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Year 2 Developmental > learning pack 5 > Flashcards

learning pack 5 Flashcards

1
Q

What is dementia?

A
  • A set of symptoms that include loss of memory, mood changes, and problems with communication and reasoning
  • Progressive –> symptoms will gradually get worse
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2
Q

Origins of dementia: Degenerative

A
  • Alzheimer type dementia
  • Lewy body dementia
  • Parkinson’s disease
  • Motor neurone disease
  • Frontotemporal dementia
  • Huntington’s disease
  • Multiple sclerosis
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3
Q

Origins of dementia: Vascular

A
  • Multi-infarct dementia
  • Lacunar state
  • Binswanger’s disease
  • Cerebral amyloid angiopathy
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4
Q

Origins of dementia: Infective

A
  • Aids-dementia complex
  • BSE/new variant creutzfeldt-jakob disease (CJD)
  • Herpes simplex encephalitis
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5
Q

Origins of dementia: Post-neurological insult

A
  • Open or closed head injury

- Carbon monoxide poisoning

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6
Q

Origins of dementia: Space occupying lesion

A
  • Chronic subdural haematoma

- Primary or metastatic intracranial tumour

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7
Q

Origins of dementia: Toxic

A
  • Alcohol related dementia

- Heavy metal poisoning (e.g. lead, mercury)

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8
Q

Origins of dementia: Metabolic/endocrine

A
  • Hypothyroidism

- Vitamin B12 deficiency.

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9
Q

Origins of dementia: Other causes

A
  • Epilepsy

- Beheet’s syndrome

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10
Q

What is Alzheimer’s disease

A
  • Physical disease named after the doctor who first described it (Alois Alzheimer)
  • During the course of the disease, proteins build up in the brain to form structures called ‘plaques’ and ‘tangles’
  • This leads to nerve cell death and loss of brain tissue
  • People with Alzheimer’s also have a shortage of certain chemicals in their brain, so signals are not transmitted as effectively
  • Alzheimer’s is a progressive disease
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11
Q

Symptoms of Alzheimer’s: Early/Mild

A
  • Lapses of memory, confusion
  • Problems with finding the right words, repetition
  • Slower at grasping new ideas
  • Finding it harder to make decisions
  • Loss of interest in other people or activities
  • Blame others for taking mislaid items
  • Unwilling to try new things/adapt to change
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12
Q

Symptoms of Alzheimer’s: Middle/Moderate

A
  • Frequently confused/disoriented in time and space/ forget names of people, places, appointments and recent events
  • Experience mood swings, scared and frustrated by their increasing memory loss
  • Become more withdrawn due to loss of confidence or to communication problems
  • Difficulty carrying out everyday activities
  • Need help with managing their daily care
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13
Q

Symptoms of Alzheimer’s: Late/Severe

A
  • Require a great deal of help, become totally dependent upon others for care
  • Very pronounced loss of memory
  • Can’t remember close family members
  • Increasingly frail/shuffling, falls, unsteady walking, confined to bed/wheelchair
  • Difficulty in eating and swallowing
  • Weight loss or over-eating
  • Incontinence
  • Loss of speech
  • Restlessness
  • Distressed/aggressive…may not understand what is happening to them
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14
Q

How do we establish the onset of Alzheimer’s

A

Main early clinical manifestation is short-term memory loss

A neuropsychological element consisting of amnesia and one or more of the following:

  1. Aphasia - problems understanding language
  2. Apraxia - inability to carry out tasks
  3. Agnosia - inability to recognise things

This can be evidenced by:

  1. Repeating of questions
  2. Forgetting birthdays/anniversaries, appointments to meet with friends or family
  3. Needing to be reminded of the day/date

However, long term memory can be preserved for some time

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15
Q

How do we establish the onset of Alzheimer’s

A

A neuropsychiatric component with symptoms such as psychiatric disturbances and behavioural disorders:

  1. Depressioin (approx. 66%)
  2. Paranoia (30%)
  3. Hallucinations (most commonly auditory, 15%)
  4. Aggression (20%)

Deficits in activities of daily living (more pronounced over time):

  1. Wandering/loss of intent -> forgetting what to do
  2. failure to wash or dress to a usual standard
  3. Self neglect of diet can lead to weight loss
  4. Neglect of household tasks lead to comments about cleanliness of the house
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16
Q

