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Clinical & Neuropsychology 2 > NP: Lecture 9 Dementia I > Flashcards

NP: Lecture 9 Dementia I Flashcards

1
Q

2 ways to look at normal cognitive aging

A

biological perspective & multidimensional perspective

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2
Q

crystallized intelligence

A

skills, abilities and knowledge that are overlearned, well practiced and familiar.
vocab and grammar
remains stable or improves with age

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3
Q

fluid intelligence

A

abilities involving problem-solving and reasoning.
processing speed and executive functioning
declines with normal aging

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4
Q

dus welke vorm van iq declines with age

A

fluid intelligence (problem solving)

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5
Q

welke vorm van iq remains stable of wordt beter over time

A

crystallized intelligence

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6
Q

kijken naar model crystallized iq en fluid

A

oke

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7
Q

wannner is fluid op het beste

A

rond 20 jaar

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8
Q

processing speed: crystallized or fluid, and decline?

A

fluid, yes

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9
Q

attention: crystallized or fluid, and decline?

A

fluid, simple tasks do not decline, complex tasks do decline

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10
Q

memory: crystallized or fluid, and decline?

A

fluid, mixed

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11
Q

language: crystallized or fluid, and decline?

A

meer crystallized dan fluid

in general no, visual confrontation naming, cerbal fluency does decline

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12
Q

visuospatial: crystallized or fluid, and decline?

A

mixed crystallized and fluid
simple tasks: no, complex tasks: yes

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13
Q

executive function: crystallized or fluid, and decline?

A

fluid, mixed

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14
Q

wat aspects of memory decline with age

A

delayed free recall (spontanous retrieval of info without a cue)
source memory (knowing the source of information)
prospective memory (remembering to perform actions in the future)

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15
Q

what aspects of memory remain stable with age

A

recognition memory (dus ability to retrieve info with a cue)
temporal order memory: memory for the correct time or sequence of past events
procedural memory: memory of how to do things

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16
Q

normal cognitive aging: structural changes

A

cortical thinning and gray matter shrinks
decreased white matter density (vooral frontal & occipital)
loss of dopaminergic receptors

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17
Q

waar leidt loss of dopaminergic receptors toe

A

attentional dysregulation
executive dysfunction
difficulty with contextual processing

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18
Q

scaffoling theory of cognitive aging model bekijken + wat is scaffolding?

A

“Scaffolding,” which is essentially a form of neuroplasticity, enables people to compensate for age-related cognitive decline through the recruitment of alternative brain regions or the generation of new brain cells.

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19
Q

protective factors for healthy aging

A

Active and healthy lifestyle
Cognitive and social stimulation
Limit cardiovascular risk

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20
Q

dementia =

A

Condition characterized with loss of cognitive functioning and
behavioral abilities which interferes with a person’s daily life
and activities

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21
Q

hoe heet dementia in dsm 5

A

major neurocognitive disorder

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22
Q

major neurocognitive disorder dsm 5

A

significant cognitive decline from previous level, in one or more cognitive domains.

  1. concern of person or surrounding, 2. decline needs to be documented and quantified.

interfere with independence
do not occur exclusively in context of a delirium

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23
Q

age > 65 years dementia prevalences

A

ad 54%
vad 16%
dlb 5%
ftd 2%
other 23%

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24
Q

age < 65 years

A

ad 34%
vad 18%
ftd 12%
alcohol related 10%
dlb 7%
hd 5%
other 14%

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25
Q

general risk factors dementia

A

age
female gender
low education
lazy lifestyle
cardiovascular risk factors
brain injury

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26
Q

alzheimers disease

A

neurodegenerative, progressive brain disorder
most common type
most distinctive symptom; memory impairment
1/9 individuals > 65 year
incidence increases with advancing age

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27
Q

prevalence alzheimers in europe

A

5%

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28
Q

gender alzheimers

A

women more than men

29
Q

one new case of dementia every …

A

3 seconds

30
Q

wat wordt geconsidered als early-onset ad

A

<65 jaar

31
Q

inherited forms of ad =

A

rare, caused by mutation. usually onset before 50 years

32
Q

welke genen kunnen tot inherited ad leiden

A

mutations in APP, PS-1 and PS-2

33
Q

ad onset bij downs syndrome

A

onset 10-20 years earlier than in the general population

34
Q

3 changes of ad in the brain

A

shrinkage of cortex
enlarged ventricles
shrinkage of hippocampus

35
Q

amyloid plaques =

A

insoluble threads of misfolded amyloid protein in the spaces between nerve cells

36
Q

neurofibrillary tangles =

A

twisted strands of mutated tau proteins inside nerve cells

37
Q

hoe ga je van app naar amyloid

A

abnormal APP cleavage - AB depositon - senile plaques - neurodegeneration - ad

38
Q

criticsm of amyloid cascade hypothesis

A
  • lack of evidence
  • not clear if plaques and tangles are a cause or consequence of AD
  • no effective treatment with this
39
Q

vascular hypothesis evidence

A
  • typical ad pathology is observed with cerebrovascular damage
  • inadequate blood flow to brain (= brain hypoperfusion) is likely involved in the pathogenesis
40
Q

wat is de vascular hypothesis

A

advanged ageing and vascular risk factors - brain hypoperfusion - neuroglial energy crisis - mild cognitive impairment - neurodegeneration - ad

