1. what are the clinical features of dementia?
    • 1. loss of memory and higher brain functions eg planning, decision making, problem solving
    • 2. loss of ADLs
    • 3. psychiatric symptoms and behavioural difficulties eg aggression, wandering, sexual disinhibition
  2. where is short term memory stored/made?
    frontal lobe
  3. what is the other name for short term memory?
    working memory - for immediate recall
  4. where is long term memory stored?
    limbic system
  5. what are the 3 main types of long term memory? and which part of brain?
    • procedural: learnt tasks eg driving, playing instrument - basal ganglia, cerebral cortex
    • episodic: personally experienced (what you've done) - limbic system
    • semantic: general knowledge, names, meaning of words - temporal neocortex
  6. which lobe and hemisphere has verbal memory?
    temporal: dominant (rational side)
  7. which lobe and hemisphere has visual memory?
    temporal: non-dominant (emotional side)
  8. if writing and calculation and R-L orientation is impaired, which lobe and hemisphere is that?
    • parietal lobe
    • dominant hemisphere
  9. what does the non-dominant hemisphere of parietal lobe control?
    • visuospatial perception
    • location in space
  10. how do you test dominant hemisphere of parietal lobe?
    'touch right ear with left hand'
  11. what is dyspraxia? give eg
    • inability to carry out a task in the absence of motor or sensory loss
    • eg making a cup of tea - sequences
  12. what is agnosia?
    inability to recognise, despite normal perception
  13. how can age associated memory impairment be distinguished from dementia? 2 ways
    • 1. late stage of dementia: reduced INSIGHT
    • 2. AAMI: forget DETAILS of event rather than the event itself
  14. what are the psychiatric complications of dementia?
    • delusions, persecution (they forget where they put things so blame someone else), theft
    • misidentification, depression
    • hallucinations: auditory (functional), visual (organic)
    • challenging behaviour: agitation, restlessness, sundowning, wandering, aggression - verbal, physical
  15. what is sundowning?
    when the day gets darker as the sun goes down, symptoms get worse
  16. which types of hallucinations are more common in organic illnesses?
  17. give 6 different presentations in patients with dementia?
    • 1. death of a partner / inability to cope
    • 2. self neglect - hygiene, dehydration (not eat/drink)
    • 3. behavioural problems
    • 4. physical problems - weight loss, exposure
    • 5. accidental harm, fires, car accident (visuo-spatial disorientation)
    • 6 loss of memory
  18. which lobes of the brain does AD mainly affect?
    • temporal
    • parietal
    • some frontal
  19. what are the 2 pathological hallmarks of AD?
    • neurofibrillary tangles
    • beta amyloid plaques
  20. which NT is deficient in AD?
    ACh so treatment acts to inhibit cholinesterase (stop the breakdown)
  21. where is beta amyloid protein derived from?
    Amyloid precursor protein (APP) and apolipoprotein E4
  22. what is sporadic AD due to?
    involvement of many different genes and combination of environmental risk factors
  23. what are some forms of early onset (before 65) familial AD due to?
    • autosomal dominant inheritance of one of 3 genes:
    • APP: chr 21
    • presenilin-1: chr 14
    • presenilin-2: chr 1
  24. what implications of neuropathology do patients with Downs syndrome have?
    • changes like AD by middle age
    • due to triplication and over expression of gene APP
  25. in late onset AD, which allele of a gene increases susceptibility to develop AD?
    • Apolipoprotein E: 4 allele
    • 1 copy increases risk by 4 and decreases age of onset but not enough to certainly develop AD
  26. what are the Risk factors for AD?
    • age
    • genetic mutation
    • APP, ApoE
    • presenilin
    • head injury
    • Down's syndrome
    • Female gender
  27. what are the protective factors for AD?
    • oestrogens
    • NSAIDs
    • antioxydants, vit E
    • education (increased cognitive reserve)
  28. what are the treatment options for AD?
    • cholinesterase inhibitors: donezepil, rivastigmine, galantamine
    • memantine (NMDA antagonist)
  29. what is the pathological hallmark of DLB?
    lewy bodies: intracellular inclusions, aggregates of alpha-synuclein
  30. what is the difference in the lewy body placements between PD and DLB?