How do we diagnose Alzheimer’s

A
  1. History
    - Perspectives on impairment from the patient, close friend or a relative is recounted to the GP to corroborate symptoms and impact on daily functioning
  2. Cognitive tests
    - Assessing mental processes
    - Referral of patient to memory clinic
  3. Physical examination
    - Blood tests include kidney and liver function, thyroid gland activity, vitamin levels
  4. Brain scan
    - MRI examination
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17
Q

What are the causes of Alzheimer’s

A
  • No single factor has been identified
  • It is likely that a combination of factors are responsible, including: age, genetic inheritance, environmental factors, lifestyle, general health
  • Progressive neurodegenerative changes due to an abundance of plaques (made of an abundance amyloid) and tangles (made an abundance of tau)
  • Reduction of neurotransmitters contribute to the profile of symptoms (acetylcholine, glutamate, GABA)
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18
Q

What is the amyloid cascade hypothesis?

Hardy and Higgins (1992)

A
  • There are two hallmark pathologies identified in. Alzheimer’s
    1. Beta amyloid peptide (ABeta)
    2. Neurofibrillary tangles (NFT) of the binding protein tau
  • An excess of ABeta triggers the disease which leads to the formation of NFTs, neuronal cell death and dementia
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19
Q

What is the cholinergic hypothesis

Bowen et al (1976)

A
  • Acetylcholine is used in arousal, memory and attention
  • Projections from the basal forebrain influence activity in the rest of the brain (including hippocampus)
  • Amyloid deposits prevent effective neurotransmission and receptor binding which produces deficits in plasticity
  • Alzheimer’s treatment options target nicotinic acetylcholine receptors e.g. Aricept, Exelon and Reminyl
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20
Q

Risk factors for dementia: Age

A
  • Greatest risk factor for dementia
  • Increased risk may. be due to factors associated with ageing:
  1. Higher blood pressure in mid-life
  2. Increased incidence of heart disease and stroke
  3. Changes to nerve cells, DNA, cell structure
  4. Weakening of the body’s natural repair systems
  5. Changes in the immune system
  6. Myelin model of neurodegeneration
  • Age-related breakdown in the protective membrane of axons from mid-life can increase the likelihood of developing AD (Bartzokis, 2004)
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21
Q

Risk factors for dementia: Genetics

A
  • Apolipoprotein E (APOE)
  • The influence of inherited genes for late-onset AD is small: most people do not have a genetic predisposition for/against AD development (as opposed to early-onset AD)
  1. APOE e2 –> rare (present in 7% of people)
    - -> Appears to be neuroprotective
    - -> If AD occurs, it usually develops much later in life
  2. APOE e3 –> most common allele (79%)
    - -> neither decreases nor increases risk
  3. APOE e4 –> increases risk for AD, earlier onset (14%)
    - -> Cumulative risk (e4/e4) - far more likely to develop AD
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22
Q

Risk factors for dementia: Environment

A
  • Recent speculation on pollution levels ‘causing’ 11% of dementia cases (Chen et al, 2017)
  • Likely to be other factors at play, and the precise contributory factors to such results are largely to be determines
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23
Q

Risk factors for dementia: Activity levels (Health/Medical history)

A
  • High blood pressure, cholesterol levels, diabetes, miid-life obesity, and stroke put individuals at increased risk
  • Medical status and cognitive decline appear related (Leoutsakos et al, 2012)
  • Physical exercise as protective (Lindsay et al, 2002)
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24
Q

Risk factors for dementia: Activity levels (Social activity)

A
  • People who are more socially active have a slightly reduced risk of developing dementia
  • Interaction with others boosts hippocampal neurogenesis and reverses memory. decline in mice (Hsiao et al, 2014)
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25
Q

Risk factors for dementia: Activity levels (Mental activity)

A
  • People who take part in mental activities, reading, learning, doing puzzles are less likely to develop dementia compared with those who do not engage in these activities (Baumgart et al, 2015).
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26
Q

What is mild cognitive impairment?

