3 Mild Cog Impairment and Alzheimer´s Flashcards
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Mild Cognitive Impairment (MCI)
DEF= A stage between normal, age-appropriate functioning and dementia
Some degree of cognitive decline is associated with ageing this is inevitable.
The also consists variability in when these changes begin. These inter-individual changes tend to increase with age
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What remains intact in normal aging?
- Implicit memory;
- Vocabulary;
- Storage of general knowledge.
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What declines in normal aging?
- Speed of processing;
- Reaction time;
- Executive control (inhibition);
- Working Memory capacity; o The working memory decline is possibly the result of reduced inhibitory mechanisms (a decreased ability to suppress irrelevant stimuli, fulfilled by executive functioning).
- Short term memory;
- Verbal fluency;
- Poorer effortful and controlled processing (automatic processing remains intact); - Decreased phonological retrieval (resulting in word finding difficulties: Tott-phenomenon); - Semantic fluency decline.
Structural brain changes in normal aging
- Volumetric shrinkage;
- Decreased white matter density; o Leads to age-related cognitive slowing (speed of processing).
- Loss of dopamine receptors; o Lead to attentional dysregulation, executive dysfunction. - The emerge of neurofibrillary plaques and tangles; - Increases in ventricular volume.
There seems to be variability per individual in the relationship between brain pathology and cognitive presentation. A possible explanation for this is cognitive reserve=
How much one is affected by the pathology of the brain depends on the size of one’s cognitive reserve. Studies of blood flow in the brain reveal an increase of bilateral activation with age, when performing in cognitive tasks. This suggests that the older brain engages in more widely distributed compensatory processing by activating bilateral regions to achieve greater cognitive benefits.
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Theories of aging
- Dedifferentiation= Sensory functioning predicts performance on cognitive tasks in older, but not in younger adults. It is proposed that abilities function independent in early life, bit become more interrelated with old age: a decrease in neural specify. Neuroimaging studies show that older people use greater frontal activity during cognitive tasks, suggesting that this greater frontal activity may be a compensatory mechanism for decreased mesi-temporal activation (which is seen in younger adults).
- Processing Speed Theory
Cognitive tasks are limited by constraints on speed of processing. Slower speed of processing limits cognition in two ways:
o Cognitive operations are executed too slowly to be completed in the available time. o The amount of simultaneously available information is reduced (early processing is no longer available when new processing occurs). Complex operations are most affected by the slow processing speed, because these tasks need simultaneously processing of information. - Scaffolding Theory=
Structural brain changes are accompanied by efforts of neural networks to maintain homeostatic cognitive functioning. This leads to brain changes: strengthening, formation of new and disuse of old neural connections. ‘Scaffolding’ is the brain’s normal response to a challenge. It maintains healthy cognitive functioning in face of neural degeneration. Because of the fact that scaffolding networks are less efficient and more prone to error, you still see some decline during ageing of older adults
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Individual factors
- Education=
Higher education leads to a preserved cognitive performance over time. - Occupational complexity=
Related to better cognitive functioning with age. - Physical heath=
Clinical and subclinical medical disorders are better predictors of neuropsychological performance than age. For example: hypertension and obesity. - Diet
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MCI definition
A decline in cognitive performance, greater than would be expected for a person’s age, but not sufficient to meet the criteria for the diagnosis of dementia’. It is conceptualized as a pathological condition.Prevalence rates: 1-19% of the population suffers from MCI. MCI has a heterogeneous clinical presentation.
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Clinical criteria of MCI
- Concern regarding change in cognition;
Compared to previous level of functioning. The concern comes from the individual self or another person. - Impairment in one or more cognitive domains;
- Preservation of independence in functional abilities; Only mild problems in carrying out complex tasks.
- Not demented.
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Subtypes of MCI
- Single Domain Amnestic MCI (a-MCI) =
Impairment in memory, all other cognitive domains functioning is still intact. - Single Domain Non-Amnestic MCI (na-MCI) = Impairment in a single, non-memory cognitive domain.
- Multiple Domain Amnestic MCI (md-MCI+a).
- Multiple Domain Non-Amnestic MCI (md-MCI-a).
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Prognosis of MCI
MCI in general is an increased risk factor for developing dementia in the future. But, this doesn’t necessarily have to be the case: some patients with MCI remain stable or even revert to normal.The na-MCI subtype is most likely to revert to normal, but in case of developing dementia: the Lewy body subtype of dementia is the most likely. The a-MCI subtypes are more likely to develop Alzheimer’s Disease in case of dementia. The multiple domain subtypes of MCI are most predictive to the progression to dementia in general
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Etiology
- Degenerative;
- Vascular;
- Psychiatric;
- Traumatic.
