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Neurology > Dementia > Flashcards

Dementia Flashcards

1
Q

What is dementia

A

An acquired and persistent generalised disturbance of higher mental functions in an otherwise fully alert person
Neurodegenerative condition - loss of neurons

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2
Q

Is dementia always pathological?

A

YES

It is not part of the ageing process

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3
Q

What are the primary dementias

A

Alzheimer’s
Lewy body dementia
Pick’s disease - fronto-temporal dementia
Huntington’s

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4
Q

What are the secondary dementias

A 
Multi-infarct - vascular 
Infection - HIV, syphilis 
Trauma
Drugs and toxins - alcohol 
Vitamin deficiencies - thiamine 
SOL's and paraneoplastic
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5
Q

What is the most common types of dementia

A

Alzheimer’s

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6
Q

Describe the trends in prevalence of Alzheimer’s

A

Get more common with age

Later the onset, the more rapid and severe the changed tend to be

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7
Q

Is Alzheimer’s genetic

A

Yes and No
Usually sporadic
Some cases are familial - APP, Presenilin 1&2
Increased risk in Down’s syndrome

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8
Q

Why is Alzheimer’s more common in trisomy 21

A

The amyloid precursor protein gene is found on chromosome 21
This is implicated in the disease and leads to early onset

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9
Q

How does Alzheimer’s present

A

Insidious impairment of higher intellectual function, with alterations in mood and behaviour
General forgetfulness is common initially
Also have visuospatial difficulties

Later – progressive disorientation, memory loss and aphasia indicate severe cortical dysfunction

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10
Q

Does Alzheimer’s usually cause death

A

It is usually due to a secondary cause such as bronchopneumonia

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11
Q

What is the macroscopic pathology of Alzheimer’s

A

Cortical atrophy
Widening of the sulci
Narrowing of the gyri
Compensatory dilation of ventricles

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12
Q

Which areas of the brain are usually spared in Alzheimer’s

A

Occipital lobe
Brainstem
Cerebellum

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13
Q

What are the microscopic features of Alzheimer’s

A

Neuronal loss - atrophy and gliosis
Disruption of the cholinergic pathways
Neurofibrillary tangles - insoluble tau protein which disrupts neurons
Neuritic plaques - amyloid plaques extracellularly
Amyloid angiopathy

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14
Q

What is amyloid angiopathy

A

Extracellular accumulation of amyloid protein

Disrupts the BBB - oedema, local hypoxia and serum leaking

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15
Q

How does Lewy body dementia present

A

Progressive dementia alongside visual hallucinations and fluctuating attention
Memory is affected later
Fluctuation in severity of condition on a day‐to‐day basis
Features of Parkinsonism present at onset, or emerge shortly after
Symmetrical tremor
Visual spatial defect

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16
Q

Does everyone with Parkinson’s get Lewy body dementia

A

NOPE

However, everyone with Lewy body dementia will have features of parkinsonism

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17
Q

What are the features of Parkinsonism

A 
Loss of facial expression 
Stooping 
Shuffling gait 
Slow initiation of movement 
Pill rolling tremor
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18
Q

What are the pathological features of Lewy body dementia

A

Degeneration of the substantia nigra
Disrupts the cholinergic and dopaminergic pathway
Will appear pale - loss of pigmented neurons
Reactive gliosis and accumulation of microglia
Lewy bodies present

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19
Q

How is Huntington’s inherited

A

Autosomal dominant
Mutation on the Huntington’s gene causes CAG repeats
Disease occurs when more than 35 repeats
Produces a neurodegenerative protein

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20
Q

What are the clinical features of Huntington’s

A

Triad of emotional, cognitive and motor disturbance

Chorea (dance‐like movements), myoclonus, clumsiness, slurred speech, depression, irritability and apathy.
Develop dementia later

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21
Q

Huntington’s has a long disease process - true or false

A

True

Often around 15 years from symptoms starting until death

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22
Q

Describe the pathology seen in Huntington’ s

A

Atrophy of the basal ganglia (caudate nucleus and putamen)

Cortical atrophy occurs later and corresponds to the onset of dementia

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23
Q

What is the other name for Pick’s disease

A

Fronto-temporal dementia

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24
Q

How does Pick’s disease/FTD present

A

Personality and behavioural change - including social deterioration
Speech and communication problems
Impairment of intellect, memory and language
Changes in eating habits
Reduced attention span
Fast loss of insight - no idea their behaviour is abnormal