A
  • The presence of acquired cognitive abnormality greater than expected in relation to age and education
  • But it has to be in the absence of dementia and detrimental effects upon daily living
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27
Q

Mild cognitive impairment statistics

A

According to Alzheimer’s society:

  • Between 5 and 20% of older people (65+) have MCI
  • Depends on how MCI is defined and whether such patients were recruited from the general public or from those attending memory clinics
28
Q

Characteristics of mild cognitive impairment

A
  • MCI can be transitory, with normal functional integrity eventually resumed, or stable over time
  • Some people can have ‘permanent MCI: function doesn’t revert back to normal but cognitive declines do not substantially progress and dementia does not develop
  • for some patients, MCI represents the early or prodromal stages of Alzheimer’s (or other form of dementia), for others it is caused by. something else
29
Q

What are the types of mild cognitive impairment?

A

1) Amnesic mild cognitive impairment: Primarily memory-related dysfunction
2) Amnesic multi-domain mild cognitive impairment: Impacts on multiple aspects of cognition as well as memory (e.g. reasoning, language)
3) Non-amnesic mild cognitive impairment: Influences multiple aspects of cognition but not memory

30
Q

What is the diagnostic criteria for mild cognitive impairment?

A
  • Significant subjective decrease in short or long-term memory (documented also by another individual)
  • An objective decline from the age and education appropriate mean scores on tests of cognitive assessment
  • Should demonstrate preserved daily living (Albert et al, 2011)
31
Q

How do they diagnose mild cognitive impairment at a memory clinic?

A
  • Lab tests (bloods etc)
  • CT/MRI scan
  • History
  • Medical examination
  • Neuropsychological test battery
32
Q

What are the issues with diagnosing mild cognitive impairment?

A
  • MCI is characterised by subtle changes in day to day memory, planning, language and perception which can all be attributed to ageing in general
  • This is exacerbated by the relative insensitivity of current neuropsychological tests and neuroimaging and biomarkers
33
Q

What are the issues with sensory impairment and diagnosing MCI

A

Vision:
- poor sight can lead to poor neuropsychological test performance… many instructions are written and some tests are visually based (e.g. drawing)

Hearing:
- Hearing loss in older adults can cause the misunderstanding of questions and/or prevent appropriate responses to verbal instructions

34
Q

Why is accurate diagnosis of mild cognitive impairment so important?

A
  • To help identify people at increased risk of developing dementia
  • To ensure that any available treatment for dementia or memory dysfunction is put in place as soon as possible, together with early access to support and advice
  • Better clinical trials (validity increases when one can be more confident about a person’s diagnosis)
  • To understand the characteristics of the disease and what problems a person may be experiencing
35
Q

How can mild cognitive impairment be an early sign for dementia

A
  • For some people (approx. 15%) mild cognitive impairment is a prodromal stage of dementia (it signals the presence of degenerative changes)
  • The risk factors and lifestyle choices that may affect. the development of Alzheimer’s disease/other dementias can also lead to MCI
  • Clearly, there may be an overlap but not everyone with MCI will develop dementia
36
Q

What are the risk factors for MCI

A
  • Age
  • Biological e.g. blood pressure, medication (warfarin prescribed to many older people, is linked to cognitive impairment)
  • Psychological e.g. depression, anxiety, stress
  • Social factors e.g. life events, lack of support (reasons for potential transient/reversible diagnoses of MCI)
37
Q

How does secondary ageing effect MCI

A
  • Factors such as these may exacerbate normal ageing deficits
  • Cognitive function is worse in such older adults compared to those who don’t smoke, eat a balanced diet, get enough exercise etc
  • Such individuals then appear to be undergoing a process that mimics the early stages of dementia
  • For those without neurodegenerative pathology/biomarkers of dementia, altering lifestyle factors could alleviate mCi
38
Q

Linking the brain to MCI behaviour

A
  • In MCI, tissue volume was reduced in the fornix
  • Shift of memory. load/processing resources from the fornix to parahippocampal cingulum
  • Alternative pathways contribute to episodic memory performance, which is likely to remain quite high due to such compensatory neural mechanisms
  • This makes detection of MCI from a behavioural perspective highly problematic
39
Q

What could help to minimise the effects of Alzheimer’s

A
  1. Lifestyle interventions
    - Increasing physical/mental/social activity
  2. Maintaining/restoring plasticity
    - Modifying neurotransmission and Brain Derived Neurotrophic Factor (BDNF)
  3. Reducing pathology
    - Clearing the amyloid/tau burden
40
Q

What are the symptomatic drugs used for Alzheimer’s?

