Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical and Neuropsychology 2 > NP Ch19: Alzheimer's disease > Flashcards

NP Ch19: Alzheimer's disease Flashcards

1
Q

Normal aging

What is crystallized intelligence? How does it change in normal aging?

A

It is skills, abilities, and knowledge that are overlearned, well-practiced, and familiar.
Vocabulary and general knowledge

It remains stable or improves with normal aging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Normal aging

What is fluid intelligence? How does it change in normal aging?

A

Abilities involving problem-solving and reasoning
Processing speed and executive functions

It declines with normal aging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Normal aging

What are some components of memory that decline with age?

A
  • Delayed free recall: spontaneous retrieval of information from memory without a cue
  • Source memory: knowing the source of learned info
  • Prospective memory: Remembering to perform intended actions in the future
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Normal aging

What are some components of memory that remain stable with age?

A
  • Recognition memory: Ability to retrieve information when given a cue
  • Temporal order memory: Memory for the correct time or sequence of past events
  • Procedural memory: Skills
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Normal aging

What are some structural and functional changes?

A
  • Cortical thinning and gray matter volumetric brain shrinkage
  • Decreased white matter density
    • Especially frontal and occipital regions of the brain
      • Therefore if you see a decrease in the temporal lobe, this isn’t normal
  • Loss of dopaminergic receptors
    • Attentional dysregulation
    • Executive dysfunction
    • Difficulty with contextual processing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Normal aging

What are protective factors for “successful” cognitive aging

A
  • Lifestyle
    • Active and healthy lifestyle
    • Cognitive and social stimulation
    • Limit cardiovascular risk
  • Cognitive reserve
    • The flexibility and adaptability of the brain or -networks to cope with brain damage
    • Positively associated with levels of education
    • Look at Figure 19.1 to see a graph showing effect of cognitive reserve.
  • Cognitive retraining
    • Teaching strategies to improve memory, reasoning, and speed of processing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Dementia (General) (up until flashcard 15)

What is dementia?

A

Dementia is the umbrella term for a number of neurological conditions, of which the major symptom is the decline in cognitive function due to physical changes in the brain. It is distinct from mental illness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Does dementia provide information about the causes?

A

Dementia says nothing about the cause, just the symptoms.
The types of dementia are what defines the cause.
E.g. AD is a type of dementia, and it can be characterised by specific brain damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What term does the DSM-5 use?

A

Neurocognitive disorder
DSM-5 definition: Minor (Mild cognitive impairment) and Major (dementia) neurocognitive disorders (NCD)
Used to be called just dementia, but it is now changed to NCD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does the DSM-5 classify NCDs?

A
  • There is evidence of substantial cognitive decline from a previous level of performance in one or more cognitive domains, based on the concerns of the individual, a knowledgeable informant, or the clinician; and a decline in neurocognitive performance, typically involving test performance in the range of two or more standard deviations on formal testing
    • This basically just says theres cognitive decline in specific domains, and decline in general performance
  • The cognitive deficits are sufficient to interfere with independence
    +
  • Not due to delirium
  • Not due to other mental disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the neurocognitive domains that the DSM-5 names?

A
  • Perceptual-motor function
  • Language
  • Learning and memory
  • Social cognition
  • Complex attention
  • Executive function

See figure 19.2 for a mindmap of these and further subpoints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

The DSM-5 uses specifiers for the possible cause of a NCD
What are the ‘Classical Neurodegenerative diseases’ specifiers?

A
  • Alzheimer’s disease
  • Vascular disease
  • Frontolobar degenerations
  • Lewy bodies
  • Huntington’s disease
  • Parkinson’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some other possible causes of NCDs?

A
  • HIV infections
  • Prion disease
  • Traumatic brain injury
  • Medication/substance use
  • Other somatic causes
  • Multiple aetiologies
  • Unspecified
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the prevalence of dementia?

A

Book says over 46 million people are estimated to have Alzheimer’s or a related dementia
This number will increase rapidly over the next few decades due two factors that have created a phenomenon called double ageing.

