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Neurology > Cognitive Aging And Dementia > Flashcards

Cognitive Aging And Dementia Flashcards

1
Q

What is normal cognitive ageing?

A

Slower to think
Slower to do
Hesitates more
More likely to ‘look before you leap’
Know the person but not the name
Pause to find words
Reminded of the past

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2
Q

What is cognitive ageing not?

A 
Can’t think the same
Can’t do like before
Can’t get started
Can’t seem to move on 
Doesn’t think it out at all 
Can’t place the person 
Words won’t come – even later 
Confused about past versus now
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3
Q

What is there in healthy ageing?

A

JLoss f brain volume 
Expansion of the ventricles

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4
Q

What is the pattern of change in healthy ageing?

A

Heterogeneous

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5
Q

At what age does grey matter begin to decrease?

A

Age 20

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6
Q

Where is there greater decreases in grey matter?

A

In cortical structures

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7
Q

Where is atrophy most prominent in grey matter?

A

The prefrontal cortex

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8
Q

What does more moderate age related changes in the temporal lobe involve

A

Decreases hippocampus volume

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9
Q

What I has greater decrease than grey matter with increasing age?

A

White matter

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10
Q

What does Decreased parahippocampal white matter lead to?

A

decreased communication with hippocampal structures
 Suggests a possible mechanism for age-associated memory declines.

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11
Q

Where are the Most marked age-related declines?

A

the anterior white matter
 Associated with deficits in executive function.

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12
Q

What may Loss of integrity of the central portion of the corpus callosum mediate

A

age-related cognitive decline.

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13
Q

What are possible causes of cognitive ageing?

A

Accumulation of Beta-amyloids
 High levels of beta-amyloid associated with decreased hippocampal volumes and episodic memory in cognitively normal individuals.
Morphologic changes in neurons likely contribute directly to the reduction of synaptic density.
 Including a decrease in the complexity of dendrite arborisation, decreased dendrite length, and decreased neuritic spines (the major sites for excitatory synapses).
A decrease in neuron size and the number of connections between them.
Neuronal Death

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14
Q

What is cognition?

A

JThe mental action or process of acquiring knowledge and understanding through thought, experience, and the senses. (Oxford Dictionary, 2016)
Refers to our information processing systems and stored knowledge

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15
Q

What is cognition mission?

A

Analyse sensation
Detect and remember irregularities in incoming sensory information
Use experience to guide behaviour

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16
Q

How are the Patterns of cognitive change over the lifespan described?

A

using the concepts of crystallized and fluid intelligence.

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17
Q

What is crystallised intelligence?

A

JSkills, ability, and knowledge that are well- practiced, overlearned, and familiar.
E.g. Vocabulary and general knowledge
Remains stable or gradually improves through the sixth and seventh decades of life.

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18
Q

What is fluid intelligence?

A

IAbilities involving problem-solving and reasoning about things that are less familiar and are independent of what one has learned.
Includes the innate ability to process and learn new information, solve problems, and attend to and manipulate your environment.
Executive function, processing speed, memory, and psychomotor ability are considered fluid cognitive domains.

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19
Q

What are the components of cognition?

A 
Processing speed 
Attention 
Language 
Memory 
Visuospatial abilities 
Excecutive functioning
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20
Q

What speed is processed by cognition?

A

The speed with which cognitive activities are performed as well as the speed of motor response

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21
Q

When does decline in processing speed begin?

A

third decade and continues throughout the lifespan.

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22
Q

What can rediuced processsing speed have implications across?

A

a variety of cognitive domains

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23
Q

What tends to be as a result of slowed processing speed?

A

Many of the cognitive changes reported in healthy older adults

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24
Q

What is attention?

A

The ability to concentrate and focus on specific stimuli.

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25
Q

Simple auditory attention span (immediate memory) measured by repetition of a string of digits shows only a slight decline when?

A

In later life

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26
Q

What are signs for decreased attention?

A

Noticeable age effect on more complex attention tasks, e.g. selective and divided attention.
• Older adults also perform worse than younger adults on tasks involving working memory,

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27
Q

What is Visuospatial Abilities/ Construction?

A

The ability to understand space in two and three dimensions.

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28
Q

How do visuospatial albilities decline?

A

Over time - generally stay intact

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29
Q

What is Executive Functioning?

