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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
What is the commonest form of CJD?
Sporadic
26
What causes sporadic CJD?
* ? erroneous production of PrPSc * ? Somatic mutation of PRNP * ? exposure to unidentified source
27
What are the clinical features of variant CJD?
Painful sensory disturbance + neuropsychiatric decline
28
What is the duration of illness of variant CJD?
14 months
29
What causes variant CJD?
Exposure to BSE (*Bovine spongiform encephalopathy*) (or comnaminate d blood)
30
What are the clinical features of iatrogenic CJD?
Cerebellar/visual onset Multifocal neurological decline
31
What is the duration of iatrogenic CJD?
\< 2 years
32
What causes iatrogenic CJD?
99% hGH+ dura mater
33
What are the clinical features of genetic CJD?
May mimic sporatic CJD Specific subtypes; * GSS (prolonged ataxic syndrome) * FFI (insomnia)
34
What is the duration and cause of genetic CJD?
Variable \<2 years Mutation of PRNP
35
What is alzheimers disease?
Neurodegenerative proteinopathy
36
Describe the pathogenesis of alzheimer's disease?
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
Why do symptoms progress from forgetfulness in alzheimers disease?
Degeneration of medial hippocampus + later parietal lobes: forgetfulness -\> apraxia/visuospatial difficulties
38
What age defines early onset alzheimers
65
39
What are the atypical presentations of alzheimers disease?
**Posterior cortical atrophy** - visuospatial disturbance - commonly referred from ophthalmology **Progressive primary aphasia** - semantic (naming) - logopenic aphasia (repeating) - non-fluent aphasia (effortful)
40
What are the investigations for alzheimers disease?
**MRI**: atrophy of temporal/parietal lobes **SPECT**: temporoparietal (decreased metabolism) **CSF**: Decreased amyloid : increased tau ratio **Research**: amyloid ligand imaging
41
What is the treatment for alzheimers disease?
Address vascular risk factors Acetylcholine boosting Rx - cholinesterase inhibitors (eg rivastigmine/galantamine) - NMDA receptor blocker (eg memantine)
42
What is frontotemporal dementia?
early onset dementia \<65 years old Neurodegenerative proteinopathy
43
What is the pathophysiology of frontotemporal dementia?
Tau \> TDP-43 \> ubiquitin Protein aggregation --\> cell damage
44
What are the early frontal features of frontotemporal dementia?
- disinhibition, apathy, loss of empathy, stereotyped or compulsive behaviours, hyperorality) - early loss of insight (collateral history vital)
45
What are the investigations for frontotemporal dementia?
MRI: atrophy of frontotemporal lobes SPECT: frontotemporal decreased metabolism CSF: increased tau/normal amyloid
46
What is the treatment for frontotemporal dementia?
Trial of trazadone/antipsychotics to help behavioural features
47
Describe unique features of management of FTD?
Safety management - controlled access to food/money/internet - structured activities Power of attorney - support: MND nurse specialise if co-existent MND/CPN
48
Vascular dementia is typically a ___ onset dementa (\>\_\_years old) The core criteria are (2)
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
What are the different presentations of vascular dementia
Subcortical Post-stroke dementia
50
What is subcortical vascular dementia?
Small vessel disease: decreased attention, excecutive dysfunction and slowed processing
51
What may occur alongside vascular dementia
Co-existent amyloid pathology
52
What is the management of vascular dementia?
Vascular risk factors +/- cholinesterase inhibitor CPN
53
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
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
What are the core criteria of dementia with lewy bodies?
1) Fluctuating cognition 2) recurrent well-formed visual hallucinations +/- 3) presence of extrapyramidal features (75%) Additional: neuroleptic sensitivity
55
What are the investigations for dementia with lewy bodies?
DaT (dopamine transporter imaging) New (research) techniques: alpha-synuclein ligand imaging / alpha- synuclein in CSF
56
What is the treatment for dementia with Lewy bodies?
Small dose levodopa / decreased acetylcholine (amongst other neurotransmitters) -\> trial cholinesterase inhibitors
57
What is parkinsons disease dementia?
Late onset dementia (\>65 years old) 80% Develop dementia after 20 years of PD
58
DLB __ year of presentation PDD __ year of presentation
DLB \<1 year of presentation PDD \>1 year of presentation
59
What is the management of PDD?
The same as DLB
60
Huntington's disease is an _____ onset dementia (mean age of onset is \_\_-\_\_ years)
Huntington's disease is an early onset dementia (mean age of onset is 30-50 years)
61
What causes huntingtons disease?
Expanison of the CAG trinucleotide repeat on the huntingin gene - produces neurodegenerative protein huntingtin
62
Describe huntingtons dementia
Dysexecutive syndrome + slowed speed of processing Eventual involvement of memory Associated changes in mood/personality, and chorea +/- psychosis
63
What are the investigations for HD?
Genetic testing MRI- loss of caudate heads
64
What are the treatment options for HD?
Mood stabilisers Rx for chorea HD nurse specialist
65
**- Referral?** 1 ) \>65 years old gradual onset dementias / no additional neurology 2 ) \<65 years old / any unusual features (including speed of onset) / additional neurology
1. old age psychiatry 2. neurology
66
what history is taken in neurology memory clinic?
History from patient Collateral history: What were the first deficits; what has happened since then; what are their functional difficulties
67
What cognitive assesement is undergone in neurology memory clinic?
Addenbrooke's cognitive assessment
68
What imaging is done in neurology memory clinic?
MRI (patterns of atrophy) SPECT
69
What bloods are taken in neurology memory clinic?
‘Dementia screen’ – B12, TFTs, syphilis, HIV, Ca2+ etc(+/- genetic panel)
70
What is done in neuropsyhcology at neurology memory clinic?
more in depth assessment of deficits / strengths (for management strategies)
71
What is checked for in CSF in neurology memory clinic?
Amyloid/tau/+/- prion

Neurology (41 decks)

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