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Neurology > Dementia > Flashcards

Dementia Flashcards

1
Q

What is cognition?

A

A mental action of acquiring knowledge, and understanding, through thought, experience and sense.

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2
Q

What is required to diagnose dementia?

A

Significant decline in atleast 1 domain of cognition which must be to such an extent that independence and ability to carry out everyday activities is impaired.

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3
Q

Is dementia a progressive disorder or is it an acute presentation?

A

It is a progressive disorder.

Delirium is an acute presentation.

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4
Q

Is age a risk factor for dementia?

A

Yes, over 65s are more susceptible to dementia.

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5
Q

What is the most common form of dementia?

A

Alzheimer’s disease

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6
Q

What occurs in AD?

A

There is deposition of amyloid outside nerve cells, at the neurofibrillary tangles. This disrupts normal nerve function and eventually leads to cell death.

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7
Q

What are produced from new memories?

A

Synapses

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8
Q

What are early signs of AD?

A

Forgetfulness

Visuospatial difficulties

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9
Q

Are environmental or genetic factors more important in the development of AD?

A

Environmental (particular vascular) factors are of more importance.

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10
Q

In which age group is dementia defined as of early-onset?

A

When it occurs in those aged under 65 years.

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11
Q

Which area of the brain is degenerated in early AD?

A

The medial hippocampus, and wil later affect the parietal lobes.

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12
Q

Is AD a clinical diagnosis?

A

Yes

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13
Q

What may an MRI show in those with AD?

A

Atrophy of the temporal and/or parietal lobes.

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14
Q

What will be seen on a PET scan in an individual suspected to have AD?

A

Reduced metabolism.

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15
Q

What is low in a CSF sample of an AD patient?

A

Amyloid.

This is due to it being used up in plaque formation.

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16
Q

How would you treat AD?

A

Address vascular risk factors.

Give drugs that boost acetylcholine (e.g. cholinesterase inhibitors or NMDA receptor blockers).

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17
Q

What is frontotemporal dementia?

A

A dementia of early onset, producing character changes and social deterioration, resulting in impaired intellect, memory and language.

It is also known as Pick’s disease.

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18
Q

What is the pathology of FTD?

A

Protein aggregation, resulting in cell damage. Leads to gliosis, with the development of Pick’s bodies and Pick’s cells.

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19
Q

What protein is most commonly involved in FTD?

A

Tau

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20
Q

What are features of FTD?

A 
Disinhibition
Apathy
Loss of empathy
Hyperorality
Loss of insight
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21
Q

What is disinhibition?

A

The inability to inhibit inappropriate behaviour.

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22
Q

Is there a genetic link in FTD?

A

Yes, 25% are linked.

23
Q

On an MRI, how will FTD present?

A

Frontotemporal lobe atrophy (this occurs more anteriorly in AD).

24
Q

What will a CSF tap show in FTD?

A

Raised tau levels.

Amyloid levels will be normal.

25
Q

How is FTD treated?

A

Anti-psychotics

Safety management

26
Q

Of which onset is vascular dementia most commonly seen?

A

Usually of late onset.

27
Q

What is required for a diagnosis of vascular dementia to be reached?

A

The presence of cerebrovascular disease.

PLUS

A clear temporal relation between the onset of dementia and cerebrovascular disease.

28
Q

What is the presentation of vascular dementia?

A

Vascular dementia has a variable presentation.

Can be subcortical.

29
Q

What are common features of vascular dementia?

A

Decreased attention
Executive dysfunction
Slowed processing

30
Q

Which type of vascular event may precede the onset of vascular dementia?

A

A stroke.

31
Q

What are the different types of dementia?

A 
Alzheimer's disease (AD)
Frontotemporal dementia (FTD)
Vascular dementia (VD)
Dementia with Lewy bodies (DwLB)
Huntington's disease (HD)
32
Q

How is vascular dementia treated?

A

Control vascular risk factors.

Similar to the management of AD.

If there is any signs of amyloid deposition, give cholinesterase inhibitors.

33
Q

Is it common for patients with VD to have co-existent amyloid pathology?

A

Yes

34
Q

Which form of late onset dementia is associated with changes in alpha-synuclein protein?

A

Dementia with Lewy bodies

35
Q

What is the pathology linked to DwLB?

A

Aggregation of alpha-synuclein protein, causing cell dysfunction and damage.

Disrupts cholinergic and dopaminergic pathways.

36
Q

Disruption of cholinergic pathways is associated with what?

A

Memory issues.

37
Q

What is disruption of dopaminergic pathways associated with?

A

Parkinsonian features.

38
Q

To diagnose DwLB, what is needed?

A

Fluctuating levels of cognition
Recurrent, well-formed, visual hallucinations
The presence of extrapyramidal features (seen in 75% of cases)

39
Q

What are examples of extrapyramidal features?

A

Bradykinesia
Tremor
Postural instability

40
Q

Are any diagnostic tests required in DwLB?

A

No it is a clinical diagnosis as it is a parkinsonian syndrome.

A DaT scan can be of benefit, showing reduced levels of dopamine within the presynaptic area.

41
Q

How is DwLB treated?

A

Small doses of levodopa and a cholinesterase inhibitor.

42
Q

What differs between PDD and DwLB?

A

In DwLB, the patient will have dementia symptoms prior to the onset of motor symptoms.

In PDD, motor symptoms will precede the onset of cognitive impairment by atleast a year.

43
Q

What is PDD?

A

A form of late onset dementia (occurs after 65 years of age).

Overlaps with DwLB clinically and pathologically (both affect alpha-synuclein protein).

44
Q

What is HD?

A

A form of early onset dementia, caused by expansion of the CAG nucleotide repeat in the huntington gene.

This results in a neurodegenerative protein being produced.

45
Q

How is PDD managed?

A

Small dose of levodopa and a cholinesterase inhibitor (the same as DwLB).

46
Q

Which age group is affected by HD?

A

30-50 year olds.

47
Q

Is HD autosomal recessive?

A

No, it is an autosomal dominant condition.

48
Q

What is the triad of components involved in HD?

A

Motor symptoms
Cognitive changes
Emotional issues

49
Q

How does HD present?

A 
Decline in executive function
Slowed speed
Chorea
Myoclonus
Mood alteration
Psychosis (at late stage)
50
Q

What tests can be used to diagnose HD?

A

Genetic testing

MRI

51
Q

What does MRI show in an individual with HD?

A

Loss of caudate heads.

52
Q

What are features of late stage HD?

A 
Rigidity
Bradykinesia
Severe chorea
Weight loss
Inability to walk/speak
Impaired muscle control
Swallowing issues
53
Q

How is diagnosis reached in HD?

A

Mainly clinical, genetic testing can aid this.

54
Q

How is HD treated?

A

Mood stabilisers and symptomatic treatment.

Neurology (22 decks)

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