Look at Figure 19.3 for prevalences of the types of dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the two factors that cause double aging

A

First, the demographic structure of western society, ∴ number of elderly people will increase
Second, the average life expectancy has increased, ∴ more elderly people, and they live longer.
It’s predicted that by 2040, the number will have increased to over 80 million worldwide.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mild Cognitive impairment (Until flashcard 19)

What is Mild Cognitive Impairment (MCI)

A

Often (not always), MCI represents a transitional phase between normal aging and dementia
Presents with impairment in one or more cognitive domains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the diagnostic criteria for MCI?

A
  • Concern regarding cognitive change by the patient
  • Impairment in one or more cognitive domains based on neuropsychological exam
  • Impairment does not interfere with activities of daily living
    • This point is important, it kinda distinguishes MCI from dementia dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the rates of progression from MCI to dementia?

A

20-40% of cases of MCI progress to dementia within 3 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the treatment for MCI?

A

No intervention, including AD medication, has proven to be effective in decreasing MCI, or delaying or preventing the progression of MCI to dementia
Reassessment if needed to monitor the progression of MCI
Psychoeducation & cognitive training
Main takeaway is that MCI allows for intervention in the neurodegenerative process before irreversible dementia has kicked in, so that plans can be made early.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Alzheimer’s disease (Until flashcard 47)

What is Alzheimer’s disease (AD)

A

It is a type of dementia.

  • Neurodegenerative, progressive brain disorder
  • Memory impairment most distinctive symptom
    • But another cognitive domain has to be affected for diagnosis (at least 2 domains)
  • Global cognitive deterioration is involved in a later stage of AD.
  • Most common cause of dementia/NCD for up to 80% of cases
  • Clinical duration of AD has been estimated at 8-10 years
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does cortical atrophy look like?

A

Extreme shrinkage of cerebral cortex
Severely enlarged ventricles
Extreme shrinkage of hippocampus

Look at figure 19.4 for picture.

21
Q

What causes cortical atrophy in AD?

A

Neuronal death results from the accumulation of protein fragments of amyloid beta (plaques) outside neurons
Twisted strands of tau protein (tangles) inside neurons

Look at figure 19.5 to see plaques and tangles

22
Q

What are the two proteins related to plaques?

A

Amyloid precursor protein (APP) and Amyloid beta protein (ABP) are related to plaques.
They aren’t unique to Alzheimer’s, but usually there’s a balance between the quantity of ABP produced and the quantity of ABP released.

23
Q

What is the Amyloid cascade hypothesis?

A

A hypothesis for the development of Alzheimer’s disease, involving APP and ABP

  • First step is the abnormal cleavage of the APP
  • Imbalance in production and breakdown of ABP
    • ABP starts to aggregate and form plaques
  • Later on, tangles of the tau protein are added.
    • The number of tangles has been shown to correlate with the severity of dementia.
24
Q

What is the criticism of the amyloid cascade hypothesis

A

Lack of coherent evidence
Not yet clear whether plaques and tangles are a cause of AD or just a consequence
Failure to provide an effective treatment

25
Q

How is AD related to vascular problems?

A

Typically AD pathology is frequently observed together with cerebrovascular damage (remember the stroke chapter, vascular dementia)
Known as mixed pathology, which is commonly seen in older patients.

26
Q

What is the Vascular hypothesis?

A

It is a potential explanation for AD, it’s typically used in addition to the amyloid cascade hypothesis, rather than replacing it.

Inadequate blood flow to the brain is likely involved in the pathogenesis of AD
Due to subsequent hardening and decreased flexibility of blood vessels, making them more susceptible to damage.

27
Q

What is the criticism of the vascular hypothesis?

A

Unclear whether the vascular component of AD constitutes the cause or rather the effect of the disease
Unclear whether typical AD pathology and vascular pathology are two simultaneously yet unrelated processes or two processes that affect and amplify each other.

28
Q

What are the age brackets for early onset AD and late onset AD?

