family history, genetics (ApoE4 allele) |
| Risk factors (modifiable) | Cardiovascular risk, physical inactivity, social isolation |
| Structural imaging | Bilateral medial temporal lobe / hippocampal atrophy (CT/MRI) [1] |
| Functional imaging (FDG-PET) | Bilateral temporoparietal hypometabolism [1] |
| Pathological imaging | Heavy amyloid loading on Pittsburgh Compound B (PiB) PET [1] |
Early-onset AD (< 65 years, < 5% of AD cases): May have atypical presentations – language variants, visuospatial, behavioural. Often has autosomal dominant mutations (PSEN1, PSEN2, APP) [1, 2].
The lecture shows a specific example: Phe386Ile PSEN1 novel mutation in a Chinese family with early-onset AD [1].
Hippocampal Atrophy Grading (MRI coronal): The lecture shows Duara grading – Grade 1 (mild widening of choroid fissure) → Grade 4 (severe volume loss of hippocampus with marked temporal horn dilation) [1].
What the coronal MRI series shows: Grades 1→4 medial temporal/hippocampal shrinkage with expanding CSF spaces — the AD structural signature you match to progressive episodic memory loss. [1]
| Feature | Detail |
|---|---|
| Onset | Can be acute (post-stroke) or insidious (small vessel disease) |
| Progression | Stepwise decline (each stroke event causes a step down) |
| Predominant deficit | Executive dysfunction (planning, sequencing, multitasking) |
| Risk factors | Hypertension, diabetes, AF, hyperlipidaemia, smoking – i.e. vascular risk factors |
| Imaging | White matter changes (leukoaraiosis), lacunar infarcts, strategic infarcts |
| Management | No specific dementia Rx; manage vascular risk factors to prevent further strokes |
Lecture case: Artery of Percheron infarction – An 85/F with DM, HT, AF presented with sudden stupor. MRI showed acute bilateral thalamic infarct. This is a classic "strategic infarct" causing vascular cognitive impairment [1]. The artery of Percheron is a rare anatomical variant where a single artery supplies both medial thalami – occlusion causes bilateral thalamic infarction with devastating cognitive consequences.
Subtypes of VaD [2]:
- Multi-infarct dementia
- Subcortical VaD / Binswanger disease (diffuse white matter ischaemia)
- Strategic infarct dementia (e.g., thalamic, angular gyrus)
| Feature | Detail |
|---|---|
| Pathology | Lewy bodies (α-synuclein inclusions) in cortex and brainstem |
| Core features (need ≥2 for probable DLB) | 1. Fluctuating cognition with variations in attention |
| 2. Recurrent well-formed visual hallucinations | |
| 3. Parkinsonism (occurring ≥1 year after cognitive onset) | |
| 4. REM sleep behaviour disorder (RBD) | |
| Supportive features | Recurrent falls/syncope, severe sensitivity to antipsychotic EPSE, delusions, depression |
| Functional imaging | Mild hypometabolism over bilateral occipital & posterior parietal lobes; NORMAL posterior cingulate cortex ("cingulate island sign") [1] |
| Amyloid PET | Amyloid NEGATIVE on PiB imaging [1] – this distinguishes DLB from AD |
| Treatment | AChEI (especially rivastigmine), cautious atypical antipsychotics, L-dopa for parkinsonism (but can worsen psychosis), melatonin/clonazepam for RBD |
Critical Exam Point: DLB vs AD on PET
DLB has OCCIPITAL hypometabolism with PRESERVED posterior cingulate; AD has TEMPOROPARIETAL hypometabolism. DLB is amyloid NEGATIVE; AD is amyloid POSITIVE. Students frequently confuse the PET patterns. Remember: Lewy bodies are NOT amyloid – they are α-synuclein [1].
Antipsychotic Sensitivity in DLB
Patients with DLB have pronounced sensitivity to antipsychotic extrapyramidal side effects. Giving haloperidol (a typical antipsychotic) to a DLB patient can cause severe rigidity, immobility, and even death. If an antipsychotic is absolutely needed, use low-dose quetiapine [2, 3].
