Old age psychiatry accounts for approximately 10% of Paper B marks (roughly 15 of 150 questions). The content covers dementia subtypes and their management, delirium, depression in older adults, late-life psychosis, and service organisation for older people’s mental health. The number of effective treatments is small, so the exam tests distinctions between dementia subtypes, appropriate pharmacological management, risk assessment, and the interface between mental health and social care.
Dementia: Classification and Diagnosis
Dementia is a clinical syndrome characterised by progressive cognitive decline that interferes with daily function, in a clear sensorium (unlike delirium), with onset in later life. The most common early-onset dementia is Alzheimer’s disease, despite the common belief that frontotemporal dementia is more frequent in younger patients.
Alzheimer’s Disease (~60% of dementias)
Core features: Insidious onset, gradual progression over years. Early and prominent impairment of episodic memory (hippocampal dysfunction) — the patient forgets recent events while remote memories are relatively preserved early on. As the disease progresses, language impairment (anomia, then aphasia), visuospatial deficits, and executive dysfunction emerge. Behavioural and psychological symptoms occur in 80-90% over the course of the illness: apathy (most common), agitation, aggression, depression, psychosis, sleep disturbance.
Pathology: Extracellular amyloid-beta plaques, intracellular neurofibrillary tangles (hyperphosphorylated tau protein), and neuronal loss. The earliest changes occur in the entorhinal cortex and hippocampus (Braak stages), then spread to temporal, parietal, and frontal cortex. ApoE4 is the strongest genetic risk factor (not causal). Early-onset familial Alzheimer’s (<65 years) is associated with mutations in amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2) genes.
Investigations: CT/MRI shows hippocampal atrophy, particularly on coronal sections. CSF shows reduced amyloid-beta 42 and increased total tau and phospho-tau. FDG-PET shows temporoparietal hypometabolism.
Vascular Dementia (~15% of dementias)
Core features: Stepwise deterioration corresponding to cerebrovascular events. Cognitive deficits are variable depending on the location of the infarcts. Executive dysfunction (slow processing, poor concentration, impaired planning) is often more prominent than memory loss, in contrast to Alzheimer’s. Focal neurological signs are common. Risk factors are those for cerebrovascular disease: hypertension, diabetes, smoking, atrial fibrillation, hypercholesterolaemia.
Subtypes: Multi-infarct dementia (multiple cortical infarcts), strategic infarct dementia (single infarct in a critical area like thalamus), small vessel disease (Binswanger’s disease: widespread subcortical white matter changes, more gradual progression). A recall question described a patient with memory loss, hypertension, and MRI showing infarcts — answer: Binswanger’s disease.
Imaging: CT/MRI shows evidence of infarcts, white matter hyperintensities (leukoaraiosis). The key distinction from Alzheimer’s is relative preservation of hippocampal volume.
Dementia with Lewy Bodies (DLB, ~10% of dementias)
Core features: The clinical triad is fluctuating cognition (marked variation in attention and alertness over hours to days), recurrent well-formed visual hallucinations (detailed, vivid images of people or animals), and parkinsonism (rigidity, bradykinesia, postural instability — less prominent tremor than Parkinson’s disease). REM sleep behaviour disorder (acting out dreams) is a supportive feature. Dysautonomia is common.
Diagnostic significance: DLB is the dementia most likely to present with psychiatric symptoms first (hallucinations, depression, behavioural disturbance). This is important when the exam presents a patient with visual hallucinations and cognitive fluctuations — the answer is DLB, not primary psychotic disorder.
Management: First-line for psychosis in DLB is rivastigmine (a cholinesterase inhibitor that may improve cognition and hallucinations). Antipsychotics are used with extreme caution and only when necessary, as patients with DLB are exquisitely sensitive to D2 blockade — up to 50% will develop severe neuroleptic sensitivity (parkinsonism, sedation, confusion, autonomic instability, can be fatal). If an antipsychotic is necessary, risperidone or olanzapine (low starting dose) is used, but quetiapine is often preferred for its lower D2 occupancy. This is a recurring question.
