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Y2 CONTROL & MOVEMENT > Dementia > Flashcards

Dementia Flashcards

1
Q

What is the definition of dementia?

A

a progressive and largely irreversible syndrome that is characterised by a widespread impairment of mental function

sufficiently severe to impair social and occupational functioning

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2
Q

What care needs are implicated in dementia?

A

dementia is associated with complex needs and high levels of dependency and morbidity

care needs often challenge the skills and capacity of carers and available services

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3
Q

What are the 6 types of neurodegenerative dementia?

Which is the most common and least common?

A

most common - Alzheimer’s disease

  • vascular dementia
  • mixed dementia
  • lewy body disease
  • fronto-temporal dementia

least common - Parkinson’s dementia

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4
Q

In which 3 ways can dementia be classified?

A
  • site in the brain
  • age
  • pathology
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5
Q

What kind of symptoms are produced from disease of the frontal lobes?

A

it produces abnormalities in several behavioural domains

abnormality leads to impaired:

  • judgement
  • abstract reasoning
  • strategic planning
  • emotional restraint
  • control of appetite and continence
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6
Q

What does disease of the medial temporal lobe, hippocampus, amygdala and limbic system lead to?

A

disorders of memory and hallucinations

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7
Q

What are the symptoms of disorders of the temporal neocortex?

A

receptive dysphasia and automatisms

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8
Q

What is receptive dysphasia and expressive dysphasia?

A

receptive dysphasia:

  • difficulty in comprehension and understanding
  • can speak words fluently, but they do not make sense

expressive dysphasia:

  • difficulty putting words together to make meaning
  • comprehension is intact
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9
Q

What symptoms arise due to disorders of the occipital lobe?

A

failure of the visual and sensory systems

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10
Q

What symptoms arise from disease of the parietal lobe?

Why do they occur?

A

impairment of visuospatial skills and integration of sensory inputs

this leads to sensory agnosias and apraxias

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11
Q

What is meant by an automatism?

A

an action that is performed unconsciously or involuntarily

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12
Q

What are the 4 categories of classification of dementia based on site?

A
  1. anterior
  2. posterior
  3. subcortical
  4. cortical
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13
Q

What are the symptoms of a condition affecting the anterior region?

What are examples of conditions which arise?

A

frontal premotor cortex

  • behavioural changes / loss of inhibition
  • antisocial behaviour
  • facile and irresponsible

seen in normal pressure hydrocephalus, Huntington’s chorea and metabolic disease

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14
Q

What symptoms arise from a problem in the posterior region?

What condition results from this?

A

parietal and temporal lobes

  • disturbance of cognitive function (memory & language) without marked changes in behaviour

seen in Alzheimer’s disease

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15
Q

What are the symptoms of a problem in the subcortial site?

What conditions results from this?

A
  • apathetic
  • forgetful and slow with poor ability to use knowledge
  • associated with other neurological signs and movement disorders

seen in Parkinson’s disease and AIDS dementia complex

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16
Q

What are the symptoms associated with a problem in the cortical region?

A

higher cortical abnormalities including:

  • dysphasia
  • agnosia
  • apraxia

this is seen in Alzheimer’s disease

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17
Q

What is meant by agnosia and apraxia?

A

agnosia:

  • inability to interpret sensations and recognise things

apraxia:

  • individual has difficulty with the motor planning to perform tasks or movements when asked
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18
Q

What is meant by young onset dementia?

A

a young onset age is < 65 years

it is not always memory that is affected

this may be genetic or metabolic

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19
Q

What types of dementia are present in people aged above and below 65?

A

age above 65:

  • alzheimer’s
  • vascular
  • lewy body

age less than 65:

  • alzheimer’s
  • vascular
  • fronto-temporal
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20
Q

What are the three categories in the molecular-genetic classification of neurodegenerative diseases?

A

tauopathies:

  • characterised by neuronal and/or glial inclusions composed of the microtubule-binding protein, tau

synucleinopathies:

  • characterised by abnormal accumulation of aggregates of alpha-synuclein protein in neurones, nerve fibres or glial cells

ubiquinopathies:

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21
Q

What are examples of tauopathies?

