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Neurology Key Info > Dementia > Flashcards

Dementia Flashcards

1
Q

what is cognition?

A

mental action of acquiring and understanding information

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2
Q

what is dementia?

A

un-doing of the mind

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3
Q

what is the biggest risk factor for dementia?

A

age

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4
Q

causes of acute cognitive decline

A

focal injuries such as viral encephalitis, head injury and stroke

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5
Q

acute cognitive disorder examples

A
  1. transient global amnesia

2. transient epileptic amnesia

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6
Q

what is transient global amnesia?

A

abrupt onset of antegrade amnesia with preserved knowledge of self

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7
Q

presentation of transient global amnesia

A

4-6 hours
antegrade amnesia
>50
triggered by change in temperature or emotion

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8
Q

what is transient epileptic amnesia?

A

associated with temporal lobe seizures causing forgetfulness

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9
Q

management of transient epileptic amnesia

A

AED response

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10
Q

causes of sub-acute cognitive disorders

A 
toxins
metabolic changes
inflammation
mood disorders
infection (HIV, syphilis)
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11
Q

examples of sub-acute cognitive impairments

A
  1. functional/ subjective cognitive impairment
  2. Prion disease
  3. Limbic encephalitis
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12
Q

what is functional/ subjective cognitive impairment?

A

everyday forgetfulness impacting on function
fluctuation in symptoms
exclude mood disorder

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13
Q

what is prion disease?

A

CJD is a neurodegenerative proteinopathy with prion building up in the brain

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14
Q

examples of gradual onset disorders of cognition

A 
Alzheimer's
FTD
vascular dementia
dementia with LB
PD dementia
Huntington's disease
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15
Q

what is the most common form of dementia?

A

Alzheimer’s disease

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16
Q

what is Alzheimer’s disease?

A

neurodegenerative proteinopathy of amyloid which disrupts cholinergic pathways with synaptic loss due to extracellular amyloid plaques

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17
Q

what do intracellular neurofibrillary tangles in Alzheimer’s cause?

A

disruption to the cytoskeleton and cell death

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18
Q

presentation of Alzheimer’s

A

forgetfulness

apraxia primary progressive aphasia

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19
Q

diagnosis of Alzheimer’s

A

screening tests e.g. MOCA
MRI (atrophy in temporal and parietal lobes)
SPECT (reduced metabolism in temporal and parietal lobes)
CSF= low amyloid with high TAU
amyloid ligand imaging

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20
Q

management of Alzheimer’s

A

ACh boosting= cholinesterase inhibitors e.g. rivastigmine or NMDA blocker e.g. memantine
vascular RF

21
Q

adverse of cholinesterase inhibitors such as rivastigmine

A 
D&V
HA
cramps
bradycardia
worsen COPD/ asthma
22
Q

what should be checked before prescribing cholinesterase inhibitors e.g. rivastigmine?

A

pulse and before any dose change

23
Q

when should you not use cholinesterase inhibitors?

A

active peptic ulcer

severe asthma/ COPD

24
Q

adverse of NMDA blocker e.g. memantine

A 
hypertension
sedation
dizziness
HA
constipation
25
Q

what should be checked before starting NMDA blockers e.g. memantine?

A

BP

26
Q

what is FTD?

A

early onset dementia caused by neurodegenerative proteinopathy involving the TAU protein which aggregates and causes cell damage

27
Q

presentation of FTD

A

personality/ behaviour change first, then dementia
primary progressive aphasia
frontal lobe symptoms
MND-FTD spectrum

28
Q

what are some examples of frontal lobe symptoms?

A

disinhibition
apathy
empathy lost
compulsive behaviour

29
Q

3 syndromes of FTD

A
  1. behavioural variant (frontal)
  2. primary progressive aphasia (temporal)
  3. semantic dementia (temporal)
30
Q

behavioural variant of FTD

A 
behaviour change
executive dysfunction
disinhibition
impulsivity
loss of social skills
apathy
obsessions
change in diet
31
Q

presentation of primary progressive aphasia

A

effortful non-fluent speech
speech errors
lack of grammar and words

32
Q

presentation of semantic dementia in FTD

A

impaired understanding of meaning of words
fluent but empty speech
difficulty retrieving names

33
Q

diagnosis of FTD

A

MRI shows atrophy of FT lobes
SPECT has reduced metabolism in FT lobes
CSF= high TAU and normal amyloid
check FH for MND spectrum

34
Q

management of FTD

A

trial of trazadone/ antipsychotics to help behavioural features
safety management with controlled access to food, money, etc.

35
Q

what is vascular dementia

A

late onset dementia >65 with the presence of cerebrovascular disease

36
Q

presentation of vascular dementia

A

memory and personality change in someone with a history of cardiovascular disease
step-wise deterioration
small vessel disease= reduced attention, slowed processing
post-stroke dementia <3 months
dysphasia
dyscalculi

37
Q

management of vascular dementia

A

vascular RF +/- cholinesterase inhibitors

38
Q

what is dementia with lewy bodies?

A

late onset dementia due to neurodegenerative proteinopathy with alpha-synuclein protein

39
Q

what does the alpha-synculein protein in DLB cause?

A

it is an insoluble protein that disrupts cholinergic and dopaminergic pathways leading to Parkinsonian features

40
Q

presentation of DLB

A 
fluctuating cognition
vivid visual hallucinations normally of children and not threatening
REM disturbance
dementia <1 year
TRAP features for <1 year
41
Q

diagnosis of DLB

A

clinical
DaT
protein in CSF or ligand imaging

42
Q

management of DLB

A

levodopa/ reduced ACh (cholinesterase inhibitors)

43
Q

what is PD dementia?

A

late onset and have had PD for a number of years before cognitive decline

44
Q

presentation of PD dementia

A

TRAP features
REM disturbance
dementia >1 year

45
Q

management of PD dementia

A

levodopa/ reduced ACh (cholinesterase inhibitors)

46
Q

what is Huntington’s disease dementia?

A

early onset 30-50 years due to expansion of CAG trinucleotide producing neurodegenerative protein (Huntingtin protein)

47
Q

presentation of HD

A

dementia

associated changes in mood/ personality and chorea +/- psychosis

48
Q

diagnosis of HD

A

genetics

MRI shows loss of caudate heads

49
Q

management of HD

A

mood stabilisers

Rx for chorea

Neurology Key Info (51 decks)

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