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PSY325 - Neuropsychology & Clinical Neuroscience > Week Six - Dementia & Alzheimer's > Flashcards

Week Six - Dementia & Alzheimer's Flashcards

1
Q

What is dementia?

A

An overarching term defining a wide range of memory problems.

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2
Q

What are progressive dementias?

A

A condition that has a continuous/step-wise decline over time

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3
Q

3 forms of progressive dementias?

A

Cortical
Subcortical
Mixed

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4
Q

What are examples of cortical dementia?

A

Alzheimer’s
Pick’s disease
FTD

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5
Q

What are some examples of subcortical dementias?

A

PD

Huntington’s

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6
Q

Who diagnoses dementia?

A

Usually by a geriatrician or neurologist - CNP opinion is essential however as behaviour observation help define type of dementia

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7
Q

What do we need to make a diagnosis?

A 
past/present history
family history
psych assessment/evaluation
brain imaging
other medical testing
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8
Q

What is important for dementia?

A

Early diagnosis

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9
Q

Why is early diagnosis important in dementia for every case?

A

It provides a diagnostic answer and education

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10
Q

Why is early diagnosis important in for patients with reversible or static dementia?

A

To:
Relieve the fear of irreversibility
Treatment
Initiate prevention/rehab

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11
Q

Why is early diagnosis important in for patients with irreversible or progressive dementia?

A

To:
Treat cognitive and behavioural symptoms
Plan legal and financial future while patient still can
Initiate management strategies to postpone dependence

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12
Q

How is dementia reflected in the DSM-5?

A

It is defined as a Neurocognitive Disorder
can be:
- mild or major

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13
Q

Diagnostic criteria for major NCD in dsm-v?

A

A) Evidence of decline from previous level in one + cog domains (must be noted by others and with testing)

B) Deficits must be substantial enough to require assistance (decline in everyday functioning)

C) Deficits do not occur in the context of delirium

D) Deficits are not better explained by another disorder

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14
Q

What diagnosing someone with major CND, you need to do what?

A 
Specify what type/cause
Specify with/without behavioural disturbance and to what extent
Specify severity (mild/moderate)
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15
Q

What is cortical dementia characterised by and what is the progression to subcortical (if any)?

A

It is characterised by preferential neuronal loss to cortical regions of the brain. Involvement in subcortical regions is rare but if it does occur, it won’t be until later stages of the disease course

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16
Q

What is AD?

A

An irreversible cortical progressive dementia

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17
Q

What is the strongest predictor of AD?

A

Age (incidence increases with age) - but there is no identifiable cause

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18
Q

What is the average duration of AD?

A

8-10 years after diagnosis - rarely survive past 15 years

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19
Q

Why might AD symptoms go unnoticed until later?

A

Because the brain is so good at using cognitive reserve to compensate for losses until a certain point

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20
Q

Sporadic Vs Familial AD

A

Sporadic is most common and has a mean age of onset of 80 yrs.

Familial is rare but has an early onset <50 yrs

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21
Q

Where does preferential cell loss occur in AD?

A

In the cortical grey matter of the brain and also in the limbic structures (hippo and amygdala)

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22
Q

What are the 2 key features of AD?

A
  1. Targets specific brain regions

2. Targeted structures sustain massive cell loss

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23
Q

What lobes experience the most cortical atrophy in AD? What % of neurons/cells are lost in these areas and why?

A

Frontal, temporal and parietal

50% of neuronal loss due to loss of dendritic arborisation

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24
Q

What does cortical thinning of the brain result in?

A

Ventricular enlargement

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25
Q

What are the 2 primary markers of AD?

A

Amyloid/senile plaques

Neurofibrillary tangles

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26
Q

What are Amyloid/senile plaques?

A

Clump like deposits, round aggregates of cellular trash.

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27
Q

What two proteins do Amyloid/senile plaques contain?

A

b-amyloid protein and apolipoprotein (ApoE)

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28
Q

What do neurofibrillary tangles resemble?

A

Resemble entwined and twisted pairs of rope

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29
Q

Where are neurofibrillary tangles located?

A

Throughout the brain (temporal and parietal), within the cytoplasm of swollen cell bodies

30
Q

What are neurofibrillary tangles made of?

A

Tau proteins (they become dislodged causing the twists)

31
Q

Where are senile plaques located?

A

In the frontal and temporal regions of the brain and in the hippocampal complex

32
Q

In AD what part of brain is affected initially?

A

The temporal lobe

33
Q

Signs and symptoms associated with AD onset are? (5)

A 
Memory problems (recent)
Depression/irritability
Seizures (occasionally)
Language problems
Disorientation/confusion (due to sudden disruptions eg work, life)
34
Q

What functions are affected in AD?

A

Memory deficits - LT declarative (episodic/semantic, anterograde, increasing retrograde, WM/STM)

Attention deficits

Slowed info processing

Impaired abstract reasoning

Impaired visuospatial skills

Impaired language

Fluent aphasia/apraxia/agnosia

35
Q

In late AD, what happens to speech?

