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Neuro > 12. Dementia > Flashcards

12. Dementia Flashcards

1
Q

what is the typical progression to dementia

A

normal age-related decline –> subjective cognitive decline –> mild cognitive impairment –> dementia

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2
Q

Outline normal age related decline:

A

our thinking skills peak between mid 20s and early 30s (they decline at an increased rate after our 60s)

lifelong declines (skills that decline right after they peaking in their early 30s) - processing speed, working memory, encoding of new information

late life declines (skills that are maintained pretty well till at least the 60s) - general knowledge and semantic memory, word finding

lifelong stability (these remain really good even in the context of normal aging) - autobiographical memory, emotional processing, procedural memories

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3
Q

How much of the population between 65-74 report memory problems?

A

Half

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4
Q

What is subjective cognitive decline?

A

Older adult’s perceived experience of decline in cognition despite cognitive testing and daily functioning showing no evidence of objective cognitive impairment.

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5
Q

Prevalence of subjective cognitive decline?

A

1/4 of people over 60

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6
Q

Criteria for SCD

A
  • subjective experience of decline in cognitive capacity (unrelated to an acute event)
  • normal age, gender and education adjusted performance on standardized cognitive tests used to classify mild cognitive impairment

Exclusion criteria;
- can’t meet criteria for mild cognitive impairment / dementia / prodromal AD
- can’t be explained by medication

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7
Q

Outline the progression of Subjective Cognitive Decline:

A
  • Most people with SCD will not show progressive cognitive decline, but they are at greater risk of developing MCI and dementia than those who don’t have SCD
  • 27% of people with SCD progress to MCI
  • 14% of people with SCD progress to dementia (but SCD starts 10-15 years before dementia diagnosis)
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8
Q

What factors predict progression of SCD to MCI and dementia

A
  • subject decline in memory (irrespective of function in other cognitive domains)
  • onset of SCD in last 5 years rather than longer ago
  • onset of SCD at or after 60 years of age
  • concerns and worry associated with SCD
  • persistence of SCD over time
  • seeking of medical help
  • confirmation of cognitive decline by an observer
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9
Q

How to manage SCD

A
  • reassure individual that their cognition is intact on objective assessment and a good baseline has been established if they have concerns about further cognitive decline
  • most people with SCD will not experience objective cognitive decline in near future
  • strategies to help promote healthy brain ageing
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10
Q

What is mild cognitive impairment?

A
  • Cognitive decline greater than expected for age / education but does NOT interfere with daily life
    –> (note: can be normal for their age but inconsistent with their premorbid functioning)
  • increased risk of progressing to dementia
  • high cognitive functioning people tend to function at a reasonable level for a much longer time (brain can withstand effects of pathology for a while)

NOT a transitional state between normal aging and dementia –> 1/3 of people’s MCI is caused by something reversible (mood disorder, side effects of medication)
- 20% of people with MCI have stable MCI
- 40^ of people with MCI develop dementia

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11
Q

What is the prevalence of MCI and conversion to dementia rates?

A
  • 11-17% in population based studies
  • vary from 3-27% of >65 years

Only 1/3 go onto develop dementia
- of clinical samples, 10-15% convert to dementia
- of community based samples, 6-10% of people transition to dementia

Note: MCI with depression doubles risk of converting to dementia

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12
Q

What are predictions of MCI conversion to dementia?

A
  • advanced age, lower education
  • cerebrovascular risks + white matter loss
  • family history of dementia
  • neuropsych: delayed recall deficits and exec dysfunction
  • informant reports of cognitive decline
  • depression, apathy
  • reduced insight
  • subtle functional changes (especially hobbies and finance)
  • biomarkers (atrophy in medial temporal lobe)
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13
Q

What are the differences between the original diagnostic criteria and current diagnostic criteria for MCI?

A

Original: focused on memory
- Having subjective concerns about memory
- memory deficits

Current:
- person is not normal but not demented (performance 1-1.5 SD below premorbid baseline)
- some subjective concerns
- evidence of some decline on cognitive tests
- remain independent in day to day functioning

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14
Q

What are the subtypes of Mild Cognitive Impairment?