A

JCapacities that allow a person to successfully engage in independent, appropriate, purposive, and self-serving behaviour.
• E.g. self-monitoring, planning, organisation, reasoning, mental flexibility, and problem-solving.

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30
Q

When does Concept formation, abstraction, and mental flexibility decline?

A

with age, especially after 70. Tendency to think more concretely.

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31
Q

What are particularly susceptible to age effects?

A

Executive abilities requiring a speeded motor component

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32
Q

What does ageing also negatively affect?

A

response inhibition, the ability to inhibit an automatic response in favour of producing a novel response.

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33
Q

What types of executive functions remain stable?

A

the ability to appreciate similarities, describe the meaning of proverbs, and reason about familiar material

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34
Q

What is language?

A

Language is everything that allows meaningful communication

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35
Q

Does vocabulary decrease over time?

A

UVocabulary remains stable and even improves over time.

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36
Q

What does decline.with age?

A

Visual confrontation naming, stable until age 70, declines in subsequent years.
Verbal fluency

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37
Q

Age-related memory changes may be related to what?

A

slowed processing speed, reduced ability to ignore irrelevant information, and decreased use of strategies to improve learning and memory.

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38
Q

What types of memory remains stable with age?

A

• Non-declarative Memory
• Retention
• Recognition memory: ability to retrieve information when given a cue
• Temporal order memory: memory for the correct time or sequence of past events
• Procedural memory: memory of how to do things
(Harada, Natelson Love and Triebel, 2013)

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39
Q

What types of memory decline with age?

A

Declarative (Explicit) Memory
• Declines in semantic and episodic memory occur with normal aging, the timing of these declines is different.
• Episodic memory shows lifelong declines while semantic memory shows late life decline
• Acquisition
• Retrieval
• Delayed free recall: Spontaneous retrieval of information from memory without a cue
• Source memory: Knowing the source of the learned information
• Prospective memory: Remembering to perform intended actions in the future

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40
Q

What structures play a role in memory?

A 
Basal forebrain
Prefrontal cortex 
Mediodorsal nucleus
Amygdala 
Rhinal cortex
Hippocampus 
Inferotemporal cortex 
Cerebellum
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41
Q

Describe the term dementia

A

Term ‘dementia’ first used in 1801 by Phillipe Pinel, a French physician with a 34 year old patient presenting with progressive loss of cognitive and physical function
 ‘Demence’ referring to incoherence or loss of mental function  On autopsy: small brain, excess fluid

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42
Q

Give O’shea, 2007’s definition of dementia.

A

Dementia refers to a group of diseases characterised by progressive and, in the majority of cases, irreversible decline in mental functioning.
The loss of cognitive abilities resulting from damage to the neurons in certain areas of the brain is often accompanied by deterioration in emotional control, social behaviour and motivation.
The effects of the damage to the brain intensify over time and are disabling and terminal.

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43
Q

What is a way to describe dementia?

A

Dementia is an umbrella term used to define over 100 different conditions that impart memory, behaviours and thinking. The most common causes of dementia are outlined below

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44
Q

Describe the prevalence of dementia

A

90,000 people living with dementia in Scotland; expected that 20,000 new cases will be diagnosed every year by 2020 (Alzheimer Scotland, 2017).
Globally, stable or declining prevalence and incidence of dementia, no single risk or protective factor has been identified that fully explains the trend (Wu et al., 2017)

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45
Q

Why is dementia sometimes called Major Neurocognitive Disorder?

A

DSM 5’s intent: Avoid “dementia’s” negative connotation
Better distinguish between disorders that have cognitive impairment as their primary feature and those that don’t
More accurately reflect the diagnostic process

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46
Q

What is the diagnostic criteria?

A

One or more acquired significant impairments (independence lost) in cognitive domains

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47
Q

What are the domains for the criteria?

A

Memory (amnesia)
Language (aphasia)
 Execution of purposeful movement (apraxia) Recognition/familiarity (agnosia)
 Visuospatial function (topographical disorientation)
 Self control/management (executive functions impairment)
 Other examples:
 Mathematics (dyscalculia)
 Emotional expression/comprehension (dysprosody)  Writing (agraphia)

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48
Q

What does neuropsychology address?

A

the link between brain and behaviour

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49
Q

What is neuropsychological assessments an objective way to do?

A

to quantify and characterise the cognitive, behavioural and emotional changes which can occur following brain disease.