A
  • Donepezil, Rivastigmine, and Galantamine are equally effective in mild/moderate AD, and can delay deterioration by 6-9 months
  • Memantine is used in more severe cases and can still improve cognition at this stage (Tariot et. al, 2004)
41
Q

Drug treatment developments for AD

A

While traditional treatments influence the cholinergic (e.g. Donepezil) and glutamergic (Memantine) systems, to target the symptoms of the disease:

  • Alternative therapeutic options seek to directly interfere with the accumulation of protein deposits, thought to be the origin of AD (Panza et al, 2016)
  • Verubecestat reached phase III trials but was recently deemed to have ‘virtually no chance of finding a positive clinical effect’
  • More promising results came from Solanezumab and Aducanumab
  • These drugs slowed cogniitive decline and reduce the presence of brain plaques, in phase II trials
  • However, they work better in preclinical/mild AD patients
42
Q

What is the use of Aducanumab in mild cognitive impairment

A
  • After one year of treatment with aducanumab, beta amyloid plaques were substantially removed with evidence of a dose response
  • Immunotherapy to reduce intracerebral amyloid seems most promising in very early, possibly still asymptomatic Alzheimer’s (Sevigny et al, 2016)
43
Q

What is cognitive reserve?

A
  • Concept or abstract idea
  • Ways to go about building resistance to detrimental neural change
  • You have a protective buffer and supplies to draw on when things get tougher
  • Individuals use alternative methods to maintain function (e.g. processing strategies or compensatory approaches)
  • There is not always an obvious relationship between brain damage and the degree of disruption in behaviour/test performance (Stern, 2002)
  • People can sustain different levels of damage before the effects are observed, which suggests there is a buffer against such damage (Stern, 2009)
44
Q

Theoretical approaches to explaining why some people have more cognitive reserve: Brain reserve

A
  • Larger brains, with more neurons, can sustain more damage

- They have greater potential to be resilient and function adequately for longer

45
Q

Explanation for brain reserve: The threshold model

Satz (1993)

A
  • A disorder or injury has to exceed the brain reserve threshold to have a visible effect
  • Only brain reserve can determine the outcome
  • Similar types of damage don’t always have the same impact to begin with
  • Cannot account for other individual differences and compensatory processing in the face of damage
  • Conceptualises brain reserve as a very narrow/rigid approach
46
Q

How does cognitive reserve differ from brain reserve

A
  • Lack of fixed thresholds
  • Levels of cognitive reserve can be enhanced, so you can actively seek to combat damage
  • Defined in relation to processing efficiency rather than in gross anatomical terms
  • Individuals have flexibility in their neural responses, so they can use the most efficient processing routes to sustain cognition
  • Two people may have the same amount of brain reserve but the person with more cognitive reserve is likely to tolerate greater damage before clinical impairment is apparent
47
Q

How is cognitive reserve active?

A
  • Dependent on choices made throughout development
  • Can be increased
  • Individual differences in modifiable lifestyle factors define age-related bran change and resilience to pathology
48
Q

How is brain reserve passive?

A
  • Dependent on brain size and neuron count which we cannot directly control
  • Maximum limit imposed
  • Individual differences in brain structure define age-related brain change and resilience to pathology
49
Q

What could damage brain reserve?

A
  • Traumatic brain injury
  • Encephalitis
  • Psychiatric illness
  • Developmental disorders
50
Q

What increases brain reserve?

A
  • Increased brain size
  • Increased neuronal count
  • Increased synaptic density
51
Q

What decreases cognitive reserve?

A
  • Sedentary mental activities
  • Malnutrition
  • Lack of education
  • Loneliness
52
Q

What increases cognitive reserve?

A
  • Cognitive engagement
  • Cognitive remediation
  • Education
  • Leisure activities
  • Nutrition
  • Social stimulation
53
Q

What is neural reserve?

A
  • Combination of brain and cognitive reserve
  • Evident that there is not such a division between cognitive reserve and brain reserve as first thought
  • Differences in cognitive processing (reserve) must have a physiological/anatomical basis
  • Integration of biological, genetic innate aspects along with psychological and social factors
  • Neural reserve: the extent of our ability to allocate neural resources and form new processing strategies to be able to keep functioning in the face of damage
54
Q

What influences cognitive reserve?

