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Neurology > Dementia > Flashcards

Dementia Flashcards

1
Q

Cognition

A

The mental action of acquiring knowledge and understanding through thought, experience and the senses

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2
Q

What does cognition ecompass

A

Attention Language ( comprehension and production) Social functioning (judgement, evaluation and reasoning) Executive functioning (problem solving/decision making) Formation of knowledge and memory

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3
Q

Define dementia

A

Undoing of the mind

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4
Q

What is the DSM criteria for dementia

A
  1. evidence of significant cognitive decline in at least 1 cognitive domain (Attention, executive, learning and memory, language, perception-motor (ie praxis ) or social cognition PLUS: the cognitive deficits interfere with independence in everyday activities PLUS: they are not better explained by another process
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5
Q

What are the three mechanisms of acute cognitive disorders

A
  • Viral encephalitis - Head injury - Stroke
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6
Q

Describe the effects of viral encephalitis

A

Memory, behaviour change and language

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7
Q

Describe the effects of head injury

A

Attention, memory, executive dysfunction

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8
Q

What are the clinical features of transient global amnesia

A

abrupt onset antegrade > retrograde amnesia (repetitive). Preserved knowledge of self Transient 4-6 hours (always <24 hours) Generally once off (c6% may recur)

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9
Q

Who is typically affected by transient global amnesia?

A

> 50 y/o generally 70s

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10
Q

What are the triggering factors of transient global amnesia

A

emotion/changes in temperature

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11
Q

What is the pathophysiology of transient global amnesia

A

Uncertain Transient changes in hippocampus

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12
Q

What are the clinical features of transient epileptic amnesia?

A

Forgetful/repetitive questioning Can carry out complex activities with no recollection of events Short lived (20-30 minutes)

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13
Q

What is transient epileptic amnesia associated with?

A

Associated with temporal lobe seizures - 30% seizures not witnessed - Response to anti-epileptic medication should be seen

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14
Q

What is the differential diagnosis for sub-acute cognitive disorders

A
  • Toxins (alcohol, carbon monoxide) - Neurodegeneration (CJD) -Metabolic (B12, calcium, thyroid) - Inflammatory: limbic encephalitis - mood disorders - functional - Infection: HIV syphillis
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15
Q

What are the clinical features of sub-acute cognitive disorders?

A

Everyday forgetfulness impacting on functioning

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16
Q

What is pathognomic of subjective cognitive impairment?

A

Fluctuation of symptoms Mismatch between: symptoms and reported function / symptoms + symptoms of known neurodegenerative disorders

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17
Q

What may subjective cognitive impairment be a part of?

A

Generalised functional disorder (reduced concentration/attention/reaction time and subsequent memory difficulties)

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18
Q

What is the treatment for subjective cognitive impairment

A

Exclude a mood disorder (deficits in attention, executive function, and memory can be seen) plus neuropsychology

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19
Q

What is the most common human prion disease?

A

Creutzfeldt-Jakob disease

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20
Q

What is CJD?

A

Neurodegenerative proteinopathy

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21
Q

What are the four kinds of CJD?

A

Sporadic Variant Iatrogenic Genetic

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22
Q

_____ CJD presents at age 60 _____ CJD presents at age 20 _____ CJD presents at age 30 _____ CJD presents at any age

A

sporadic CJD presents at age 60 variant CJD presents at age 20 iatrogenic CJD presents at age 30 genetic CJD presents at any age

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23
Q

What are the clinical features of sporadic CJD?

A

Rapid onset dementia + neurological signs + myoclonus

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24
Q

What is the duration of illness of sporadic CJD?

A

4 months

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25
Q

What is the commonest form of CJD?

A

Sporadic

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26
Q

What causes sporadic CJD?

A
  • ? erroneous production of PrPSc
  • ? Somatic mutation of PRNP
  • ? exposure to unidentified source
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27
Q

What are the clinical features of variant CJD?

A

Painful sensory disturbance + neuropsychiatric decline

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28
Q

What is the duration of illness of variant CJD?

A

14 months

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29
Q

What causes variant CJD?

A

Exposure to BSE (Bovine spongiform encephalopathy) (or comnaminate d blood)

30
Q

What are the clinical features of iatrogenic CJD?

A

Cerebellar/visual onset

Multifocal neurological decline

31
Q

What is the duration of iatrogenic CJD?

A

< 2 years

32
Q

What causes iatrogenic CJD?

A

99% hGH+ dura mater

33
Q

What are the clinical features of genetic CJD?

A

May mimic sporatic CJD

Specific subtypes;

  • GSS (prolonged ataxic syndrome)
  • FFI (insomnia)
34
Q

What is the duration and cause of genetic CJD?

A

Variable <2 years

Mutation of PRNP

35
Q

What is alzheimers disease?

A

Neurodegenerative proteinopathy

36
Q

Describe the pathogenesis of alzheimer’s disease?

A

Disruption of cholinergic pathways in the brain + synaptic loss: extracellular amyloid plaques (? disrupts normal cell function/ induces apoptosis)

Intracellular neurofibrillary tangles (?disruption of cytoskeleton -> cell death)

37
Q

Why do symptoms progress from forgetfulness in alzheimers disease?

A

Degeneration of medial hippocampus + later parietal lobes: forgetfulness -> apraxia/visuospatial difficulties

38
Q

What age defines early onset alzheimers

A

65

39
Q

What are the atypical presentations of alzheimers disease?

A

Posterior cortical atrophy

  • visuospatial disturbance
  • commonly referred from ophthalmology

Progressive primary aphasia

  • semantic (naming)
  • logopenic aphasia (repeating)
  • non-fluent aphasia (effortful)
40
Q

What are the investigations for alzheimers disease?

A

MRI: atrophy of temporal/parietal lobes

SPECT: temporoparietal (decreased metabolism)

CSF: Decreased amyloid : increased tau ratio

Research: amyloid ligand imaging

41
Q

What is the treatment for alzheimers disease?

A

Address vascular risk factors

Acetylcholine boosting Rx

  • cholinesterase inhibitors (eg rivastigmine/galantamine)
  • NMDA receptor blocker (eg memantine)
42
Q

What is frontotemporal dementia?

A

early onset dementia <65 years old

Neurodegenerative proteinopathy

43
Q

What is the pathophysiology of frontotemporal dementia?

A

Tau > TDP-43 > ubiquitin

Protein aggregation –> cell damage

44
Q

What are the early frontal features of frontotemporal dementia?

A
  • disinhibition, apathy, loss of empathy, stereotyped or compulsive behaviours, hyperorality)
  • early loss of insight (collateral history vital)
45
Q

What are the investigations for frontotemporal dementia?

A

MRI: atrophy of frontotemporal lobes

SPECT: frontotemporal decreased metabolism

CSF: increased tau/normal amyloid

46
Q

What is the treatment for frontotemporal dementia?

A

Trial of trazadone/antipsychotics to help behavioural features

47
Q

Describe unique features of management of FTD?

A

Safety management

  • controlled access to food/money/internet
  • structured activities

Power of attorney

  • support: MND nurse specialise if co-existent MND/CPN
48
Q

Vascular dementia is typically a ___ onset dementa (>__years old)

The core criteria are (2)

A

Vascular dementia is typically a late onset dementa (>65 years old)

The core criteria are;

  1. Presence of cerebrovascular disease
  2. A clear temporal relationship between the onset of dementia and cerebrovascular disease
49
Q

What are the different presentations of vascular dementia

A

Subcortical

Post-stroke dementia

50
Q

What is subcortical vascular dementia?

A

Small vessel disease: decreased attention, excecutive dysfunction and slowed processing

51
Q

What may occur alongside vascular dementia

A

Co-existent amyloid pathology

52
Q

What is the management of vascular dementia?

A

Vascular risk factors +/- cholinesterase inhibitor

CPN

53
Q

Dementia with Lewy bodies is a ____ onset dementia (majority >__yrs)

It is also neurodegenerative proteinopathy;

_-_____ aggregates = insoluble -> cell ______ -> cell _____

Leads to disruption of ______ and _________ pathways

A

Dementia with Lewy bodies is a late onset dementia (majority >65 yrs)

It is also neurodegenerative proteinopathy;

alpha-synuclein aggregates = insoluble -> cell dysfunction -> cell damage

Leads to disruption of cholinergic and dopaminergic pathways

54
Q

What are the core criteria of dementia with lewy bodies?

A

1) Fluctuating cognition
2) recurrent well-formed visual hallucinations

+/- 3) presence of extrapyramidal features (75%)

Additional: neuroleptic sensitivity

55
Q

What are the investigations for dementia with lewy bodies?

A

DaT (dopamine transporter imaging)

New (research) techniques: alpha-synuclein ligand imaging / alpha- synuclein in CSF

56
Q

What is the treatment for dementia with Lewy bodies?

A

Small dose levodopa / decreased acetylcholine (amongst other neurotransmitters) -> trial cholinesterase inhibitors

57
Q

What is parkinsons disease dementia?

A

Late onset dementia (>65 years old)

80% Develop dementia after 20 years of PD

58
Q

DLB __ year of presentation

PDD __ year of presentation

A

DLB <1 year of presentation

PDD >1 year of presentation

59
Q

What is the management of PDD?

A

The same as DLB

60
Q

Huntington’s disease is an _____ onset dementia (mean age of onset is __-__ years)

A

Huntington’s disease is an early onset dementia (mean age of onset is 30-50 years)

61
Q

What causes huntingtons disease?

A

Expanison of the CAG trinucleotide repeat on the huntingin gene - produces neurodegenerative protein huntingtin

62
Q

Describe huntingtons dementia

A

Dysexecutive syndrome + slowed speed of processing

Eventual involvement of memory

Associated changes in mood/personality, and chorea +/- psychosis

63
Q

What are the investigations for HD?

A

Genetic testing

MRI- loss of caudate heads

64
Q

What are the treatment options for HD?

A

Mood stabilisers

Rx for chorea

HD nurse specialist

65
Q

- Referral?

1 ) >65 years old gradual onset dementias / no additional neurology

2 ) <65 years old / any unusual features (including speed of onset) / additional neurology

A
  1. old age psychiatry
  2. neurology
66
Q

what history is taken in neurology memory clinic?

A

History from patient

Collateral history: What were the first deficits; what has happened since then; what are their functional difficulties

67
Q

What cognitive assesement is undergone in neurology memory clinic?

A

Addenbrooke’s cognitive assessment

68
Q

What imaging is done in neurology memory clinic?

A

MRI (patterns of atrophy)

SPECT

69
Q

What bloods are taken in neurology memory clinic?

A

‘Dementia screen’ – B12, TFTs, syphilis, HIV, Ca2+ etc(+/- genetic panel)

70
Q

What is done in neuropsyhcology at neurology memory clinic?

A

more in depth assessment of deficits / strengths (for management strategies)

71
Q

What is checked for in CSF in neurology memory clinic?

A

Amyloid/tau/+/- prion

Neurology (41 decks)

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