A

Onset before age 65 is defined as early onset AD (EOAD)
Therefore, after age 65 is late onset AD (LOAD)

29
Q

Whats the percentage of late onset AD cases?
What is the risk of AD at different ages?

A

95% of AD cases is LOAD
AD risk increases with age

  • 65-74: 5%
  • 75-84: 13%
  • > 84: 35%
30
Q

If people live long enough are they guaranteed to get AD?

A

Tt isn’t known if everyone would get AD if they lived long enough, but there are people age 110 whose brains show no signs of AD.
This is because Alzheimer’s is a disease, not an accelerated type of aging

31
Q

What are the risk factors for AD?

A
  • Age
  • Female gender
  • Genetics
  • Brain injury
  • Cardiovascular risk factors (hypertension, diabetes, smoking, etc.)
  • Inactive lifestyle
  • Lower level of education
32
Q

Whats the role of genetics in AD

A

A small minority of cases are caused by a familial type of AD, in which over half of the children of an affected parent will develop the disease.
Familial AD is caused by mutations in three specific genes
However most cases aren’t caused by an autosomal dominant mutation, but genetics still plays a role

33
Q

What does the book say you need to diagnose AD?

^ All this above is extra info, go off the slides info/DSM-5 part

A

First the severity of symptoms is determined (dementia syndrome diagnosis)
Second, the type of dementia is determined (aetiological diagnosis)
To make a specific diagnosis of the type of dementia, the criteria of the National institute of aging and the Alzheimer association (NIA-AA) can be used as they ascribe the clinical diagnosis with low-high probability to underlying Alzheimer pathology, using findings from additional investigations.
Definite diagnosis can be made post-mortem during autopsy.

^ All this above is extra info, go off the slides info/DSM-5 part.

34
Q

SLIDES: What is the clinical diagnosis based on?

A

Currently based on medical history of patient, clinical examination, neuroimaging, and neuropsychological testing

Diagnostic cycle appears again for diagnosis
1. Complaints analysis
2. Problem analysis
3. Diagnosis
4. Indication for treatment

35
Q

Complaints analysis: Who do you perform a clinical interview with? and why?

A

Both with patient and close relative
Why?

  • Patient has reduced insight into deficits (anosognosia)
  • Patients with dementia/AD commonly deny or trivialise their complaints
  • Initial rough impression of global cognitive functioning is obtained through a screening test, such as the Mini-Mental State Examination
36
Q

Problem analysis: Neuropsychological assessment

A

What areas of cognitive deterioration are essential for assessment?

  • Memory
    • Declarative episodic: Most commonly impaired.
  • Executive function and problem solving
    • Cognitive flexibility and planning problems
  • Attention
    • Mental flexibility and divided attention problems (becomes more complex in later stages)
  • Other cognitive problems , e.g., visuospatial perception, language, or apraxia
    • Decreased sense of orientation with regard to time and place and language impairments may be present during the initial stage
37
Q

In what stages do you see different kinds of memory impairment?

A

Early stages: typically anterograde long-term memory impairment
Because atrophy of the MTL and hippocampus is present at an early stage.
Later stages: also retrograde memory impairment and semantic memory problems

38
Q

What is the most sensitive measure for detecting cognitive deterioration in AD?

A

The delayed memory condition of a memory test
Which can be evaluated using the verbal learning tests, such as the Rey Auditory Verbal Learning Test for incoherent verbal information.

39
Q

Problem analysis: What are some Neuropsychiatric symptoms commonly seen

A
  • Depression
  • Anxiety (Seen commonly in early stage as well as depression)
  • Apathy, social disengagement and/or irritability
  • Psychosis
  • Agitation, aggression and/or wandering
  • Motor unrest (more common in evening)
  • Sleeping problems
  • Eating problems

95% of patients with dementia experience one or more neuropsychiatric symptoms.

40
Q

Problem analysis: What are some other symptoms seen in AD patients?

A

Olfactory dysfunction
Seizures (10-20% of cases, usually in later stages)
Motor signs (typically in later stages)

41
Q

Diagnosis: What are the DSM-5 criteria for AD?

