3 Mild Cog Impairment and Alzheimer´s Flashcards
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Mild Cognitive Impairment (MCI)
A
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?
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- Implicit memory;
- Vocabulary;
- Storage of general knowledge.
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What declines in normal aging?
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- 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.
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Structural brain changes in normal aging
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- 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
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- 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
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- 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
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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
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- 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
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- 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
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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
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- Degenerative;
- Vascular;
- Psychiatric;
- Traumatic.
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Pathology and neuro diagnostic findings= Typical differential diagnosis focusses on
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- Normal cognitive ageing;
- Dementia;
- Depression (‘pseudo-dementia’) or delirium; - Reversible causes (for instance medication).
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Clinical interview
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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
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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
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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
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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
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- 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
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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
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- 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
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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)
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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
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- 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
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An optimal neuropsychological battery assesses:
- Learning and retentive memory;
- Executive functioning;
- Language;
- Visuo-spatial skills.
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Assessment of Memory
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The most important measure is the List Learning Task, which measures difficulties with delayed recall and the rate of forgetting. These are important features of AD, but not every patient will have these symptoms
A flat learning curve=
Will point to the direction of AD.
- Proactive interference: old learning interferes with new learning.
- Retro-active interference: new learning interferes with old learning.
- Pro-active interference is associated with MCI patients who progress to dementia within 2-3 years
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| Assessment of non-memory functions
- Language;
- Executive functioning;
- Visuo-spatial skills and constructional praxis (the ability to perform skilled motor movements);
- Attention;
- Psychomotor speed.
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| When do you use a neuropsychological test?
- With any older adult in which it is important to establish the presence or absence of cognitive deficits, or where the clinician is unsure about the nature and extend of certain cognitive deficits.
- Neuropsychological tests only provide a snapshot of a person’s performance. Longitudinal assessment may be necessary to define accurately a particular condition.
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| Depression
Depression may be a primary mood disorder, but it could also be the early sign of dementia.
The prevalence of depression in older adults is 3-14 %. Approximately 1 in 15 older adults experiences a major depressive disorder in the course of 1 year.
Depression in late life can be associated with significant cognitive impairments.
These depression related impairments are often similar to those seen in dementia, which gave it the name ‘pseudo-dementia’, and later ‘reversible dementia’.
The first pseudo-dementia patients were described as followed= - Highlighting their failures, emphasizing their disabilities.
- Their functional deficits were incongruent with the mildness of their cognitive deficits.
- They didn’t know responses to closed questions (yes/no), but showed detailed responses to open questions.
- There was a clear onset of the cognitive impairments
- They showed no attempts to compensate for their difficulties.
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| Dementia
- Patients show a lack of insight in their dysfunctions.
- Try to minimize their symptoms.
- Show temporally graded deficits (no clear onset).
- Try to compensate for their difficulties.
Currently, the term pseudo-dementia is not used anymore. The term implies that it is a mutually exclusive process (pseudo-dementia ór dementia) while it is also possible that both conditions are present. Reversible dementia implies that it is a reversible condition and that it lacks pathology. While the cognitive deficits may actually not be truly reversible: the treatment of depression may lead to improvements but true reversibility of the cognitive symptoms is uncommon.
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| Depression as a symptom of dementia
Depressive symptoms can be a manifestation of an underlying progressive dementing illness. Depression is the most common psychiatric symptom in individuals with dementia or cognitive impairment. This depression is not a reaction to the illness itself. There is no association between the severity of the dementia and the depression.
Depression may be a risk factor for developing dementia, but it could also be a behavioral manifestation of the dementia process itself, this relationship remains unclear.
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| Clinical assessment
Neuropsychological evaluations can have a significant contribution to the diagnosis.
Depression in older adults is often difficult to assess. The reasons why:
- Symptoms of depression are easily confounded by the effects of age or a medical disorder.
- Older adults are more likely to underestimate their depression symptoms (the common misconception is that depression is a normal part of ageing while ageing isn’t an increased risk for developing depression).
- Older adults are less likely to deport dysphoric mood than younger adults (they often only report vague symptoms).
When older adults report cognitive problems, they should be screened for a depression, regardless of the referral question. Possible screenings for depression are:
- Beck Depression Inventory (BDI-II);
- Hamilton Depression Rating Scale (HDRS);
- Geriatric Depression Scale (GDS) (specifically for depression screening in older adults).
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| Differential Diagnosis
It is important to rule out diagnoses with both cognitive and psychiatric symptoms.
- Primary psychiatric disorders=
Anxiety, depression and bipolar disorder (onset of the last one in late adulthood is unusual)
- Dementia subtypes=
AD, Lewy Body dementia, frontotemporal dementia and vascular dementia.
