Dementia Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Robert Walsh is a 79-year-old retired accountant presenting with a 3-year history of progressive cognitive decline, now complicated by behavioural disturbance, falls, and carer strain. He lives with his wife, who is his main carer and who is exhausted. [1]

His past history includes ischaemic heart disease with a drug-eluting stent 5 years ago, hypertension, benign prostatic hyperplasia, and osteoarthritis. His medications are aspirin, atorvastatin, amlodipine, oxybutynin, regular paracetamol, and codeine as needed. [1]

Over 3 years he has developed progressive forgetfulness, difficulty managing finances (he has paid the same bill three times), and repetition of questions. Three months ago he was admitted with a urinary tract infection and was confused. Over the last 2 months he has become agitated in the evenings, accuses his wife of stealing his wallet, and has tried to leave the house at night. He had a fall last week. On examination he is oriented to person only, his MoCA is 14 out of 30, and he has a slow shuffling gait and brisk reflexes. His CT brain shows mild cerebral atrophy with a few small 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 directly opposing any cholinergic strategy, and codeine contributing to sedation and falls
4. Fall risk
5. Vascular risk factor management — hypertension and ischaemic heart disease
6. Driving safety and capacity — he is no longer safe to drive
7. Carer strain — his wife is exhausted and is the pillar of his care [1]

My integrated plan is to make the diagnosis on the clinical history and the collateral, exclude reversible causes with a B12, folate, TSH, and the imaging he has already had, and conduct a structured medication review — I will stop the oxybutynin and switch to mirabegron, minimise the codeine, and review the amlodipine for orthostatic hypotension. I will start donepezil 5 mg at night after a baseline ECG, titrating to 10 mg, and add memantine as the disease progresses. I will manage his BPSD by searching for precipitants, using non-pharmacological strategies, and reserving a time-limited low-dose risperidone only for severe aggression. I will counsel him and his wife about driving cessation and report to the licensing authority, and I will initiate advanced care planning — power of attorney, enduring guardianship, and an advance care directive — while he retains some capacity. I will support his wife with education, respite, and community services." [1]

Examiner probing questions and model answers

Q1: "You mentioned stopping the oxybutynin. Explain why, and what would you use instead for his bladder?" [1]

"Oxybutynin is a potent antimuscarinic anticholinergic with high blood-brain barrier penetration — it directly blocks acetylcholine at central muscarinic receptors, worsening cognition and opposing the mechanism of the donepezil I am about to start. It is among the highest-anticholinergic-burden drugs in common use, and reducing anticholinergic burden is one of the most effective and safest interventions I can make in this patient. For his bladder, I would switch to mirabegron, a beta-3 adrenergic agonist that relaxes the detrusor without anticholinergic activity, or manage with timed voiding, fluid management, and bladder training. If an antimuscarinic is essential, I would choose one with lower central penetration, such as trospium or darifenacin, but the principle is to minimise anticholinergic burden — and the evidence is that higher anticholinergic burden is associated with faster cognitive decline in dementia." [1]

Q2: "How would you distinguish his dementia from delirium, given he was confused during his recent admission?" [1]

"The distinction rests on the temporal pattern and the cognitive domains. His underlying dementia is a 3-year, insidious, progressive decline with a stable — though declining — baseline and preserved attention in the early stages. The confusion during his admission for a urinary tract infection was an acute change superimposed on that baseline — that was delirium on dementia, confirmed by the acute onset, the inattention, and the improvement with treatment of the infection. The key clinical question is always: is this an acute change from the patient's baseline? If yes, it is delirium until proven otherwise, even in a patient with established dementia. I would document his baseline cognition from his wife, and plan a repeat MoCA after any acute illness to track the return to baseline. The two conditions coexist in the majority of hospitalised older patients with dementia, and the management of both — the precipitant search, the non-pharmacological care, the avoidance of sedatives — is the same." [1]

Q3: "He was driving until recently. How do you approach driving assessment in dementia?" [1]

"My clinical assessment is that he is no longer safe to drive — the MoCA of 14, the impaired orientation, the visuospatial and executive impairment, the falls, and the nocturnal wandering all indicate that he lacks the judgement, reaction time, and attention required for safe driving. The conversation should be honest, compassionate, and documented. In Australia, there is a legal obligation to report — the patient must notify the licensing authority, and in some states the doctor has a mandatory or discretionary reporting obligation. I would provide a medical certificate advising against driving, recommend a formal on-road driving assessment if there is any doubt, and pair the conversation with a plan for alternative transport to preserve his autonomy and social engagement. The position statement of the Australian and New Zealand Society for Geriatric Medicine and the Austroads guidelines are the reference. I would not let him continue driving on the grounds of autonomy, because the risk to him and to others outweighs it, and because there is a legal duty." [1]

