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Flashcards in Cognitive Neurology Deck (43):
1

what generally causes dementias

neurodegenerative proteinopathies

2

what is cognition

the mental action of acquiring knowledge and understanding through thought, experience ans the scenes
encompases
- formation of knowledge and memory
-executive function (problem solving/ decision making)
-language (comprehension and production of language)
-social functioning (judgement, evaluation, reasoning)
-attention

3

what is dementia

significant cognitive decline in at least 1 cognitive domain (attention, executive, learning and memory, language, perceptuo-motor (ie praxis) or social cognition


generally progressive/ pervasive and generally associated with neurodegeneration

4

what cognitive problems arise from viral encephalitis

frontal temporal problems
-memory, behaviour change, language

5

what cognitive problems can arise from head injury

attention
memory
executive dysfunction

6

what is transient global amnesia

an acute cognitive disorder
abrupt onset antegrade>retrograde amnesia that is repetitive
will have preserved knowledge of self
lasts 4-6 hours (always <24hrs)

7

what causes a transient global amnesia

triggering factors inc emotion/ changes in temperature
transient changes in the hippocampus

8

what are the clinical features of a transient epileptic amnesia

forgetful/ repetitive questioning
can carry out complex activities with no recollection of events
short lived(20-30 mins)
recurrent problems

9

what is transient epileptic amnesia associated with

temporal lobe seizures

10

what can cause sub acute cognitive disorders

toxins- alcohol, CO
neurodegeneration (CJD)
metabolic- B12, calciulm, thyroid etc
inflammatory- limbic encephalitis
mood disorders
functional
infection- HIV, syphilis

11

what are the clinical features of functional/ subjective cognitive impairment

everyday forgetfulness impacting on functioning
fluctuation of symptoms
mismatch of symptoms (symptoms vs reported symptoms/ function, or symptoms vs symptoms of known neurodegenerative disorders)
(will think symptoms are worse than they actually are)

12

what can a functional/ subjective cognitive impairment be a part of

generalised functional disorder (decreased concentration/ attention/ reaction time and memory problems)

13

what is the treatment for a functional cognitive impairment

exclude a mood disorder
neuropsychology

14

what is creutzfeldt-jakob disease

the most common human prion disease

15

what causes prion disease

neurodegenerative proteinopathy (prion)
prion protein in misfolded

16

what are the types of CJD

sporadic (60s, rapid onset dementia + neuro signs + myoclonus, lasts 4 months)

variant (20s, painful sensory disturbance + neuropsychiatric decline, lasts 14 months)

iatrogenic

genetic (any age onset, may mimic sporadic, duration <2 years)

17

what is seen pathologically in prion disease

spongiform change

18

what is the pathology of alzheimers

is a neurodegenerative proteinopathy (amyloid)
disruption of cholinergic pathways in the brain + synaptic loss
-extracellular amyloid plaques
-intracellular neurofibrillary tangles

19

what parts of brain are affected in alzheimers

degeneration of medial hippocampus + later parietal lobes

(forgetfullness -> apraxia/ visuospatial difficulties)

20

what are the symptoms of posterior cortical atrophy (atypical presentation of AD)

visuospatial disturbance
problems recognising death

21

what are the features of progressive primary aphasia (an atypical presentation of AD)

semantic (naming difficulties)
logopenic aphasia (repeating)
non fluent aphasia (effortful speech)

22

what is seen on investigations in AD

MRI- atrophy of temporal/ parietal lobes
SPECT - temporoparietal decreased metabolism
CSF- decreased amyloid : increased tau ratio

23

what is the treatment for alzheimers

address vascular risk factors
acetylcholine boosting treatments:
- cholinesterase inhibitors (rivastigmine/ galantamine)
-NMDA receptor blockers (memantine)

24

what are the features of frontotemporal dementia

early onset dementia (<65y/o)
Early frontal features (disinhibition, apathy, loss of empathy, stereotyped or compulsive behaviours, hyperorality)
Early loss of insight (collateral history vital)

25

what causes frontotemporal dementia

Neurodegenerative proteinopathy

protein aggregation -> cell damage

26

what is seen in investigations in FTD

MRI: Atrophy of frontotemporal lobes
SPECT: Frontotemporal ↓metabolism
CSF: ↑ tau / normal amyloid

27

what is the management for FTD

Trial of Trazadone / antipsychotics to help behavioural features

Safety management
Controlled access to food / money / internet
Structured activities

Power of attorney
Support: MND nurse specialist if co-existent MND / CPN

28

what are the features of vascular dementia

late onset dementia (>65)
presence of cerebrovascular disease (vascular changes on MRI)
co existent amyloid pathology
slow progression
prognosis similar to AD

29

what is the presentation of vascular dementia

subcortical (small vessel disease)= decreased attention, executive dysfunction, slowed processing
post stroke dementia

30

what is the management for vascular dementia

vascular risk factors +/- cholinesterase inhibitor

31

what are the features of lewy bodies dementia

late onset dementia (>65)
fluctuating cognition
recurrent well formed visual hallucinations +/-
presence of extrapyramidal features

neuroleptic sensitive (gets worse when you give halopuridol)

32

what causes lewy body dementia

Neurodegenerative proteinopathy (α-synuclein)
α-synuclein aggregates = insoluble → cell dysfunction → cell damage
Leads to disruption of cholinergic and dopaminergic pathways

33

what is seen on investigations in lewy body dementia

dopamine transporter imagine
alpha-synuclein ligand imaging
alpha synuclein in CSF

34

what is the treatment for dementia with lewy bodies

small dose levodopa
cholinesterase inhibitors

35

what are the features of parkinsons disease dementia

late onset >65
clinically and pathologically overlap with LBD (LBD has quicker onset of dementia after presentation< PD usually dementia 20 years after presentation)

36

what is the management for parkinsons disease dementia

small dose levodopa
cholinesterase inhibitors

37

what are the symptoms of parkinsons disease dementia

Parkinson’s disease (bradykinesia + rigidity + tremor) + dementia (↓attention + slowness of processing, impaired visuospatial functions + memory) +/- hallucinations

38

what are the features of huntingtons disease dementia

early onset 30-50
Dementia: Dysexecutive syndrome + slowed speed of processing. Eventual involvement of memory
Associated changes in mood / personality, and chorea +/- later psychosis

39

what causes huntingtons

Expansion of the CAG trinucleotide repeat on the huntingtin gene
produces neurodegenerative protein (Huntingtin)

40

what is seen in investigations in huntingtons

CAG trinucleotide repeat
MRI- loss of caudate heads

41

what is the treatment for huntingtons

mood stabilisers
Tx for chorea
nurse specialist

42

what is the apo34 gene associated

amyloid deposition with age- alzheimers

43

what proteins are associated with the different types of dementias IMPORTANT

AD +/- VaD – amyloid,
PDD / DLB – α-synuclein,
CJD – prion,
FTD – tau,
HD – huntingtin