| Feature | Detail |
|---|---|
| Onset | Often < 65 years (unlike AD) |
| Predominant deficit | Personality & behavioural changes, language (not memory initially) |
| Behavioural variant | Disinhibition, apathy, loss of empathy, socially inappropriate behaviour, compulsive behaviours |
| Language variants | Semantic dementia (loss of word meaning), progressive non-fluent aphasia |
| Functional imaging | Bilateral anterior temporal lobe hypometabolism (semantic dementia) [1]; frontal ± temporal hypometabolism (behavioural variant) |
| Amyloid PET | Amyloid NEGATIVE – no cortical amyloid retention [1] |
| Treatment | No specific disease-modifying therapy; symptomatic management of BPSD |
The lecture's QMH data showed FTD had only 14.3% accuracy on initial clinical diagnosis, dramatically improving to 85.7% after FDG-PET ± PiB imaging [1]. This shows how difficult FTD is to diagnose clinically and why functional imaging is so valuable.
| Feature | AD | VaD | DLB | FTD |
|---|---|---|---|---|
| Age of onset | Usually > 65 | Any age | Usually > 65 | Often < 65 |
| Onset | Insidious | Acute/stepwise or insidious | Insidious | Insidious |
| Progression | Gradual | Stepwise | Fluctuating | Gradual |
| Primary deficit | Memory | Executive function | Attention (fluctuating) | Personality/language |
| Hallucinations | Late | Uncommon | Early, well-formed VH | Uncommon |
| Motor features | Late | Focal neuro signs | Parkinsonism | Late |
| CT/MRI | Hippocampal atrophy | White matter changes, infarcts | Relatively preserved | Frontal/temporal atrophy |
| FDG-PET | Temporoparietal ↓ | Variable | Occipital + posterior parietal ↓ | Frontal ± anterior temporal ↓ |
| Amyloid PET | Positive | Usually negative | Usually negative | Negative |
4. Approach to Cognitive Impairment: The Workup
High Yield: The lecture's systematic approach slide is likely the basis for SAQ questions. [1]
- Obtain history from main caregivers [1] – patients with dementia often lack insight into their deficits. A caregiver history is essential to document timeline, functional decline, and behavioural changes.
- Ask about:
- Onset and progression (weeks → infection/inflammation; months → NPH; years → neurodegeneration) [2]
- Predominant cognitive deficit (memory → AD; executive → VaD; behaviour/language → FTD; fluctuating cognition + VH → DLB)
- Functional status (basic ADL vs instrumental ADL)
- Family history – especially for early-onset AD (autosomal dominant mutations: PSEN1, PSEN2, APP) [1]
- BPSD: wandering, aggression, sleep disturbance, psychosis
- Vascular risk factors: DM, HT, AF, hyperlipidaemia, smoking
- Drug history: anticholinergics, sedatives, polypharmacy
- Mood: screen for depression (pseudodementia)
Use the HK version of Montreal Cognitive Assessment (HK-MoCA) [1]
The MoCA is preferred over MMSE because it is more sensitive for MCI and tests executive function and attention more rigorously. It includes:
- Visuospatial/executive (trail-making, cube copy, clock drawing)
- Naming
- Attention (digit span, serial 7s, vigilance)
- Language (sentence repetition, verbal fluency)
- Abstraction
- Delayed recall (5 words)
- Orientation
Score ≤ 25/30 suggests cognitive impairment (but education-adjusted norms apply).
Other screening tools mentioned in related GC lectures:
- Abbreviated Mental Test (AMT): 10 items, quick bedside screen
- MMSE: still widely used but less sensitive for MCI and has copyright issues
| Test | Purpose |
|---|---|
| Thyroid function test | Rule out hypothyroidism (treatable cause) |
| Vitamin B12 level | B12 deficiency → subacute combined degeneration, cognitive decline |
| Folate level | Folate deficiency → cognitive impairment |
| ±VDRL | Screen for neurosyphilis (treatable cause) |
Standard:
- Plain CT brain [1] – primarily to rule out structural causes (tumour, chronic SDH, NPH) and identify AD signature (hippocampal atrophy) or vascular changes.
Potentially useful / Advanced:
| Modality | When to use | What it shows |
|---|---|---|
| MRI brain | Better anatomical detail | Hippocampal atrophy grading, white matter disease, strategic infarcts |
| EEG | Especially for CJD (periodic sharp wave complexes) | Also useful for non-convulsive status epilepticus |
| CSF examination | Rule out CNS infection; AD biomarkers (↓Aβ42, ↑tau, ↑p-tau) | Also for CJD (14-3-3 protein, RT-QuIC) |
| Functional imaging (FDG-PET, SPECT) | Aid subtyping when clinical diagnosis uncertain | Pattern of hypometabolism/hypoperfusion |
| Pathological imaging (amyloid PET) | Confirm/exclude amyloid pathology | PiB uptake pattern |
| Plasma P-tau 217 | Newest biomarker for AD | See below |
The lecture's data shows clinical diagnosis alone is only 63.7% accurate across dementia subtypes [1]
| Final diagnosis | Initial clinical accuracy | Improvement after PET |
|---|---|---|
| AD | 81.5% | 18.5% |
| DLB | 44.4% | 55.6% |
| FTD | 14.3% | 85.7% |
| VaD | 28.6% | 71.4% |
| Mixed | 0% | 100% |
| Overall | 63.7% | 36.3% |
Key takeaway: AD is the easiest to diagnose clinically. FTD and mixed dementia are the hardest. PET imaging dramatically improves diagnostic accuracy for non-AD dementias.
