Card Set Information
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
where is short term memory stored/made?
what is the other name for short term memory?
working memory - for immediate recall
where is long term memory stored?
what are the 3 main types of long term memory? and which part of brain?
: learnt tasks eg driving, playing instrument - basal ganglia, cerebral cortex
: personally experienced (what you've done) - limbic system
: general knowledge, names, meaning of words - temporal neocortex
which lobe and hemisphere has verbal memory?
temporal: dominant (rational side)
which lobe and hemisphere has visual memory?
temporal: non-dominant (emotional side)
if writing and calculation and R-L orientation is impaired, which lobe and hemisphere is that?
what does the non-dominant hemisphere of parietal lobe control?
location in space
how do you test dominant hemisphere of parietal lobe?
'touch right ear with left hand'
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
what is agnosia?
inability to recognise, despite normal perception
how can age associated memory impairment be distinguished from dementia? 2 ways
1. late stage of dementia
: reduced INSIGHT
: forget DETAILS of event rather than the event itself
what are the psychiatric complications of dementia?
delusions, persecution (they forget where they put things so blame someone else), theft
: auditory (functional), visual (organic)
: agitation, restlessness, sundowning, wandering, aggression - verbal, physical
what is sundowning?
when the day gets darker as the sun goes down, symptoms get worse
which types of hallucinations are more common in organic illnesses?
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
which lobes of the brain does AD mainly affect?
what are the 2 pathological hallmarks of AD?
beta amyloid plaques
which NT is deficient in AD?
ACh so treatment acts to inhibit cholinesterase (stop the breakdown)
where is beta amyloid protein derived from?
Amyloid precursor protein (APP) and apolipoprotein E4
what is sporadic AD due to?
involvement of many different genes and combination of environmental risk factors
what are some forms of early onset (before 65) familial AD due to?
autosomal dominant inheritance of one of 3 genes:
: chr 21
: chr 14
: chr 1
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
in late onset AD, which allele of a gene increases susceptibility to develop AD?
: 4 allele
1 copy increases risk by 4 and decreases age of onset but not enough to certainly develop AD
what are the Risk factors for AD?
what are the protective factors for AD?
antioxydants, vit E
education (increased cognitive reserve)
what are the treatment options for AD?
: donezepil, rivastigmine, galantamine
memantine (NMDA antagonist)
what is the pathological hallmark of DLB?
lewy bodies: intracellular inclusions, aggregates of alpha-synuclein
what is the difference in the lewy body placements between PD and DLB?
: cortical therefore affects higher cognitive function
what is the main difference between AD and DLB in terms of cognition?
: fluctuations of cognition
: deterioration is gradual decline
what is the onset of DLB like?
often executive function
parietal lobe deficits
what are the main symptoms of DLB?
parkinsonism including falls (postural instability)
: visual hallucinations in 60-70%
REM sleep behaviour disorder (RBD)
: when you act out your dreams
is memory more affected in AD or DLB?
which drugs is DLB very sensitive to? and what implications does this lead to?
so don't use eg chlorpromazine or haloperidol as risk of catatonia/muscle rigidity, sedation, worsening confusion, irreversible parkinsonism, NMS like, death!
what are the DAT scan results of DLB?
low dopamine transporter uptake
what is vascular dementia due to?
small vessel disease
emboli - recurrent strokes
what are the RF for vascular dementia?
carotid artery stenosis
what is the onset of vascular dementia?
what is the course of vascular dementia typically like?
associated with TIA or CVA
how is examination of vascular dementia different from eg AD?
focal neurological signs
what is the cognitive impairment like in vascular dementia?
what are the other features of vascular dementia?
where is Brocas area?
inferior frontal gyrus
where is Wernickes area?
superior temporal gyrus
what functions relevant to dementia are there in frontal lobe?
executive functions ie organising, planning, problem solving, sequencing
regulation of social behaviour
Brocas area - speech (inferior frontal gyrus)
cortical inhibition of bowels/bladder
what are the main features of frontotemporal dementia?
inappropriate social behaviour
loss of empathy, insight
NB memory relatively preserved
what % of FTLD is genetic?
which age group does FTD affect more?
how is the MMSE different between AD and FTD?
: score goes down with every time u do it
: relatively preserved score until late stage
what is pseudodementia?
symptoms consistent with dementia but the cause is a psychiatric illness ie depression rather than a degenerative cause.
what is the difference in terms of illness duration between dementia and depression?
what is the difference in terms of progression between dementia and depression?
: more rapid
what is the difference in terms of complaining of poor memory and the history given and response between dementia and depression?
: don't ℅ poor memory, vague hx and reactive response
: do ℅ poor memory, detailed hx, flat response
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
what are the reversible causes of dementia? split into intracranial lesions, infections/inflam, metabolic and toxic
: tumour, subdural haematoma, NPH
: encephalitis, neurosyphilis, cerebral sarcoid/sle/rheum
: thyroid, uraemia, liver failure, B12/folate/thiamine deficiency
: alcohol or heavy metal poisoning
what are the Ix used in dementia?
: bloods - FBC, U&E, CRP, ESR, TFT, LFT, VDRL, B12, folate
reversible causes exclude
genotyping chromosome 1, 14, 21, ApoE (allele4)
what are non-drug treatments of dementia?
Environmental modifications and activities
Social aspects – Needs assessments, services (GP vital)
Carers and families
Financial / Power of Attorney
Occupational (esp younger patients)