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Neuroimaging > MRI & Dementia > Flashcards

MRI & Dementia Flashcards

1
Q

What is dementia?

A

The progressive decline of someone’s cognitive functions that impact the person’s daily functioning and social skills

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2
Q

What is required for a diagnosis of dementia?

A

Objective impairment in standard cognitive assessment
Documentation of decline over time
Ruling out of other causes notably depression of delerium
Impaired daily activities of living
Impaired social cognition

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3
Q

What two categories of disease can cause dementia?

A

Neurodegenerative and vascular

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4
Q

What is the name of the disease that precedes dementia but does not always lead to dementia

A

Mild Cognitive Impairment

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5
Q

What are the symptoms of MCI?

A

Subjective impairment in one or more cognitive functions such as memory
Objective impairment in one or more cog functions
Preserved independent everyday and social functioning
No dementia
Exclusion of other causes

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6
Q

What are the 4 common types of dementia, what category of disease do they come under?

A

Neurodegenerative = Alzheimer’s Disease, Lewey Body disease, fronto-temporal demetia
Vascular = vascular dementia

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7
Q

What is the most common screening tool for dementia? What scores classify MCI and dementia?

A

The Mini-Mental State Examination (MMSE)
24-26 = MCI
<24+

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8
Q

What are the 8 clinical presentations of Alzheimer’s Disease?

A
  1. Memory loss that disrupts daily like
  2. Challenges in planning and problem-solving
  3. Difficulty completing familiar tasks
  4. Confusion with time/place
  5. Misplacing things and trouble retracing steps
  6. Problems with words and writing
  7. Withdrawal from work and social activities
  8. Personality and mood changes
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9
Q

What 4 factors can affect Late-onset alzheimers?

A

Age, Genes, lifestyle and envrionment

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10
Q

What causes early onset alzheimers?

A

Inherited through mutations in:
Amyloid Precursor Protein (APP)
Presenilin 1 and 2 (PSEN1/PSEN2)

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11
Q

What two proteins in the brain are thought to contribute to the progression of AD?

A

Amyloid Beta Plaques and tau tangles

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12
Q

What is a Amyloid Beta Plaques and what happens to them in those with AD?

A

A by-product of myelin that normally gets cleared out but doesn’t in those with AD
Starts in the medial temporal lobe and spreads to the back of the brain

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13
Q

What can MRI and PET do in regards to AD?

A

Can possibly identify early biomarkers to AD but there is only a very small window before onset

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14
Q

What is the Alzheimer’s Disease Neuroimaging Intiative (ADNI) developed by Weiner et al (2015)?

A

An initiative all over north america to investigate how predictive certain biomarkers were of cognitive decline using CSF/Blood and imaging

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15
Q

What are the challenges of multi-centre trials that were part of the ADNI?

A

Standardisation/Harmonisation of study protocols and data analysis
Accounting for confounds such as differing hardware/software, tesla strengths, miscalibration etc

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16
Q

How can we account for the challenges of multi-centre trials?

A

Phantom scanning after each ptp to quantify and correct for differences - altho not humans so can be affected by temp

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17
Q

What did Fennema-Notestine et al’s (2009) cross-sectional study find about cortical thinning and MCI and AD

A

Differences shown between controls and MCI/AD using T1 weighted MRI.
Similar spread to plaques and tangles
Can’t assume this correlates with decline due to being a cross-sectional design

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18
Q

What did Cho et al’s (2013) longitudinal study show about cortical thinning and cognitive decline?

A

EOAD had a more rapid decline which correlated with more rapid cortical thinning in all associated areas
LOAD showed more decline only in the parahippocampal gyrus compared to EOAD

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19
Q

What was the difference between the pattern of annual grey matter decline in those with MCI/AD and controls?

A

MCI/AD = posterior to anterior
Control/healthy = Anterior to posterior

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20
Q

What area of the brain is shown to demonstrate atrophy first with AD and what symptom does this correlate with?

A

Hippocampus and short-term memory

21
Q

What was found in Bozzali et al’s (2006) study about grey matter atrophy in those with MCI that progresses to AD?

A

For those that developed into AD, they showed greater grey matter atrophy at the MCI stage compared to those that did not develop into AD

22
Q

What two factors determine how good a biomarker is as a predictor?

A

Specificity; How many healthy people are identified as not having the disease?
Sensitivity; How many patients are identified correctly

23
Q

What is the ideal specificity and sensitivity of a biomarker?

A

Sensitivity= 80-85%
Specificity = >80%

24
Q

What is the specificity and sensitivity of hippocampus atrophy as a biomarker?

A

AD and Control = 63% sensitivity and 80% Specificity
MCI and COntrol = 73% sen and 74% Spec

25
Q

What pattern was found in regards to hippocampal subfields and atrophy from Wisse et al (2014)? What was the limitation to this study?

A

AD = all subfields except CA2 showed atrophy
MCI = no sig differences but trends
Small sample size

26
Q

What pattern was found in regard to hippocampal subfields and atrophy from Wisse et al (2014)? What was the limitation to this study?

A

AD = all subfields except CA2 showed atrophy
MCI = no sig differences but trends
Small sample size

27
Q

Which white matter structure was shown to be disproportionately impaired for those with Amnestic MCI? What does it connect?

A

Fornix
Hippocampus with frontal cortex

28
Q

What other areas are connected by white matter tracts that show impairment?

A

Frontal anterior cingulate, Posterior cingulate and temporal culnus (cingulum bundle)

29
Q

What relationship has been found between brain connectivity and MCI/AD that differs from brain atrophy?

A

Atrophy was only shown in AD but not MCI whilst brain connectivity is clearly shown in MCI
Could suggest brain connectivity precedes atrophy and atrophy is a result of the disconnection

30
Q

What has different PET techniques shown us about AD?

A

PDG PET = reduction in metabolism
PiB Amyloid PET = Increased metabolism
Tau PET = increased metabolism

31
Q

What is the specificity and sensitivity like for FDG and amyloid PET? What is a possible explanation to this?

A

Varies widely
Lack of standardised thresholds for defining positive PDG and Amyloid PET

32
Q

What is an alternative biomarker other than imaging that can be used for AD/MCI?

A

Cerebrospinal fluid to analyse amyloid and tau

33
Q

What other disease can co-occur and precede with Dementia with Lewy Bodies?

A

Parkinson’s disease

34
Q

What is the neuropathological hallmark of lewy body disease?

A

a-synulein containing lewy bodies

35
Q

What is the pattern of distribution for Lewy body dementia?

A

From the vagus nerve through the olfactory bulb (bottom up)

36
Q

What are two essential cognitive features of DLB?

A

Attention-executive
visuo-perceptual

37
Q

what can Dementia with Lewy Bodies be misdiagnosed as? What can be the implications of this?

A

AD or Parkinsons
- Not get the correct medication = they response well to antipsychotic drugs and won’t get this if misdiagnosed
- Show adverse affects to neuroleptic drugs that people with AD are given

38
Q

Why do DLB patients get diagnosed?

A

Overlapping symptoms at early stages = memory and attention-executive problems
Overlap in motor symptoms for parkinsons
Overlap in neuropathology

39
Q

What neuropathology overlaps with AD, PD, PDD and DLB?

A

DLB and PDD = Tau and Alpha-synuclein
DLB and AD = Tau and Amyloid beta
DLB and PD = Alpha-synuclein

40
Q

What imaging technique was used to investigate reduced Dopamine Transporter uptake in Walker et al’s (2007) study? Which dopamine pathway was affected?

A

SPECT
Nigrostriatal

41
Q

What was the specificity and sensitivity of DAT as a biomarker in DLB?

A

Specificity = 100%
Sensitivity = 88%

42
Q

What did FDG-PET show in those with DLB compared to AD?

A

Reduced glucose metabolism in occipital areas and visual association areas

43
Q

what would be the benefit of looking at brain metabolism?

A

Differential diagnosis

44
Q

What’s the difference in overall hippocampal atrophy in DLB compared with AD?

A

Relatively compared only 62% of DLB patients have it compared to 100% in AD

45
Q

Whats the difference in subfield hippocampal atrophy in DLB compared with AD?

A

AD = all subfields except CA1 and subiculum
DLB = pre-subiculum, subiculum, CA2/3 and CA4/DG

46
Q

Whats the differences in cortical thinness for prodromal DLB and AD?

A

DLB = Insular and anterior cingulate
AD = parietal and temporal areas and precuneus

47
Q

Whats the differences in white matter integrity between DLB and AD?

A

DLB = reduced integrity in left thalamus and pons
AD = Reduced integrity in fornix, parahippocampal gyrus and frontal gyrus

48
Q

What percentage of accuracy of diagnosis can the combination of imaging techniques cause?

A

98%

49
Q

What two imaging techniques did Burke et al (2011) use for distinguishing AD and DLB?

A

Amyloid and Dopamine PET

Neuroimaging (11 decks)

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