The lecture lists 7 indications from the 2025 Alzheimer's Association update:
- MCI/dementia < 65 years with suspected AD pathology
- MCI/dementia ≥65 with amnestic presentation consistent with AD
- MCI/dementia with atypical features (non-amnestic, rapid/slow progression, mixed aetiology)
- Equivocal CSF biomarkers
- To inform prognosis of MCI due to suspected AD
- To determine eligibility for anti-amyloid therapy
- To monitor response to anti-amyloid therapy
High Yield: This is flagged as a "new advance" in the lecture [1]
- Plasma P-tau 217 reflects amyloid pathology [1]
- Measured by immunoprecipitation mass spectrometry (IP-MS), Meso Scale Discovery (MSD), or Single Molecule Array (SIMOA) platforms
- Elevated by 250-600% in AD patients compared with non-AD patients [1]
- This is a game-changer because it is a blood test – far less invasive than CSF or PET
- Potential future role: population-level screening, monitoring treatment response, and selecting patients for anti-amyloid therapy
Why P-tau 217 specifically?
P-tau 217 (phosphorylated at threonine-217) outperforms P-tau 181 because it rises earlier in the disease course and correlates more strongly with brain amyloid burden. It reflects AD-specific pathology rather than general neurodegeneration.
6. Management of Alzheimer's Disease
For mild to moderate AD [1]
Mechanism: In AD, there is degeneration of cholinergic neurons in the nucleus basalis of Meynert, leading to acetylcholine deficit. AChEIs inhibit acetylcholinesterase, increasing synaptic ACh levels and temporarily improving or stabilizing cognition.
They do NOT modify the disease course – they are symptomatic treatments [2].
| Drug | Starting dose | Titration | Notes |
|---|---|---|---|
| Donepezil | 5 mg daily | ↑ to 10 mg daily after 4-6 weeks | Most commonly used; once daily |
| Galantamine (IR) | 4 mg BD | → 8 mg BD after 4 wk → 12 mg BD after 4 wk | Max 16 mg daily for moderate renal impairment |
| Galantamine (ER) | 8 mg daily | → 16 mg daily after 4 wk → 24 mg daily after 4 wk | Extended-release formulation |
| Rivastigmine (oral) | 1.5 mg BD | → 3 mg BD → 4.5 mg BD (each step 4 wk apart) | Also has transdermal patch |
| Rivastigmine (patch) | 4.6 mg/24hr | → 9.5 mg/24hr after 4 wk | Patch has ↓ GI side effects, ↑ compliance |
Major side effects: anorexia, nausea, vomiting, diarrhoea, bradycardia [1]
AChEI Side Effects – First Principles
All the GI side effects (nausea, vomiting, diarrhoea) are due to increased cholinergic activity in the gut (parasympathetic stimulation → ↑ peristalsis, ↑ secretions). Bradycardia is from vagal stimulation of the heart. Be cautious in patients with COPD/asthma (bronchoconstriction), PUD (↑ acid secretion), and sick sinus syndrome/heart block (bradycardia).
For moderate to severe AD [1]
| Drug | Starting dose | Titration | Notes |
|---|---|---|---|
| Memantine | 5 mg daily | → 5 mg BD (wk 2) → 5 mg OM + 10 mg PM (wk 3) → 10 mg BD (wk 4) | Max 10 mg daily if CrCl < 30 mL/min |
Mechanism: In AD, there is excessive glutamate signalling leading to NMDA receptor overactivation → excitotoxicity → neuronal death. Memantine is a non-competitive, moderate-affinity NMDA receptor antagonist that blocks pathological tonic activation while still allowing physiological phasic activation needed for learning and memory.
