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Neurology > Dementia > Flashcards

Dementia Flashcards

1
Q

What is dementia?

A

A condition characterised by evidence of significant cognitive decline in at least 1 cognitive domain (attention, executive, learning and memory, language, perceptuo-motor (ie praxis) or social cognition, interfering with independence and unexplained by any other process

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2
Q

What is the main environmental risk factor of dementia?

A

Ageing

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3
Q

What are some genetic causes of dementia?

A

ApoE4 in Alzheimer’s increases risk

Huntington’s disease is a monogenetic inherited dementia

Autosomal dominant Alzheimers caused by Presenilin 1 and 2 mutations

Trisomy 21 increases Alzheimers risk between 3rd and 4th decade due to 3 copies of the APP gene on chromosome 21

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4
Q

What are some forms of potentially treatable dementia?

A
  • Metabolic e.g. uraemia
  • Toxic e.g. alcohol
  • Vitamin deficiency - B12and thiamine
  • Traumatic - severe or repeated brain injury
  • Intracranial lesions e.g. subdural haematoma, tumours
  • Infections e.g. HIV
  • Endocrine e.g. hypothyroidism
  • Psychiatric - depression causing ‘pseudodementia’
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5
Q

What are the main forms of dementia?

A

Alzheimer’s disease
Frontotemporal dementia
Vascular dementia
Lewy-body dementia

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6
Q

What is the most common form of dementia?

A

Alzheimers disease

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7
Q

How does having a 1st degree relative with AD increase risk of AD?

A

It doubles it

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8
Q

What is AD occurring in those under 65 known as?

A

Early onset AD (Possibly atypical or genetic)

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9
Q

What is AD occurring in those over 65 known as?

A

Sporadic AD (Mostly environmental)

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10
Q

What are the 2 main atypical sub-types of AD?

A
  • Posterior cortical atrophy (Terry Pratchet)
  • Progressive primary aphasia (Bruce Willis) - A form of frontotemporal dementia, but can cause an atypical form of AD
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11
Q

Describe the pathophysiology of AD

A

Alzheimer’s disease is a neurodegenerative proteinopathy, in which there is a build up of Amyloid-ß proteins

This causes the formation of:

  • Extracellular amyloid plaques
  • Intracellular neurofibrillary tangles

These cause disruption to cholinergic pathways in the brain and synaptic loss, causing cognitive impairment

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12
Q

What do extracellular amyloid plaques cause in the brain?

A

Disruption of normal cell functional and induced apoptosis

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13
Q

What do intracellular neurofibrillary tangles cause in the brain?

A

Disruption of the cell cytoskeleton leading to cell death

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14
Q

Describe the pathway that AD symptoms usually take?

A

Alzheimer’s disease usually presents initially with general forgetfulness, caused by degeneration of the medial hippocampus and later parietal lobes

This can then progress into apraxia and visuospatial difficulties

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15
Q

What are the main symptoms of AD?

A
  • Gradual onset, decline of particularly short-term memory
  • Autobiographical and political memory often well preserved
  • Poor concentration, poor sleep, low mood
  • Personality change - disinhibited, aggression, lack of self-care
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16
Q

What are some end stage symptoms of AD?

A

hallucinations, poor dentition, skin ulcers, loss of verbal communication

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17
Q

What is a symptom of posterior cortical atrophy (Sub-type of AD)?

A

Visuospatial disturbance

18
Q

What investigations are required in AD?

A
  • MRI: Atrophy of temporal / parietal lobes
  • SPECT: temporoparietal ↓metabolism
  • CSF : ↓amyloid : ↑ tau ratio
  • Research: amyloid ligand imaging
19
Q

How is AD managed?

A

Address vascular risk factors

ACh boosting treatments:
- Cholinesterase inhibitors (eg Rivastigmine / Donepezil)
- NMDA receptor blocker (eg Memantine)
- Amyloid monoclonal (Lecanemab – not NICE/SMC approved)

20
Q

Describe the pathophysiology of frontotemporal dementia

A

Frontotemporal dementia is a neurodegenerative proteinopathy, in which there is a build up of Tau or TDP-43 proteins in the brain

Specific degeneration/atrophy occurs in the frontal and temporal lobes of the brain

21
Q

What are the 3 syndromes of frontotemporal dementia?

A

Behavioural variant
Primary progressive aphasia
Semantic dementia

22
Q

What are some symptoms of behavioural variant frontotemporal dementia?

A

Behavioural changes
Executive dysfunction
Disinhibition
Impulsivity
Loss of social skills
Apathy
Obsessions
Change in diet

23
Q

What are some symptoms of primary progressive aphasia?

A
  • Logopenic aphasia (repeating)
  • Non-fluent aphasia (effortful)
    Effortful non-fluent speech, speech sound/articulatory errors, lack of grammar, lack of words
24
Q

What are some symptoms of semantic dementia?

A

Impaired understanding of meaning of words, fluent but empty speech
Difficulty retrieving names

25
Q

What investigations are required in frontotemporal dementia?

A
  • MRI: Atrophy of frontotemporal lobes
  • SPECT: Frontotemporal ↓metabolism
  • CSF: ↑ tau / normal amyloid
26
Q

What are some management options for frontotemporal dementia?

A
  • Trial of trazadone/antipsychotics to help behavioural features
  • Safety management - controlled access to food/money/internet, structured activities
  • Power of attorney
  • Environmental / safety management
  • Controlled access to food / money / internet
  • Structured activities
  • Support: MND nurse specialist if co-existent MND / CPN
27
Q

What causes vascular dementia?

A

Brain damage due to cerebrovascular disease: either major stroke, multiple smaller unrecognised strokes (multi-infarct) or chronic changes in smaller vessels (subcortical dementia)

28
Q

What are some symptoms of vascular dementia?

A
  • Dysphasia
  • Dyscalculia
  • Frontal lobe symptoms
  • Affective symptoms (more common than in Alzheimers)
29
Q

Describe the pattern of decline in vascular dementia

A

Stepwise decline

30
Q

What are some symptoms of subcortical (Small vessel) vascular dementia?

A

↓ attention, executive dysfunction, and slowed processing

31
Q

What are the core criteria for vascular dementia diagnosis?

A
  1. Presence of cerebrovascular disease plus
  2. A clear temporal relationship between the onset of dementia and cerebrovascular disease
32
Q

How is vascular dementia managed?

A

Manage vascular risk factors +/- cholineresterase inhibitor

33
Q

What causes Lewy-body dementia?

A

Lewy-body dementia is a neurodegenerative proteinopathy, in which there is a build up of Alpha-synuclein proteins in the neurons of the brain stem and neocortex

34
Q

How does alpha-synuclein cause dementia in Lewy-body dementia?

A

α-synuclein aggregates are insoluble and so lead to cell dysfunction and therefore cell damage

This leads to disruption of cholinergic and dopaminergic pathways

35
Q

What are some early symptoms of Lewy-body dementia?

A

Common early involvement of reduced attention, executive function and visuospatial skills

36
Q

What are some other symptoms of Lewy-body dementia?

A
  • Visual hallucinations
  • Fluctuating cognition (delirium-like)
  • REM sleep behaviour disorder
  • Extrapyramidal features (Parkinsonism) seen in 75% (Not more than 1 year prior to onset of dementia)
37
Q

What are the core criteria for diagnosis of Lewy-body dementia?

A
  1. Fluctuating cognition plus
  2. Recurrent well-formed visual hallucinations +/-
  3. Presence of extrapyramidal features (seen in 75%)
38
Q

What are some investigations for Lewy-body dementia?

A

DaT (dopamine transporter imaging) if atypical features

New (research) techniques: αsynuclein ligand imaging / αsynuclein in CSF

39
Q

How is Lewy-Body dementia managed?

A

Small dose Levodopa /↓ acetylcholine (amongst other neurotransmitters) → trial cholinesterase inhibitors

Support: PD nurse specialist / CPN

40
Q

What are some generalised investigations for suspected dementia?

A

CT (Standard)
MRI (If young or fast progressing)
Bloods (Dementia screen)
SPECT
DAT

41
Q

What are some blood tests involved in the dementia screen?

A

B12, TFTs, syphilis, HIV, Ca2+

42
Q
A

Neurology (28 decks)

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