- Stroke;
- Medications;
- Chronic medical illness
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| Differences between depression and dementia
1. Onset=
Dementia: gradual (often over the course of years).
Depression: more acute (over the course of days/weeks).
2. Complaints=
Dementia: lack of insight into their symptoms, minimizing their cognitive difficulties.
Depression: subjective cognitive complaints, complaining more and the complaints are out of proportion.
3. Apathy and dysphoric mood=
Dementia: more likely to show apathy (a loss of motivation, indifference). Depression : more likely to show dysphoric mood (self-criticism, sadness, guilt and hopelessness) and a loss of self-esteem.
4. Number of symptoms and prominence=
Dementia: presence of minimal 3 depressive symptoms + social isolation and irritability. Not necessarily present every day.
Depression: presence of minimal 5 depressive symptoms, present nearly every day.
5. Age of onset=
Dementia: later age of onset during older adulthood.
Depression: early age of onset during older adulthood.
6. Sleep=
Dementia: difficulty awakening in the morning, poor sleep efficiency and later sleepiness. Depression: early morning awakenings, difficulty staying asleep in the morning, higher number of night awakenings.
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| Neuropsychological profiles of depression and dementia= Objective assessment of cognitive functioning
1. Effortful – automatic hypothesis= Depression: shows deficits in effortful processing, and will therefore be showing difficulties on tasks requiring a high degree of cognitive resources. Performance will be adequate on automatic tasks (less effort is needed).
Dementia: decrements in the ability rather than the effort of processing. This will lead to difficulties in tasks that are independent of effort.
2. Progression vs. stabilization=
Depression: the deficits stabilize or even improve over time. Dementia: deficits are progressive.
3. Cues in recall=
Depression: executive functioning deficits are most prominent, therefore: cues in delayed recall will lead to improvement.
Dementia: memory deficits are most prominent, so there will be no benefit from cues in delayed recall.
4. Recognition performance
Depression: adequate performance on recognition tasks. Depressed individuals take a more conservative approach to recognition tasks, leading to ‘I don’t know’ answers and false negatives.
Dementia: impaired performance on recognition tasks (no encoding of information). Demented individuals will show a more liberal approach to recognition tasks, leading to more falsepositives.
5. Serial position effects
Depression: depressed individuals will show advantages from the recency and primacy effects, the middle words of a list will have poorer recall, leading to a U-shaped curve. Dementia: demented individuals will show an advantage of the recency effect (the last words) but not from the primacy effect (first words), leading to an upward slope line
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| Dementia
Latin: “madness” or “without mind”
Definition: Dementia is a syndrome due to disease of the brain, usually chronic, characterized by a
progressive, global deterioration in intellect including memory, learning, orientation, language,
comprehension and judgement.
Consequence: loss of independent living skills (both social an work-related)
35,6 million people with dementia world wired / 5% od population 65+ / Prevalence double with
every 5 year increment in age: 20-40% in 85+
Main risk factor: age
2-10% of all dementia cases 65-
More women than men with dementia!
No treatments available that cure, or even alter the progressive course of dementia. Partially effective
treatments are available, but these treatment are symptomatic.
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| Alzheimer´s Disease
- A degenerative brain disorder characterized by progressive intellectual and behavioral
deterioration
- Symptomatically usually dominated by, memory disorder, with prominent visusospatial and
language impairment in the context, at least early in the course, or preserved social skills
- Broad age range of clinical onset but usually after age65
- Life span after diagnosis generally about 10 years, but can be as long as 20 years
- Motor and primary sensory disturbances are either not present or are late manifestations
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| Alzheimer´s DSM5
- Insidious onset and gradual progression of impairment in one or more cognitive domains.
- Clear evidence of decline in memory and learning and at least one other cognitive domain
- No evidence of mixed etiology (i.e. absence of other neurodegenerative or cerebrovascular
disease or any other disease that can contribute to cognitive decline)
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| Alzheimer´s Pathology
Mediotemporal lobe atrophy. Dying back of cholinergic neurons.
- Plaque formation begins with abnormal misfolding of beta amyloid protein.
- Leads to neurofibrillary tangles
- Consequence: synatptic disruption and neurodegeneration
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| Alzheimer´s Memory
AD: progressive memory impairment!
