Dementia Flashcards
what is cognition?
mental action of acquiring knowledge and understanding through thought, experience and the senses
cognition encompasses what?
attention memory executive function (problem solving/decision making) language social functioning
criteria for dementia?
evidence of significant cognitive decline in at least 1 cognitive domain or social cognition
plus - cognitive defects interfere with independence in everyday activities
plus - they are not better explained by another process/do not occur exclusively in context of delirium
is the incidence of dementia increasing or decreasing?
decreasing
what can cause acute cognitive dysfunction?
brain insult
- viral encephalitis (memory, behaviour, language change)
- head injury (attention, memory, executive dysfunction)
- stroke
- transient global amnesia
- transient epileptic amnesia
what is transient global amnesia?
cannot lay down new memory
abrupt onset antegrade > retrograde amnesia (repetitive)
preserved knowledge of self
how long does transient global amnesia last?
transient (4-6 hours)
always less than 24 hours
what can trigger transient global amnesia?
emotion/changes in temperature
what is transient epileptic amnesia?
similar to transient global but happens repetitively?
forgetful/repetitive questioning
can carry out complex activities with no recollection of events
associated with temporal lobe seizures
should respond to anti-epileptic medication
differentials for subacute cognitive disorders?
toxins neurodegeneration metabolic (B12, calcium, thyroid etc) inflammatory mood disorders functional infection
describe the functional/subjective cognitive impairment seen in sub-acute cognitive disorders?
everyday forgetfulness impacting on functioning
fluctuation of symptoms
mismatch between symptoms and reported function/symptoms and symptoms of known neurodegenerative disorders
may be a part of generalised functional disorder (reduced concentration/attention/reaction time and subsequent memory difficulties)
how is sub-acute cognitive disorder managed?
exclude mood disorder
refer to neuropsychology
what is prion disease?
neurodegenerative proteinopathy (prion) most common type = CJD abnormally folded prion proteins leads to enurodegeneration
describe the most common form of CJD?
sporadic = most common type
rapid onset dementia + neurological signs and myoclonus (twitchy movements)
progresses over few weeks to 4 months
causes death
other types of CJD?
variant
iatrogenic
genetic
what is seen on pathology of all types of CJD?
spongiform change on pathology
what causes alzheimers?
neurodegenerative proteinopathy (amyloid) disruption of cholinergic pathways in brain + synaptic loss causes - extracellular amyloid plaques (disrupts normal cell functioning/induces apoptosis) - intracellular neurofibrillary tangles (disruption of cytoskeleton leading to cell death)
how does alzheimers progress in most cases?
initial symptoms = forgetfulness
degeneration of medial hippocampus + later parietal lobes = forgetfulness > apraxia/visuospatial difficulties later
types of alzheimers depending on age?
<65 = early onset (genetic influence) >65 = sporadic (environmental)
describe 2 atypical presentations of alzheimers?
posterior cortical atrophy - visuospatial disturbance - commonly referred from ophthalmology progressive primary aphasia - semantic (naming difficulty) - logopenic aphasia (repeating) - non-fluent aphasia (effortful)
how is alzheimers investigated?
MRI - shows atrophy of temporal/parietal lobes
SPECT - shows tempoparietal reduced metabolism
CSF - shows reduced amyloid and increased tau ratio
amyloid ligand imaging (new research)
how is alzheimers managed?
address vascular risk factors
acetylcholine boosting treatment
- cholinesterase inhibitors
- NMDA receptor blocker
examples of cholinesterase inhibitors?
rivastigmine
galantamine
examples of NMDA receptor blockers?
memantine
what causes frontotemporal dementia?
neurodegenerative proteinopathy
- Tau > TDP43 > ubiquitin > protein aggregation > cell damage
25% are genetic, may be part of MND
how does frontotemporal dementia present?
early onset (<65) early frontal features (disinhibition, apathy, loss of empathy, stereotyped or compulsive behaviours, hyperorality) early loss of insight behavioural variant more common than primary progressive aphasia
how is frontotemporal dementia investigated?
MRI - shows atrophy of frontotemporal lobe
SPECT - frontotemporal reduced metabolism
CSF - increased tau/normal amyloid
how is frontotemporal dementia managed?
trial trazadone/antipsychotics to help behavioural features
safety management - control access to food/money/internet etc
power of attorney
core criteria for vascular dementia?
presence of cerebrovascular disease plus a clear temporal relationship between onset of dementia and cerebrovascular disease
how does vascular dementia present?
subcortical (small vessel disease) - reduced attention - executive dysfunction - slowed processing post stroke dementia can have co-existent amyloid pathology (slow progression, similar prognosis to AD)
how is vascular dementia managed?
manage vascular risk factors +/- cholinesterase inhibitors
CPN
what causes lewy body dementia?
neurodegenerative protienopathy (alpha synuclein) - alpha synuclein aggregates (insoluble) > cell dysfunction > cell damage > disruption of cholinergic and dopaminergic pathways
core criteria of lewy body dementia?
fluctuating cognition + recurrent well formed visual hallucinations +/- presence of extramyramidal features (seen in 75%)
may also have neuroleptic sensitvity
how is lewy body dementia investigated?
DaT (dopamine transporter imaging)
new research = alpha synuclein ligand binding imaging/alpha synuclein in CSF
how is lewy body dementia managed?
small dose levodopa/ increase acetylcholine (cholinesterase inhibitors)
support from PD nurse specialist
describe parkinsons disease dementia
late onset
most develop after 20 years of disease
overlaps clinically and pathologically with lewy body
features of parkinsons disease dementia?
parkinsons (bradykinesia + rigidity + tremor) + dementia (reduced attention + slow processing, impaired visuospatial functions and memory) +/- hallucinations
how is parkinsons disease dementia managed?
same as lewy body
describe huntingtons disease dementia?
early onset
dysexecutive syndrome + slowed speed of processing
eventual involvement of memory
associated changes in mood/personality and chorea +/- later psychosis
what causes huntingtons disease dementia?
expansion of CAG trinucleotide repeat on huntingtin gene produced neurodegenerative protein (huntingtin)
how is huntingtons disease dementia investigated and managed?
investigations = genetic, MRI (shows loss of caudate heads) management = mood stabilisers, Rx for chorea, HD nurse specialist)
how can genetics be involved in gradual onset disorders of cognition (dementia)?
can be polygenic + environmental (e.g apoe4 in alzheimers)
can be monogenetic inherited disorders
where do you refer cognitive dysfunction to?
> 65 with gradual onset dementia and no additional neurology = old age psychiatry
<65 with any unusual features