Frontotemporal Dementia (FTD, ~5% of dementias)
Core features: Earlier onset than Alzheimer’s (typically 45-65 years). Two main presentations: behavioural variant (bvFTD — personality change, executive dysfunction, loss of empathy, disinhibition, apathy, stereotyped behaviours) and primary progressive aphasia (language variant — progressive loss of language function, classified as non-fluent/agrammatic, semantic, or logopenic). A recall question described Pick’s disease (FTD with Pick bodies on histology) as presenting with no insight, cognitive decline, and primary motor dysphasia (non-fluent aphasia). Insight is notably impaired early in bvFTD.
Pathology: Tau protein inclusions (Pick bodies) or TDP-43 inclusions. Atrophy is most prominent in the frontal and anterior temporal lobes (on CT/MRI), with the characteristic “knife-edge” gyral atrophy. SPECT shows frontal and anterior temporal hypoperfusion, which helps distinguish FTD from Alzheimer’s (which shows temporoparietal changes).
Management: No pharmacological treatments are approved for FTD. Cholinesterase inhibitors (donepezil, rivastigmine, galantamine) are NOT effective in FTD and may worsen behavioural symptoms. Management is non-pharmacological: behavioural interventions, environmental modification, carer support. SSRIs may help with disinhibition and repetitive behaviours.
Pharmacological Management of Dementia
Cholinesterase inhibitors (donepezil, rivastigmine, galantamine): Licensed for mild to moderate Alzheimer’s disease. NICE recommends them as options for managing Alzheimer’s (reviewed at 3-6 month intervals). Donepezil (once daily) is most commonly used. Rivastigmine is the only one licensed for DLB and Parkinson’s disease dementia. Galantamine is also a nicotinic receptor modulator. Side effects: nausea, vomiting, diarrhoea, bradycardia, and muscle cramps donepezil can cause bradycardia and hypotension (recall question: patient on donepezil 10mg, hypotensive, ankle oedema — ECG shows sinus bradycardia).
Memantine: NMDA receptor antagonist. Licensed for moderate to severe Alzheimer’s disease (NICE recommends it as an option for managing Alzheimer’s in people with moderate or severe disease). Can be used alone or in combination with a cholinesterase inhibitor. Side effects: constipation, headache, dizziness, hypertension.
BPSD management (Behavioural and Psychological Symptoms of Dementia): First-line is non-pharmacological (ABC approach: Antecedent, Behaviour, Consequence — identifying triggers and modifying the environment, carer training, structured activities). Medication is reserved for severe distress or risk to self/others. The first-line antipsychotic is risperidone (licensed for up to 6 weeks for persistent aggression in Alzheimer’s). Haloperidol is used for severe agitation or psychosis but carries higher EPS risk. Antipsychotics increase stroke risk (all antipsychotics, approximately 2-fold) and mortality in dementia, and should be used at the lowest effective dose for the shortest possible time.
Delirium
Delirium is an acute, fluctuating disturbance in attention and awareness caused by an underlying medical condition. It is the most common acute neuropsychiatric syndrome in hospitalised older adults and is associated with increased length of stay, institutionalisation, and mortality. The detection and management of delirium is a mandatory competency and appears regularly in Paper B.
Clinical features (ICD-11 criteria): Disturbance in attention (reduced ability to direct, focus, sustain, and shift attention) and awareness (disorientation, reduced orientation to environment), developing over hours to days, fluctuating during the day. Additional features: cognitive disturbance (memory, language, orientation), perceptual disturbances (illusions, hallucinations — often visual or tactile), delusions (often persecutory, poorly formed), psychomotor disturbance (hyperactive: agitation, restlessness; hypoactive: lethargy, reduced movement; mixed), emotional disturbance (anxiety, fear, irritability, apathy).
Hyperactive vs hypoactive delirium: Hyperactive delirium is more likely to be recognised (agitation, wandering, shouting, hallucinations). Hypoactive delirium (withdrawn, quiet, lethargic, reduced speech) is more common but frequently missed. Both types are equally serious in prognosis. Between the two, hypoactive delirium has higher mortality but is less easily detected. A standard question asks about the hypoactive subtype being missed in clinical practice.