Major side effects: headache, dizziness, sedation, agitation, constipation [1]
High Yield as "new advance" from the lecture [1]
| Feature | Detail |
|---|---|
| Indications | MCI or early dementia due to AD (NOT moderate-severe AD) |
| Mechanism | Monoclonal antibodies targeting amyloid-β |
| Efficacy | Slow down cognitive decline by ~30% |
| Examples | Lecanemab, Donanemab |
| Route | Regular IV infusion in hospital |
| Cost | Expensive and self-paid |
| Major risk | ARIA (Amyloid-Related Imaging Abnormalities) – cerebral oedema (ARIA-E) and microhaemorrhages (ARIA-H). Higher risk in ApoE4 homozygotes |
Anti-Amyloid Therapy: Key Exam Points
These are the first disease-modifying therapies for AD. They work by clearing amyloid plaques from the brain. However, they are only for EARLY disease, require IV infusion, are very expensive, and carry the risk of ARIA (brain swelling/bleeding that requires MRI monitoring). They do NOT cure AD – they only slow the decline by about 30%.
| Severity | First-line pharmacotherapy | Notes |
|---|---|---|
| MCI due to AD | Consider anti-amyloid therapy (if eligible and affordable) | No AChEI for MCI (insufficient evidence) |
| Mild-moderate AD | AChEI (donepezil, rivastigmine, galantamine) | Can combine with memantine for moderate AD |
| Moderate-severe AD | Memantine ± AChEI | |
| Vascular dementia | No specific Rx | Manage vascular risk factors |
| DLB | AChEI (esp. rivastigmine) | Avoid antipsychotics if possible |
| FTD | No specific Rx | Symptomatic BPSD management |
This is a perennial exam topic. The comparison table from GC 037 is highly tested [4]:
| Feature | Delirium | Dementia | Depression |
|---|---|---|---|
| Onset | Acute | Insidious | Insidious |
| Course | Fluctuating | Progressive | Diurnal variations |
| Duration | Days-weeks | Months-years | Variable |
| Consciousness | Altered | Clear | Generally unimpaired |
| Attention | Impaired (hallmark) | Normal unless severe | Unaffected |
| Psychomotor | ↑ or ↓ | Often normal | Psychomotor slowing |
| Reversibility | Usually | Rarely | Control with medications |
The hallmark of delirium that distinguishes it from dementia is ACUTE ONSET AND FLUCTUATING COURSE [5, 6]
Pseudodementia
Depression can mimic dementia ("pseudodementia") – the 2020 MCQ Q24 tested this directly [8]. Key discriminators: depression has more defined onset, patient complains MORE about memory (unlike dementia patients who lack insight), gives "don't know" answers rather than wrong answers, and has classical depressive features (morning dysphoria, anhedonia, sleep/appetite changes).
The final slide lists topics NOT covered today [1]:
- Behavioural and psychological symptoms of dementia (BPSD) – pharmacological and non-pharmacological
- Advanced directives and advanced care planning
- Feeding issues
These are covered in other GC lectures (GC 045 End-of-life care, GC 038 CGA and rehabilitation) and are testable from those sources.
While not extensively covered in the primary lecture, the lecture mentions EEG is especially useful for CJD [1], and CJD appears as a distractor in the 2018 MCQ EMQ [7]. Key facts:
- Rapidly progressive dementia (weeks to months)
- Prion disease (misfolded PrPSc)
- Features: myoclonus, cerebellar ataxia, pyramidal/extrapyramidal signs, akinetic mutism
- EEG: periodic sharp wave complexes
- CSF: 14-3-3 protein, RT-QuIC assay
- MRI: cortical ribboning, caudate/putamen DWI hyperintensity
- Fatal, no treatment
Exam Intelligence
- Pattern-matching EMQ/MCQ: Given a vignette, identify the dementia subtype (AD vs VaD vs DLB vs FTD vs CJD). Focus on the discriminating features in section 3.
- Workup SAQ: "List the investigations for a patient presenting with cognitive impairment." Follow the lecture's sequence: bloods (TFT, B12, folate, ±VDRL) → CT brain → advanced if needed.
- Treatment SAQ/MCQ: Know drug names, indications by severity, and side effects.
