Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neurology > Dementia > Flashcards

Dementia Flashcards

1
Q

What is cognition?

A

Mental action of acquiring knowledge and understanding through thought, experience and sense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What processes does cognition encompass?

A

Attention, social functioning, language, memory and executive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the literal definition of dementia?

A

Undoing of the mind = generally progressive/persuasive and associated with neurodegeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is needed to diagnose dementia?

A

Evidence of significant cognitive decline in at least one cognitive domain = cognitive deficits interfere with independence and can’t be explained by another process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the cognitive domains?

A

Attention, executive, learning and memory, perceptuo-motor, social cognition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the epidemiology of dementia?

A

Prevalence in >= 65 y/o = 670000 cases

Incidence in >= 65 y/o = 210000 new cases per year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the greatest risk factor for dementia?

A

Ageing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What do focal deficits depend on?

A

The area of the brain that has been affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the acute cognitive disorders?

A

Focal injury to brain, transient global amnesia and transient epileptic amnesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some examples of focal injuries to the brain?

A

Viral encephalitis, head injury, stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some features of viral encephalitis?

A

Memory and language affected
Behaviour change
Patient pyrexial and unwell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some features of a head injury?

A

Attention, memory and executive dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the clinical features of transient global amnesia?

A

Abrupt onset antegrade > retrograde amnesia (repetitive), preserved knowledge of self, transient changes in the hippocampus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the duration of transient global amnesia?

A

4-6hr duration (always <24hrs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the epidemiology of transient global amnesia?

A

Patients >50 = generally in 70s

Triggering factors = emotion, changes in temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some features of transient epileptic amnesia?

A

Short lived = forgetful with repetitive questioning, can carry out complex activities with no recollection of events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is transient epileptic amnesia associated with?

A

Temporal lobe seizures = 30% seizures not seen

Should respond to anti-epileptic medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some causes of subacute cognitive disorders?

A 
Toxins = alcohol, carbon monoxide
Infection = HIV, syphilis
Inflammatory = limbic encephalitis
Neurodegeneration and mood disorders
Metabolic and functional
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is functional cognitive impairment?

A

Everyday forgetfulness impacting on functioning = more extreme cases may result in fugue state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do the symptoms vary in functional cognitive impairment?

A

They fluctuate = mismatch between symptoms and reported function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What may functional cognitive impairment be part of?

A

A generalised functional disorder = decreased concentration, attention and reaction time with subsequent memory difficulties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

In what group of people is functional cognitive impairment more common in?

A

Those with previously good memories

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is functional cognitive impairment different from a mood disorder?

A

Functional cognitive impairment doesn’t have deficits in attention, executive function and memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is functional cognitive impairment treated?

A

Explanation +/- neuropsychology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the most common human prion disease?

A

Creutzfeldt-Jakob disease = misfolded PrPsc causes neurodegenerative proteinopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the four types of Creutzfeldt-Jakob disease?

A

Sporadic, variant, iatrogenic and genetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are some features of sporadic Creutzfeldt-Jakob disease?

A

Usually aged 60
Rapid onset dementia and neurological signs with myoclonus = lasts 4 months
Most common type and cause unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are some features of variant Creutzfeldt-Jakob disease?

A

Usually aged 20 = due to exposure to BSE
Painful sensory disturbance and neuropsychiatric decline = lasts 14 months
Least common type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are some features of iatrogenic Creutzfeldt-Jakob disease?

A

Usually aged 30 = lasts <2 years

Cerebellar or visual onset and multifocal neurological decline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are some features of genetic Creutzfeldt-Jakob disease?

A 
Occurs at any age = may mimic sporadic type 
GSS type = prolonged ataxic syndrome
FFI type = insomnia
Variable duration but usually <2years 
Due to mutation in PRNP
31
Q

How is limbic encephalitis identified?

A

Inflammatory changes on MRI or in CSF

Antibodies identified in CSF or serum

32
Q

What are some features of limbic encephalitis?

A

Short term memory deficits +/- seizures +/- behavioural changes
May be associated with underlying malignancy or autoimmune disease

33
Q

How is limbic encephalitis treated?

A

Treat tumour and give immunosuppressants

34
Q

What are the most common dementia syndromes?

A

Alzheimer’s disease, vascular dementia and mixed dementia

35
Q

What is Alzheimer’s disease?

A

Neurodegenerative proteinopathy = extracellular amyloid plaques disrupt normal cell function and induce apoptosis

36
Q

What occurs in Alzheimer’s disease?

A

Disruption of cholinergic pathways in the brain and spinal cord = intracellular neurofibrillary tangles disrupt cytoskeleton and cause cell death

37
Q

What is the initial symptom of Alzheimer’s disease?

A

Generally forgetfulness

38
Q

What lobes of the brain are affected by Alzheimer’s disease?

A

Degeneration of the medial hippocampus and later parietal lobes = forgetfulness then apraxia and visuospatial difficulties

39
Q

What are some features of early onset Alzheimer’s disease?

A

Age <65, genetic influences, may be atypical presentation

40
Q

What are some features of sporadic Alzheimer’s disease?

A

Age >65, more due to environmental influences, usually typical initial forgetfulness

41
Q

What are the atypical presentations of Alzheimer’s disease?

A

Occur in 15%
Posterior cortical atrophy = visuospatial difficulty
Progressive primary aphasia = semantic, logopentic aphasia (repeating), non-fluent aphasia

42
Q

What investigations may be done for Alzheimer’s disease?

A

MRI = atrophy of temporal/parietal lobes
SPECT = decreased tempoparietal metabolism
CSF = decreased amyloid:increased TAU ratio
Amyloid ligand imaging

43
Q

How is Alzheimer’s disease treated?

A

Address vascular risk factor
Cholinesterase inhibitors = rivastigmine, galantamine
NMDA receptor blocker = memantine

44
Q

When does frontotemporal dementia usually present?

A

Early onset dementia = most age <65

45
Q

What is the pathogenesis of frontotemporal dementia?

A

Neurodegenerative proteinopathy = TAU-TDP43-ubiquitin

Protein aggregation causes cell damage

46
Q

What are the three types of frontotemporal dementia?

A

Behavioural variant (60%), primary progressive aphasia, genetic cause (25%)

47
Q

What are some features of frontotemporal dementia?

A

Early frontal features = disinhibition, apathy, loss of empathy, stereotypes/compulsive behaviours
Early loss of insight
May be part of MND-FTD spectrum

48
Q

What investigations can be done for frontotemporal dementia?

A 
MRI = atrophy of frontotemporal lobes
SPECT = decreased frontotemporal metabolism
CSF = increased TAU, normal amyloid
49
Q

What is the treatment for frontotemporal dementia?

A

Trial trazadone or anti-psychotics

50
Q

What age does vascular dementia present?

A

Late onset dementia = majority aged > 65

51
Q

How is vascular dementia diagnosed?

A

Presence of cerebrovascular disease plus a clear temporal relationship between the onset of dementia and cerebrovascular disease

52
Q

How can vascular dementia present?

A

Subcortical (small vessel) = decreased attention, executive dysfunction and slowed processing
Post stroke dementia = 25% develop vascular dementia <3 months after stroke

53
Q

What pathology is associated with vascular dementia?

A

Co-existent amyloid pathology = slow disease progression

54
Q

How is vascular dementia treated?

A

Manage vascular risk factors +/- cholinesterase inhibitor, CPN

55
Q

When does Lewy body dementia present?

A

Late onset dementia = majority aged >65

56
Q

What is the pathogenesis of Lewy body dementia?

A

Neurodegenerative pathology = alpha-synuclein aggregates are insoluble which leads to cell dysfunction and damage

57
Q

What effect do alpha-synuclein aggregates have on brain pathways in Lewy body dementia?

A

Disrupt cholinergic and dopaminergic pathways

58
Q

How does Lewy body dementia present?

A

Fluctuating cognition plus recurrent well formed hallucinations +/- presence of extrapyramidal features
May have additional neuroleptic sensitivity

59
Q

What is the treatment for Lewy body and Parkinson’s disease dementia?

A

Small dose levodopa, decrease acetylcholine

60
Q

What investigations cane be done for Lewy body dementia?

A

Dopamine transport imaging

Alpha-synuclein ligand imaging

61
Q

When does Parkinson’s disease dementia present?

A

Late onset dementia = usually >65 years old

62
Q

What does Parkinson’s disease dementia overlap with clinically?

A

Lewy body dementia

63
Q

How does Parkinson’s disease dementia present?

A

Parkinson’s = bradykinesia, rigidity, tremor

Decreased attention, slowness of processing, impaired visuospatial function and memory, hallucinations

64
Q

When does Huntington’s disease present?

A

Early onset dementia = mean age of onset is 30-50 years old

65
Q

What causes Huntington’s disease?

A

Expansion of the CAG nucleotide repeat on huntingtin gene produces neurodegenerative protein

66
Q

What is dementia?

A

Dysexecutive syndrome and slowed speed of processing = eventual involvement of memory

67
Q

What are some features of Huntington’s disease?

A

Associated changes in mood, personality and chorea +/- later psychosis

68
Q

What investigations are done for Huntington’s disease?

A

Genetic testing

MRI = loss of caudate heads

69
Q

How is Huntington’s disease managed?

A

Mood stabilisers, drugs for chorea, HD nurse specialist

70
Q

Who do you refer an >65 y/o with gradual onset dementia and no additional neurology to?

A

Old age psychiatry

71
Q

Who do you refer an <65 y/o with additional neurology or any unusual features to?

A

Neurology

72
Q

What are some features of the collateral history taken in the neurology memory clinic?

A

What were the first deficits?
What has happened since?
What are their functional difficulties?

73
Q

How are patients assessed in the neurology memory clinic?

A

Cognitive assessment = Addenbrooke’s +/- FAB
Imaging = MRI, SPECT if MRI unrewarding
Bloods = B12, TFTs, syphilis, HIV, Ca2+ +/- genetic panel

Neurology (48 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions