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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
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where is short term memory stored/made?
frontal lobe
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what is the other name for short term memory?
working memory - for immediate recall
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where is long term memory stored?
limbic system
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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
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which lobe and hemisphere has verbal memory?
temporal: dominant (rational side)
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which lobe and hemisphere has visual memory?
temporal: non-dominant (emotional side)
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if writing and calculation and R-L orientation is impaired, which lobe and hemisphere is that?
- parietal lobe
- dominant hemisphere
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what does the non-dominant hemisphere of parietal lobe control?
- visuospatial perception
- location in space
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how do you test dominant hemisphere of parietal lobe?
'touch right ear with left hand'
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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
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what is agnosia?
inability to recognise, despite normal perception
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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
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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
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what is sundowning?
when the day gets darker as the sun goes down, symptoms get worse
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which types of hallucinations are more common in organic illnesses?
visual
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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
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which lobes of the brain does AD mainly affect?
- temporal
- parietal
- some frontal
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what are the 2 pathological hallmarks of AD?
- neurofibrillary tangles
- beta amyloid plaques
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which NT is deficient in AD?
ACh so treatment acts to inhibit cholinesterase (stop the breakdown)
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where is beta amyloid protein derived from?
Amyloid precursor protein (APP) and apolipoprotein E4
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what is sporadic AD due to?
involvement of many different genes and combination of environmental risk factors
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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
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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
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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
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what are the Risk factors for AD?
- age
- genetic mutation
- APP, ApoE
- presenilin
- head injury
- Down's syndrome
- Female gender
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what are the protective factors for AD?
- oestrogens
- NSAIDs
- antioxydants, vit E
- education (increased cognitive reserve)
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what are the treatment options for AD?
- cholinesterase inhibitors: donezepil, rivastigmine, galantamine
- memantine (NMDA antagonist)
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what is the pathological hallmark of DLB?
lewy bodies: intracellular inclusions, aggregates of alpha-synuclein
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what is the difference in the lewy body placements between PD and DLB?
- PD: subcortical
- DLB: cortical therefore affects higher cognitive function
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what is the main difference between AD and DLB in terms of cognition?
- DLB: fluctuations of cognition
- AD: deterioration is gradual decline
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what is the onset of DLB like?
- insidious onset
- often executive function
- parietal lobe deficits
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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
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is memory more affected in AD or DLB?
AD
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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!
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what are the DAT scan results of DLB?
low dopamine transporter uptake
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what is vascular dementia due to?
- small vessel disease
- emboli - recurrent strokes
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what are the RF for vascular dementia?
- HTN
- AF
- Smoking
- diabetes
- carotid artery stenosis
- hypercholesterolaemia
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what is the onset of vascular dementia?
abrupt, sudden
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what is the course of vascular dementia typically like?
- stepwise
- associated with TIA or CVA
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how is examination of vascular dementia different from eg AD?
focal neurological signs
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what is the cognitive impairment like in vascular dementia?
patchy
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what are the other features of vascular dementia?
emotional lability
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where is Brocas area?
inferior frontal gyrus
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where is Wernickes area?
superior temporal gyrus
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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
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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
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what % of FTLD is genetic?
30-50%
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which age group does FTD affect more?
yonger
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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
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what is pseudodementia?
symptoms consistent with dementia but the cause is a psychiatric illness ie depression rather than a degenerative cause.
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what is the difference in terms of illness duration between dementia and depression?
- dementia longer
- depression short
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what is the difference in terms of progression between dementia and depression?
- dementia: slower
- depression: more rapid
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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
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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
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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
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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)
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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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