- Delirium vs Dementia distinction: The single most tested concept – acute onset + fluctuating course = delirium.
| Trap | Why students fall for it | Correct answer |
|---|---|---|
| Choosing AD for a patient with early behavioural/personality changes | AD is the commonest, but personality change = FTD | FTD |
| Saying MCI when ADL is impaired | MCI by definition has preserved independence | Dementia (major NCD) |
| Thinking all dementias are amyloid-positive on PET | Only AD is typically amyloid-positive | DLB and FTD are amyloid-negative |
| Prescribing haloperidol for agitation in DLB | DLB has severe antipsychotic sensitivity | Use quetiapine cautiously; prefer non-pharmacological first |
| Using AChEI for severe AD monotherapy | AChEI is for mild-moderate; memantine for moderate-severe | Memantine |
| Confusing temporoparietal hypometabolism with occipital | AD = temporoparietal; DLB = occipital | Check the lobe |
- "Gradual memory loss over years" + hippocampal atrophy → AD
- "Stepwise decline" + vascular risk factors + white matter changes → VaD
- "Swearing, disinhibited, personality change" + frontal atrophy → FTD (behavioural variant) [7]
- "Fluctuating alertness + vivid visual hallucinations + parkinsonism" → DLB
- "Sudden stupor + bilateral thalamic infarct" → Strategic infarct VaD (artery of Percheron) [1]
- "Rapid progression over weeks-months + myoclonus" → CJD
Geriatrics AOS Practice Question [5]
Question
"78-year-old female with Alzheimer's disease admitted for UTI. Nursing staff reports increased agitation, disorientation, confusion. Symptoms worse in evening, consciousness fluctuates. Delayed recall 0/5. Which feature is consistent with delirium rather than exacerbation of dementia?"
- A. Score 0/5 on delayed recall
- B. Disorientation to time and place
- C. Increased agitation during evening
- D. Acute onset and fluctuating course of symptoms → CORRECT
Rationale: Poor delayed recall is a hallmark of AD (not delirium-specific). Disorientation occurs in both. Sundowning occurs in dementia. Only acute onset and fluctuating course distinguishes delirium from dementia.
- GC 037 (Common neurological problems in older people): Provides the delirium-dementia-depression comparison table used above [4].
- GC 038 (CGA and rehabilitation): Covers functional assessment (ADL scales) and multidisciplinary team approach.
- GC 079 (Prescribing in older people): AChEI side effects and dose adjustments feature here; also anticholinergic burden concept.
- GC 045 (End-of-life care): Covers advanced care planning and feeding issues in advanced dementia.
- GC 169 (Geriatric psychiatry/Dementia): Overlapping content on BPSD management and non-pharmacological approaches.
- GC 091 (Movement disorders/Parkinsonism): Parkinsonism in DLB vs PD with dementia (the "1-year rule" – if dementia precedes parkinsonism by ≥1 year, it's DLB; if parkinsonism precedes by ≥1 year, it's PD with dementia).
High Yield Summary
-
DSM-5
- Major NCD = cognitive decline + functional impairment (not during delirium). Minor NCD (MCI) = cognitive decline WITHOUT functional impairment.
-
Always subtype
- AD (memory, hippocampal atrophy, amyloid+), VaD (executive, stepwise, vascular lesions), DLB (fluctuating cognition, VH, parkinsonism, RBD, amyloid−, occipital hypometabolism), FTD (personality/language, amyloid−, frontal/temporal atrophy).
-
Workup
- Caregiver history → HK-MoCA → TFT, B12, folate, ±VDRL → plain CT brain → advanced imaging/biomarkers if unclear.
-
Treatment
- AChEIs (donepezil, rivastigmine, galantamine) for mild-moderate AD; memantine for moderate-severe AD. Side effects: GI (nausea, vomiting, diarrhoea) + bradycardia. Anti-amyloid (lecanemab, donanemab) for early AD – slow decline by ~30%, IV, expensive, risk of ARIA.
-
Plasma P-tau 217
- Blood biomarker elevated 250-600% in AD vs non-AD.
-
Key discriminator
- Delirium = acute onset + fluctuating course + impaired attention/consciousness. Dementia = insidious + progressive + preserved consciousness. Depression = pseudodementia (treatable mimic).
-
DLB caution
- Severe antipsychotic sensitivity – avoid typical antipsychotics.
Active Recall - Lecture Notes
[1] Lecture slides: GC 241. A short course of dementia.pdf [2] Senior notes: Maksim Medicine Notes.pdf (Geriatrics section, pp. 112-115) [3] Senior notes: Ryan Ho Psychiatry.pdf (pp. 77-88) [4] Lecture slides: GC 037. Common neurological problems in older people.pdf (p. 29) [5] AOS material: Geriatrics AOS.pdf (pp. 3-4); AOS - Geriatrics.pdf (pp. 1, 4) [6] Senior notes: Ryan Ho Fundamentals.pdf (pp. 325-326) [7] Past papers: 2018 Fourth Summative MCQ.pdf (Geriatrics EMQ, Q24-25) [8] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q23, Q24)
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