Q4: "What is the role of cognitive enhancers in his management, and what benefit can his family expect?" [1]

"Donepezil, rivastigmine, and galantamine are cholinesterase inhibitors that increase acetylcholine in the cerebral cortex and produce a modest symptomatic benefit in mild to moderate Alzheimer dementia (Birks 2006, PMID 16437532) — a mean improvement of about 2 to 3 points on the ADAS-cog, sustained for 6 to 12 months before the underlying decline resumes. They do not halt or cure the disease. I would start donepezil 5 mg at night, check a baseline ECG for bradycardia or heart block, and titrate to 10 mg after 4 weeks. As his disease progresses into the moderate-severe range, I would add memantine, an NMDA receptor antagonist, which has a modest additional benefit. I would counsel the family honestly — the drug may stabilise him for a time, may slightly improve his function, but will not reverse the dementia, and the response is individual and unpredictable. I would review at 3 to 6 months with a structured assessment and continue only if there is perceived benefit or stabilisation." [1]

Q5: "The nurses want to prescribe risperidone for his evening agitation. What is your response?" [1]

"My response is that risperidone is a last resort, not a first step. The BPSD escalation ladder starts with searching for and treating precipitants — pain, infection, constipation, urinary retention, dehydration, sensory deprivation, a new drug — and with non-pharmacological strategies: a structured evening routine, adequate lighting as dusk falls to reduce sundowning, reassurance and redirection around the delusional beliefs, and a safe environment. If these are exhausted and the behaviour is causing severe distress or risk, I would consider a time-limited trial of risperidone 0.25 to 0.5 mg in the evening, reviewed every 2 to 4 weeks, with the family informed of the increased mortality (about 1.6 to 1.7 times placebo, Schneider 2005) and stroke risk. The key exclusion before any antipsychotic is Lewy body dementia — the fluctuation, the detailed visual hallucinations, and the spontaneous parkinsonism are not the dominant features in this patient, who fits the mixed Alzheimer and vascular picture, so an antipsychotic is not absolutely contraindicated here — but the principle is caution, lowest dose, shortest time, regular review, and stop if ineffective." [1]

DCE Short-Case Viva — Cognitive Assessment

Examiner instruction: "This 76-year-old woman on the ward is said to be confused. Please assess her cognition." [1]

Candidate's examination routine (narrated)

"I would begin by confirming the patient's identity, introducing myself, explaining what I am going to do, and ensuring she is comfortable, not in pain, and that she has her glasses and hearing aids if she uses them — these are essential for a valid cognitive assessment and are frequently missing on the ward. I would also note the time of day, because cognition and confusion fluctuate, and I would establish, from the nursing staff or a family member, what her baseline cognition is. [1]

First, I assess her level of consciousness and alertness. I observe whether she is alert, drowsy, hypervigilant, or fluctuating. An altered level of consciousness is a red flag for delirium superimposed on dementia. [1]

Next, I assess attention, the cardinal cognitive domain. I ask her to recite the months of the year backwards — December, November, October, September. Impaired attention suggests delirium; preserved attention with memory loss suggests a pure dementia. [1]

I then assess orientation — to time (day, date, month, year, season), to place (the hospital name, the floor, the city), and to person (her name and date of birth). I document each item individually. [1]

I assess registration and recall — I name three objects (an apple, a table, a penny), ask her to repeat them to confirm registration, and then ask her to recall them after 3 to 5 minutes. Failure of registration suggests attentional impairment; failure of recall with preserved registration is the hallmark of an amnestic deficit (Alzheimer). [1]

I assess language — naming (a watch, a pencil), repetition ('no ifs, ands, or buts'), comprehension (a three-step command), and fluency. Naming difficulty (anomia) is an early sign of Alzheimer; non-fluent or halting speech suggests a primary progressive aphasia. [1]

I assess executive function and visuospatial ability with the clock-drawing test — I ask her to draw a clock face, put in all the numbers, and set the hands to ten past eleven. This tests planning, organisation, spatial layout, and frontal-executive function, and is very sensitive to both dementia and delirium. An executive-predominant pattern with a poor clock but preserved memory suggests vascular or frontotemporal pathology. [1]

