Vascular, Lewy body & frontotemporal dementia flashcards
19 high-yield MRCP Part 1 cards from the Intellect Medicos Geriatrics & Palliative Care course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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What pattern of progression is classic for vascular dementia?
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Stepwise deterioration.
Why? Each new infarct causes a sudden drop in function, followed by a plateau.
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Which imaging supports a diagnosis of vascular dementia?
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MRI showing infarcts and/or white matter (small vessel) changes.
Why? The NINDS-AIREN criteria need imaging evidence of cerebrovascular disease linked to the cognitive decline.
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When should cholinesterase inhibitors or memantine be used in vascular dementia?
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Only if there is suspected co-existing Alzheimer's disease, Lewy body dementia or Parkinson's disease dementia.
Why? They have no proven benefit in pure vascular dementia (NICE NG97). Management is otherwise symptomatic plus vascular risk-factor control.
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Which protein forms Lewy bodies?
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α-synuclein.
Why? Dementia with Lewy bodies and Parkinson's disease are both α-synucleinopathies.
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Name three core clinical features of dementia with Lewy bodies.
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Any three of: fluctuating cognition, recurrent well-formed visual hallucinations, parkinsonism, REM sleep behaviour disorder.
Why? These are the core diagnostic features; attention and visuospatial function are hit early, memory later.
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Which scan helps confirm dementia with Lewy bodies when the diagnosis is uncertain?
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123I-FP-CIT SPECT (DaTscan), showing reduced striatal dopamine transporter uptake.
Why? Low dopaminergic uptake separates DLB from Alzheimer's disease. The tracer is iodine-123 labelled ioflupane.
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What is the first-line drug treatment for mild to moderate dementia with Lewy bodies?
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Donepezil or rivastigmine.
Why? The cholinergic deficit in DLB is often greater than in AD, so response can be good. NICE NG97: galantamine only if these are not tolerated; memantine if AChE inhibitors cannot be used.
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A 76-year-old man with fluctuating confusion, vivid visual hallucinations and mild parkinsonism is given haloperidol for agitation. Within days he becomes rigid, drowsy and falls repeatedly. What has happened?
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Severe neuroleptic sensitivity reaction in dementia with Lewy bodies.
Why? DLB patients are very sensitive to D2 blockade; reactions include severe parkinsonism, sedation, NMS-like states and death. Avoid antipsychotics.
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One-year rule: if dementia starts before or within 1 year of parkinsonism the diagnosis is ______; if parkinsonism has been present for more than a year first, it is Parkinson's disease dementia.
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dementia with Lewy bodies
Why? The two share pathology, so timing is used to label them. Fluctuating cognition and hallucinations are more prominent in DLB.
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One-year rule: if dementia starts before or within 1 year of parkinsonism the diagnosis is dementia with Lewy bodies; if parkinsonism has been present for more than a year first, it is ______.
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Parkinson's disease dementia
Why? The two share pathology, so timing is used to label them. Fluctuating cognition and hallucinations are more prominent in DLB.
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Name the three clinical subtypes of frontotemporal dementia.
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Behavioural variant (Pick's), semantic dementia and progressive non-fluent aphasia.
Why? Semantic dementia and progressive non-fluent aphasia are the two primary progressive aphasias.
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How does the typical age of onset of frontotemporal dementia compare with Alzheimer's disease?
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Younger — usually before 65.
Why? FTD is a leading cause of young-onset dementia.
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Name three early features of behavioural-variant frontotemporal dementia.
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Any three of: personality change, disinhibition, apathy, loss of empathy, hyperorality/food fads, repetitive behaviours, poor insight.
Why? Frontal (orbitofrontal and anterior cingulate) damage affects social conduct before memory.
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Which cognitive domains are relatively preserved early in frontotemporal dementia?
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Memory and visuospatial function.
Why? This is the opposite of Alzheimer's disease, where memory loss comes first.
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What is the classic imaging finding in frontotemporal dementia?
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Focal frontal and/or anterior temporal lobe atrophy ("knife-blade" atrophy), often asymmetric.
Why? PET shows frontal/temporal hypometabolism.
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What are Pick bodies made of?
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Aggregated tau protein.
Why? They are intraneuronal inclusions in Pick's disease, a tauopathy within the FTD spectrum.
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Should cholinesterase inhibitors or memantine be offered in frontotemporal dementia?
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No — NICE says do not offer them. Management is supportive.
Why? There is no cholinergic deficit to correct and they can worsen behaviour.
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Which FTD variant gives fluent speech but loss of word meaning and object knowledge?
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Semantic dementia.
Why? Grammar, articulation and repetition are spared; MRI shows marked anterior temporal atrophy, usually left-sided.
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In progressive non-fluent aphasia, where is the atrophy on MRI?
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Left posterior frontal lobe and insula (around Broca's area).
Why? Speech is effortful, apraxic and agrammatic, with comprehension and object knowledge spared.