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50
Q

Move from viewing Dementia as a generalised impairment of function to what?

A

distinct profiles of change depending on the distribution of neuropathology

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51
Q

What domains are examined in dementia?

A 
Premorbid function 
Memory 
Attention 
Visuospatial 
Language 
Effort/motivation 
Executive functions 
Praxis 
Mood
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52
Q

In the early stages neurodegenerative diseases show what?

A

a preference for certain brain regions with relative sparing of others

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53
Q

As a result of the preference for certain brain regions with relative sparing of others what happens?

A

they have discernible cognitive profiles associated with the distribution of the neuropathology

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54
Q

Profiles help with what?

A

diagnosis and differentiation from other dementias

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55
Q

What 5 things are involved in diagnosis?

A 
Detailed medical history 
Onset and course of progression 
Profile of cognitive impairment 
Presence of non- cognitive symptoms such as behavioural disturbance, hallucinations and delusions
Career involvement
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56
Q

What is differential diagnosis?

A

Reversible causes
Progressive decline may be slowed/stopped
Differing impairments and retained abilities results in need for different:
 Advice to carers
 Informed management
Facilitate legal processes and advanced care planning

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57
Q

What does the clinical dementia rating distinguish?

A

a stage of questionable dementia (CDR 0·5) from people termed healthy (CDR 0) and those with mild dementia (CDR 1).

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58
Q

How many stages are there in the global deterioration scale scale for ageing and dementia (GDS)?

A

7

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59
Q

What does the GDS do?

A

Identifies seven clinical stages, of which four range from normality to mild dementia.

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60
Q

What is stage one of GDS?

A

free of both subjective and objective clinical deficits.

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61
Q

What is stage 2 of GDS?

A

subjective deficits only, e.g. self-perceived difficulties remembering names.

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62
Q

What is stage 3 of the GDS?

A

subtle deficits in cognition and may have some impairment in executive functioning have that affects complex occupational and social activities.

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63
Q

What is stage 4 of GDS?

A

clear deficits in cognition and functioning with reduced performance in instrumental activities of daily life, such as preparing meals and managing personal financial affairs. People at GDS stage 4 fulfil criteria for mild dementia.

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64
Q

What are the five pillars of management?

A 
Planning for future decision-making 
Supporting community connections 
Peer support 
Planning for future care
Understanding the illness and managing symptoms
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65
Q

What are the eight pillars of community support?

A 
Dementia practice 
Support for careers
Personalised support 
Community connections 
Environment 
Mental health care and treatment 
General health care and treatment 
Therapeutic interventions to tackle symptoms of the illness
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66
Q

What are the aims of management?

A

Prevention
Pharmacological
Behavioural
Rehabilitation
Psychosocial interventions
Caregiver Support, Training and Education

67
Q

What art examples of pharmacological interventions?

A

Cholinesterase Inhibitors (e.g. donepezil, rivastigmine & galantamine) for cognitive functioning
Memantine
Ginkgo
Salvia
Antidepressants
Antipsychotics
Trazodone
Clinically ineffective interventions (anti-inflammatories; melatonin; oestrogen; physostigmine; selegiline)
Interventions lacking evidence (anticonvulsants; aspirin; benzodiazepines; lithium)

68
Q

Psychosocial intervention is a broad term to describe different what?

A

ways to support people to overcome challenges and maintain good mental health

69
Q

Psychosocial interventions maintain what?

A

independence, quality of life, maintain cognitive function and reduce anxiety and depression

70
Q

What are some non pharmacological interventions?

A

Cognitive Behavioural Therapy (CBT) Environmental Design
Multisensory Stimulation
Physical Activities
Orientation programmes
Arts therapy (music, art)
Simulated Presence
Validation therapy
Reminiscence therapy
Family/Caregiver Intervention Programmes

71
Q

What are the 4 types of dementia?

A 
Cortical 
- AD, CJD
Subcortical 
- PSP, IPD, HD
Mixed cortical-subcortical 
-FTD, VaD, LBD, CBD
Treatable
-NpH, subdural, SoL, metabolic/endocrine, deficiency, infections
72
Q

What is Alzheimer’s disease?

A

‘A chronic neurodegenerative disease with an insidious onset and progressive but slow decline’ (BMJ, 2017)

73
Q

What is the most common type of dementia?

A

Alzheimer’s

74
Q

What is the aetiology of Alzheimer’s?

A

Non-genetic aetiology yet to be confirmed; some studies linking serum cholesterol and homocysteine levels are risk factors; controversial association between Vitamin E and Vitamin C and development of dementia.

75
Q

What is the neuropathology of Alzheimer’s?

A

Plaques, neurofibrillary tangles and neuronal loss.

76
Q

How do deficits progress in AD?

A

A relatively predictable pattern

77
Q

What are some symptoms of AD?

A

Symptoms include memory problems (recent), language problems (verbal fluency & word finding), visuospatial dysfunction, progressive deterioration in ability to perform basic ADLs, and behavioural disturbance (aggression, wandering, agitation, inappropriacy, apathy).

78
Q

What are signs of early/mild AD?

A 
Episodic memory (esp delayed recall) 
 Semantic memory
 Attention/executive function
79
Q

What are some risk factors of AD?

A

Down’s syndrome
Advanced Age
Female (might be changing)
Genetic predisposition
Family history
Elevated homocystine levels
History of TBI
Lifestyle Factors

80
Q

What are protective factors of AD?

A

Education (confounding with social class, diet) Cognitive stimulation
Possibly tobacco (nicotinic effect on cholinergic transmission)
Wine and coffee
Exercise
Foods containing vitamin E (not supplements)
? Non steroidal anti-inflammatory drugs and aspirin
? HRT

81
Q

What are some behavioural and psychosocial symptoms of AD?

A 
Anxiety 
Agitation 
Aggression 
Wandering 
Hallucinations 
Delusions
Depression
82
Q

The diagnosis of probable AD dementia should not be applied when there is evidence of what?

A

a) substantial concomitant cerebrovascular disease; or
b) core features of dementia with Lewy bodies; or
c) prominent features of behavioural variant frontotemporal dementia; or
d) prominent features of semantic variant primary progressive aphasia or non-fluent/agrammatic variant progressive aphasia; or
e) evidence for another concurrent, active neurological disease, or a non- neurological medical comorbidity, or use of medication that could have a substantial effect on cognition

83
Q

What is definite AD?

A

meets the criteria for probable AD and has histopathological evidence of AD on autopsy or brain biopsy.

84
Q

What is probable AD?

A

dementia established by clinical and neuropsychological examination and involves:
• Progressive deficits in 2 or more areas of cognition, including memory
• Onset between the ages of 40 and 90 years
• Absence of systemic or other brain diseases capable of
producing a dementia syndrome, including delirium

85
Q

What is possible AD?

A

a dementia syndrome with an atypical onset, presentation, or progression and without a known aetiology.
Any comorbid diseases capable of producing dementia are not believed to be the cause.

86
Q

What is unlikely AD?

A

a dementia syndrome with any of the following: sudden onset, focal neurological signs, seizures, or gait disturbance early in the course of the illness.

87
Q

What are the major AD pharmacological treatment goals?

A

• Slow symptoms of disease progression by preserving memory and functional abilities
• Reduce behavioural disturbance
• Delay entry into institutional care settings.

88
Q

What is treatment of AD based on?

A

fact that neurons that use acetylcholine to transmit messages through choline acetyltransferase are primary locus of damage.

89
Q

What is the medical management of AD focussed on?

A

 Increasing availability of precurers (acetyle CoA and choline)
 Direct stimulation of receptors
 Preventing breakdown of acetylcholine (acetylcholinesterase)

90
Q

What is there some evidence that medications do with AD?

A

slow the rate of progression but no solid evidence of improving cognitive function

91
Q

What is mild cognitive impairment?

A

An intermediate state of cognitive function between the changes seen in ageing and those fulfilling the criteria for dementia and often Alzheimer’s disease (Peterson, 2011).
A syndrome defined as cognitive decline greater than that expected for an individual’s age and education level but that does not interfere notably with activities of daily life (Gauthier et al., 2006).

92
Q

What is the transition stage of mild cognitive impairment?

A

normal aging and dementia

93
Q

What are the subtypes of mild cognitive impairment?

A

amnestic and non-amnestic

94
Q

What can mild cognitive impairment affect?

A

many areas (language, attention, judgment) but most commonly affects memory
Usually normal perception and reasoning skills and usually normal activities of daily living

95
Q

What may people with mild cognitive impairment also have?

A

depression, irritability, anxiety, aggression

96
Q

What are the changes in mild cognitive impairment?

A

Same type of changes as for Alzheimer’s, but to a lesser extent
 Plaques
 Tangles
 Shrinkage of hippocampus (memory)

97
Q

Elevated beta-amyloid in people with MCI predicts what?

A

Conversion to AD

98
Q

What are the risk factors for mild cognitive impairment?

A

 Genetic predisposition
 High blood pressure
 Diabetes
 Low levels of physical, social and mental activity  Few years education

99
Q

What are some factors that can affect cognitive performance in elderly populations?

A

 education,
 vascular risk factors,
 psychiatric status,
 genetic background,
 hormonal changes,
 use of anticholinergic drugs,

100
Q

What differentiates vascular dementia from other types?

A

Executive functions more affected than memory – motor and mood changes seen early

101
Q

Hope do symptoms arise in vascular dementia?

A

Symptom onset may be abrupt & there may be periods of sudden decline followed by relative stability
 Stair-step decline

102
Q

Vascular pathology cause to what?

A

Grey and whit matter:

Infarction, ischaemia, haemorrhage, and small-vessel changes

103
Q

What 4 types of Vascular dementia are there?

A

Infarction
Leukoaraiosis
Haemorrhage
Mixed

104
Q

What is infarction in vascular dementia?

A

 Multiple large infarcts
 Small infarcts in strategic areas

105
Q

What is leukoaraiosis in vascular dementia?

A

 Loss of axons, myelin and oligodendrocytes.
 Perivascular tissue loss and dilation of perivascular spaces.
 Damage to the capillaries with breakdown of blood-brain barrier and protein leakage

106
Q

What is a haemorrhage in vascular dementia?

A

 Large parenchymal haemorrhages in the BG often secondary to hypertension
 Small haemorrhages in the cortex and white matter usually secondary to amyloid angiopathy

107
Q

What is mixed dementia in vascular dementia?

A

Often co-occurs with Alzheimer’s disease

108
Q

What is the criteria for dementia?

A

Impairment in memory and at least 2 other domains:

• Orientation
• Attention
• Language
•Visuospatial functions
•Executive functions, motor control, and praxis.

109
Q

What is the criteria for cerebrovascular disease?

A

Focal signs on neurological examination (haemiparesis, lower facial weakness, Babinski’s sign, sensory deficit, haemianopia and dysarthria) •Evidence of relevant cerebrovascular disease by brain imaging (CT):
•Large-vessel infarcts
•Single strategically placed infarct
•Multiple basal ganglia and white matter lacunes •Extensive periventricular white matter lesions •Combinations thereof.

110
Q

What are clinical features constituent with a diagnosis of probable vascular dementia?

A

Early presence of a gait disturbance
•History of unsteadiness or frequent, unprovoked falls
•Early urinary incontinence
•Pseudobulbar palsy
•Personality and mood changes.

111
Q

What are subtypes of vascular dementia?

A

Multi-infarct
Progressive small vessel disease (Binswanger’s)
CADASIL
Congophilic amyloid angiopathy

112
Q

What is multi-infarct dementia?

A

Step wise deterioration

Cortical and sub cortical lesions

113
Q

What is progressive small vessel disease?

A

Sub cortical frontal executive dysfunction

•Gait apraxia
•Psuedobulbar palsy
•Urinary incontinence
•Insidious onset often without stroke

114
Q

What is CADASIL?

A

CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)
•Genetic
•History of migraine
•Onset 30-60 years

115
Q

What is congophilic amyloid angiopathy?

A

Repeated brain haemorrhages and then dementia supervenes

116
Q

What are people with vascular dementia most likely to have?

A

 Abrupt onset
 Fluctuating course
 May include some degree of recovery post an episode
 History of stroke
 Focal neurological symptoms and signs

117
Q

What is there a high incidence of with VAD and AD?

A

Co-occurrence

118
Q

What are cognitive functioning of people with VAD?

A

Preserved recent memory
More diverse language profiles than AD Test scores decline less than AD over time

119
Q

What does subcortical VAD present with?

A

 Poor general cognitive functioning

 High insight
 Depression

120
Q

What kind of term in dementia with lewy bodies?

A

An umbrella term – includes LBD with and without Parkinson’s Disease

121
Q

What is the aetiology of dementia with lewy bodies?