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Pathology and neuro diagnostic findings= Typical differential diagnosis focusses on
- Normal cognitive ageing;
- Dementia;
- Depression (‘pseudo-dementia’) or delirium; - Reversible causes (for instance medication).
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Clinical interview
In the ideal case, a collateral source is brought by the client to provide extra insight in the situation. Further: history & emerge of symptoms, evaluating functional abilities, changes in behavior or personality (often MCI and depression go hand in hand, a-MCI and md-MCI: higher rates of depression), medical history and current health status, family history of dementia.
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Functional Impairment
Assessing Activities of Daily Living (ADL’s), by individual him or herself and an informant. Optional to use self-report and ADL’s scales in addition to the interview, but these scales don’t pick up subtle changes, while the interview does.
MCI patient report some decline in their abilities to handle daily tasks
More forgetful, less able to multitask, planning difficulties, organization difficulties and subtle decline in driving skills.
They are also a little impaired in learning and retaining new information, and performing higher order executive skills. Their impaired memory and psychomotor speed are most strongly related to functional abilities.
They are still able to function independently, but will do this less efficient and with the use of compensatory strategies
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Cognitive impairment
Using objective measurements, besides the self- and family reports. 1-1,5 standard deviations below age norms is used as a guideline (and not as a cut off score) for an indication of MCI. It is important to view the cognitive decline relative to the patient’s baseline (previous cognitive functioning).
Measurements of:
- All major cognitive domains;
- Multiple measurements of memory (essential for differential diagnosis); - Self-report measures of mood functioning
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Common neurocognitive deficits
MCI patients that convert to Alzheimer’s Disease (AD):
- Show decline in episodic memory and learning, early in the disease process (due to deficits in the medial temporal lobe)
- Show poorer immediate recall and divided attention
Md-MCi patients show the most severe impairments.
The breakdown of semantic knowledge doesn’t occur during MCI, but does occur in the AD stage. MCI patients suffer from poorer semantic memory, due to the decrease of executive functioning.
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Highlights
- Degree of cognitive impairment;
- Increased risk for developing dementia, particularly a-MCI and md-MCI;
- Cognitive strength can be used as a compensatory strategy;
- All the amnestic subtypes of MCI should be tested again one year later; - Determining the follow-up evaluation based on:
o Severity and number of cognitive domains impaired; o The patient’s functional status.
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Characteristic neuropathology of AD= Plaques and tangles
5,5 million adults in the US suffer from Alzheimer’s Disease (AD). AD was first discovered in 1906.
Characteristic neuropathology of AD= Plaques and tangles.
- First=
The formation of plaques (which are abnormal formations of the protein ‘beta amyloid’) this process can start 20-30 years before the symptoms of the AD are manifested. These plaques eventually result in neurofibrillary degeneration, seen as neurofibrillary tangles.
- These changes lead to synaptic disruption and neurodegeneration of brain structures (primarily the hippocampus and entorhinal cortex).
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The first clinical manifestations of AD
- Disruptions in short-term memory;
- When the disease progresses: more severe memory deficits (losing abilities in daily living and eventually total disability and death).
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Diagnosis
Diagnosis=
There is made a distinction between possible and probable AD.
Probable AD=
- Memory impairment and impairment in at least 1 other cognitive domain;
- Impairment in social or occupational functioning;
- Ruling out all other possible dementias;
- So: probable AD is a diagnosis of exclusion. The final diagnosis can only be made by an autopsy.
Possible AD=
- The clinical core criteria;- An atypical course, or:
- Insufficient evidence of cognitive decline.
New proposed criteria add biomarkers to the diagnosis. This will make it not a diagnosis of exclusion anymore.
Cognitive impairments are not always clearly present and can be quite mild and difficult to detect. Also: individuals with a high cognitive reserve can use other brain sources to mask overt deficits.
The current treatment of AD doesn’t treat the pathology of the disease, but does work better when AD is detected earlier
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Mild Cognitive Impairment (MCI)
Is an intermediate state between normal ageing and dementia. Criteria:
1. Subjective memory complaint;
2. Objective evidence of memory impairment;
3. Intact intellectual functioning;
4. No impairment in daily functioning.
Best cognitive marker for AD: episodic memory impairment.
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Clinical Interview
- With patient and collateral informant, the best way to conduct the clinical interview is to speak to them separately.
- Early AD: often recent memory deficits, while still being able to recall info from the recent past.
- Sometimes, the cognitive symptoms of AD will first become apparent, often due to a stressful life events
- Determine whether the symptoms show a sudden or a slowly onset. AD show almost always a progressive course and gradual worsening symptoms.
- The clinical interview provides a context in which to view and interpret neuropsychological findings.
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Neuropsychological assessment
An optimal neuropsychological battery assesses:
- Learning and retentive memory;
- Executive functioning;
- Language;
- Visuo-spatial skills.