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25
Q

Describe the disease pattern of Pick’s disease/FTD

A

Starts in middle life (50-60) which is younger than most dementias
Rapidly progressing - lasts between 2-10 years

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26
Q

Describe the underlying pathology of Pick’s disease

A

Extreme atrophy of the frontal lobes and later in the temporal lobes
Tau protein problem, aggregate within neuronal cells which causes death and neurodegeneration
Neuronal loss and gliosis
Will see Picks cells and Picks bodies on histology

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27
Q

What causes multi-infarct dementia

A

Successive, multiple cerebral infarctions cause increasingly larger areas of cell death and damage
Damage is cumulative and caused by hypoxia as a result of infarcts

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28
Q

Who gets multi-infarct dementia

A

More common in men
Usually seen after age 60
Also seen in younger hypertensives
Post-stroke

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29
Q

What characterises multi-infarct dementia

A

Insight

Sufferers aware of their mental deficits and are prone to depression and anxiety.

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30
Q

How does mutli-infarct dementia present

A

Similar to Alzheimer’s symptom wise
Abrupt onset with a stepwise progression
Progresses slowly
History of hypertension or stroke (evidence on CT)
Patient has insight into deficits
Depression is common

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31
Q

What are the risk factors for multi-infarct dementia

A

Same as CVD
Hypertension, smoking etc
Previous stroke

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32
Q

Describe the morphological appearance of multi-infarct dementia

A

See large vessel infarcts scattered through the hemispheres

May have smaller lacunar infarcts

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33
Q

What is cognition

A

The mental action of acquiring knowledge and understanding through thought, experience, and the senses

Split into: Memory
Attention (ability to be alert enough to take info in)
Social functioning; how to evaluate and reason
Language: ability to produce, and understand language
Executive function; problem solving, decision making

34
Q

What are the criteria for a diagnosis of dementia

A

Evidence of significant cognitive decline in at least 1 domain
Must interfere with everyday activities and independence
Must not be diagnosable as something else

35
Q

Is forgetfulness always a sign of dementia

A

NO

Everyone has days of poor cognitive function such as forgetting names

36
Q

What is the greatest risk factor for dementia

A

Ageing

Most occur above the age of 65

37
Q

List acute cognitive disorders

A

Brain insults/injury
Transient global ischaemia
Transient epileptic amnesia

38
Q

Describe the effects of brain insults

A

Deficits depend on the area of brain affected
Includes:
Viral encephalitis (memory, behaviour change, and language)
Head injury (memory, executive dysfunction)
Stroke

39
Q

How does transient global amnesia

A 
Abrupt onset 
More commonly anterograde amnesia 
Preserved knowledge of self - name, age etc 
Transient - 4-6hours 
Generally a once off
40
Q

What triggers transient global amnesia

A

Emotion
Changes in temperature
Uncertain pathophysiology

41
Q

Who gets transient global ischaemia

A

The over 50s

usually in 70s

42
Q

What is anterograde amnesia

A

Can’t lay down new memories

43
Q

What is retrograde amnesia

A

Cannot remember things from the past

44
Q

What are the clinical features of transient epileptic amnesia

A

Forgetful / repetitive questioning
Can carry out complex activities with no recollection of events
Short lived (20 – 30 minutes)
Recurrent problem

45
Q

What is transient epileptic amnesia associated with

A

Temporal lobe seizures

46
Q

How can you treat transient epileptic amnesia

A

Should respond to anti-epileptic medication

47
Q

List some common sub-acute cognitive disorders

A 
Functional disorders 
Mood disorders 
Metabolic - B12, thyroid etc 
Inflammatory - encephalitis 
Toxins - alcohol 
CJD 
Infection - HIV etc
48
Q

What is functional/subjective cognitive impairment

A

Everyday forgetfulness that starts to impact upon ability to function
Losing keys, forgetting names etc
Fluctuating symptoms - good and bad days
Mismatch between symptoms + reported function (feel they should remember more than they do, even if normal and no one has reported concern)

49
Q

How can you treat functional/subjective impairment

A

Exclude a mood disorder and Alzheimer’s

Neuropsychology

50
Q

What is the most common human prion disease

A

Creutzfeldt-Jakob Disease
Still very rare
Leads to neurodegenerative conditions due to prion abnormality in the brain

51
Q

What are the 4 types of CJD

A

Sporadic
Variant - from BSE in cows
Iatrogenic
Genetic

52
Q

What are the symptoms of sporadic CJD

A

Rapid onset dementia, neurological signs and myoclonus
Lasts around 4 months
Often fatal

