Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neurology > Cognitive Neurology > Flashcards

Cognitive Neurology Flashcards

1
Q

what generally causes dementias

A

neurodegenerative proteinopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is cognition

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is dementia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what cognitive problems arise from viral encephalitis

A

frontal temporal problems

-memory, behaviour change, language

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what cognitive problems can arise from head injury

A

attention
memory
executive dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is transient global amnesia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what causes a transient global amnesia

A

triggering factors inc emotion/ changes in temperature

transient changes in the hippocampus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the clinical features of a transient epileptic amnesia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is transient epileptic amnesia associated with

A

temporal lobe seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what can cause sub acute cognitive disorders

A 
toxins- alcohol, CO 
neurodegeneration (CJD)
metabolic- B12, calciulm, thyroid etc 
inflammatory- limbic encephalitis 
mood disorders 
functional 
infection- HIV, syphilis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the clinical features of functional/ subjective cognitive impairment

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the treatment for a functional cognitive impairment

A

exclude a mood disorder

neuropsychology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is creutzfeldt-jakob disease

A

the most common human prion disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what causes prion disease

A 
neurodegenerative proteinopathy (prion) 
prion protein in misfolded
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the types of CJD

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is seen pathologically in prion disease

A

spongiform change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the pathology of alzheimers

A

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

19
Q

what parts of brain are affected in alzheimers

A

degeneration of medial hippocampus + later parietal lobes

forgetfullness -> apraxia/ visuospatial difficulties

20
Q

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

A

visuospatial disturbance

problems recognising death

21
Q

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

A

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

22
Q

what is seen on investigations in AD

A

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

23
Q

what is the treatment for alzheimers

A

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

24
Q

what are the features of frontotemporal dementia

A

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
Q

what causes frontotemporal dementia

A

Neurodegenerative proteinopathy

protein aggregation -> cell damage

26
Q

what is seen in investigations in FTD

A

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

27
Q

what is the management for FTD

A

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
Q

what are the features of vascular dementia

A 
late onset dementia (>65)
presence of cerebrovascular disease (vascular changes on MRI)
co existent amyloid pathology 
slow progression 
prognosis similar to AD
29
Q

what is the presentation of vascular dementia

A

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

30
Q

what is the management for vascular dementia

A

vascular risk factors +/- cholinesterase inhibitor

31
Q

what are the features of lewy bodies dementia

A

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

neuroleptic sensitive (gets worse when you give halopuridol)

32
Q

what causes lewy body dementia

A 
Neurodegenerative proteinopathy (α-synuclein)
α-synuclein aggregates = insoluble → cell dysfunction → cell damage
Leads to disruption of cholinergic and dopaminergic pathways
33
Q

what is seen on investigations in lewy body dementia

A

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

34
Q

what is the treatment for dementia with lewy bodies

A

small dose levodopa

cholinesterase inhibitors

35
Q

what are the features of parkinsons disease dementia

A

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
Q

what is the management for parkinsons disease dementia

A

small dose levodopa

cholinesterase inhibitors

37
Q

what are the symptoms of parkinsons disease dementia

A

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

38
Q

what are the features of huntingtons disease dementia

A

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
Q

what causes huntingtons

A

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

40
Q

what is seen in investigations in huntingtons

A

CAG trinucleotide repeat

MRI- loss of caudate heads

41
Q

what is the treatment for huntingtons

A

mood stabilisers
Tx for chorea
nurse specialist

42
Q

what is the apo34 gene associated

A

amyloid deposition with age- alzheimers

43
Q

what proteins are associated with the different types of dementias IMPORTANT

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

Neurology (35 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions