Dementia — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Robert Walsh, 79 years old, retired accountant. ^[1]

Presenting complaint: Progressive cognitive decline over 3 years, with recent behavioural disturbance, falls, and carer strain, assessed in the memory clinic. ^[1]

History of the presenting complaint: Mr Walsh's wife first noticed changes about 3 years ago — he began misplacing his keys, repeating questions he had just asked, and forgetting recent conversations. The decline has been gradual and progressive. Two years ago he made errors managing the household finances (he paid the same electricity bill three times in one month), and his wife took over the banking. One year ago he stopped driving after getting lost in a familiar suburb. Six months ago his general practitioner diagnosed hypertension and commenced amlodipine. Three months ago he was admitted to hospital with a urinary tract infection and was noted to be confused; this improved with antibiotic treatment, but his cognition did not return to his pre-admission baseline. ^[1]

Over the last 2 months, his wife reports a new behavioural disturbance. He becomes agitated in the early evening ("sundowning"), paces the house, and on several occasions has accused her of stealing his wallet and his watch. Twice in the last month he has tried to leave the house at night in his pyjamas. He has become unsteady on his feet and had a fall in the bathroom last week, without loss of consciousness. His appetite has decreased and he has lost 3 kilograms. ^[1]

Past history:

• Ischaemic heart disease — drug-eluting stent to the left anterior descending artery 5 years ago. No angina since.
• Hypertension — diagnosed 6 months ago.
• Benign prostatic hyperplasia — on oxybutynin for overactive bladder symptoms for 4 years.
• Osteoarthritis of the knees and lumbar spine.
• No history of stroke, diabetes, atrial fibrillation, or psychiatric illness.
• No history of alcohol misuse. ^[1]

Current medications:

• Aspirin 100 mg daily
• Atorvastatin 40 mg daily
• Amlodipine 10 mg daily
• Oxybutynin 5 mg twice daily
• Paracetamol 1 g three times daily
• Codeine 30 mg every 6 hours as needed (he takes it 2 to 3 times daily for back and knee pain) ^[1]

Social history: Lives with his wife (76, in good health) in their own single-storey home. Two adult children who live interstate and visit several times a year. He was driving until 12 months ago. He is a former accountant, retired at 67. He does not smoke and drinks alcohol rarely. His wife is his sole carer and reports exhaustion. ^[1]

Examination findings (trainee elicits):

• Alert, cooperative, but orientated to person only. Speech is slow with word-finding pauses. Mood is flat.
• MoCA 14 out of 30 — points lost on orientation (day, date, month, year, place all incorrect), delayed recall (0 of 5 words), serial sevens (2 of 5 correct), and clock-drawing (numbers crowded on the right, hands misplaced).
• Attention tested with months of the year backwards — completed with two errors (mildly impaired).
• Cardiovascular: pulse 72 and regular, blood pressure 138/82 lying, 124/76 standing (a 14 mmHg systolic drop). No cardiac murmurs.
• Respiratory and abdominal examination: unremarkable.
• Neurological: cranial nerves intact. Tone increased with mild rigidity in all four limbs (more marked on the left). Power 5/5 throughout. Reflexes brisk bilaterally, more so on the left. Plantars downgoing. Sensation intact. Gait slow and shuffling with reduced arm swing. No tremor. No myoclonus.
• Bladder scan: 80 mL (not in retention).
• Cognitive profile: an amnestic and executive impairment pattern, with mild attentional impairment. ^[1]

Investigations:

• Full blood count: haemoglobin 138 g/L, white cell count 7.2, normal differential, platelets 230.
• Urea and electrolytes: sodium 136, potassium 4.2, urea 7.1, creatinine 95 (baseline 88). eGFR 62. Calcium normal. Glucose 6.2. Liver function normal. Albumin 38.
• TSH 3.1 (normal).
• Vitamin B12 280 pmol/L (normal range 150 to 700). Folate 15 (normal).
• CRP 4.
• Syphilis serology: negative.
• Urinalysis: clear. Urine culture: negative.
• Chest X-ray: clear.
• ECG: sinus rhythm 68, normal intervals, no acute changes.
• CT brain: mild generalised cerebral atrophy, more prominent in the medial temporal lobes. A few small white matter hypodensities in the periventricular region. No infarct, haemorrhage, mass, or hydrocephalus. ^[1]

Candidate's long-case presentation (SASPOP)

"Mr Robert Walsh is a 79-year-old retired accountant presenting with a 3-year progressive cognitive decline, now with behavioural disturbance, falls, and carer strain. ^[1]

His past history includes ischaemic heart disease with a drug-eluting stent 5 years ago, hypertension, benign prostatic hyperplasia, and osteoarthritis. ^[1]

His medications are aspirin, atorvastatin, amlodipine, oxybutynin, regular paracetamol, and codeine as needed. ^[1]

On examination he is oriented to person only, his MoCA is 14 out of 30 with an amnestic and executive impairment pattern, he has mild orthostatic hypotension, mild rigidity with brisk reflexes and a slow shuffling gait, and his CT shows medial temporal atrophy with a few white matter changes. ^[1]

His main problems are:

1. Mixed Alzheimer and vascular dementia, moderate stage
2. Behavioural and psychological symptoms — evening agitation, accusatory delusions, nocturnal wandering
3. High anticholinergic and opioid drug burden — oxybutynin and codeine both worsening cognition and contributing to falls
4. Orthostatic hypotension and fall risk
5. Vascular risk factor management — hypertension and ischaemic heart disease
6. Carer strain — his wife is exhausted and is the sole carer
7. Advanced care planning — driving (already ceased), power of attorney, guardianship, future care ^[1]

My integrated plan is: confirm the clinical diagnosis of mixed Alzheimer and vascular dementia, noting the B12, folate, TSH, and syphilis serology are all normal and the reversible causes are excluded; conduct a structured medication review — stop the oxybutynin and switch to mirabegron, minimise and eventually stop the codeine in favour of regular paracetamol and topical NSAIDs, and reduce the amlodipine to address the orthostatic drop; start donepezil 5 mg at night after the baseline ECG I have, titrating to 10 mg; manage his BPSD with a precipitant search and non-pharmacological strategies, reserving a time-limited low-dose risperidone for severe aggression; arrange falls prevention and an occupational therapy home assessment; refer his wife for carer support, respite, and a community home care package; and initiate advanced care planning — enduring power of attorney, enduring guardianship, and an advance care directive." ^[1]

Discussion questions

Q1: "Why do you say mixed Alzheimer and vascular, rather than Alzheimer alone?" ^[1]

"Three reasons. First, the cognitive profile has an executive and processing-speed component (the poor serial sevens and the shuffling gait with brisk reflexes) alongside the amnestic deficit (the zero recall and the anomia), which suggests more than pure temporoparietal Alzheimer pathology. Second, the imaging shows white matter changes alongside the medial temporal atrophy — the combination of hippocampal atrophy and white matter disease is the radiological signature of mixed pathology. Third, the vascular risk factor burden — hypertension and ischaemic heart disease — makes coexistent cerebrovascular disease likely. In practice, pure subtypes are uncommon in a 79-year-old, and mixed Alzheimer and vascular dementia is the most likely real-world diagnosis. The management combines the approaches: a cholinesterase inhibitor plus aggressive vascular risk factor control." ^[1]

Q2: "What would make you reconsider the diagnosis and think of dementia with Lewy bodies?" ^[1]

"The rigidity, the brisk reflexes, and the shuffling gait could fit DLB, and the visual hallucinations and the fluctuation of DLB are not absent here. The discriminating features would be: prominent, detailed visual hallucinations (people or animals, reported spontaneously), marked day-to-day fluctuation in cognition and alertness (not just the sundowning pattern), a history of REM sleep behaviour disorder (acting out vivid dreams), and a more prominent parkinsonian picture with a resting tremor. The clock-drawing would be relatively preserved early in DLB, and the memory deficit less dominant. The reason this matters urgently is that an antipsychotic — which I might consider for his evening agitation — would be absolutely contraindicated if the diagnosis were DLB, because of the risk of catastrophic neuroleptic sensitivity (McKeith 2017, PMID 28592453). The clinical picture here is more consistent with mixed Alzheimer and vascular — the visual hallucinations are not reported, the fluctuation is not the core feature, and the parkinsonism is mild and could be explained by vascular small-vessel disease — but I would keep the possibility of DLB in mind and specifically ask about hallucinations and sleep behaviour, and I would use any antipsychotic with extreme caution." ^[1]

Q3: "How will you manage his wife's exhaustion?" ^[1]

"Carer strain is the commonest reason for institutionalisation, and supporting her is central to his community care. I would offer education about the diagnosis, the trajectory, and the practical management (structured routines, managing the delusions without arguing, the sundowning strategies); a formal carer assessment; referral to Dementia Australia for a support group and a carer advisory service; regular in-home respite and a day programme; a community home care package for assistance with shopping, cleaning, medications, and personal care; an identification bracelet or GPS tracker for the wandering; a crisis respite number; and active monitoring of her own health, including a depression screen. I would also encourage the two adult children to increase their involvement — regular phone calls, more frequent visits, and shared decision-making — to share the load. The Lancet Commission (Livingston 2020, PMID 32738937) identifies social isolation and carer intervention as modifiable factors in the dementia care pathway." ^[1]