    • PD: subcortical
    • DLB: cortical therefore affects higher cognitive function
  31. what is the main difference between AD and DLB in terms of cognition?
    • DLB: fluctuations of cognition
    • AD: deterioration is gradual decline
  32. what is the onset of DLB like?
    • insidious onset
    • often executive function
    • parietal lobe deficits
  33. what are the main symptoms of DLB?
    • fluctuating cognition
    • parkinsonism including falls (postural instability)
    • psychotic features: visual hallucinations in 60-70%
    • REM sleep behaviour disorder (RBD): when you act out your dreams
  34. is memory more affected in AD or DLB?
  35. which drugs is DLB very sensitive to? and what implications does this lead to?
    • neuroleptics
    • so don't use eg chlorpromazine or haloperidol as risk of catatonia/muscle rigidity, sedation, worsening confusion, irreversible parkinsonism, NMS like, death!
  36. what are the DAT scan results of DLB?
    low dopamine transporter uptake
  37. what is vascular dementia due to?
    • small vessel disease
    • emboli - recurrent strokes
  38. what are the RF for vascular dementia?
    • HTN
    • AF
    • Smoking
    • diabetes
    • carotid artery stenosis
    • hypercholesterolaemia
  39. what is the onset of vascular dementia?
    abrupt, sudden
  40. what is the course of vascular dementia typically like?
    • stepwise
    • associated with TIA or CVA
  41. how is examination of vascular dementia different from eg AD?
    focal neurological signs
  42. what is the cognitive impairment like in vascular dementia?
  43. what are the other features of vascular dementia?
    emotional lability
  44. where is Brocas area?
    inferior frontal gyrus
  45. where is Wernickes area?
    superior temporal gyrus
  46. what functions relevant to dementia are there in frontal lobe?
    • executive functions ie organising, planning, problem solving, sequencing
    • personality
    • regulation of social behaviour
    • Brocas area - speech (inferior frontal gyrus)
    • cortical inhibition of bowels/bladder
  47. what are the main features of frontotemporal dementia?
    • behavioural syndrome
    • personality change
    • inappropriate social behaviour
    • disinhibition
    • apathy
    • loss of empathy, insight
    • reduced speech
    • executive dysfunciton
    • NB memory relatively preserved
  48. what % of FTLD is genetic?
  49. which age group does FTD affect more?
  50. how is the MMSE different between AD and FTD?
    • AD: score goes down with every time u do it
    • FTD: relatively preserved score until late stage
  51. what is pseudodementia?
    symptoms consistent with dementia but the cause is a psychiatric illness ie depression rather than a degenerative cause.
  52. what is the difference in terms of illness duration between dementia and depression?
    • dementia longer
    • depression short
  53. what is the difference in terms of progression between dementia and depression?
    • dementia: slower
    • depression: more rapid
  54. what is the difference in terms of complaining of poor memory and the history given and response between dementia and depression?
    • dementia: don't ℅ poor memory, vague hx and reactive response
    • depression: do ℅ poor memory, detailed hx, flat response
  55. what is the difference in terms of orientation, apraxia and test performance between dementia and depression?
    dementia: poor orientation, apraxia present, always poor test performance
  56. what are the reversible causes of dementia? split into intracranial lesions, infections/inflam, metabolic and toxic
    • intracranial lesions: tumour, subdural haematoma, NPH
    • infec/inflam: encephalitis, neurosyphilis, cerebral sarcoid/sle/rheum
    • metabolic: thyroid, uraemia, liver failure, B12/folate/thiamine deficiency
    • toxic: alcohol or heavy metal poisoning
  57. what are the Ix used in dementia?
    • dementia screen: bloods - FBC, U&E, CRP, ESR, TFT, LFT, VDRL, B12, folate
    • reversible causes exclude
    • MRI CT
    • EEG
    • genotyping chromosome 1, 14, 21, ApoE (allele4)
  58. what are non-drug treatments of dementia?
    • Environmental modifications and activities
    • Establishing routines
    • Safety,
    • mobility,
    • special senses,
    • diet,
    • continence
    • Social aspects – Needs assessments, services (GP vital)
    • Carers and families
    • Day centres
    • Financial / Power of Attorney
    • Driving
    • Occupational (esp younger patients)
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