Mild stages:
- Inconsistent but more-than-before forgetful
- Forgetting names, phone numbers, recent conversations, misplacement of personal stuff
- Missing appointments and forgetting to remember tasks in the future (prospective
memory)
Mild stages:
- Housekeeping, most activities of daily living are usually reasonably well maintained – if other
people “cover” for diminished capacity
- Clues, cues and multiple choices usually improve retrieval and recognition of forgotten items
Moderate stages:
- Often starts when memory impairment affects daily living
- Forgetting becomes more persistent, resulting in repetitive iterations of the same questions
and statements, often accompanied by irritable insistence that he/she is doing no such thing
- Patients can neither store new information for more than a few minutes or maintain a
coherent stream of thought
- Increased reliance on spouse, children or friends
Severe stages:
- Even the most overlearned memories are starting to be lost or inaccessible, including
recognition of close family or even of personal identity
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Alzheimer
Memory impairments
-Related to degeneration of hippocampus and entorhinal cortex
Long term memory - assessment
- Word list: e.g. Rey Auditory Verbal Learning Test
o 15 common words, recalling, after 20 minutes again
- Evaluation of:
o Encoding – acquisition of information
o Consolidation – storing information in long term memory
o Retrieval – retrieving information from memory
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Alzheimer
Working Memory
- Early stages in AD: working memory is relatively spared
| - Moderate to sever: working memory is affected
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Alzheimer
Visuospatial and perceptual functions
Clinical manifestations:
- Environmental and geographic disorientation: getting lost, aimless wandering
- Dressing disturbances (apraxia): inability to locate shirt or pant legs or to match socks
- Impaired contrast and figure-ground discrimination: consistently missing the toilet, difficulty
locating misplaced objects, inability to segregate clothes properly withing a closet
- Various viusal agnosias: non-recognition of common objects and their use (eating utensils)
and familiar faces, including one’s own, inability to discriminate among members of a given
class (e.g. animal species)
Associated with pathology in visual association cortex. Occurs early but in general it is clinically
apparent until memory and attentional disturbances are fully established.
Assessment:
- Copy of complex figure of Rey (werid house)
- Clock drawing
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Alzheimer
Lanuage
Aphasia: the acquired disturbance of language secondary to brain damage
Importan feature of AD!
Earlies manifestation:
- Word finding difficulties, speech becomes less spontaneous, speech becomes emtpy (“it,
things”)
Moderate stages:
- Auditory comprehension deteriorates, significantly anomic in confrontation naming tasks
- Language remains fluent with preserved repition but semantic (whole word) and neologistic
(non-word) paraphasia litter the output
- Basic language structure is intact: nouns are placed where nouns should go and verbs and
other tyoes of words are placed where they should go
Severe stages:
- Patients become more dysprosodic
- Some patients develop reiterative speech disturbances
o Echolalia: repeating others words and phrases
o Palilalia: repeating his/her own words and phrases
- Finally patient becoms mute
General conclusion:
In AD: both output (speech and writing) and input (auditory and reading comprehension) are affected
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Alzheimer
Apraxia
Definition: a family of cognitive motor disorders that entail the loss or impairment of the ability to
program motor systems to perform purposeful skilled movements
Two types:
- Ideational: failure to pantomime correctly the sequence of events of a complex motor act,
such as selecting and lighting a cigarette
- Idiomotor: inability to do on command or imitate an act that can be performed automatically,
such as brushing one’s teeth
Assessment by giving commands
- Pretend to comb you hair, brush your teeth
- Rarely an early disabling symptom in AD
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Alzheimer
Attention and executive functioning
Attention
- Divided, selective and sustained attention (vigilance)
- Sustained attention is preserved in early stages of AD
- Patients eventually become distractible and have poor concentration
Executive functioning
- Planning, set-shifting, inhibition, working memory, initiation, etc
- Executive functions are mainly applied in non-routine situations
- Impairments in executive functions are already present in the mild stages of AD
- Impairments in executive functions often underlie problems with activities of daily living
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Alzheimer´s
Neuropsychiatric issues
- Core feature of AD
- Occur earlier in some patients than in others
- Once established, some evolve, some remain stable, some recede
- Behavioral deterioration may be triggered suddenly by an acute stressor, e.g. change in
environment
- Changes range from apathy and social withdrawal to disinhibition, agitation, eating disorder
and psychosisvvvv
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Alzheimer´s
Personality and social beh
Early stages:
- Personality and social behavior broadly preserved (subtle indifference or emotional
detachment may be present)
- Many AD patients function well socially -> Consequence: others underestimate or excuse cognitive impairments
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Alzheimer´s
Aphaty
Definition:
- Lack of motivation relative to patient’s baseline state. Ranges from mild passivity and loss if
interest to abulic immobilization
- Most common neuropsychiatric manifestation in AD
- Can be misdiagnosed as depression
o Low mood and apathy frequently go hand in hand
Separate phenomena with different neuroanatomic substrates
Half of the apathetic patients with AD are not depressed
Strongly associated with anosognosia (deficit of self-awareness) and executive dysfunctions.
