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NEUROPSYCH & CLINICAL NEURO > Week 6: Dementia > Flashcards

Week 6: Dementia Flashcards

1
Q

Is dementia a specific disease?

A

No, it is not a specific disease but rather an overall term that describes a wide range of symptoms associated with declines in memory or other cognitive skills that reduce everyday abilities

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2
Q

What are progressive dementias?

A

They are characterised by a continual decline in functioning overtime

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3
Q

What categories of dementia are considered to be progressive?

A

Cortical dementias
Subcortical dementias
Mixed dementias

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4
Q

Examples of cortical dementias?

A

AD
Picks disease
Frontal lobe dementia

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5
Q

Examples of subcortical dementias?

A

Huntingtons disease

Parkinsons disease

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6
Q

Examples of mixed dementias?

A

Lewy body dementia

Multi-infarct (vascular) dementia

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7
Q

What are potentially static dementias?

A

These dementias are not progressive

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8
Q

What categories of dementia are considered to be potentially static?

A

Toxic conditions - heavy metal poisoning
Infectious conditions - herpes encephalitis
Miscellaneous - tumour, trauma

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9
Q

What are some potentially reversible dementias?

A

Systematic illnesses - amnesia
Deficiency states - vit b12
Endocrine disorder - addisons disease, thyroid disorders
Drug toxicity - antipsychotics

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10
Q

What is an example of psuedodementia?

A

Depression

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11
Q

What is the most prevalent dementia?

A

Alzheimers disease

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12
Q

Who diagnoses dementia?

A

Geriatrician, neurologist or medical practitioner

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13
Q

Whos opinion is essential for dementia diagnosis?

A

Clinical neuropsychologists

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14
Q

Why is early diagnosis important for every case?

A

Provided with a diagnostic answer and possible education for the patient and family to relieve fear

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15
Q

Why is early diagnosis important for static dementia?

A

You can then treat the underlying disease and initiate prevention and rehabilitation strategies

Relieve the patients fear of an irreversible disease

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16
Q

Why is early diagnosis important for progressive dementia?

A

You can begin to treat behavioural and cognitive symptoms (eg. memory strategies)

Can also make legal and financial plans while the patient is still competent

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17
Q

What is dementia labelled in the DSM-5?

A

Neurocognitive disorder (NCD)

  • much broader classification
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18
Q

Diagnostic criteria for NCD?

A

Evidence of significant cognitive decline from a previous level of performance

  • Has to be notable by others
  • Need testing to assess

Deficits interfere with independence in everyday life

The deficits do not occur exclusively in the context of a delirium

The deficits are not better explained by another mental disorder

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19
Q

When diagnosing someone with MND, you need to…

A
  • Specify what type/cause
  • Specify the extent of behavioral disturbances
  • specify severity
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20
Q

Cortical to subcortical dementia?

A

Cortical dementia is characterized by preferential neuronal loss to the cortical regions of the brain

This can progress and start to affect subcortical regions of the brain (later stages of the disease)

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21
Q

Why is there a lot more deficits in movement with subcortical dementia?

A

Involves areas important for movement such as the basal ganglia

E.g. Parkinsons dementia is dementia of the subcortical type

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22
Q

What is the strongest predictor for AD?

A

Age - incidence increases with age

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23
Q

Are there any gender differences in AD?

A

Twice as many women as men

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24
Q

What is the average duration of AD?

A

8-10 years

Those with AD rarely survive more than 15 years post-diagnosis

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25
Q

Why may AD symptoms not be noticed until later on?

A

May not know because the brain is so good at using cognitive reserves to compensate for loses - however it gets to a point where you just can’t compensate anymore

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26
Q

Sporadic vs. familial AD?

A

Sporadic: most common type, not a strong genetic basis (APOE34 gene) - typical onset after 80 years

Familial: rare - but strong genetic trait
Early onset dementia - after 50 years

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27
Q

Where does cell loss occur in AD?

A

Cortical grey matter of the brain and limbic structures (hippocampus, amygdala)

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28
Q

Which lobes are the most atrophied in AD?

A

Frontal, temporal and parietal

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29
Q

How many cells are lost in affected lobes (AD)? and why?

A

Estimated 50% of large neurons in these areas
Due to a loss of dendritic arborisation (decreases and declines in dendritic branching that allows the brain to form connections)

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30
Q

Cortical thinning results in….

A

Ventricular enlargement

31
Q

What are the primary markers of AD brains?

A

Amyloid/senile plaques

Neurofibrillary tangles

32
Q

What are amyloid/senile plaques?

A

Clump like deposits, round aggregates of cellular trash

Made of b-amyloid protein and apolipoprotein (ApoE)

Toxic to neurons

33
Q

What are neurofibrillary tangles?

A

Resemble entwined and twisted pairs of rope within the cytoplasm of swollen cell bodies

Made of the protein tau

34
Q

Where are senile plaques typically found?

A

Frontal and temporal regions of the brain

Hippocampal complex

35
Q

Where are neurofibrillary tangles found?

A

All throughout the brian but concentrated in temporal-parietal areas as well as the hippocampal complex

36
Q

Much of AD pathology begins in the….

A

temporal regions

37
Q

Onset symptoms of AD?

A

Failing recent memory

Depression and irritability

Occasionally a seizure (when neurons are dying it can trigger a miscommunication in the brain)

One or more language problems

Disorientation and confusion when sudden disruption to work or social life occurs (struggles with forming new association in new environment)

38
Q

Cognitive functions affected in AD are…

A

Memory - long term declarative, anterograde amnesia, STM

Attention - 7+/-2 may become less

Slowed information processing

Abstract reasoning

Language

Visuospatial skills

Fluent aphasia becomes prominent - non-words and incorrect words

39
Q

Speech in AD progression?

A 
Naming difficulties 
Dysfluency 
Bizarre word combinations 
Non-fluent, repetitive and non-communicative speech becomes apparent 
May have partial or complete mutism
40
Q

What may reemerge at the end stage of AD?

A

Primitive reflexes

  • sucking
  • grasping

Really go back to an infant state

41
Q

Aside form cognitive changes, what behavioural and personality changes are associated with AD?

A 
May cling to the caregiver, be easily distracted
Be disinterested 
Have poor self-care 
Agitation and restlessness - bursts of violence and destructiveness 
Wandering 
Suspiciousness and paranoia 
Incontinence 
Depression
42
Q

Which areas of the brain are affected by frontal-lobe dementia?

A

Frontal lobes

  • significant atrophy in frontal and temporal lobes
  • some changes to the parietal lobes

However, subcortical structures, as well as the cerebellum and brain stem are affected

43
Q

What is frontal-lobe dementia often called?

A

Picks disease

44
Q

What is the pathology of frontal lobe dementia?

A

Abnormal collections of tau protein in the brain

Deterioration of the caudate nucleus (BG - timing, ordering and sequencing movement)

Cerebellum deterioration

45
Q

What happens in the initial stages of frontal-lobe dementia?

A

Socially disinhibited behaviour, silliness and poor judgement

Incontinence may also occur

46
Q

What happens in the middle stages of frontal-lobe dementia?

A

Progressive apathy, blunted affect and cog dysfunction

47
Q

What happens in the late stages of frontal-lobe dementia?

A

May become mute and display motor rigidity

48
Q

How does frontal-lobe dementia end?

A

In a terminal vegetative state

49
Q

What is the disease duration for frontal-lobe dementia?

A

2-17 years

50
Q

What percentage of dementia does frontal-lobe dementia account for?

A

12%

51
Q

What are some of the cognitive deficits in those with frontal-lobe dementia?

A 
Empty speech 
Dysnomia - object naming difficulties 
Dysfluency 
Lack of self-awareness 
Executive dysfunction - frontal lobes
52
Q

What is huntingtons disease?

A

A progressive sub-cortical dementia that is fatal

53
Q

Is huntingtons prevalent?

A

No it is rare

54
Q

Which gene is the cause of huntingtons disease?

A

ITI5 on chromosome 4

55
Q

What age do people get symptoms of huntingtons?

A

30-40 years

56
Q

How long following the onset of symptoms do those with huntingtons survive?

A

10-20 years

57
Q

How likely are you to inherit huntingtons disease?

A

It is autosomal dominant - affecting 50% of offspring will have the trait

100% of people with the trait will go on to develop the disease = dominant

58
Q

Chorea is a symptom of huntingtons. What is it?

A

Involuntary, spasmodic and torturous movements that become disabling

59
Q

Cognitive deficits of those with huntingtons?

A

Disturbances to eye movements

Attention span

Memory

Speech production

Visuospatial

Cannot regulate own behaviour

Planning and organisation

60
Q

What is the 2nd largest type of dementia?

A

Multi-infarct (vascular) dementia

61
Q

What causes multi-infarct dementia?

A

Multiple infarctions of brain tissue from repeated strokes or blockages to blood vessels

62
Q

is multi-infarct dementia cortical or subcortical?

A

Can be either - it depends on where the strokes are occurring

Deterioration is step wise occurring with strokes

63
Q

What is an example of dementia from infection?

A

Creutzfeldt-Jakob disease (CJD)

64
Q

What is CJD?

A

A rapidly Progressive sub cortical dementia affecting one person in 1 million per year = extremely rare

65
Q

What is the pathology of CJD?

A

Results in spongiform encephalopathy (SE) - sponge like holes throughout the brain

Typically caused by infectious agent does not produce usual symptoms of acute infection

Transmitted by consuming infected meat both within and across species

Astrogliosis following death of neurons

Small, rusted, stick-like fibres - scrapie associated fibrils (SAFs)

66
Q

The Karu people?

A

Related to CJD

They were cannibals ingesting prions which are abnormally folded proteins in the brain they ate deceased family members especially their brains in which women and children eat

67
Q

Sporadic CJD?

A

This is the most common it occurs despite no risk factors being apparent

68
Q

Variant CJD?

A

Like mad cow disease it is a cross species infection via consumption of tainted meat containing neural tissue

69
Q

Familial CJD?

A

An extremely rare familial variant only found in a handful of families this results in fatal insomnia

Eg. Gerstmann-straussker-scheinker syndrome (GSSS)

70
Q

Why do researchers believe it is possible for it to be years before CJD is detected

A

They believe it is a slow virus that incubates over years possibly in the hosts spleen it is camouflaged in cells so it is not to be recognised by the immune system

71
Q

Which areas of the brain are targeted by the spongy tissue

A

The Cerebellum and cerebrum

72
Q

Motor symptoms in CJD?

A

Uncoordinated

Slurred speech and inarticulate

Involuntary tremors and grimaces

Cannot swallow - may eventually die of starvation

73
Q

Emotional/cognitive symptoms of CJD?

A

Mood disorders (depression, anxiety, hypo mania)

Fatigue

Sleep difficulties

Attention and concentration problems

74
Q

Progression of CJD?

A

Very rapid. Typically less than a year, usually within 3-4 months

NEUROPSYCH & CLINICAL NEURO (12 decks)

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