41
Q

criticism vascular hypothesis

A
  • unclear wether the vascular component of ad is cause or effect
  • unclear if typical ad pathology and vascular pathology are unrelated or related
42
Q

3 stages of diagnostic criteria of AD

A

syndrome diagnosis
specific diagnosis
definite diagnosis

43
Q

syndrome diagnosis=

A

dementia present or not

44
Q

specific diagnosis =

A

probable ad or not

45
Q

definite diagnosis

A

neuropathological characteristics of ad -> post mortem

46
Q

specific diagnosis stages

A
  • probable ad dementia
  • probable ad dementia with increased level of certainty
  • possible ad dementia
  • probable or possible ad dementia with evidence of ad pathophysiological process
47
Q

probable ad

A

neurocognitive presentation, gradual onset and worsening of cognitive deficits and functioning

48
Q

probable ad dementia with increased level of certainty

A
  • documented progressive cognitive decline
  • genetic mutation (APP, PS-1, PS-2)
49
Q

possible ad dementia

A

atypical course
mixed presention

50
Q

probable or possible AD dementia with evidence of AD pathophysiological process

A

Evidence from biomarkers

51
Q

biomarkers=

A

A (medical) sign that can be used as an objective indication of medical
state observed from outside the patient, which can be measured
accurately and reproducibly.

medical signs =/= medical symptoms

52
Q

definite diagnosis =

A

A definite diagnosis can only be made post-mortem when neuropathological characteristics of AD have been demonstrated during an autopsy.

53
Q

agreement between clinical and autopsy diagnosis =

A

80%

54
Q

hoe diagnosticeren ze nu ad

A

Currently, the clinical diagnosis (specific diagnosis) is based on the
(medical) history of patient, clinical examination, neuroimaging (CT,
MRI or PET) and neuropsychological testing.

55
Q

neuropsychiatric symptoms of AD

A
  • Depression
  • Anxiety
  • Apathy, social disengagement and/or irritability
  • Psychosis (including hallucination and/or delusions)
  • Agitation, aggression and/or wandering
  • Motor unrest
  • Sleeping problems
  • Eating problems
56
Q

other symptoms of AD

A
  • Olfactory dysfunction
  • Seizures (10-20% of cases, usually in later stages of disease)
  • Motor signs (typically in later stages of disease)
57
Q

wat is de prognosis bij older age of onset

A

older age of onset is slower late of decline. dus latere onset is beter! jongere onset is slechter.

58
Q

what about prognosis and neuropsychiatric symptoms

A

neuropsychiatric symptoms = faster rate of decline

59
Q

high level of education prognosis

A

later onset, but faster rate of decline

60
Q

life expectancy after AD diagnosis =

A

8-10 jaar

61
Q

medication to inhibit cognitive symptoms bij AD

A
  • Cholinesterase inhibitors (for patients with mild to moderate AD)
  • N-Methyl D-aspartate (NMDA) antagonist (for patients with moderate to severe AD)
62
Q

psycho treatment bij ad

A

psychoeducation
cognitive training
manage behavioural symptoms

63
Q

criteria for mci

A

cognitive concern
objective evidence
nog steeds independence
not demented

64
Q

prevalence of MCI > 60 years

A

rond de 20%

65
Q

protective factors for mci

A

zelfde als ad: active and healthy lifestyle ,cognitive and social
stimulation, limit cardiovascular risk

66
Q

subtypes of mci

A

memory loss -> amnestic MCI -> single domain or multiple domain

absence of memory impairment -> non amnestic MCI -> single domain or multiple domain

67
Q

mci progression

A

20% reversion to normal cognition
30-55% remains stable
20-40% progression to dementia (first year: 10-15% per year)

68
Q

reversion to normal cognition bij wie?

A

Younger age, male sex, single domain MCI, absence of medical conditions, lower level of education

69
Q

progression to dementia bij wie

A

Severity of underlying pathology and cerebral dysfunction (e.g., degree of functional impairment at time of diagnosis) + neuroimaging abnormalities (e.g., hippocampal atrophy)

Clinical & Neuropsychology 2 (30 decks)

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