Y4 - Dementia Flashcards
What is required for the diagnosis of dementia?
Evidence of cognitive decline (e.g. MOCA/MMSE) and functional decline with a clear consciousness and duration > 6months
What are some examples of cognitive dysfunctions common in dementia?
Dysmnesia (tends to be short term)
Dysphasia
Dysgnosia
Dyspraxia
Problems with orientation (in time, place, person)
Constructional ability issues
Executive dysfunction (initiation, inhibition, abstraction, problem solving etc.)
What activities of daily living may be affected in dementia?
Finances Food - eating food that is in date? buying food? cooking? Care of children/pets Health/medication Use of telephone/television Basic ADL - washing, dressing, eating Driving
When assessing someone’s functional ability for a diagnosis of dementia what must you do?
Consider a change from baseline
What must you do in relation to driving when someone is diagnosed with dementia?
Tell them to inform the DVLA
If they do not, you can go above their head if you feel their driving would put them/others at risk
Name some reversible types of dementia
Normal pressure hydrocephalus Subdural haematoma (tends to be fluctuating) Tumours Neurosyphillis/HIV Vitamin deficiencies Hypothyroidism
When might you think of a vitamin deficiency causing a reversible dementia?
Poor cognition, low mood
This is why GPs must always check haematinics and FBC
What vitamin deficiencies can lead to a reversible dementia?
B12
Folate
How are dementias typed?
Based on clinical decision
Scans may be used to back it up
What are the types of dementia?
Alzheimer's Vascular Mixed AD and VD Lewy body dementia Frontotemporal/Pick's Alcohol related brain damage - e.g. Korsakoff's Subcortical, e.g. Parkinson's, Huntington's, HIV Prion protein, e.g. CJD
What is typical in the presentation of Alzheimer’s?
Progressive deterioration over a long period of time
V. little insight
Confabulation
Memory issues
What is typical in the presentation of vascular dementia?
Step wise deterioration
What is typical in the presentation of Lewy body dementia?
Dementia
Parkinsonism
Hallucinations (visual)
Fluctuation
What is Pick’s disease?
Type of frontotemporal dementia
Neurodegeneration of frontal and temporal lobes due to accumulation of proteins in the brain
Tends to affect behaviour and personality a lot (e.g. become hypersexualised, rude)
What causes ARBD?
Thiamine deficiency
What is the pathology of Alzheimer’s?
Abnormal accumulation of proteins (beta-amyloid plaques, tau tangles)
Atrophy of key brain regions (temporal in Alzheimer’s)
Neurochemical disruption - acetylcholine is reduced
What is the aetiology of Alzheimer’s?
Genetic and environmental factors
Early onset more associated with genetic factors, late onset more associated with environmental factors
What are RFs for Alzheimer’s?
Age
F>M
Vascular RFs
Head injury
What are risk factors for vascular dementia?
Age HTN Smoking Hyperlipidaemia M IHD DM
How do you treat vascular dementia?
No specific Rx
Modify RFs
What is the difference between LBD and dementia in Parkinson’s?
Onset of motor and cognitive decline within 1y = LBD
Onset of cognitive decline 1y after motor symptoms = DPD
What is the pathology of LBD?
Lewy body accumulation leads to reduced dopamine due to alpha synucleic protein
Why can people with LBD get differing symptoms?
Predominant site in brain confers symptoms
What are classical features of LBD?
Visual hallucinations
Fluctuating course
Parkinsonism
What drug should be avoided in those with LBD?
Antipsychotics
Makes motor symptoms a lot worse
How do you treat LBD?
Cholinesterase inhibitors (e.g. rivastigime)
What are some differentials for dementia?
Normal
Delirium
Depression
Mild cognitive impairment
What things may make you lean towards delirium as a diagnosis as opposed to dementia?
Rapid onset & decline Very fluctuant Worse at night Psychomotor disturbance Disrupted sleep wake cycle Florid psychotic symptoms Clouding of consciousness
What things may make you lean towards depression as a diagnosis as opposed to dementia?
Trigger/life event Subjective complaints of memory loss Sleep/appetite disturbance Worse in morning Distressed & unhappy 'Don't know answers'
What is involved in the clinical assessment of someone with suspected dementia?
Hx, collateral Hx Functional ability Ex - physical, MSE, cognitive Ex Risks Bloods - FBC, UE, LFTs, glucose, B12, folate CT/SPECT
How should you treat Alzheimer’s?
Anticholinesterase inhibitors for mild to moderate AD (MMSE 10+)
NMDA antagonist, GABA for moderate to severe AD (14 or less on MMSE) or second line if AChI not tolerated
How do anticholinesterases work?
Reduce breakdown of ACh
What are the anticholineasterases?
Donepezil
Galantamine
Rivastigime
What is the NMDA antagonist used for moderate-severe Alzheimer’s?
Memantime
How is the severity of dementia assessed/
Consider functional level MMSE: Mild - 21-30 Moderate - 10-20 Moderately severe - 10-14 Severe <10
What are BPSD?
Behavioural and psychological symptoms in dementia
Challenging behaviours (unreasonable and challenging the norms and rules of the context in which they occur)
What are the kinds of BPSD?
Lack of behaviour
Exaggerated normal behaviour
Abnormal/undesirable behaviours
What are the five major BPSD symptoms?
Agitation (restlessness, wandering)
Psychosis
Affective (depression, lability, anxiety, hypomania, apathy)
Disinhibition (aggression, sexual)
Behaviour (eating, toileting, dressing, sleep wake cycle)
What is involved in BPSD management?
Hx, Obs, monitoring Environment Personal history and personality Physical health Intervention
What is the ABC approach to BPSD management?
