Dementia Flashcards
What are the subtypes of dementia?
MCI (mild cognitive impairment)
Anterograde Amnesic syndrome of AD
Dementia due to CVD
Dementia with Lewy Bodies (DLB)
Fronto-temporal dementia (FTD)
Progresssive aphasia
Creutzfeld-Jakob Disase (CJD)
What is the diagnostic criteria for dementia?
- decline from previously higher levels of functioning
- significant interferance with ADL
- cognitive dysfunction in recent memory, language (comprehension and expression), visuospacial function, executive function
What is the most common cause of dementia?
Alzheimer’s Dementia
What investigations may indicate AD?
MRI showing parietal lobe (hippocampal) atrophy
PET scan showing hypometabolism in fronto-parietal area
CSF showing high tau and low beta
How do you treat AD?
- Manage HTN and DM
- Manage cognitive impairment with cholinesterase inhibitors (neostigmine)
What is the diagnostic criteria for Alzheimer’s disease?
- Memory loss
- one or more of: aphasia, apraxia, agnosia/anomia, disturbed executive functioning
- behavioural and personality canges
- loss of insight
What are the changes seen in FTD?
aphasia, seantics, loss of insight and affect, sexually inappropriate behviour, OCD
What is the most common group that FTD presents in?
<65yos
What screening tools are there for AD?
- history
- MMSE
- Montreal Cognitive Assessment (MoCA)
- PET scan - showing hypometabolism in frontoparietal area)
- spinal fluid markers - high tau, low beta
what is dementia?
a group of brain disorders that msot commonly occur in old age, although sometimes can dvelop earlier. They are a result in brain tissue deterioration. Common features include decline inthe ability to recall recent and past events, decine in mental functioning and the person behaving in ways that are out of character for her/him.
what is the second most common cause of dementia?
vascular dementia
what is the pathology of AD?
- neurofibillary tangles (tau protein)
- neuritic plaques (B amyloid protein)
- loss of cortical acetylcholine
- neuronal loss
how does AD present?
gradual onset and steadily progressiv memory impairment
affects new learning, praxis and language
what is the pathology of vascular dementia?
large or small vessels disease
how does vasccular dementia present?
of abrupt onset and “stepwise” progression. first features are gait dysfunction and uniranry incontinence.
how does LBD present?
fluctuating attention and concentration, detailed visual hallucinations and parkinsonism.
with “supportive features” - history of falls, REM sleep disorder, sensitivity to antpsychotics
memory loss usually presents later
what is the typicla age of onset of FTD?
45-65 yo
what is the typical presentation of FTD?
behavioural and personality changes (disinhibition, loss of empathy, poor judgment), also language disturbance and executive dysfunction.
new learning is relatively well rpeserved
What are the subtypes of FTD?
- behavioural variant
- semantic dementia (SD)
- progressive non-fluent aphasia (PNFA)
what is te pathology of FTD?
genetic mutation affecting tau protein (family history in 10-50% of cases)
what investigation for FTD?
MRI shows atrophy of frontal regions
what two types of dementia are intimately linked?
AD and vascular dementia. often overlap, most AD cases show significant CVD and people with vascualr dementia have coeisting AD pahtology at autopsy
what are the potentially reversible causes of dementia?
- alcohol related
- hydrocephalus
- hypothyroidism
- B12 deficiency
- neurosyphilis
- medication
what conditions often seem like dementia?
- normal cognitive changes associated with ageing
- MCI
- depression
- delirium
- moderate intellectua disability
how do you manage dementia?
- educate patient and family
- initiate community support
- plan lifestyle issues and legal issues (e.g. Will)
- assess driving capacity
- prevent further insult (e.g. ETOH, vascualr risk factors)
- treatment with cholinesterase inhibitors
What is the medical treatment for dementia and name some examples?
cholinesterase inhibities (galantamine, donepezil, rivastigmine, neostigmine)
potentially slow preogression of AD. also evidence for use in LBD and vascular dementia
