Cognitive Neurology Flashcards by Louise Emerson

what generally causes dementias

neurodegenerative proteinopathies

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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

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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

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what cognitive problems arise from viral encephalitis

frontal temporal problems

-memory, behaviour change, language

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what cognitive problems can arise from head injury

attention
memory
executive dysfunction

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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)

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what causes a transient global amnesia

triggering factors inc emotion/ changes in temperature

transient changes in the hippocampus

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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

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what is transient epileptic amnesia associated with

temporal lobe seizures

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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

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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)

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

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

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what is the treatment for a functional cognitive impairment

exclude a mood disorder

neuropsychology

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what is creutzfeldt-jakob disease

the most common human prion disease

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what causes prion disease

neurodegenerative proteinopathy (prion) 
prion protein in misfolded

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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)

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what is seen pathologically in prion disease

spongiform change

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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

what parts of brain are affected in alzheimers

degeneration of medial hippocampus + later parietal lobes

forgetfullness -> apraxia/ visuospatial difficulties

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

visuospatial disturbance

problems recognising death

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

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

what is seen on investigations in AD

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

what is the treatment for alzheimers

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

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)

what causes frontotemporal dementia

Neurodegenerative proteinopathy protein aggregation -> cell damage

what is seen in investigations in FTD

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

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

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 ```

what is the presentation of vascular dementia

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

what is the management for vascular dementia

vascular risk factors +/- cholinesterase inhibitor

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)

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 ```

what is seen on investigations in lewy body dementia

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

what is the treatment for dementia with lewy bodies

small dose levodopa | cholinesterase inhibitors

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)

what is the management for parkinsons disease dementia

small dose levodopa | cholinesterase inhibitors

what are the symptoms of parkinsons disease dementia

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

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

what causes huntingtons

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

what is seen in investigations in huntingtons

CAG trinucleotide repeat | MRI- loss of caudate heads

what is the treatment for huntingtons

mood stabilisers Tx for chorea nurse specialist

what is the apo34 gene associated

amyloid deposition with age- alzheimers

what proteins are associated with the different types of dementias IMPORTANT

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