53
Q

What are the symptoms of variant CJD

A

Painful sensory disturbance
Neuropsychiatric decline - personality changes
Duration of around 14 months before death

54
Q

How does iatrogenic CJD present

A

Cerebellar or visual onset
Multifocal neurological decline
Illness duration of less than 2 years before death

55
Q

How does genetic CJD present

A

Similar to sporadic
May have ataxia or insomnia
Variable duration but usually less than 2 years

56
Q

How do you diagnose CJD

A

EEG and MRI

Gold standard is a brain biopsy - becomes spongiform

57
Q

What is posterior cortical atrophy

A

Unusual form of Alzheimer’s
Part of the visual field deteriorates
Cannot recognise faces and has difficulty going down stairs
Memory symptoms appear later

58
Q

What is progressive primary aphasia

A

Unusual for of Alzheimer’s
Can’t name something correctly, can’t repeat something back, very difficult to talk
memory and behavioural symptoms come later

59
Q

What investigations would you do for Alzheimer’s

A

MRI - shows atrophy
SPECT - shows decreases in metabolism
CSF will show reduced amyloid

60
Q

How can you treat Alzheimer’s

A

Address vascular risk factors - reduced risk of progression

ACh boosting treatment - cholinesterase inhibitors or NMDA blockers

61
Q

How would frontotemporal dementia appear on investigations

A

MRI would show atrophy of frontotemporal lobes (later sign)
SPECT would show decreased metabolism in the frontotemporal areas
CSF will have increased tau

62
Q

How can you manage frontotemporal dementia

A

Trials of anti-psychotics to help behavioural symptoms
SSRIs may help behaviour
Mainly safety management - controlled access to food, money, internet
Support for family - power of attorney

63
Q

How can you manage vascular dementia

A

Reduce CVS risk factors- stop smoking, reduce cholesterol,

Give cholesterase inhibitors if clear also have AD

64
Q

How can you investigate Lewy body dementia

A

DaT scan - dopamine transporter imaging
Will show reduced uptake in the basal ganglia
Will look like dots instead of commas

65
Q

How can you treat Lewy body dementia

A

Small dose of levodopa - will help motor but not cognitive symptoms
Community and nursing support

66
Q

What generally causes dementias

A

Neurodegenerative proteinopathies

67
Q

What is Parkinson’s disease dementia

A

Dementia that present in someone who already has Parkinson’s
The dementia will present over one year after the appearance of Parkinson’s symptoms

68
Q

How does dementia present in Huntington’s

A

Early onset dementia (30-50)
Slow processing
Eventual involvement of memory
Changes in mood and personality

69
Q

How can you manage Huntington’s

A

Mood stabilisers
Treat chorea
Specialist Huntington’s nurse

70
Q

Who do you refer dementia patients to

A

If over 65 and no additional features - old age psychiatry

If under 65, unusual features or additional neurology - neurology

71
Q

What tests are found in a dementia blood screen

A 
FBC, LFT and U&E
B12 and folate 
Thyroid function 
HIV and syphilis 
Calcium 
\+/- genetic panel
72
Q

When is SPECT imaging used

A

Done if MRI normal but clear cognitive changes

73
Q

What is the most common type of vascular dementia

A

Multi-infarct dementia

74
Q

What comes first in Lewy body dementia - cognitive decline or Parkinsonism

A

The cognitive decline starts first

Parkinsonism will appear shortly after

75
Q

What is the issue in cortical dementia

A

The problem is with storing memories

Alzheimer’s is a type of cortical dementia

76
Q

What is the issue in subcortical dementia

A

The problem is with retrieving memories - may remember with a prompt
Lewy body and vascular dementia are in this category

77
Q

Which drugs increase mortality in Lewy body dementia

A

Anti-psychotics

78
Q

What is a REM sleep disorder

A

Shouting out or purposeful movement when asleep

Seen in Lewy body dementia and Parkinson’s

79
Q

Which other disease can frontotemporal dementia be seen in

A

Motor neurone disease

80
Q

How is memantine used in dementia

A

Its a glutamate inhibitor used in moderate to severe dementia
May help with behavioural issues

81
Q

What is the contraindication to using cholinesterase inhibitors

A

Can slow the heart rate so need to check pulse first

Do an ECG if you suspect bradycardia or heart block

Neurology (18 decks)

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