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lesson 17 Flashcards

1
Q

three main points of dementia

A

Not all cognitive declines are dementia

Not all dementias are Alzheimer’s disease

Not all dementias mean memory loss as the main symptom

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2
Q

Dementia

A

acquired and progressive cognitive impairment in multiple domains, which interferes with functioning in everyday living

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3
Q

Prevalence

A

increases with age; 10% of people 65 – 70 –> increases to ~ 20 – 50% of people over 85

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4
Q

Most common condition

A

Alzheimer’s disease –> vascular and Lewy body demential, btu may be caused by at least 80 different disorders

Conditions worsen over time

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5
Q

Diagnostic Criteria for Dementia:

A

Memory impairment

One or more of the following: aphasia, apraxia, Disturbance in executive function

The cognitive deficits result in functional impairment (social/occupational)

The cognitive deficits do not occur exclusively during a delirium

NOT due to other medial or psychiatric conditions

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6
Q

Memory impairment

A

impaired ability to learn new information or to recall old information

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7
Q

Aphasia

A

language disturbance

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8
Q

Apraxia

A

impaired ability to carry out motor activities despite intact motor function

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9
Q

Disturbance in executive functions

A

impaired ability to plan, organize, sequence, abstract

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10
Q

Conditions that can lead to cognitive decline in ageing (other than dementia):

A

Physiological ageing

Mild cognitive impairment (MCI)

Other conditions

—> Different diagnosis is required!

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11
Q

Mild cognitive impairment (MCI)

A

impairment in one (or some) cognitive domain(s) and does not interfere with everyday living

Note: it is not necessary a prodromal phase of dementia, since in a high percentage of people, MCI does not convert to dementia – BUT it constitutes a risk state for the development of dementia

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12
Q

Other conditions

A

as delirium, depression or other mood disorders, aphasia, auditory or visual loos, psychosis –> dementia related to other neurological or psychiatric disorders

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13
Q

Ageing is associated with many neurophysiological changes

A

e.g. gray matter and white matter atrophy or decay in the connectivity of large-scale networks

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14
Q

HEALTHY AGING does not typically lead to

A

marked cognitive decline

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15
Q

In healthy elderly person can observe

A

sychomotor slowing, difficulty in divided attention (dual tasks), episodic learning, deficit, anomia, accentuation of pseudo depressive behavioral traits

Dementia occurs if all these symptoms are excessive and interferes with daily life activities

Note: many factors influence the performance (e.g. pre-existing disabilities, level of education, job placement, physical as well as mental exercise) –> this constitutes the patient’s so-called “cognitive reserve”

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16
Q

A health human brain compared to the brain of a 90-year old

A

which is only 2/3rds the size of the young brain

Over time, white matter decreases, and the brain shrinks – this gradual shrinkage is most extreme between age 70 - 80

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17
Q

Mild Cognitive Impairment (MCI)

A

neurocognitive disorder which involves cognitive impairments beyond those expected based on an individual’s age and education, but which are not significant enough to interfere with activities of daily living

May include both memory and non-memory impairments

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18
Q

50% of people diagnosed with MCI turns into

A

Alzheimer’s disease within five years

Other 50%, MCI may remain stable or even remit

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19
Q

MCI classification

A

Amnestic MCI (aMCI), Nonamnestic MCI (naMCI)

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20
Q

Nonamnestic MCI (naMCI)

A

mild cognitive impairment in which impairments in domains other than memory (for example, language, visuospatial, executive) are more prominent

Patients are believed to be more likely to convert to other dementias –> nonamnestic single- or multiple-domain MCI

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21
Q

Amnestic MCI (aMCI)

A

mild cognitive impairment with memory loss as predominant symptom

frequently seen as a prodromal stage of Alzheimer’s disease

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22
Q

Causes of Dementia

A

Degenerative diseases (neurological diseases)

Trauma (diffuse axonal degeneration)

Outcomes of childhood encephalitis or other infectious diseases (AIDS, syphilis)

Vascular

Hypoxia

Paracarcinomatous (lung or bronchial tumor; limbic encephalitis)

Collagenopathies (lupus)

Alcoholic (Korsakoff syndrome

iatrogenic

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23
Q

Crucial questions - Classifications of Different Types of Dementia

A

Which is the pathogenesis of the cognitive deterioration?

Had the dementia an instrumental versus dysexecutive onset?

Which was/were the first domain(s) to show cognitive impairment?

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24
Q

Which is the pathogenesis of the cognitive deterioration?