A

Aetiology is unknown, almost all cases are sporadic with some indicators of genetic involvement

122
Q

How is dementia with lewy bodies characterised?

A

by cognitive decline with a combination of fluctuating cognition, recurrent visual hallucinations, spontaneous extrapyramidal signs, rapid eye movement (REM) sleep behavioural disorder, and antipsychotic sensitivity.

123
Q

What do people with DLB exhibit?

A

exhibit a prominent dysexecutive syndrome and visuo-perceptive disturbances.
 Attention and visual perception more affected than in AD

124
Q

When many detectable memory loss occur?

A

Detectable memory loss may not occur early in the disease
 More severe procedural memory and motor-skill-learning impairment; Less-impaired episodic memory

125
Q

How is DLB marked?

A

day to day fluctuations in functioning- transitory episodes of confusion

126
Q

What else may occur with DLB?

A

Paranoid delirium

127
Q

How is the pathology of DLB characterised?

A

Characterised by an accumulation of Lewy bodies in vulnerable sites. Lewy bodies displace nerve cell structures leading to impairments.
Lewy bodies are β-Amyloid plaques aggregates of α-Synuclein protein. Other proteins include neurofilament and ubiquitin.

128
Q

What are the distribution and density of lewy bodies are thought to be correlated with?

A

clinical symptoms, although the distribution of Alzheimer’s disease pathology in DLB may have a bearing on phenotype.
 In DLB, co-existing Alzheimer’s disease pathology is common, especially amyloid pathology. Neurofibrillary tangles tends to be less severe than in typical cases of Alzheimer’s disease.

129
Q

In DLB where does lewy bodies start?

A

In cortical areas

130
Q

Describe DLB in Parkinson’s disease dementia.

A

Lewy Bodies begin to accumulate in upper brainstem (Substantia Nigra)
 leading to tremor, rigidity, and slowed movement
 In 25% of cases, Lewy bodies spread to cortical areas (especially frontal) and to Basal Nucleus to cause cognitive decline

131
Q 
Describe management of DLB. 
Treatment type 
Main goal 
Increase sensitivity 
Limitations
A

Treatment is symptomatic
Main goal: Stabilise cognition, behaviour and ADLs
Increased sensitivity to antipsychotic medication – should be avoided
Limited clinical trials = uncertainty around medications
 Cholinesterade inhibitors may be used to improve cognition and behaviour without exacerbating extrapyramidal symptoms (EPS)

132
Q

What is the prognosis is DLB?

A

Progressive disease course with steady decline in functioning Survival of 5-7 years after symptom onset

133
Q

What is the second most frequent type of dementia?

A

Frontotemporal dementia

134
Q

What is FTD?

A

a spectrum – includes behavioural and language variants

135
Q

When does FTD typically appear?

A

appear in mid-life, mean age of onset 53-58

136
Q

What are some prominent early symptoms in FTD?

A

include progressive coarsening of personality, social behaviour, self-regulation (of emotions, drives, and behaviour), and language.

137
Q

What are some gross changes in social behaviour and language that are often seen?

A

including indifference to self-care and others’ needs, loss of speech and comprehension, loss of empathy, distractibility, impulsiveness, disinhibition, stereotyped behaviours and rigid routines, and compulsions

138
Q

What are the two groups in FTD?

A

FTD-tau

FTD-ubiquitin

139
Q

What is FTD-tau?

A

intra-neuronal and glial inclusions of tau are observed on microscopic examination

140
Q

What is FTD-U?

A

cytoplasmic and intra-nuclear inclusions that are immunoreactive to ubiquitin and negative for tau.
 Also referred to as TDP-42 proteinopathies

141
Q

How is A distinction between taupathies and TDP-43 proteinopathies emerging?

A

by correlating neuropathological findings with clinical features

142
Q

What are there major changes in with frontal variant FTD?

A

personality with stereotyped behaviour, change in eating preferences, disinhibition, and loss of empathy
Presents with an insidious disorder of personality and behaviour

143
Q

Frontal variant FTD has the prescience of two or more of what features?

A

 Loss of insight, disinhibition, restlessness, distractibility, emotional lability, reduced empathy or unconcern for others, lack of foresight, poor planning or judgement, impulsivity, social withdrawal, apathy or lack of spontaneity, poor self-care, reduced verbal output, verbal stereotypes or echolalia, perseveration, features of Kluver-Bucy syndrome (gluttony, pica, sexual hyperactivity)

144
Q

In frontal variant FTD what is there relative preservation of?

A

day-to-day (episodic) memory

145
Q

What is the treatment for FTD?

A

The treatment of frontotemporal dementia (FTD) is based on the need to ensure the safety of the patient and others, to provide reassurance and support for patient and carers, and to provide adequate guidance and supervision of a care team faced by problems in the management of behavioural complications and their practical consequences. (BMJ, 2017)
Treatment is supportive care and symptom management. No available disease modifying treatments.

146
Q

What is the prognosis of FTD?

A

Disease progression differs across the variants. Median survival from diagnosis is 6-7 years

147
Q

What are some other causes of dementia?

A 
HIV dementia 
Huntington's Disease
Prion Disease 
Traumatic Brain Injury 
Substance-Induced (alcohol) Major Cognitive Disorder
148
Q

What is HIV dementia?

A

Viral Induced toxins and opportunistic infectious/cancerous tumours

149
Q

What is huntington’s disease creating dementia?

A

Autosomal dominant gene leads to degeneration in basal ganglia. 50% chance of passing to offspring

150
Q

What is Prion Disease creating dementia ?

A

DSM-IV described only one (Creutzfeld-Jacob Disease). Slowly infectious agent (prion) spreads in brain. Mad Cow Disease is an animal form of this disease

151
Q

What is a Traumatic Brain Injury creating dementia?

A

Fibres (axons) connecting brain cells are snapped during impact and withdraw into “retraction balls”. Frontal areas most vulnerable because axons are longer

152
Q

What is Substance-Induced (Alcohol) Major Cognitive Disorder (DSM-IV TR) creating dementia?

A

Persisting Amnesia (aka Korsakoff’s Dementia). Thiamine deficiency develops in some chronic abusers and damages the brain’s “mammillary bodies” leading to virtually discrete impairment in forming new memories and the manifestation of confabulation
•Persisting Dementia (aka Alcoholic Dementia). Chronic alcohol toxicity causes generalized shrinkage of brain. This disease (including shrinkage) may be reversible with abstinence.
•DSM 5 does not distinguish between Persisting Amnesia and Persisting Dementia. However, Alcohol-Induced Major NCD can be embellished with written descriptions such as ICD-10’s “Amnestic-confabulatory type” and “Non-amnestic type

153
Q

What are some treatable causes of dementia?

A 
Normal pressure Hydrocephalus 
Chronic Subdural Haematoma 
Benign Tumors 
Metabolic & Endocrine Disturbances
Infections
154
Q

What is Normal Pressure Hydrocephalus creating dementia?

A

Gait apraxia, subcortical dementia, urinary dysfunction

• Worse when walking than when on bed
• Gait invariably precedes or accompanies dementia
• Treatment: shunt

155
Q

What is chronic Subdural Haematoma creating dementia?

A

Fluctuations, focal signs

156
Q

What is benign tumours creating dementia?

A

Subfrontal meningiomas, colloid cysts of III ventricle, pituitary tumours

157
Q

What is Metabolic & endocrine disturbances creating dementia?

A
  • Chronic hypocalcaemia, recurrent hypoglycaemia
    • Hypothyroid, Addison’s disease, hypopituitarism, Cushing’s Disease
  • Wilson’s Disease
    • Alcohol Deficiency state
158
Q

What are infections creating dementia?

A

AIDS-dementia complex
• Neurosyphilis
• SSPE
• Whipple’s
• Dementia, ophthalmoplegia, myoclonus
• B12, folate, B1

159
Q

Dementia should be differentially diagnosed from what?

A

Depression
Acute confusional state

160
Q

What can dementia present as?

A

pseudodementia

161
Q

What is the role of the SLT in dementia?

A

Our training allows us to assess and manage cognitive, communicative and swallowing disorders

162
Q

What is delirium?

A

Delirium is an acute (hours to days), usually reversible, metabolically induced state of fluctuating consciousness. It involves rapid changes in the level of consciousness, and in level of orientation rather than a slow progression of memory and functioning as is found in dementia (BMJ, 2017)

163
Q

What type of onset does delirium have?

A

Abrupt onset of marked attentional abnormalities

164
Q

What are there fluctuations in, in delirium ?

A

Cognitive performance and behaviour

Neurology (8 decks)

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