A
  • FTD and FTDP-17
  • progressive supranuclear palsy (PSP)
  • corticobasal degeneration
  • Alzheimer’s disease
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22
Q

What are examples of synucleinopathies?

A
  • parkinson’s disease
  • dementia with lewy bodies
  • multiple system atrophy (MSA)
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23
Q

What are examples of ubiquinopathies?

A
  • motor neurone disease (MND) and MND / dementia
  • semantic dementia
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24
Q
A
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25
Q

What steps are required in the diagnosis of dementia?

A
  • history - GP, memory clinic, neurologist, psychiatrist
  • examination
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26
Q

What type of information is crucial when diagnosing dementia?

A

collateral information (from other people)

time-scale is also important to identify whether it is a rapidly progressive dementia

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27
Q

What are the 2 stages involved in cognitive assessment for dementia?

A

screening tests:

  • MMSE
  • ACE-III
  • MoCA

neuropsychological assessment:

  • objective vs subjective deficit
  • how many cognitive domains are affected
  • which cognitive domains are affected
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28
Q

What additional tests may be performed when diagnosing dementia?

A
  • blood tests
  • structural brain imaging (CT, MRI)
  • functional brain imaging (PET, DaT)
  • lumbar puncture (biomarkers)
  • genetic blood tests
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29
Q

What is the 2 main features that are affected in Alzheimer’s disease?

A

episodic memory:

  • patients are forgetful and repetitively ask the same questions

orientation:

  • patients get lost in familiar places
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30
Q

What is meant by episodic memory?

A

the memory of every day events such as:

  • times
  • location geography
  • associated emotions
  • who, what, where, when, why knowledge

that can be explicitly stated or conjured

it is a collection of past personal experiences that occurred at a particular time and place

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31
Q
A
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32
Q

How does a patient with Alzheimer’s present initially?

How does this change with disease progression?

A
  • in early stages the personality is unchanged and they maintain a good social facade
  • the patient lacks insight and head-turning sign is present
  • there are eventually more widespread deficits
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33
Q

What is meant by head-turning sign in Alzheimer’s disease?

A

patients who turn their head toward their caregiver for assistance or cues to help them answer questions are more likely to have Alzheimer’s dementia

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34
Q

What are useful questions to ask patients with Alzheimer’s disease?

A
  • how did you get here?
  • what did you do this morning?
  • what has been happening in the news lately?
35
Q

What investigations are performed in Alzheimer’s disease and what are the expected results?

A

cognitive assessment

examination:

  • may have myoclonus or UMN signs

CT/MRI brain scan:

  • medial temporal lobe atrophy

FDG-PET scan:

  • posterior hypometabolism

CSF biomarkers:

  • raised tau
  • low a-beta
36
Q

What is meant by myoclonus?

A

spasmodic jerky contraction of groups of muscles

37
Q

What is posterior cortical atrophy?

What causes the symptoms?

A

a form of dementia that is usually considered an atypical variant of Alzheimer’s disease

it causes atrophy of the posterior part of the cerebral cortex

this results in decline in visuo-spatial processing skills with relatively intact memory

38
Q

What are some of the symptoms and signs of posterior cortical atrophy?

A
  • vague hemianopia - tend to get lost whilst reading
  • reverse size phenomenon - small print is easier to read than large
  • cannot judge distances so problems with driving / parking
  • difficultly identifying a static object (can still catch a ball)
  • difficulty reading fragmented letters
  • visual crowding (easier to read letters when they are spaced out)
  • light sensitivity and distortion - difficulty with glass / mirror surfaces and prolonged colour after-images
39
Q

What is hemianopia?

A

blindness over half the field of vision

40
Q

What is fronto-temporal dementia?

What are the typical symptoms and areas affected?

A

a group of non-Alzheimer’s neurodegenerative disorders

memory is intact but language, behaviour and personality are affected

41
Q

When is the typical onset of fronto-temporal dementia?