A

Based primarily on the phenotype rather than the pathogenesis (biomarkers)

Crucial to distinguish between: primary and secondary form

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25
Q

neurodegeneration

A

neuronal loss

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26
Q

cellular apoptosis

A

a natural process of self-destruction by degradative enzymes in the cell

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27
Q

Primary forms

A

neurodegeneration (neuronal loss) due to cellular apoptosis (a natural process of self-destruction by degradative enzymes in the cell) associated with different processes

e.g. amyloid deposits possibly leading to neurofibrillary degeneration in AD

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28
Q

Secondary form

A

dementia is due to necrosis generated by a non-neurodegenerative process

e.g. vascular pathology in vascular dementia

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29
Q

Had the dementia an instrumental vs dysexecutive onset?

A

Deficits in memory –> aphasic, apraxic, and agnosic disorders

Primary deficits in fronto-executive functions

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30
Q

Primary deficits in fronto-executive functions

A

= impairment of executive function due to pre-frontal dysfunction

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31
Q

Deficits in memory –> aphasic, apraxic, and agnosic disorders

A

= impairment of instrumental functions due to temporo-parietal dysfunction

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32
Q

Which was/were the first domain(s) to show cognitive impairment?

A

Memory

Executive functions/socially appropriate behavior

Language

Visuo-spatial

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33
Q

Memory

A

Alzheimer’s disease (AD)

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34
Q

Executive functions/socially appropriate behavior

A

FTD, Lewy body dementia, Cortico-basal degeneration (apraxia and lateralized parkinsonism), progressive supranuclear palsy (atypical parkinsonism, vertical eye movement paralysis), Parkinson’s dementia, vascular dementia

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35
Q

Language

A

Primary Progressive Aphasias (PPA) – nonfluent/agrammatic type, logogenic type, semantic type (semantic dementia)

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36
Q

Visuo-spatial

A

posterior cortical atrophy (frequently associated with atypical AD)

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37
Q

The brains of people with AD have an abundance of two abnormal structures:

A

Beta-amyloid plaques and Neurofibrillary tangles

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38
Q

Neurofibrillary tangles

A

twisted fibers that build inside the nerve cell

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39
Q

Beta-amyloid plaques

A

dense deposits of protein and cellular material that accumulate outside and around nerve cells

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40
Q

Suspicion of AD

A

Memory disorder with insidious onset (~3 – 6 months before the diagnosis) and progressive evolution

At short distance instrumental disturbances (aphasia, apraxia, agnosia)

Executive function disorders

Psychiatric disorders (later during the disorder)

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41
Q

20% of patients initially show

A

no atrophy –> cortical and subcortical atrophy

Diagnosis: two observations separated by at least 6 months

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42
Q

Alzheimer’s Disease – Symptoms

A

Memory loss

Misplacing items

Difficulty in decision making, problem solving and judgements (executive functions)

Difficulty in completing complex or even familiar tasks

Repetitive speech, difficulties in words and in communication (language functions)

Reading and writing issues

Reduced ability to understand visual images

Confusion with time and location

Mood swing, unfounded emotions, impulsive behaviors, aggressiveness (mood and behavior changes)

Inability to recognize people

Social isolation and/or withdrawal from social activities

Changes in vision

Sleep disorders

Etc…

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43
Q

Down syndrome

A

a genetic disorder caused by the presence of a complete or partial extra copy of chromosome 21

Most constant and typical features of down syndrome are intellectual disability and craniofacial dysmorphisms + other symptoms in a variety of organs and systems

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44
Q

Cognitive phenotype usually characterized by

A

more pronounced language and verbal memory challenges

relatively stronger non-verbal abilities and implicit memory skills but high interindividual variability has been registered in the syndrome related to the level of intellectual disability

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45
Q

when do patients develop AD-like plaque

A

Develop Alzheimer’s-like plaque and tangles deposits early – often before 40 years old

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46
Q

Neuro- and functional profile similar to

A

AD patients

With alterations in parietal, lateral temporal and frontal regions –> memory loss, executive functions but also behavioral problems (as indifference and inappropriateness)

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47
Q

Lewy-body dementia

A

due to abnormal deposits of Lewy bodies in the brain (i.e. abnormal collections of alpha-synuclein protein within diseased brain neurons, manifesting as Lewy bodies and Lewy neurites)

Constituted by 2 different syndromes: (1) dementia with Lewy bodies, (2) Parkinson’s dementia

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48
Q

Dementia with Lewy bodies (DLB) is characterized by:

A

Fluctuating cognition and alertness

Recurrent visual hallucinations

Rapid eye movement (REM) sleep behavior disorder (RBD)

Parkinsonism (slowness of movement, rigidity, postural instability, and tremor)

Neuropsychiatric symptoms (aggression, anxiety, apathy, depression, …)

Changes in regular of automatic bodily functions

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49
Q

DLB has

A

Has widely varying symptoms and is more complex than many other dementias

Prodromal phase of disease may start 15 years + before dementia develops

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50
Q

DLB earliest symptoms

A

constipation and dizziness from autonomic dysfunction, hyposmia (reduced ability to smell), RBD, anxiety, depression

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51
Q

Parkinson’s disease

A

due to a progressive atrophy in the substantia nigra (dopamine hypoactivity) –> determines an unbalance in the direct pathway

52
Q

Onset is characterized by specific motor deficits:

A

Akinesia, Hypokinesia and bradykinesia, Muscle stiffness (hypertone)

Resting tremor

Shuffling gait

Posture in flexion

Reduced facial expressions

Reduced blinking movements

Poor speech articulation

53
Q

Akinesia

A

difficulty initiating voluntary movement

54
Q

Hypokinesia and bradykinesia

A

slowness of movement

55
Q

Symptoms improve taking specific medications aimed at

A

increasing dopamine concentrations

56
Q

Important reduction in

A

dopamine metabolism in basal ganglia –> symptoms appear when the reduction is >70%

57
Q

how is dopamine activity measured and what is it proportional to

A

The reduction in dopamine activity (measured by the number of receptors responsible for the re-uptake of the NT) is proportional to motor deficits

58
Q

over time, PD patients also present

A

Loss of automaticity in motor control and loss of procedural learning because implicit memory depends on the basal ganglia circuits –> progressive higher requirement for voluntary control

Cognitive symptoms: dysexecutive syndrome due to fronto-striatal dysfunction

Psychiatric symptoms (depression, anxiety, sleep disturbances)

Dementia often develops in long-term patients

59
Q

The three deficits are due to the several functions of dopaminergic circuits:

A

Nigrostriatal, Mesolimbic, Mesocortical

60
Q

Mesocortical

A

cognitive control (executive functions, dorsal frontal regions and social cognition (medial frontal regions)

61
Q

Mesolimbic

A

mood and emotional regulation, reward processes, addiction

62
Q

Nigrostriatal

A

motor control

63
Q

Lewy-body dementia – Parkinson’s dementia %

A

~80% of PD people have dementia

64
Q

Similar features PD dementia with Lewy bodies

A

motor, cognitive and executive dysfunctions

65
Q

differences between PDD than DLB

A

delusions and visual hallucinations are less common in PDD than in DLB + higher incidence of tremor at rest in PD than DLB and signs of parkinsonism in PDD are les symmetrical than in DLB

66
Q

Compulsive behaviors

A

due to impulse control disorders, these behaviors may include compulsive gambling or shopping or hyper sexuality

67
Q

DLP is diagnosed when

A

cognitive symptoms begin before or at the same time as parkinsonism

68
Q

PDD is the diagnosis when

A

Parkinson’s disease is well established before dementia occurs (more than a year after onset of parkinsonian symptoms

69
Q

Huntington’s disease

A

an inherited genetic condition that causes dementia

70
Q

Huntington’s disease causes

A

Causes a slow and progressive decline in a person’s movement, memory, thinking and emotional state

71
Q

Huntington’s patients may be less able to

A

May be less able to recognize other people’s emotions (theory of mind) - difficulty in concentration, planning

72
Q

HD - emotional, memory and recognition

A

Emotional difficulties can lead to difficulties in their relationships and work

Preserved explicit memory but difficulties in procedural memory

Patients may continue to recognize people and places until the very late stages of the disease

73
Q

Huntington’s disease neural correlates

A

subcortical involvement - enlarged ventricles, atrophy of cerebral nerve tissue and basal ganglia

74
Q

what is HD due to

A

A degenerative disease due to a progressive atrophy in caudate and putamen structures –> determines an unbalance in the indirect pathway

determined by a mutation of a dominant gene on chromosome 4

75
Q

HD is the most common

A

Most common autosomal dominant neurological disease of adulthood

76
Q

HD patients

A

Affects 5 – 10/100,000 individuals

Most cases occur between 20 – 40 years of age:

77
Q

HD symptoms

A

motor, cognitive, psychiatric

78
Q

HD motor symptoms

A

chorea, athetosis, and later rigidity and dysarthria

79
Q

HD cognitive symptoms

A

cognitive slowing and dysexecutive deficits

80
Q

HD psychiatric symptoms

A

anxiety, irritability, aggressive, psychotic behavior

81
Q

HD differences between patients

A

Some patients exhibit poor judgements and socially inappropriate behaviors, others are apatic and abulic

