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Clinical Neuroscience > Dementia > Flashcards

Dementia Flashcards

1
Q

Sequence of events (symptoms) as dementia progresses (5 steps)

A
  1. Loss of short term memory (unable to take in new information) with preservation of long term memo and knowledge.
  2. Loss of motor skills and language
  3. Loss of long term memory (esp episodic memo)
  4. Disoriented (getting lost, not sure where they are)
  5. Bedridden
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2
Q

What happens during normal pressure hydrocephalus?

A

Enlarged ventricles are filled with CSF. Cure is to implant shunt to divert excess CSF to abdomen.

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3
Q

How will the neuroimaging brain of a AD patient looks like?

A

Reduced blood flow and glucose metabolism in the posterior temporo-parietal regions and hippocampus. Medial temporal lobe is generally affected.

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4
Q

What are the “symptoms” of an AD brain?

A

Cortical thinning, enlarged ventricles, hippocampal atrophy and overall progressive brain atrophy.

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5
Q

What are the symptoms of an AD brain with regards to reasoning and language?

A
  1. Lack of problem solving ability and abstract reasoning

2. Word finding difficulties and reduced verbal fluency (initial stages) & loss of verbal comms (advanced stages)

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6
Q

What are the symptoms of an AD brain with regards to Visospatial problems? Which part of the brain is affected?

A
  1. Lost in familiar places and forget where they place things.
    2a. Entorhinal cortex and hippocampus - spatial navigation and formation of episodic memory
    2b. Parietal lobe atrophy - difficulty in understand spatial relationship (getting dressed)
    2c. Temporal lobe (visual memory, fusiform area) - difficulty in recognising objects and people
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7
Q

What are the psychiatric symptoms of an AD patient?

A
  1. Depression or anxiety
  2. Disinhibition with inappropriate child-like behaviour
  3. Apathy
  4. hallucinations, paranoid
  5. Frustrations and irritability
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8
Q

What are the most important risk factors for AD?

A
  1. Ageing
  2. Possession of one or more copies of APOE4 allele
  3. Lower SES
  4. Head injury
  5. Ischemic heart disease
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9
Q

What is cerebral amyloid angiopathy (CAA)?

A

Deposits of amyloid beta in cortical blood vessels. Happens to more than 90% of AD patients

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10
Q

What are the disease modifying treatments for dementia?

A
  1. inhibition of beta secretase to reduce Amyloid Beta production
  2. Interference in amyloid fibril formation (blocking them)
  3. Immunotherapy (amyloid beta vaccination) - triggering active immune response that will remove amyloid beta plaques peptide from the brain.
  4. Inhibition of tau aggregation.
  5. Inhibition/modulation of gamma secretase - altering the ration of ABeta 40 and Abeta 42
  6. Cholinesterase inhibitiors to potentiate cholinergic transmission by inhibition acetycholine degradation (acetycholine helps in working memory, muscles)
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11
Q

What are the main differences between dementia with lewy bodies (DLB) and AD?

A
  1. Reduced blood flow and glucose metabolism in occipital AND posterior temporoparietal lobe - resulting in hallucinations
  2. Fluctuations in cognitive performances
  3. Features of Parkinsonism
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12
Q

What are patients DLB most sensitive to?

A

Neuroleptics (antipsychotic agents) which acts to antagonise dopamine receptors resulting in muscular rigidity and immobility and confusion.

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13
Q

Is Parkinson’s disease dementia similar to DLB?

A

Differences are purely clinical. microscopic features are the same. Stages of DLB are the same as Parkinson’s disease dementia.

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14
Q

What are the stages of progression of pathology of DLB?

A
  1. Affect olfactory and brain stem (medulla, pons, midbrain)
  2. then affects limbic lobe (amygdala and entorhinal cortex)
  3. then higher order association cortices and lastly pri and sensory areas.
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15
Q

What does vascular cognitive impairment usually refers to?

A

Non progressive decline in intellectual ability and vascular causes.

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16
Q

What are the symptoms of vascular dementia that are different from AD?

A
  1. Emotional incontinence (inappropriate laughter)
  2. Stepwise loss of cognitive abilities (not progressive like AD)
  3. More mood swings when sun goes down
  4. Some may display parkisonian features and neurological signs consistent with strokes
17
Q

What are the symptoms of FTD that are different from AD?

A
  1. Disinhibition (inappropriate behaviour)
  2. Relative preservation of memory and language with striking personality change
  3. recognised by anatomical distribution of pathological changes and neuronal loss in neurons and glial cells rather than protein involved.
  4. May be found together with Motor Neuron Disease (muscle weakness, lost of speech, slurr speech etc)
18
Q

Wich part of the brain affects FTD patients?

A

Front and temporal lobe

19
Q

What is the number 1, 2 & 3 form of Dementia?

A

AD, mixed dementia, other dementia (then FTD, vascular, parkinson’s dementia)

20
Q

What is MCI

A

MCI refers to the state of cognition and functional ability between normal aging and very mild AD.

21
Q

What are the diagnostic tools for dementia?

A

Biomarkers, psychometric tests and Mrt/MRS/PET

22
Q

How is dementia being diagnosed?

A
  1. Cognitive problems
  2. Problems with daily activities
  3. Orientation
    With all these can be diagnosed as dementia.
23
Q

Know the process of amyloidhypothesis.

A

NIL

24
Q

Soluble oligomeres are produced by after cutting APP (amyloid precursor protein) and they are toxic to synapeses

A

NIL

25
Q

Patients with dementia are associate with reduce no of A-Beta42 (cos need it to form plaques)

A

NIL

26
Q

Is P-TAU a disease or progression marker?

A

Progression marker(patients who develop AD faster has HIGHER amt as those who develop slower)

27
Q

Is A-Beta42 a disease or progression marker?

A

Disease marker (patients who develop AD faster has same amt as those who develop slower)

28
Q

Is P-TAU a disease or progression marker?

A

Progression marker(patients who develop AD faster has HIGHER amt as those who develop slower)

29
Q

Do healthy individuals have A-Beta 42 in their brain (or detectable through scans?)

A

No

30
Q

A-Beta are not plaques. But are used to form plaques

A

NIL

31
Q

A-Beta is a risk factor for TAU and is also needed for TAU to spread. In healthy controls, extra TAU (without A-beta, no effect)

A

NIL

32
Q

What is passive immunisation?

A

ADministration of antibodies to person to develop immunity

33
Q

What is active immunisation for dementia?

A

Activating body’s own antibodies or production of these antibodies to actively clear off amyloid plaques when its occuring

34
Q

What is active immunisation for dementia?

A

Activating body’s own antibodies or production of these antibodies to actively clear off amyloid plaques when its occuring

35
Q

What is another approach to stop progression of AD (apart form active and passive immunisation)?

A

Inhibition of beta secretase

Clinical Neuroscience (4 decks)

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