A

Becomes non-fluent, repetitive and largely non-communicative. Many display partial or complete mutism.

36
Q

What can no longer be measured in the end stages of AD and may reemerge?

A

Can no longer measure neuropsychological functions Primitive reflexes such as sucking, grasping

37
Q

What does the progression of AD resemble?

A

A reversal of development from infancy to childhood with high level skills being lost, returning to a reflexive state

38
Q

What are some behavioural and personality changes associated with AD? (7)

A 
clinging to caregiver
easily distracted
disinterest/passive
poor self care
agitation
bursts of violence (decreases with disease progression)
paranoia/suspicious
39
Q

What parts of the brain are affected in FTD?

A

Mostly affects frontal lobe

Atrophy in frontal and temporal lobes with some change in parietal.

40
Q

What parts of the brain are unaffected in FTD?

A

subcortical structures and cerebellum and brain stem

41
Q

What happens in the initial stages of FTD?

A

Silliness, socially disinhibited behavior and poor judgement.

42
Q

What happens in the middle stages of FTD?

A

Characterised by progressive apathy, blunted affect and significant cognitive dysfunction

43
Q

What happens in the late stages of FTD?

A

Patients become more muste and display motor rigidity, ending in a terminal vegetative state

44
Q

What is the disease durations of FTD?

A

2-17 years

45
Q

What % of dementia is FTD

A

12%

46
Q

What are some of the cognitive deficits in those with FTD? (5)

A 
empty speech
dysnomia
dysfluency
executive dysfunction
hyperorality
47
Q

What is Huntington’s Disease?

A

A progressive subcortical dementia that is always fatal

48
Q

HD prevalence and age of onset

A

5-10 in 100,000

onset of symptoms 30-40 yrs

49
Q

What is HD linked to?

A

Gene ITI5 on chromosome 4

50
Q

Is there is cure for HD

A

no known cure or treatment

51
Q

Describe the heritability of HD

A

It is a hereditary condition and is the only known autosomal dominant condition (affecting 50% of all children with one parent with the disorder)

52
Q

Chorea is a symptom of HD, what is it?

A

involuntary, spasmodic and torturous movements that become disabling

53
Q

The primary neuropathological change in HD is what?

A

Bilateral deterioration of the caudate nucleus

54
Q

What neuropathology occurs with disease progression in HD?

A

There is a deterioration of multiple systems involving white matter structures and areas of the cerebellum

55
Q

What is the caudate nucleus?

A

A component of the BG involved in timing, ordering, and sequencing of movement

56
Q

What are some cognitive profiles of HD? (8)

A 
eye movement deficits (delayed)
decreased attention span
memory difficulties
language stays in tact
deteriorating speech production
visuo-spatial orientation impaired
impaired behaviour regulation
depression
57
Q

What is the second largest type of dementia?

A

Multi-infarct vascular dementia

58
Q

MIVD is a result of what?

A

Multiple infarction of brain tissue, from repeated strokes or blockages to blood vessels

59
Q

is MIVD cortical or subcortical?

A

can present with both or combination of the two

60
Q

How is MIVD different from AD?

A 
It is acute and rapid
cog deficits proceed personality changes
people tend to be aware of deficits
frontal lobe compromise is early
deteriorating is step-wise, AD is slow/insidious
61
Q

Example of dementia from infection?

A

Creutzfeldt-Jakob Disease (CJD)

62
Q

What is CJD?

A

A rapidly progressive subcortical dementia

63
Q

What does CJD result in?

A

Spongiform encephalopathy (SE) in which sponge-like holes appear throughout the brain

64
Q

CJD is related to what other forms?

A

Minks in sheep

Cows - mad cows disease

65
Q

What are the 4 types of CJD and what are their characteristics?

A
  1. Sporadic: most common - occurs with no risk factors
  2. Variant (mad cow disease): cross species infection via consumption of meat containing neural tissue
  3. Familial: GSSS - found in handful of families result in fatal insomnia
  4. Iatrogenic: transmission through affected neuronal tissue, contamination via medical procedures
66
Q

Why is it hard to identify CJD?

A

As it’s a transmissible agent which does not produce usual symptoms of acute infection as it is camouflaged in cells and therefore is not recognised by the immune system

67
Q

CJD produces SE targeting what areas of the brain?

A

cerebellum and cerebrum

68
Q

What is found in human and sheep brains with kuru and CJD but not AD?

A

scrapie-associated fibrils (SAF) which is the disease agent

69
Q

Hallmark features of CJD are what?

A

Motor symptoms deficits such as uncoordination, slurred speech, tremors

70
Q

What are some emotional/cognitive symptoms of CJD?

A

mood disorders
fatigue
sleep problems
attention

71
Q

what is the progression of CJD like?

A

Very rapid - usually less than a year (approx 3-4 months)

PSY325 - Neuropsychology & Clinical Neuroscience (12 decks)

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