A
  • Variation in cognitive reserve is likely due to lifestyle factors, which provide resilience to damage
  • Assessed in terms of abstract markers or ‘proxies’
55
Q

Cognitive reserve influencers: Education

A
  • Higher education produces greater cognitive reserve
  • Cognition in latter life is best predicted by educational attainment
  • Education delays observable signs of pathology (Jefferson et al, 2011)
  • Linked to markers of brain reserve (larger brains, increased thickness of the cortex –> Liu et al, 2012)
  • Quality vs. quantity: role of literacy, standard of education as opposed to years of schooling
56
Q

Cognitive reserve influencers: Literacy/Intelligence

A
  • National Adult Reading Test (NART)
  • Better NART = higher cognitive reserve
  • Reading ability can protect older adults from cognitive impairment in later life, particularly in regard to working memory
57
Q

Cognitive reserve influencers: Knowing a second language

A
  • Life-long bilingualism leads to more efficient use of neural resources, which attenuates cognitive decline in Alzheimer’s disease
  • Other contributing factors: age of onset, proficiency and frequency of language use
58
Q

Cognitive reserve influencers: Socioeconomic status

A
  • Those lower on the scale are more susceptible to the behavioural effects of brain damage
  • Likely to relate more to the impact it has on opportunities to engage with education or cognitively stimulating activities
59
Q

Cognitive reserve influencers: Exercise

A
  • Improved vascular physiology forms a barrier to cognitive decline in the face of damage
  • We know it can prevent damage but what about attenuating the effects of damage
  • Exercise increases resting cerebral blood flow and “cerebrovascular reserve”, to promote greater neurogenesis and cognitive performance
  • In particular, aerobic exercise that makes you think e.g. dancing
60
Q

Cognitive reserve influencers: Social activity/cognition in leisure

A
  • Social networks modify the relationship between Alzheimer’s pathology and cognition. Less impact of pathology with larger social networks
  • Such individuals have an average of 24/30 on the Mini Mental State Exam
  • Past. and present activities count. Prevention of cognitive decline in those with AD pathology - 14% of variability in cognitive change
61
Q

How is cognitive reserve related to Alzheimer’s?

A
  • Differences in cognitive reserve can account for findings related to Alzheimer’s
  • There is a mismatch between pathology and test scores
  • An individual may have a high load in relation to AD brain pathology (plaques and tangles) but not demonstrate deficits on neuropsychological tests
  • Their level of cognitive reserve prevents symptoms from emerging until the late stages
62
Q

How does cognitive reserve relate to AD diagnosis

A
  • individuals with the greatest cognitive reserve will have more advanced pathology at the onset of observable cognitive decline/at diagnosis
  • They will have less time until they reach the point when pathology overwhelms function and thus a more rapid rate of decline
  • Cognitive reserve can help by attenuating the experience of AD but this can be viewed as a hinderance with respect to diagnosis, where an individual will be unable to make use of early stage interventions
63
Q

How does IQ effect Alzheimers diagnosis

A
  • Risk of inaccurate assessment affects older adults wiith high or low premorbid intelligence
  • Older adults with high premorbid IQ are more likely to be misclassified as normal
  • Older adults with low premorbid intelligence are more likely to be misclassified as demented
  • IQ influences MMSE and MoCA scores: Premorbid IQ evaluation should be considered to ensure correct interpretation of scores
64
Q

How does education effect Alzheimers diagnosis

A
  • Individuals with high levels of educational attainment can be misdiagnosed as not having Alzheimer’s because of their cognitive reserve
  • Education modifies the relationship between Alzheimer’s and cognitive performance
  • Higher educational levels may inhibit the change from mild cognitive impairment to dementia
  • Link to occupation: manual work is linked with higher risk of Alzheimer’s compared to non-manual work
65
Q

What are the limitations of cognitive reserve?

A
  • Further details are needed on the physiological processes that support cognitive reserve
  • Increased research of a longitudinal and prospective nature is needed to enhance existing evidence based on retrospective data

Year 2 Developmental (5 decks)

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