- Consequence: They don’t know and they don’t care
- Underlies e.g. poor hygiene and inappropriate dressing
- Common in the moderate stages of AD
Apathetic AD patients are more dependent with regard to their activities of daily living than nonapathetic
patients
Apathetic AD patients more often develop other behavioral disturbances!
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Alzheimer´s
Other neuropsychiatric issues
- Delusions and hallucinations
o Delusions are more common than hallucinations and usually are persecutory,
involving fears of personal harm, property theft and spousal infidelity
o Hallucinations are usually visual
o Predict more rapid functional and cognitive decline
- Depression
o AD and depression often coexist and symptoms overlap
o Depression often precedes the development of AD
- Aggression and agitation provoked by:
o Confusions due to cognitive, memory or language impairments
o Delusions, depression, sleep disturbances, pain, infections, etc.
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| AD SUMMARY
Core feature: impairments in memory
- Learning new information
Other cognitive impairments in:
- Language, visuospatial and perceptual functions, praxis, attention and executive functions
Neuropsychiatric disturbances are often present
- Most common: apathy!!
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| Mild cognitive impairment
MCI: subjective and objective cognitive symptoms greater than expected for an individual’s age and
education level which do not interfere with activities of daily life
- MCI is a transitional stage between normal aging and dementia!
Diagnostic criteria:
1. Concern regarding cognition
a. Concern for change in patients cognitive status as compared to previous lecel and
concern on part of the patient, informant who knows the patient well or clinician
2. Impairment in one or more cognitive domains
a. Lower performance than what would be expect for age and educational level,
impairment may be in a variety of cognitive domains
3. Perservation of independence in functional abilities
a. Maintains his/her independence of function in daily live without assistance and may
have mild problems with complex functional tasks
4. Not demented
a. Cognitive changes are so mild that there is no evidence of significant impairment in
social or occupational functioning
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| MCI subtypes
- Single VS Multiple domain
| - Amnesic VS Non-amnesic
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| Etiology
```
Different subtypes = Different etiologies
Most likely etiologies:
- Neurodegenerative disease (e.g. AD)
- Vascular (e.g. cerebrovascular disease)
- Psychiatric (e.g. depression)
- Traumatic (e.g. head injury)
Other potential etiologies:
- Medication side effects
- Metabolic effects
o Thyroid dysfunction
o Dysfunction of other hormones
o Vitamin B12 deficiency
- Infection
```
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| Mild conitive impairment
General prevelance: 19%+ until 75 and 29%+ for 85+
Conversion rates:
10-19% of MCI to AD per year
Comparison: 1-2§ of general population develop AD per year
Study 6 year follow up:
- 65-80% converted to dementia
- 48% to AD / 15% to DLB / 3% to other types of dementia
MCI patients who do not develop a dementia over a time remain stable or show an improve in
cognition
- Cause of cognitive dysfunction is reversible (e.g. metabolic factors or medication use)
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| MCI Differential Diagnosis
- Normal cognitive aging
- Dementia (AD, DLB, FTD)
- Depression
- Delirium
- Metabolic factors, medication use, etc
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| Depression as differential MCI diagnosis
Patients with a depression can show impairments in:
Memory, executive functions, attention,
psychomotor speed
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| Delirium as differential MCI diagnosis
Delirium: an acute clinical condition of any origin that manifests itself with a disturbed consciousness,
and cognitive dysfunction, sometimes followed by psychotic and affective symptoms and the
fluctuations of such symptoms during the course of the day
Possible causes:
- Alcohol abuse, surgery, medication use, multiple etiologies
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| Delirium DSM
1. Disturbance in attention and awareness
2. Develops over a short period of time (hours to days) and fluctuates in severity
3. Additional disturbance in cognition (memory, language, disorientation, etc.)
4. 1 and 3 not better explained by other disorders
5. Evidence that disturbance is not due to other effects (medication, drugs, etc)
Prevelance:
1-2% in population
Increases with age, rising to 14% in individuals 85+
Older adults admitted to hospitels: 14-24%
- 15-53% postoperatively and 70-87% at the intensive care
Development and course: Majority of patients have a full recovery and treatment can shorten the
duration of a delirium
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| SUMMARY
MCI
- MCI is a transitional stage between normal aging and dementia
- There are different subtypes of MSI
o Single and multiple domain amnestic MCI
o Single and multiple domain non-amnestic MCI
- In clinical practice, one should be aware of possible differential diagnosis:
o Types of dementia, depression, delirium
- The majority of MCI patients convert to dementia (AD most common in this context)
- Some MCI patients remain stable or their cognition improves over time
AD
- Memory impairment are most prominent
- Impairments in executive function, attention, visuospatial and perceptual skills, praxis and
language are also often present
- Many patients have neuropsychiatric disturbances
o Apathy is most often present