Causes (PINCH ME mnemonic): Pain, Infection (UTI, chest), Nutrition (dehydration, electrolyte imbalance), Constipation, Hypoxia, Medication (anticholinergics, sedatives, opioids, steroids), Environment (sensory impairment, sleep deprivation). Polypharmacy and anticholinergic burden are the most common reversible contributing factors.
Assessment: Confusion Assessment Method (CAM) is the validated screening tool: acute onset and fluctuating course, inattention, and either disorganised thinking or altered level of consciousness. Additional investigations: FBC, U&Es, glucose, calcium, LFTs, TFTs, B12/folate, infection screen (blood cultures, urine, chest X-ray), ECG, CT head if indicated.
Management: Identify and treat the underlying cause. Environmental measures: frequent orientation cues, familiar objects, clear communication, family presence, adequate lighting, sleep hygiene. Medication if the patient is distressed or at risk (do not medicate purely for staffing convenience). First-line for severe agitation: haloperidol 0.5-2mg (lower dose than in younger patients) OR lorazepam (particularly when cause is alcohol withdrawal or if antipsychotics are contraindicated). Second-line: olanzapine or risperidone.
Depression in Older Adults
Depression in older adults presents differently than in younger adults. Somatic symptoms (pain, fatigue, gastrointestinal disturbance) are more prominent. Psychomotor change (retardation or agitation) is more common. Cognitive impairment resembling dementia (depressive pseudodementia) can occur and may be difficult to distinguish from early dementia. The key distinction: in pseudodementia, cognitive deficits improve with treatment of depression. Neuropsychological testing may show inconsistent performance (variable across assessments, unlike Alzheimer’s where deficits are consistent).
Suicide risk in older adults: Older adults (particularly older men) have the highest suicide rates of any demographic group. Risk factors: male sex, widowed/divorced, living alone, physical illness, functional decline, recent bereavement, access to means. Suicide attempts in older adults are more lethal (higher completion rate). This is a high-yield concern in old age psychiatry questions.
Treatment: SSRIs (sertraline first-line) are the pharmacological first choice at half the usual starting dose. Agomelatine is an alternative with favourable side-effect profile and no significant drug interactions. ECT is particularly effective and safe in older adults and is underutilised in this population. It should be considered early in severe depression with psychotic features, catatonia, or food/fluid refusal.
Service Organisation for Older Adults
Old age psychiatry services in the UK are community-oriented, with most patients managed at home or in care homes. The multidisciplinary team includes psychiatrists, community psychiatric nurses, occupational therapists, psychologists, social workers, and liaison with primary care. Memory clinics provide specialist assessment and diagnosis of dementia. Care home liaison services provide regular input to care homes to manage BPSD and reduce inappropriate antipsychotic prescribing.
High-Yield Recall Patterns
- Most common early-onset dementia: Alzheimer’s disease (NOT FTD)
- Alzheimer’s CT finding: Hippocampal atrophy
- Donepezil + bradycardia + hypotension: Sinus bradycardia (reduce or stop donepezil)
- Visual hallucinations + Parkinson’s: Rivastigmine first-line, or consider low-dose quetiapine
- Visual hallucinations + fluctuating cognition + parkinsonism: DLB
- DLB + antipsychotics: Extreme neuroleptic sensitivity (50% develop severe reactions). Quetiapine preferred if needed.
- Stepwise deterioration + hypertension + infarcts on MRI: Vascular dementia / Binswanger’s disease
- Early onset + personality change + loss of insight + language impairment: FTD / Pick’s disease
- Pick’s disease + language: Primary motor dysphasia (non-fluent aphasia)
- Acute confusion + fluctuating + inattention + medical cause: Delirium. Use CAM to screen.
- Hypoactive delirium: More common, higher mortality, more often missed than hyperactive
- Best dementia scale for non-English speaker with low education: RUDAS (Rowland Universal Dementia Assessment Scale)
- Becoming frail, query MCI vs dementia: Collateral history of functional impairment is key
- Depressive pseudodementia vs Alzheimer’s: Inconsistent cognitive performance, improves with antidepressant treatment
- Highest suicide rate demographic: Older men (widowed, living alone, physical illness)
PsychStar’s Paper B question bank covers old age psychiatry with questions calibrated to real exam difficulty. Start with 5 free questions at psychstar.io/try.