A

onset is in middle life (50-65 years)

up to 50% of cases are familial (consider genetic testing)

there are overlap syndromes (motor neurone disease, parkinsonism, etc.)

42
Q

What are the 4 subtypes of frontal-temporal dementia?

A
  1. behavioural
  2. semantic
  3. progressive non-fluent aphasia
  4. logopenic aphasia
43
Q

What are the features of behavioural FTLD?

A
  • disinhibited, socially inappropriate, apathy, loss of insight
  • sweet tooth
  • repetitive behaviours
  • executive dysfunction
44
Q

What are the features of semantic FTLD?

A
  • fluent but empty speech
  • anomia - inability to recall names of everyday objects
  • impaired word comprehension
  • surface dyslexia
45
Q

What are the features of progressive non-fluent aphasia?

A
  • effortful non-fluent speech
  • phonemic errors
  • articulation
  • orofacial apraxia
  • insight is retained
46
Q

What is orofacial apraxia?

A

a loss of voluntary control of facial, lingual, pharyngeal and masticatory muscles in the presence of preserved reflexive and automatic function of the same muscle

47
Q

What are the features of logopenic aphasia?

A
  • hesitant by grammatically correct speech
  • impaired phrase repetition
48
Q
A
49
Q

what are the 3 main features of progressive non-fluent aphasia?

A
  • effortful non-fluent speech
  • phonemic errors
  • orofacial apraxia (tested by asking the patient to cough or yawn)
50
Q

What are the 3 main features of semantic dementia?

A
  • fluent but empty speech
  • impaired word comprehension
  • surface dyslexia

patient may have trouble finding names for people and objects and make spelling mistakes

51
Q

what is meant by surface dyslexia?

A

a disorder characterised by the inability to read words with “irregular” or exceptional print-to-sound correspondences

e.g. “pint” or “soot”

52
Q

How would someone with behavioural variant dementia present?

A
  • disinhibited
  • impulsive
  • apathetic
  • compulsive overeating
  • executive dysfunction
53
Q

What are the stages involved in investigating dementia?

A
  • history
  • examination
  • blood tests
  • imaging
54
Q

What are “treatable” conditions that result from dementia?

A
  • depression
  • iatrogenic (anticholinergics, sedatives, narcotics, H2 blockers, multiple meds)
  • hypothyroidism
  • B12 deficiency
  • neurosyphylis
  • HIV
  • normal pressure hydrocephalus
  • subdural haematoma
  • encephalitis
55
Q

What is normal pressure hydrocephalus a triad of?

A

1. dementia

2. gait disturbance

3. urinary incontinence

occurring in conjunction with hydrocephalus and normal CSF pressure

56
Q

What are the 2 different types of normal pressure hydrocephalus?

A
  1. NPH with a preceding cause
    e. g. SAH, meningitis, trauma, radiation induced
  2. NPH with no known preceding cause (idiopathic)
57
Q

What is shown in this image?

A

normal pressure hydrocephalus

there is an accumulation of CSF that causes the ventricles in the brain to become enlarged

sometimes there is little or no increase in intracranial pressure

58
Q

What type of condition looks like this?

A

transmissible spongiform encephalopathies

under a microscope, the affected brain tissue looks like a sponge

59
Q

What is the median age of death in classic (sporadic) and variant CJD?

A

classic CJD - 68 years

variant CJD - 28 years

60
Q

What is the median duration of illness in classic and variant CJD?

A

classic CJD - 4-5 months

variant CJD - 13-14 months

61
Q

What are the clinical signs and symptoms in classic and variant CJD?

A

classic CJD:

  • dementia
  • early neurologic signs

variant CJD:

  • prominent psychiatric / behavioural symptoms
  • painful dyesthesiasis
  • delayed neurologic signs
62
Q

What types of test signs are present in sporadic and variant CJD?

A

classic CJD:

  • periodic sharp waves on electroencephalogram often present

variant CJD:

  • “pulvinar sign” on MRI present in >75% of cases
  • presence of florid plaques on neuropathology present in large numbers
63
Q

What signs are present in tissue in sporadic and variant CJD?

A

classic CJD:

  • immunohistochemical analysis of brain tissue shows variable accumulation

variant CJD:

  • immunohistochemical analysis of brain tissue shows marked accumulation of protease-resistant prion protein
  • presence of agent in lymphoid tissue is readily detected
64
Q

What would be seen in an EEG in CJD?

A

triphasic waves on repeat testing

65
Q

What would be seen on an MRI for sporadic CJD?

A

non-specific changes in the basal ganglia

66
Q

What would be seen on an MRI for variant CJD?

A

a characteristic abnormality seen in the posterior thalamic region - pulvinar sign

this is highly sensitive and specific for vCJD

67
Q
A
68
Q

What is corticobasal degeneration?

How does it usually present?

A

rare progressive neurological disorder characterised by cell loss and deterioration of a specific area of the brain

affected individuals often initially experience motor abnormalities in one limb which eventually spreads to affect all the arms and legs

69
Q

What are the signs and symptoms of corticobasal degeneration?

A
  • apraxia - difficulty with motor planning to perform tasks when asked
  • alien limb - limbs act on their own without conscious control
  • balance, co-ordination, parkinsonism / PSP
  • speech and cognitive
70
Q

What would an MRI for corticobasal degeneration show?

What is the underlying pathology?

A
  • asymmetrical atrophy
  • usually parietal and basal ganglia

the pathology is tauopathy

71
Q

What is encephalitis?

What are the 3 main categories?

A

inflammation of the brain caused by an infection or through the immune system attacking the brain in error

  1. viral
  2. autoimmune
  3. paraneoplastic
72
Q

What are the viral causes of encephalitis?

A

herpes simplex virus

seen on MRI and in CSF

73
Q

What are the autoimmune causes of encephalitis?

A

antibodies are present in the blood and CSF

this is usually the voltage gated potassium channel antibody (VGKC Ab LE)

74
Q

What is meant by paraneoplastic causes of encephalitis?

A

neuronal antibodies are present in the blood, body examination and imaging

75
Q

What are the symptoms and signs of VGKC Ab limbic encephalitis?

A
  • subacute memory loss
  • psychiatric / behavioural disturbance
  • seizures - usually partial
  • hyponatraemia
76
Q

What is present in most cases of VGKC Ab limbic encephaltis?

what tumours may be present?

A

most cases have serum and CSF antibodies to the LGI1 subunit of the K channel

others have CASPR2

thymoma/SCLC and other tumours may be present, but they are not associated

77
Q
A
78
Q

What is the difference in functions of the anterior and posterior aspects of the brain?

A

the frontal aspect of the brain is involved in executive functions such as motor, planning and strategic thinking

the posterior aspect is involved in perception / integration of sensory stimuli and encoding knowledge

79
Q

What is the role of the limbic system?

A

arousal, emotion, motivation, attention and memory

80
Q

What are the 8 different diseases of dementia?

A
  • alzheimer’s disease
  • vascular dementia
  • frontotemporal lobar degeneration
  • dementia with parkinsonism
  • idiopathic parkinson disease
  • dementia with lewy body
  • corticobasal degeneration
  • progressive supranuclear palsy
  • normal pressure hydrocephalus
  • creutzfeldt-jakob disease
81
Q

What are the 5 different proteins which may be involved in dementia?

A
  • B-amyloid
  • Tau
  • a-synuclein
  • TDP-43
  • ubiquitin
82
Q

What are the 2 things involved in the general pathology of dementia?

A
  • neurone loss from the hippocampus and cerebral cortex
  • accumulation of abnormal proteins
83
Q

Where do the abnormal proteins seen in dementia accumulate?

A

B-amyloid is in plaques and amyloid angiopathy

Tau in neurofibrillary tangles

a-synuclein in lewy bodies

ubiquitin in Pick’s bodies

84
Q
A

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