I assess mood and insight — I ask how her mood is, whether she feels low, and whether she is aware that her thinking is not as it should be. A positive depression screen raises pseudodementia. [1]

Finally, I note the need for a collateral history — I would arrange to speak with a family member to establish the baseline, the onset, and the course. The collateral history is the single most useful piece of information in distinguishing dementia from delirium and depression. [1]

I would perform the MoCA if I have not already done so, to obtain a standardised score, and I would perform a focused neurological examination for focal signs, parkinsonism, and gait, to identify the subtype." [1]

Presentation template (model answer)

"I performed a cognitive assessment on this 76-year-old woman. Her level of consciousness is normal — she is alert throughout. Attention is preserved — she recites the months of the year backwards without error. She is disoriented to time (she gives the year as 2012) and to place (she cannot name the hospital), but oriented to person. Registration of three objects is intact, but recall at 3 minutes is zero of three. Language shows anomia — she cannot name a watch, calling it 'the thing you wear' — but repetition and comprehension are preserved. Her clock-drawing shows poor spatial layout with all the numbers crowded on the right side and the hands misplaced. Mood is flat but she does not describe depression. Insight is limited — she acknowledges some forgetfulness but minimises it. [1]

The pattern is of an amnestic, temporoparietal cognitive impairment — preserved attention with disorientation, a failure of recent recall, anomia, and visuospatial impairment on clock-drawing — consistent with an Alzheimer-pattern dementia. The preserved attention excludes delirium as the sole diagnosis. A collateral history from her daughter, obtained by telephone, confirms a 2-year gradual decline in memory and function from a previously intact baseline, with no acute events — consistent with a neurodegenerative dementia rather than delirium or a rapid vascular course. [1]

My differential is Alzheimer disease first, with mixed Alzheimer and vascular dementia given her age and the need to assess her vascular risk factors. I would arrange an MRI to characterise the atrophy and vascular burden, a B12, folate, and TSH to exclude reversible causes, and I would start a cholinesterase inhibitor after a baseline ECG. I would initiate advanced care planning and carer support." [1]

Examiner discussion

Q: "How would the findings differ if this were dementia with Lewy bodies rather than Alzheimer?" [1]

"The three distinguishing features would be fluctuation, visual hallucinations, and parkinsonism. The attention would be impaired and variable — lucid one day, muddled the next — rather than preserved as in Alzheimer. The patient or the family would describe detailed, well-formed visual hallucinations of people or animals. On examination there would be bradykinesia, rigidity, and a shuffling gait. A history of REM sleep behaviour disorder — acting out vivid dreams — would be highly suggestive. The clock-drawing may be relatively preserved early, because the memory and visuospatial deficits of DLB are less prominent than in Alzheimer, but the attentional and executive impairment is greater. I would specifically avoid antipsychotic drugs in DLB because of the risk of catastrophic neuroleptic sensitivity (McKeith 2017, PMID 28592671), and I would use a cholinesterase inhibitor — rivastigmine is particularly effective in DLB." [1]

Q: "How would you distinguish depression (pseudodementia) from dementia?" [1]

"Depression in older adults can produce cognitive impairment that mimics dementia. The distinguishing features are the onset (subacute over weeks to months, not years), the variability (worse in the morning, diurnal variation), the patient's effort (they give up easily, answer 'I don't know', show poor effort rather than trying hard), the preserved orientation and attention, the prominent biological features of depression (low mood, anhedonia, sleep and appetite disturbance), and a positive depression screen. The practical rule is to screen for and treat depression in every patient with cognitive impairment and to reassess the cognition after the mood has improved — but to remember that depression and dementia coexist in up to 40 percent of cases, and that depression can be a prodrome of dementia. Treating the depression does not reliably 'cure' the cognition if an underlying dementia is present." [1]

Q: "What is the single most useful piece of information in this assessment?" [1]

"A collateral history from a family member or carer who knows the patient's baseline cognition, to establish the onset and the course of the change. It is the piece of information that transforms the assessment, because it distinguishes a chronic, progressive decline (dementia) from an acute fluctuating change (delirium) and from a subacute depressive decline (pseudodementia), and it establishes the baseline against which progression and response to treatment are measured. Without the collateral history, a single cognitive test score in isolation is uninterpretable." [1]