A

Amnestic = issues with memory
Non-amnestic = no issues with memory

Based on neuropsychological assessment

Amnestic:
- just memory problems = Amnestic Single Domain MCI
- other problems = Amnestic Multiple Domain MCI

Non-amnestic
- don’t have memory problems, but only one cognitive domain impacted = Non-amnestic single domain MCI
- more than one domain impacted = non-amnestic multi domain MCI

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15
Q

Why is the aetiology of MCI important?

A

Helps us predict which of the 3 groups of MCI someone might fall into

Non-amnestic single domain with attention issues –> likely to not get worse over time
Amnestic multi-domain cognitive impairment with language - more likely to progress onto dementia through alzheimer’s

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16
Q

Management of mild cognitive impairment:

A
  • drugs don’t help, but cognitive interventions are more helpful
  • RCTs using cognitive training in MCI: significant cognitive / psychosocial improvements (particularly in memory) –> potential capacity to prevent conversion to dementia?
  • psychoeducation regarding modifiable risk factors (i.e. change in lifestyle factors like smoking, alcohol, more exercising, brain stimulation, etc), e.g. wiseminds
  • planning ahead: they can still make decisions for themselves so its a critical time for them to express their wishes and financially plan
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17
Q

What is dementia?

A

Umbrella term used to describe a range of progressive neurodegenerative disorders

Characterised by cognitive or behavioural impairments AND functional decline

One of the most common diseases affecting older adults - and is assisted with significant healthcare and socioeconomic costs

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18
Q

What is the prevalence of dementia?

A

Worldwide:
- 47 million people living with dementia
- predicted to be 131.5 million by 2050

In Australia
- 472 000 people living with dementia in 2021
- predicted to be 590 000 by 2028 and 1 million by 2058
- 3/10 people >85 and almost 1/10 >65 have dementia
- 250 people are joining the population with dementia each day

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19
Q

What is the socioeconomic burden of dementia?

A

Formal/direct costs of medical and social care:
- average yearly healthcare costs for dementia patients is 3x greater than those of the same age without dementia
- worldwide, the global costs of dementia are estimated to cost > $15 billion in 2018 (predicted to increase to 37 billion by 2056)

Informal / indirect costs of unpaid care
- 2012: unpaid caregivers provided 17.5 billion hours of assistance (sig. increases in stress, depression, physical health problems)

20
Q

What are the criteria for dementia?

A

A. Significant cognitive decline from previous level of performance in 1+ cognitive domains (complex attention, exec function, learning and memory, language, perceptual motor, social cognition) based on:
- concern from knowledgeable informant or clinician AND
- substantial impairment in performance documented by standardised testing

B. Cognitive deficits interfere with independence in everyday activities

C. cognitive deficits do not occur exclusively in context of delirium

D. cognitive deficits are not better explained by another mental disorder

21
Q

Management of dementia:

A

Pharmacological treatments
- Alzheimer’s specific
- behaviour management: anxiety, aggression, delusions / hallucinations

Behaviour management
- common in nursing homes
- behaviour support plans

Increased level of care
- providing transport
- offering respite / nursing home

Cognitive intervention programs are useless - instead we want to manage and slow down progression

22
Q

What does ‘risk factor reduction’ include for people with dementia?

A

Often has to happen before someone is diagnosed with dementia
- strongest risk factor: previous traumatic brain injuries (exposed to explosive blasts, concussion)
- moderate risk factor: mid-life obesity, mid-life hypertension, current smoking, diabetes
- small: history of depression, sleep disturbances, hyper-lipidemia

23
Q

What are protective factors for dementia/

A

Strongest: years of education (in early life)
Moderate: physical activity
Less: Mediterranean diet and cognitive training
Smallest: moderate alcohol consumption, social engagement

24
Q

Risk factor reduction for dementia: what should we be focussing on at different stages of life?

A

Mid-life: treating hearing loss (hearing loss reduces stimulation, impacts memory and makes the individual become more disengaged) and TBI, high blood pressure, excessive alcohol consumption, obesity

Later life: smoking, depression, social isolation, physical inactivity, airpollution

25
Q

What are the subtypes of dementia?

A

Alzheimer’s disease (AD)
Vascular dementia (VaD)
Mixed dementia
Frontotemporal dementia (FTD)
Lewy Body dementia
Parkinson’s disease dementia

pathology in brain starts 10-15 years before obvious symptoms

26
Q

Comorbid pathology of dementia:

A
  • Most common = AD and Vascular –> those with AD and vascular brain changes will develop dementia earlier and decline faster
  • AD also often co-occurs with Lewy Bodies
27
Q

When is the best time to be able to diagnose dementia types?

A

When they get to the stage of dementia- their subtype is the clearest - but if you leave it too far, they all blur together because the deficits become global.

Subtypes may not matter to the patient.

28
Q

Outline Alzheimer’s disease

A
  • Most common type of dementia (approx 50% of all dementia cases)
  • onset typically after age 65 (earlier onset is usually related to genetic mutation)
  • average age at diagnosis is 75

Onset is gradual (insidious)

Typical AD presentation: primary memory impairment with later deterioration of other cognitive domains and functional decline.

Atypical ad presentation: language, visuospatial or frontal variants

29
Q

What is the prevalence of Alzheimer’s

A

4.4% of > 65 (other estimates are 1/8 people > 65)
- chances of getting it doubles every 5 years after the age 60

30
Q

What are the risk factors for alzheimer’s disease?

A
  • advancing age
  • family history
  • APP and presenlin genetic mutations
  • apolipoprotein E allele
  • down’s syndrome
  • vascular risk factors
  • head trauma
  • low education and intelligence
  • sedentary lifestyle
  • excess alcohol consumption
31
Q

What is the neuropathology underlying Alzheimer’s disease?

A

Senile / amyloid plaques
- abnormal accumulation of clumps of amyloid protein outside the neuron (interfering with communication between neurons and contributing to cell death)

Neurofibrillary tangles
- abnormal accumulations of tau protein inside neurons blocking transport of nutrients and essential molecules inside neurons contributing to cell death

What determines the presentation of AD is where in the brain these processes start.
Typical presentation = memory issues - pathology starts in hippocampi, followed by medial temporal lobe

32
Q

Outline the time delay of Alzheimer’s pathology

A

Appearance of plaques tends to occur 10-15 years before impacting cognition

The lag is even greater at younger ages
- when researchers looked at brains of autopsies, there were brains with these plaques who never had dementia
- and people with alzheimer dementia who never had these plaques

When we assess someone clinically, we should not say they have alzheimer’s disease but instead alzheimer’s clinical syndrome

33
Q

How do we diagnose alzheimer’s?

A
  • gradual (insidious) onset
  • clear history of deteriorating cognition reported by them or family member
  • objective cognitive decline (amnestic or non-amnestic)
  • evidence of biomarkers (further enhances this diagnosis)
  • is it typical or mixed (mixed could be meeting these criteria but features of lewy body dementia, concomitant cerebrovascular disease)
34
Q

Outline the cognitive profile of alzheimer’s disease?

A

Memory changes typically occur early in disease process:
- primarily storage deficit (rapid forgetting on testing)
- difficulty laying down new memories from time of illness onset due to storing difficulties
- memory loss is temporally graded
- temporal disorientation

Language:
- anomia (word finding difficulties)
- semantic fluency worse than letter fluency

Visuospatial deficits
- difficulties with construction and spatial orientation

Apraxia: inability to perform learned motor acts - occurring in later stages
Possible subtle executive dysfunction

Intact:
- attention, working memory, processing speed

35
Q

Outline vascular cognitive impairment

A
  • cognitive impairment resulting from conditions that affect cerebral circulation
  • 2nd most common cause of dementia (20% of all dementia cases)
  • onset can be insidious or abrupt
  • prevalence increases with age
  • 1/3 dementia cases demonstrate substantial vascular pathology at autopsy
36
Q

Outline the neuropathology behind vascular cognitive impairment:

A
  • stroke
  • transient ischaemic attacks
  • subcortical ischaemic vascular disease (lacunar strokes deep in white matter)
  • hereditary vascular disease
37
Q

What are the criteria for vascular cognitive impairment?

A
  • Must have had at least 1 stroke and a stepwise decline after that
  • Almost always has fronto-subcortical pattern of deficits (processing speed, attention, working memory, executive function)
  • If no stroke, they need to have numerous vascular risk factors (and white dots in brain)
  • temporal association between stroke symptoms and decline
  • more likely to have behavioural issues and more prone to depression
38
Q

Outline the cognitive profile of someone with vascular cognitive impairment

A

Cognitive pattern is frontosubcortical:
- impaired attention, working memory, processing speed
- memory characterised by poor encoding and retrieval, but not forgetting (i.e. bad at list learning task but good with recognition)
- executive dysfunction (disorganised, can’t plan well)
- increased prevalence of behavioural and mood symptoms

Intact:
- language skills and visuospatial skills (unless there’s been a stroke in this area)

39
Q

Outline dementia with lewy bodies

A

Lewy body disease causes brain atrophy leading to a range of physical, cognitive and behavioural symptoms.

M age of onset: 67 years (much younger than others)

Course = more rapidly progressive than AD

40
Q

Outline the neuropathology of dementia with lewy bodies

A

Lewy bodies: microscopic structures seen inside some of the brain cells, composed of a protein called alpha-synuclein that becomes disrupted and tangled

Lead to gradual loss of brain cells resulting in changes in movement, cognition, and behaviour.

Cortical degeneration, particularly in the temporal and parietal lobes.

Degeneration and loss of dopaminergic cells in basal ganglia (midbrain - movement, parkinsonian presentation of a tremor, slow shuffled gait, loss of balance)

41
Q

What are the key criteria of Lewy Bodies Dementia

A

Fluctuating cognition: sometimes seems completely normal, other times, demented

Visual hallucinations: usually well-formed hallucinations (seeing animals / people)

REM sleep disorder: disruption of aspect in sleep cycle (very active in their sleep)

Parkinson’s / Movement symptoms: tremor, rigid (especially with their trunks)

42
Q

Outline the cognitive profile of dementia with lewy bodies

A
  • disproportionate visuospatial deficits (impaired block design, figure copying, clock drawing)
  • severe psychomotor slowing (can’t do trail making test)
  • prominent exec dysfunction
  • attention deficits with prominent fluctuations
  • language and memory can be affected by other cognitive deficits
43
Q

Noncognitive features of dementia with lewy bodies

A

Motor features
- parkinsonian motor disorder: rigidity, bradkynesia (slowness of movement), gait disorder, falls, masked facies (expressionless appearance), hypophonic speech (speaking quietly)

Behavioural:
- depression in 40% of cases
- sleep disturbances

Psychiatric features
- complex visual hallucinations

44
Q

Outline behavioural-variant frontotemporal dementia

A
  • degeneration of frontal and temporal lobes
  • most common form of FTD
  • insidious onset around 55 years of age (young)
  • more rapidly progressive than AD

Fundamental personality changes

45
Q

Outline neuropathology of behavioural-variant frontotemporal dementia

A

2 major subtypes:
- accumulation of abnormal tau protein in frontotemporal lobes leading to nerve cell death
- OR genetic component: accumulation of the transactive DNA binding protein TDP-43 in nerve cells in the frontotemporal lobe leading to nerve cell death (shrinking in frontal lobes)

Atrophy of the pfc and anterior temporal neocortex

46
Q

Diagnosis of behavioural-variant frontotemporal dementia

A

Character change and disordered social conduct:

  • early decline in social interpersonal conduct
    Developing less empathy
    becoming rude / inappropriate
    making comments
    preference of sweets
    rigid
    trouble regulating emotions
    no insight
47
Q

Cognitive profile of behavioural-variant frontotemporal dementia

A
  • marked executive dysfunction
  • exec dysfunction may impact performance on other assessments
  • behavioural observations are important (rely on the interview a lot)

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