YearClub 2026 Neurology session (dementia) Flashcards
What is dementia?
Dementia is irreversible, progressive decline in cognitive function of atleast 1 domain without altered conscious state.
Dementia doesn’t have to be consistent or gradual. True/false?
True
Frontotemporal dementia is the commonest form of dementia. True/false?
False. Alzheimer’s dementia is most common form of dementia.
Hallmarks of Alzheimer’s dementia?
Neurofibrillary tangles (abnormal accumulations of a protein called tau that collect inside neurones).
Senile plaques (polymorphous beta-amyloid protein deposits found in the brain in Alzheimer disease and normal aging).
Loss of cortical neurones (neurones are lost in a progressive pattern that is relatively consistent among individuals).
Polymorphisms in ApoE4 decrease dementia risk. True/false?
False.
Polymorphisms in ApoE4 increase risk.
In ApoE2 decrease risk of alzheimer’s
Treatment of Alzheimer’s dementia?
Improves symptoms but doesn’t slow decline:
1st rivastigmine (Cholinesterase inhib)
2nd Memantine (NMDA receptor blocker)
What is a cholinesterase (acetylcholinesterase) inhibitor?
Example = rivastigmine
Inhibit the enzyme acetylcholine from breaking down into acetate and choline. Leading to improved communication between nerve cells to temporarily improve dementia symptoms.
What is an NMDA receptor blocker?
Examples = memantine, amantadine.
Block NMDA receoptors hence reducing glutamate production and slowing damage to nerve cells.
What is vascular dementia?
Dementia due to micro-infarction of brain tissue. Can be focal post stroke, or generalised. Generally >65.
Vascular dementia usually has a gradual progression. True/false?
False. Progression is often step-wise rather than gradual, as small strokes accumulate.
Step-wise is stable on between events.
Gradual has continuous decline (usually the case with Alzheimer’s).
What does vascular dementia show in an MRI?
MRI shows severe small vessel disease
Treatment for vascular dementia?
Treatment is to reduce vascular disease risk factors, monitor disease. Often overlap with Alzheimer’s in which case Rivastigmine can help
Frontotemporal dementia tends to develop in people younger than 65. True/false?
True
What does frontotemporal dementia present with?
Since frontal lobe often presents with behavioral symptoms, or disinhibition. Drastic personality change, hyperorality/ overeating.
Appearance of frontotemporal dementia on imaging?
MRI/Spect show atrophy/ reduced uptake but specifically in the frontal/temporal lobes
Management of frontotemporal dementia?
Aggressive disease which is hard to manage.
Trial of antipsychotics/ trazadone (serotonin antagonist and reuptake inhibitor).
Manage access to food, money, internet. Sort power of attorney.
The deposition of what protein is the underlying cause of Lewy body dementia and Parkinson’s dementia?
Alpha synuclein protein
How does Dementia with Lewy bodies and Parkinsons dementia present?
Presents usually >65 with fluctuating cognition and well formed visual hallucinations.
What differentiates Dementia with Lewy bodies from Parkinson’s dementia?
If extrapyramidal (parkinsonian) features present atleast 1 year before cognitive: parkinsons dementia
If absent or present within a year/ after cognitive- dementia with Lewy Bodies
Extrapyramidal features include resting tremor, rigidity, akinesia (loss or impairment in power of voluntary movement) and affected posture and balance.
Fluctuating cognitive impairment is a major sign in Lewy body dementia. true/false?
True
Also present in parkinson’s dementia
Fluctuating cognition is characterized by alternating periods of cognitive impairment and “normal or near-normal performance” and “pronounced variations in attention and alertness.
Preferred investigation for Lewy body and Parkinson’s dementia?
Investigation of choice is DaT scan (dopamine transporter activity on SPECT)
Some features of Lewy body dementia include hallucinations, memory problems and some parkinsonian features such as poor arm swing. true/false?
True
What is huntington’s disease?
An Autosomal Dominant Disorder causing distinctive symptoms due to degeneration of the basal ganglia and cerebrum.
Tends to affect patients at an early age, onset 30-50 years.
Underlying cause of huntington’s disease?
Mutations in the huntington gene (ch 4). Causes CAG trinucleotide expansion leading to long glutamine strings which are toxic to cells.
Investigations for huntington’s disease?
MRI: focal atrophy of caudate heads. Genetic test is gold standard
Medications for huntington’s disease?
Amantadine, antipsychotics.
Wernicke-korsakoff syndrome is the combination of wernickes encephalopathy and korsakoff syndrome. true/false?
True
What is the main cause of wernicke encephalopathy and korsakoff syndrome?
Both neurological conditions caused by thiamine deficiency (deficiency of vitamin B1) often associated with chronic alcoholism.
main difference between wernickes encephalopathy and korsakoff syndrome?
The key difference is that Wernicke encephalopathy is an acute, reversible condition that can be treated with thiamine supplementation.
Korsakoff syndrome is an irreversible, chronic condition that occurs after incomplete recovery from Wernicke encephalopathy.
Wernicke encephalopathy is characterized by a triad of eye abnormalities (ophthalmoplegia), ataxia, and confusion.
Korsakoff syndrome is characterized by anterograde and retrograde amnesia with preserved long-term memory.
What is anterograde and retrograde amnesia?
Retrograde amnesia is the inability to recall past memories while anterograde amnesia is the inability to create new memories.
What is ophthalmoplegia?
paralysis of the muscles within or surrounding the eye.
Another name for vascular dementia?
Multi-infarct dementia
What is Huntington’s disease and it’s features?
A genetic disease inherited in an autosomal dominant pattern that affects the brain.
Symptoms can include:
- Rapid involuntary movements (chorea)
- Cognitive decline
- Behavioural changes
- Confusion
- Gait disturbances (walking slowly with irregular stepping patterns, and finding it hard to initiate each step)
What is a change in the brain that can be seen in Alzheimer’s disease on post-mortem?
Widespread cerebral atrophy
What feature is typically seen in the early stages of Alzheimer’s disease?
Amnesia for recent memories
What is the triad of features for Lewy Body dementia?
REM sleep disorder
History of falls (secondary to falls)
Hallucinations
What are the anti-cholinergic side-effects of mild stage Alzheimer’s drugs?
Diarrhoea
Nausea
Vomiting
Bradycardia
Urinary incontinence
Increased salivary production
What is pseudo dementia?
the condition in which depression causes cognitive deficits that masquerade as dementia.
What are the features of pseudo dementia?
Depression mimicking dementia
Features include:
- Normal MMSE (mini mental state examination)
- Sleep disturbance
- Irritation
- Global memory loss
When is donepezil usually indicated in Alzheimer’s?
Used for symptomatic treatment of mild to moderate Alzheimer’s disease.
Main examples of acetylcholinesterase inhibitors?
Donepezil, rivastigmine and galantamine
Memantadine is an example of an acetylcholinesterase inhibitor. True/false?
False
Memantadine is an example of a NMDA receptor antagonist which slows down the progression of Alzheimer’s. Typically used near the end stages of the disease.