82
Q

HD treatment

A

Treated with drugs that reduce chorea symptoms, but the efficacy on cognitive and psychiatric symptoms is limited

83
Q

Vascular dementia

A

a general term describing different pattern of symptoms caused by brain damage from impaired blood flow to the brain

84
Q

vascular dementia symptoms variation explanation

A

Dementia symptoms vary, depending on the part of your brain where blood flow is impaired

85
Q

vascular dementia most significant symptom

A

Most significant symptoms of vascular dementia tend to involve speed of thinking and problem-solving rather than memory loss

86
Q

vascular dementia symptoms

A

Confusion

Trouble paying attention and concentrating

Reduced ability to organize thoughts or actions

Decline in ability to analyze a situation, develop an effective plan and communicate that plan to others

Slowed thinking

Difficulty with organization

Difficulty deciding what to do next

Problems with memory

Restless and agitation

Unsteady gait

Sudden and frequent urge to urinate or inability to control passing urine

Depression or apathy

87
Q

Korsakoff dementia

A

a chronic memory disorder caused by severe deficiency of thiamine (vitamin B-1)

Most commonly caused by alcohol abuse or by a diet with a deficiency in vitamin B1 assumption

88
Q

Korsakoff dementia symptoms

A

Problems learning new information, inability to remember recent events and long-term memory gaps

Implicit and semantic memory are preserved

May be present hallucinations and confabulation –> patients fill their memory gaps with delusional fantastic productions

Social skills may be relatively unaffected

For example: individuals may seem able to carry on a coherent conversation but moments later are unable to recall that the conversation took place

89
Q

Fronto-temporal Lobe Degeneration (FTLD)

A

From an anatomopathological point of view, degenerations in frontal and/or temporal lobe, due to a non-AD frontal lobe degeneration or Pick disease

90
Q

FTLD three classical behavioral syndromes

A

Fronto-temporal dementia

Nonfluent primary progressive aphasia

Semantic dementia

91
Q

FTLD what’s appropriated and not appropriate for diagnosis

A

MODA and MMSE are not appropriate for a diagnosis –> frontal tests first

10% of patients have delusions and hallucinations

92
Q

FTLD - Fronto-temporal Dementia onset and evolution

A

Insidious onset and progressive evolution – onset: age of 45 – 70y

93
Q

FTLD - Fronto-temporal Dementia symptoms

A

serious alteration of personality and social conduct

Inertia

Loss of initiative

Apathy

Social disinhibition

Distractibility

Mild memory deficit

Anosognosia

Irritability

Smoking, drinking and eating abuse

SIMILAR TO DEPRESSIVE DISORDER OR HYPOMANIC STATE

Automatic utilization of objects and imitation of behaviors (environmental dependency syndrome)

Deficit in executive functions: attention, abstraction, planning and decision-making
perception, spatial abilities and praxis abilities are preserved

Memory deficits are secondary to attentional and executive dysfunctions

Language

94
Q

fronto-temporal dementia language

A

poor verbal initiative, stereotypes, perseveration of a limited number of sentences, up to mutism (final phase of dementia)

95
Q

Primary progressive aphasia (PPA)

A

characterized by progressive language impairment without other disorders for at least 2 years –> behavioral disorders: irritability and apathy

96
Q

PPA onset

A

before age of 65

97
Q

PPA Symptoms vary based on

A

which part of the brain’s language areas are involved – has three types

98
Q

PPA symptoms types

A

Nonfluent-agrammatic variant primary progressive aphasia

Logopenic variant primary progressive aphasia

Semantic variant primary progressive aphasia, or semantic dementia

99
Q

Semantic variant primary progressive aphasia, or semantic dementia

A

progressive cognitive and language deficit, primarily involving comprehension of words and related semantic progressing

Trouble understanding spoke or written language, particularly single words

Trouble understanding the meaning of words

Not being able to name objects

Trouble formulating sentences

100
Q

Logopenic variant primary progressive aphasia

A

trouble understanding spoken language, particularly long sentences

Pausing and hesitancy during speech while searching for words

Not being able to repeat phrases or sentences

101
Q

Nonfluent-agrammatic variant primary progressive aphasia

A

effortful speech, telegraphic, agrammatic and anomic –> like Broca’s aphasia

Poor grammar in written and spoken language

Trouble understanding complex sentences

Using grammar incorrectly

102
Q

‘mixed dementia’

A

a person has more than one type of dementia

103
Q

‘mixed dementia’ - most common

A

Alzheimer’s and vascular are most common type or Alzheimer’s and dementia with Lewy bodies

104
Q

‘mixed dementia’ - predominance

A

Often someone will have a greater amount of one type of dementia than another –> this type is ‘predominant’

105
Q

‘mixed dementia’ - Behavioral and Psychological Symptoms

A

Present in 80 – 90% of patients with dementia – distressing for all involved

Psychosis (delusions o hallucinations)

Agitation/aggression

Apathy/indifference

Depression/dysphoria

Anciety

Elation/euphoria

Disinhibition

Irritability/lability

Aberrant motor behavior

Insomnia

Appetite disruption

106
Q

How to Diagnose Dementia?

A

Comprehensive clinical assessment including clinical observation, instrumental evaluations (neuroimaging, neurophysiology), blood and/or cerebrospinal fluid tests and neuropsychological testing

107
Q

Dementia assessment - first

A

First a clinical interview and administration of a brief global assessment tool = mandatory for identification of critical cases

108
Q

dementia assessment - second

A

Then complete neuropsychological testing required to identify specific neurodegenerative profiles, for differential diagnosis and correct identification of the type of dementia

109
Q

clinical interview

A

Regarding the exploration of the patient’s developmental and medical history, academic and work functioning, socialization and social support

Includes the clinical evaluation of the patient’s awareness of the deficit, subjective feelings about them, speech quality, quality of thinking, range and appropriateness of emotional expression

110
Q

Brief global assessment tools

A

e.g., the Mini-Mental State Examination (MMSE)

111
Q

The Mini-mental State Examination - PROS

A

very fair, widespread application, corrective scores for age and education are available, scores between 26 – 24 indicate ‘at risk’ conditions, score lower than 24 indicate possible dementia

In both cases the score indicated the need for a complete neuropsychological assessment

112
Q

The Mini-mental State Examination - CONS

A

low sensitivity as a stand-alone instrument, strongly influenced by education, socioeconomic status, and prior intellectual achievement, overweighted for language, underweighted for recent memory and executive function assessment

113
Q

Assessment for AD

A

Assessment of dysexecutive syndrome – FAB (Frontal Assessment Battery)

114
Q

Assessment of dysexecutive syndrome – FAB (Frontal Assessment Battery)

A

Six subtests exploring the following

Conceptualization

Mental flexibility

Motor programming

Sensitivity to interference

Inhibitory control

Environmental autonomy

115
Q

Management/Treatment of Dementia - main goal

A

Main goal is to control the symptoms of dementia

116
Q

Management/Treatment of Dementia

A

Treatment depends on the condition causing the dementia

Treatment of cognitive dysfunction but also, and above all, the behavioral and psychological symptoms of dementia

117
Q

Management/Treatment of Dementia - pharmacological treatment

A

for slowing down the disease progression

118
Q

Management/Treatment of Dementia - nonspecific cognitive activation

A

can take place informally (spontaneously during daily meetings) or as part of a structured, individual or group activity

Reality-orientation therapy

Reminiscence and life review therapies

119
Q

Management/Treatment of Dementia - Specific cognitive activation

A

Memory training, Subject performed task, Language and communication treatment

120
Q

Management/Treatment of Dementia - Doll therapy

A

recognized intervention for people living with dementia to help address cases of depression, agitation and lack of fulfilment

Dolls are introduced to residents where it is felt that they may provide a source of comfort or meet an individuals need to care for someone else

May provide structure and a sense of responsibility and has been observed to have positive effects on mood

121
Q

Management/Treatment of Dementia - Reality-orientation therapy

A

used in the initial stages of the disease to try to orient the patient to memory, space and time, trying to remember names, stimulating memories and giving space0time references

122
Q

Management/Treatment of Dementia - Reminiscence and life review therapies

A

based on the natural propensity of the elderly to recall their past, these intervention uses memory as an indispensable tool to stimulate residual memory resources and to recover emotionally pleasant experiences – process developed by enhancing remote amnestic abilities, integrating past memories with recent ones and expanding recent memory

123
Q

Management/Treatment of Dementia - Memory training

A

Examples: use of mnemonics (e.g., transform the story to be remembered into images), items categorization, vanishing cues, repetition priming, conditioning

124
Q

Management/Treatment of Dementia - Subject performed task

A

based on the assumption that you remember something better if you simultaneously perform it

125
Q

Management/Treatment of Dementia - Language and communication treatment

A

primarily based on anomia, perseverations, loss of speech, articulatory disorders

neuropsych (25 decks)

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