A
  • A. Criteria met for major or mild NCD
  • B. Insidious onset and gradual progression of impairment in one or more cognitive domains (two for major NCD)
  • C. Criteria either probable or possible AD if either of the following is present
    • Evidence of a causative AD genetic mutation from family history or genetic testing
    • All three of the following
      • Clear evidence of decline in memory and learning and at least one other cognitive domain
      • Steadily progressive, gradual decline in cognition, without extended plateaus
      • No evidence of mixed etiology
42
Q

How can Neuroimaging and other techniques be used to assist diagnosis?

A

Neuroimaging is often used initially to exclude alternative diagnoses.
Positive evidence for Alzheimer’s can also be found, like atrophy of the MTL
Biomarkers aren’t neuroimaging, but are another technique to provide evidence for the type of dementia.
They are found by taking samples of cerebrospinal fluid, which can be analysed to see what is in the brain.

43
Q

What is the progression of AD?

A

Cognitive deficits progress further over time
Older age of onset = slower rate of decline
Neuropsychiatric symptoms = faster rate of decline

44
Q

What are some points that indicate prognosis of AD?

A
  • High level of education (cognitive reserve) = later onset, but faster rate of decline
  • Life expectancy after AD diagnosis approximately 8-10 years (range 3-20 years)
    • Related to: Stage of disease and age of onset of symptoms
45
Q

What are the treatment options for AD?

A

Alzheimer’s disease cannot be cured

  • Medication to inhibit cognitive symptoms to a certain extent (More info on next card)
  • Psychoeducation
  • Cognitive training (early stages)
  • Manage behavioural symptoms
46
Q

What medications can be used for AD?

A
  • Cholinesterase inhibitors (for mild to moderate AD)
    • The cholinergic hypothesis is why we use these drugs, because it states that the loss of cholinergic neurons results in a presynaptic cholinergic deficiency.
      • Cholinesterase inhibitors ensure acetylcholine is broken down less quickly so it remains in the presynaptic cleft for longer.
  • N-Methyl D-aspartate (NMDA) antagonist (for moderate to severe AD)
47
Q

Posterior cortical atrophy (until flashcard 51)

What is Posterior Cortical Atrophy? (PCA)

A

It is a subtype of Alzheimer’s disease
Onset with atrophy of the visual cortex and sometimes also the cerebellum
Also called the visual variant of Alzheimer’s
It also involves impairment in Perceptual-motor function section of domains picture

48
Q

What is the neuropathology of PCA?
What is the course of PCA?

A
  • Neuropathology: plaques and tangles
  • This atypical course often occurs in young-onset dementia, at an average age of 55.
    • It typically has a more rapid course,
    • Its more difficult to diagnose in younger people because it might be attributed to work-/relationship-related problems.
49
Q

What are the clinical characteristics of PCA?

A

Progressive visuoperceptual problems, such as,

  • Visual field deficits
  • Not being able to recognize objects or faces
  • Problems with letter recognition and reading
  • Optic ataxia
  • Visual and spatial orientation problems
50
Q

What are some discrepancies in reported symptoms that make PCA difficult to diagnose?

A

Especially in the beginning, its difficult to diagnose due to atypical strange complaints in daily life
In the early stage, neuropsychological assessment is great.
The following are discrepancies that are confusing.

  • Patients say they can’t see while their behaviour is adequate (“blind sight”)
  • Objects that suddenly seem to appear or disappear
  • Objects that seem distorted
  • Not being able to recognise objects in close distance but no problems when far away
  • Letters that are distorted or missing
  • Patient that sometimes seem not aware of their visual problems
51
Q

What are some other types of dementia
What can you use to distinguish different types of dementia?

A

Based on the neuropsychological profile, you can distinguish different types of dementia

  • AD is characterised by memory impairment
    • This is less prominent in dementia with Lewy bodies
  • Semantic dementia and primary progressive aphasia are initially characterised by language impairment.
  • Slowness and decreased mental flexibility are often prominent in vascular dementia.

Clinical and Neuropsychology 2 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions