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Neuro > Dementia > Flashcards

Dementia Flashcards

1
Q

Why can dementia be considered a Cinderella disease?

A

Because although has a very high health and social care cost (52% vs cancer’s 23%), little research funding is allocated to it (only 6% compared to cancer’s 71%)

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2
Q

What are the 2 approaches in looking at the clinical features of dementia?

A

The historical method

The precise/deductive method -> clinical approach

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3
Q

What does the historical approaches to dementia include?

A

Looking for senility, poor memory, global decline

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4
Q

Why is the precise/deductive method of assessing the clinical features of dementia better than historical approaches?

A

It tells you more about diesease pathogenesis and allows you to identify the different types of dementia

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5
Q

What clinical assessments exist for dementia?

A 
Witness account
Blood tests
Examination
Imagine
Neuropsychology
EEG
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6
Q

Why are EEGs useful for assessing dementia?

A

Because many people suffering from epilepsy get Alzheimer’s

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7
Q

Is neuroimaging a good diagnostic tool for dementia?

A

No, but it is good at ruling out other causes (e.g. brain tumour, stroke, hydroencephalus)

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8
Q

What are the things you think about in a clinical neurological examination?

A

Where? - localisation
When? - time course of illness
What? - investigations
So what? - treatment

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9
Q

What part of the CNS does dementia affect?

A

The cortex

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10
Q

What are symptoms?

A

Something the person/witness observes

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11
Q

What are signs?

A

They can be elicited in the clinic by the clinician

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12
Q

What are the symptoms of someone with frontal lobe damage?

A 
Disinhibition
Apathy
Change in sexual/eating behaviour
OCD
Loss of insight and empathy
Difficulty with planning/multi-tasking
slowing

Frontal-language:
Poverty of speech
mutism

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13
Q

What are signs of frontal lobe damage?

A 
Verbal fluency
Frontal release signs
cognitive estimates
motor sequencing
utilization behaviour
Frontal-language:
short sentences
agrammatical 
phonemic paraphasias
oro-buccal dyspraxia
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14
Q

What are frontal release signs?

A

Primitive reflexes that are normally present in infants. include the grasp, snout, root, and suck reflexes.

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15
Q

What are utilization behaviours?

A

The appropriate usage of an object by a patient, however at an inappropriate situation.

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16
Q

What is motor sequencing?

A

The ability to move the body with appropriate sequencing and timing to perform bodily movements with refined control.

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17
Q

What are phonemic paraphasias?

A

Substitution of a word with a nonword that preserves at least half of the segments and/or number of syllables of the intended word. (maybe like “That’s a hippopotamus” –> “That’s a hippocampus”)

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18
Q

What is oro-buccal dyspraxia

A

Difficulty moving mouth

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19
Q

What is Broca’s aphasia characterised by?

A

Short sentences - agrammatic telegraphic speech

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20
Q

How do you test verbal fluency?

A

Get people to say words that e.g. start with the same letter. Most people can get 12 words per min.

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21
Q

Do the symptoms displayed by the patient help diagnose the cause of the brain damage?

A

No, only the part of the brain damaged

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22
Q

What are symptoms of left temporal damage?

A

“deaf”

Not following commands/ instructions

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23
Q

What are signs of left temporal damage?

A

Preserved grammar

Semantic paraphasias

Anomia

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24
Q

What is semantic paraphasia?

A

Substituting a related or unrelated (sometimes distinguished as verbal paraphasia) word for the apparently intended or correct word.
maybe like “I’m bipolar” –> “I’m polar-bear”)

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25
Q

Why do people with left temporal lobe damage have problems with word selection?

A

Because the left temporal lobe is involved with:

  1. processing of verbal versus non-verbal inputs
  2. word retrieval
  3. social content of the stimuli
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26
Q

What are symptoms of left parietal damage?

A

Difficulty with writing, spelling, calculations

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27
Q

What are signs of left parietal damage?

A

Dyspraxia (miming and hand positions)

Dyslexia

Acalculia

Myoclonus

Corticoal Sensory loss

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28
Q

What are symptoms of occipital lobe damage?

A

Hallucinations

Virual misperception (e.g. visual snow)

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29
Q

What are signs of occipital lobe damage?

A

Loss of colour vision

Visual disorientation (optic ataxia - can’t grab things in front of them)

Asimultanagnosia - loss over movement perception

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30
Q

What is asimultanagnosia?

A

Inability of an individual to perceive more than a single object at a time

31
Q

What are symptoms of right parietal damage?

A

Spatial inattention

Dressing apraxia

32
Q

What are signs of right parietal damage?

A

Constructional apraxia

Sensory innatention
myoclonus

Cortical sensory loss

33
Q

What are signs of right temporal damage?

A

Prosopagnosia (cannot recognise faces)

Poor topographical memory (doesn’t remember routes)

34
Q

What are the symptoms of right temporal damage?

A

Getting lost

Difficulty with face recognition

35
Q

What are symptoms of mesial temporal damage?

A

Forgetful

36
Q

What are signs of mesial temporal damage?

A

Disorientation

Poor episodic memory

37
Q

Which is the first area of the brain to be affected by alzheimers?

A

Mesial temporal (contains the hippocampus and parahippocampus

38
Q

What would you see if you did an autopsy of an alzheimer’s brain?

A

Amyloid plaques occurring diffusely through the cerebral cortex

Tau neurofibrillary tangles

Neurodegeneration- enlarged ventricals, shrinking of hippocampus, shrinkage of cerebral cortex (grey and white matter)

39
Q

Which neurons are most affected by alzheimers?

A

Cholinergic neurons are lost

40
Q

How do amyloid plaques form?

A

Amyloid molecules usually sit in cell membrane but they become sticky and form plaques

41
Q

What are neurofibrillary tangles?

A

Insoluble twisted fibers found inside the brain’s cells.

These tangles consist primarily of a protein called Tau, which forms part of a structure called a microtubule

Cholinergic neurons are the most affected

42
Q

How common is alzheimers?

A

Very (1.4% UK pop, x10 more than PD)

43
Q

What are the early clinical features of alzheimer’s disease?

A

Disorientation

Day to day memory impairment

Mild naming problems

44
Q

What are later features of Alzheimers?

A

Receptive dysphasia (difficulty understanding)

Motor retardation

Visuo-spatial disorientation

Myoclonus

45
Q

What probably causes myoclonus in alzheimers?

A

Damage to inhibitory neurones

46
Q

Name a test often used to localise the part of the brain damaged by alzheimers and explain its steps

A

Folstein Mini-Mental State Examination (MMSE):

  1. Orientation (0-10): what day is it?, what floor are we on? etc - checks mesial temporal
  2. Immediate recall (0-3): Ask them to repeat words - frontal
  3. Attention and calculation (0-5) Count back from 100 - check left parietal
  4. Recall(0-3): Remember words I said before? - mesial temporal
  5. Language(0-3): what is this? show a watch - left temporal
  6. Praxis (0-3): Take paper and fold in half - parietal
  7. Language and reading comprehension (0-1): do as it says on the paper - temporal
  8. Praxis: Write a sentence - parietal
47
Q

Discribe Alzheimers prodrome

A

Memory tests start to change about 10 years before symptoms

Amyloid markers build up starting about 20 years before onset

48
Q

How does the progression of language comprehension and memory test compare in alzheimers?

A

Memory tests begin to worsen long before onset and reach a plateau after onset

Language comprehension test begin to get worse about 5 years before onset and the continue to get worse after

49
Q

What tracks with Alzheimers progression?

A

Amyloid pathology does not track with disease process well

Tau pathology does

50
Q

What happens to the Tau and Amyloid concentration in the CSF as disease progresses?

A

You can see amyloid in spinal fluid, this decreases when the disease starts probably because they are turning into plaques

Tau pathology starts way before disease starts

Tau increases in the CSF

51
Q

Describe typical AD progression

A

Memory problems –> executive dysfunction, praxis, language, complex visual impairments –> spatial function

52
Q

What is an APP mutation

A

You will get Alzheimer’s disease (people in 20s in the families have 50% chance of getting it)

These are the people who were studied to learn about the AD prodrome

53
Q

What are the current treatments for AD?

A

Supportive care: physiotherapy, social support

Treat vascular risk factors: there is interplay between vascular risk factors and AD

Cholinesterase inhibitors

Multidisciplinary care

54
Q

Chilnesterase inhibitors increase AD life expectancy.

TRUE or FALSE

A

FALSE

They only help control symptoms

55
Q

What is Gantenerumab and what does it do?

A

It was a Mab which was meant to bind to beta-amyloid plaques, dissassemble them and stimulate phagocytosis to remove them.

It didn’t work

56
Q

Name another Mab being trialed against AD

A

Crenuzumab

Can recognize different forms of amyloid-beta aggregates and plaques.

It stimulates the cellular ingestion of amyloid plaques and limits the release of cell signalling molecules (cytokines) that promote inflammation.

57
Q

What is the amyloid cascade hypothesis

A

It proposes that the deposition of β-amyloid (Aβ) is the initial pathological event in AD, leading to the formation of plaques, tau-immunoreactive neurofibrillary tangles (NFT), neuronal loss, and ultimately, clinical dementia.

58
Q

What kills people with AD?

A

Immobility leads to pneumonia and pulmonary embolisms

59
Q

What is the most common cause of early onset dementia?

A

FTLD:AD = 1:1 ratio

60
Q

What are the clinical features of frontotemporal dementia?

A

Insidious onset and gradual progression

Early decline in social interpersonal conduct

Early impairment in regulation of personal conduct

Early emotional blunting

Early loss of insight

61
Q

What part of the brain does sematic dementia mainly affect?

A

Left temporal lobe

62
Q

What are the diagnostic features of SD?

A

Insidious onset and gradual progression

Language disorder characterised by: Progressive, fluent , empty spontaneous speech

Loss of word meaning, manifested by impaired naming and comprehension

Sematic paraphasias

63
Q

What are the clinical diagnostic features of progressive nonfluent aphasia?

A

Insidious onset and gradual progression

Nonfluent spontaneous speech with at least one of the following: agrammatism, phonemic paraphasias, anomia

II. Supportive diagnostic features -Speech and language

  1. Stuttering or oral apraxia
  2. Impaired repetition
  3. Alexia, agraphia
  4. Early preservation of word meaning
  5. Late mutism
64
Q

What area of the brain does progressive nonfluent aphasia affect?

A

Frontal lobe (Broca’s area)

65
Q

What 3 molecules are found in FTLD?

A

Tau, FUS, TDP-43

66
Q

What are the 3 phenotypes of FTLD?

A

Sematic dementia

Behavioural variant frontal temporal dementia

Progressive nonfluent aphasia

67
Q

How is FTLD different from AD?

A

Memory is usually normal at first but e.g. can’t look after kids (innapropriate punishing)

Can’t plan

Massive frontal atrophy

Onset is 50s not 60s

68
Q

What is the central feature of dementia with Lewy bodies

A

Progressive cognitive decline with resultant functional impairment

Essential features for diagnosis:

Fluctuating cognition and pronounced variations in attention and alertness

Recurrent visual hallucinations (well formed, detailed)

Spontaneous motor features of Parkinsonism

69
Q

Where else are lewy bodies found?

A

Parkinson’s

70
Q

What are features of dementia with Lewy bodies which are supportive of the diagnosis?

A

Repeated falls

Syncope

Transient loss of consciousness

Neuroleptic sensitivity

Systematized delusions

Hallucinations

71
Q

What is the most common dementia after AD?

A

DLB

72
Q

How do you treat DLB?

A

May respond to cholinesterase inhibitors

73
Q

What cells are damaged most in DLB?

A

Cholinergic neurons

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