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Neurology > Dementia > Flashcards

Dementia Flashcards

1
Q

what is cognition?

A

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

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2
Q

cognition encompasses what?

A 
attention
memory
executive function (problem solving/decision making)
language
social functioning
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3
Q

criteria for dementia?

A

evidence of significant cognitive decline in at least 1 cognitive domain or social cognition
plus - cognitive defects interfere with independence in everyday activities
plus - they are not better explained by another process/do not occur exclusively in context of delirium

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4
Q

is the incidence of dementia increasing or decreasing?

A

decreasing

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5
Q

what can cause acute cognitive dysfunction?

A

brain insult

  • viral encephalitis (memory, behaviour, language change)
  • head injury (attention, memory, executive dysfunction)
  • stroke
  • transient global amnesia
  • transient epileptic amnesia
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6
Q

what is transient global amnesia?

A

cannot lay down new memory
abrupt onset antegrade > retrograde amnesia (repetitive)
preserved knowledge of self

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7
Q

how long does transient global amnesia last?

A

transient (4-6 hours)

always less than 24 hours

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8
Q

what can trigger transient global amnesia?

A

emotion/changes in temperature

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9
Q

what is transient epileptic amnesia?

A

similar to transient global but happens repetitively?
forgetful/repetitive questioning
can carry out complex activities with no recollection of events
associated with temporal lobe seizures
should respond to anti-epileptic medication

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10
Q

differentials for subacute cognitive disorders?

A 
toxins
neurodegeneration
metabolic (B12, calcium, thyroid etc)
inflammatory
mood disorders
functional
infection
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11
Q

describe the functional/subjective cognitive impairment seen in sub-acute cognitive disorders?

A

everyday forgetfulness impacting on functioning
fluctuation of symptoms
mismatch between symptoms and reported function/symptoms and symptoms of known neurodegenerative disorders
may be a part of generalised functional disorder (reduced concentration/attention/reaction time and subsequent memory difficulties)

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12
Q

how is sub-acute cognitive disorder managed?

A

exclude mood disorder

refer to neuropsychology

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13
Q

what is prion disease?

A 
neurodegenerative proteinopathy (prion)
most common type = CJD
abnormally folded prion proteins leads to enurodegeneration
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14
Q

describe the most common form of CJD?

A

sporadic = most common type
rapid onset dementia + neurological signs and myoclonus (twitchy movements)
progresses over few weeks to 4 months
causes death

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15
Q

other types of CJD?

A

variant
iatrogenic
genetic

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16
Q

what is seen on pathology of all types of CJD?

A

spongiform change on pathology

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17
Q

what causes alzheimers?

A 
neurodegenerative proteinopathy (amyloid)
disruption of cholinergic pathways in brain + synaptic loss causes
- extracellular amyloid plaques (disrupts normal cell functioning/induces apoptosis)
- intracellular neurofibrillary tangles (disruption of cytoskeleton leading to cell death)
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18
Q

how does alzheimers progress in most cases?

A

initial symptoms = forgetfulness

degeneration of medial hippocampus + later parietal lobes = forgetfulness > apraxia/visuospatial difficulties later

19
Q

types of alzheimers depending on age?

A 
<65 = early onset (genetic influence)
>65 = sporadic (environmental)
20
Q

describe 2 atypical presentations of alzheimers?

A 
posterior cortical atrophy
- visuospatial disturbance
- commonly referred from ophthalmology
progressive primary aphasia
- semantic (naming difficulty)
- logopenic aphasia (repeating)
- non-fluent aphasia (effortful)
21
Q

how is alzheimers investigated?

A

MRI - shows atrophy of temporal/parietal lobes
SPECT - shows tempoparietal reduced metabolism
CSF - shows reduced amyloid and increased tau ratio
amyloid ligand imaging (new research)

22
Q

how is alzheimers managed?

A

address vascular risk factors
acetylcholine boosting treatment
- cholinesterase inhibitors
- NMDA receptor blocker

23
Q

examples of cholinesterase inhibitors?

A

rivastigmine

galantamine

24
Q

examples of NMDA receptor blockers?

A

memantine

25
Q

what causes frontotemporal dementia?

A

neurodegenerative proteinopathy
- Tau > TDP43 > ubiquitin > protein aggregation > cell damage
25% are genetic, may be part of MND

26
Q

how does frontotemporal dementia present?

A 
early onset (<65)
early frontal features (disinhibition, apathy, loss of empathy, stereotyped or compulsive behaviours, hyperorality)
early loss of insight 
behavioural variant more common than primary progressive aphasia
27
Q

how is frontotemporal dementia investigated?

A

MRI - shows atrophy of frontotemporal lobe
SPECT - frontotemporal reduced metabolism
CSF - increased tau/normal amyloid

28
Q

how is frontotemporal dementia managed?

A

trial trazadone/antipsychotics to help behavioural features
safety management - control access to food/money/internet etc
power of attorney

29
Q

core criteria for vascular dementia?

A

presence of cerebrovascular disease plus a clear temporal relationship between onset of dementia and cerebrovascular disease

30
Q

how does vascular dementia present?

A 
subcortical (small vessel disease)
- reduced attention
- executive dysfunction
- slowed processing
post stroke dementia
can have co-existent amyloid pathology (slow progression, similar prognosis to AD)
31
Q

how is vascular dementia managed?

A

manage vascular risk factors +/- cholinesterase inhibitors

CPN

32
Q

what causes lewy body dementia?

A 
neurodegenerative protienopathy (alpha synuclein)
- alpha synuclein aggregates (insoluble) > cell dysfunction > cell damage > disruption of cholinergic and dopaminergic pathways
33
Q

core criteria of lewy body dementia?

A

fluctuating cognition + recurrent well formed visual hallucinations +/- presence of extramyramidal features (seen in 75%)
may also have neuroleptic sensitvity

34
Q

how is lewy body dementia investigated?

A

DaT (dopamine transporter imaging)

new research = alpha synuclein ligand binding imaging/alpha synuclein in CSF

35
Q

how is lewy body dementia managed?

A

small dose levodopa/ increase acetylcholine (cholinesterase inhibitors)
support from PD nurse specialist

36
Q

describe parkinsons disease dementia

A

late onset
most develop after 20 years of disease
overlaps clinically and pathologically with lewy body

37
Q

features of parkinsons disease dementia?

A

parkinsons (bradykinesia + rigidity + tremor) + dementia (reduced attention + slow processing, impaired visuospatial functions and memory) +/- hallucinations

38
Q

how is parkinsons disease dementia managed?

A

same as lewy body

39
Q

describe huntingtons disease dementia?

A

early onset
dysexecutive syndrome + slowed speed of processing
eventual involvement of memory
associated changes in mood/personality and chorea +/- later psychosis

40
Q

what causes huntingtons disease dementia?

A

expansion of CAG trinucleotide repeat on huntingtin gene produced neurodegenerative protein (huntingtin)

41
Q

how is huntingtons disease dementia investigated and managed?

A 
investigations = genetic, MRI (shows loss of caudate heads)
management = mood stabilisers, Rx for chorea, HD nurse specialist)
42
Q

how can genetics be involved in gradual onset disorders of cognition (dementia)?

A

can be polygenic + environmental (e.g apoe4 in alzheimers)

can be monogenetic inherited disorders

43
Q

where do you refer cognitive dysfunction to?

A

> 65 with gradual onset dementia and no additional neurology = old age psychiatry
<65 with any unusual features

Neurology (53 decks)

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