Antecedent - circumstances & precipitating factors at onset of behaviour
Behaviour - description of behaviour
Consequences - what occurs after behaviour, how everyone responds to behaviour
How is BPSD managed pharmacologically?
Antipsychotics, e.g. risperidone
What are the SEs of using antipsychotics in dementia patients?
Sedation, falls, confusion, postural hypotension
Make EPSE worse
Which part of the brain does Alzheimer’s largely affect?
Temporal lobes
What are the two main theories of Alzheimer’s pathology?
Beta-amyloid plaques which interfere with neuronal signalling, cause inflammation –> neuron damage, and deposit in BVs weakening their walls and predisposing to haemorrhage
TAU tangles - TAU proteins become misshapen, cannot support the cytoskeleton & clump together to form neurofibrillary tangles
Non-functioning neurons cannot signal and undergo apotosis –> brain atrophy, sulci and ventricles widen, gyri shrink
What are the main clinical features of Alzheimer’s?
Loss of short term memory Loss of motor skills Language problems Long term memory problems Disorientation Bed ridden
How is the definitive diagnosis of Alzheimer’s made?
Brain biopsy on autopsy
What is Parkinson’s?
Movement disorder where dopamine producing neurons in the substantia nigra undergo degeneration
Give two risk factors for PD
Pesticide exposure
DNA variants in genes
Where are the SN?
One either side of midbrain
They are part of the basal ganglia
What is the role of the basal ganglia?
Control movement via its connections to the motor cortex
What part of the brain tends to disappear in PD?
Substantia nigra
What is the pathophysiology of PD?
Lewy bodies appear in the affected substantia nigra before they die
What are Lewy bodies?
Eosinophilic, round lesions made of alpha synuclein proteins
What other disease are Lewy bodies found in?
LBD among others
What are the two parts of the SN?
Pars reticulata - receives signals from the striatum, relays messages via GABA neurons to the thalamus
Pars compacta - sends messages to the striatum via dopamingeric neurons (nigrostriatal pathway)
What is the nigrostriatal pathway involved in?
Stimulating cerebral cortex to initiate movement and calibrating/fine tuning movement
What is the striatum?
Caudate and putamen
What are some clinical features of PD?
Resting, asymmetric, pill rolling tremor Cogwheel rigidity Stooped posture Expressionless face Bradykinesia, hypokinesia, akinesia Shuffling gait Postural instability (can lead to falls)
Depression, dementia, sleep disturbances/difficulties
What are some PD treatments?
Levodopa/carbidopa Amantadine Dopamine agonists COMT inhibitors MAO-B inhibitor Anticholingerics Deep brain stimulation
Can dopamine cross the BBB?
No but levodopa (its precursor can)
How is levodopa converted into dopamine?
By dopa decarboxylase in the nigrostriatal neurons
NB peripheral dopa decarboxylase is found elsewhere in the body
What may lead to some of the unwanted SEs associated with levodopa?
May be broken down elsewhere in the body to adrenaline, which can lead to arrhythmias
What drug is levodopa always given with and why?
Carbidopa (dopa decarboxylase inhibitor that can’t cross the BBB to stop it breaking down before it reaches the brain)
How does amatadine work?
Increases endogenous dopamine production
Give examples of dopamine agonists?
Bromocriptine
Pramiprexole
Ropinirole
What does the COMT enzyme do?
Degrade dopamine and levodopa
When are COMT inhibitors given?
With levodopa
Used to prevent it being broken down outside the CNS
How do MAO-B inhibitors work?
MAO-B is an enzyme that metabolises dopamine
Why might anticholingeric drugs be given in the treatment of PD?
Relative increase in amount of ACh compared to dopamine
This tries to reset the balance
Often helps the tremor
What is deep brain stimulation?
Implanted device that directly sends electrical signals to the basal ganglia that counteracts the aberrant signalling in PD
What is parkinsonism?
Symptoms of Parkinson’s, e.g. in other diseases or due to drugs, e.g. antipsychotics or metacloperamide
What is vascular dementia?
Progressive loss of brain function due to long term poor blood supply (usually a series of strokes)
What are the functions of the frontal lobe?
Movement Personality Counting Spelling Decision making
What are the functions of the parietal lobe?
Processes sensory information to allow us to know where we are physically
Guides movement in 3D space
What are the functions of the temporal lobe?
Hearing
Smell
Memory
Recognition of faces
What is the main function of the occipital lobe?
Visual information processing
What is the pathophysiology of vascular dementia?
Neurons are aerobic & have no longer term energy supply
Atherosclerosis leads to gradual decrease in BF to the brain –> chronic ischaemia
Small parts of atherosclerosis can break off & occlude small arteries
Once tissue demand > supply ==> ischaemic stroke & tissue damage (which can undergo liquefactive necrosis)
–> loss of mental function
What is atherosclerosis?
Build up of plaque that thickens the artery wall
What are the symptoms of vascular dementia like?
Depends on area affected
Symptoms appear suddenly and function decreases with each stroke
How do you diagnose vascular dementia?
Neuropsychological tests
CT/MRI can show multiple cortical/subcortical infarct & atrophy confirming ischaemia
What causes lewy body dementia?
Misfolded alpha-synuclein proteins that aggregate to form Lewy bodies that deposit in neurons, especially those in the cortex/SN
What are the symptoms of LBD?
Early cognitive - difficulty focusing, poor memory, visual hallucinations, disorganised speech, depression
Later motor - resting tremor, stiff movements, reduced facial movements
Sleep disorders
How is the definitive diagnosis of LBD made?
Brain biopsy
How do you manage LBD?
Alzheimer’s meds for the cognitive aspects, e.g. donepezil
PD medications for the motor aspects, e.g. levodopa
