CSI - Emily Wilkins and MCI Flashcards
What is mild cognitive impairment?
mild cognitive impairment is cognitive decline beyond what is expected for age and education but doesn’t affect normal daily function
amnestic MCI - affects memory loss
How many people MCI progress to dementia annually?
10 - 15%
What is dementia?
Dementia is a chronic neurodegenerative disease leading to cognitive decline BEYOND what is expected for age and education. It is an umbrella term for a range of conditions affecting normal every day life due to deterioration of higher interllectual brain function
Difference between MCI and dementia
- MCI does not affect day to day life
- MCI is associated with the normality of ageing
- MCI are sets of symptoms, dementia has an underlying pathophysiology
- There is no approved drug treatment for MCI whereas there is for Alzheimers
similarities between MCI and dementia
- both affects cognitive abilities
- both do not affect consciousness
factors which affect risk of dementia
- physical activity
- mediterranean diet
- smoking
- drinking
- socially active
- cognitive stimulation
6 item cognitive impairment test
- can quickly assess the scale of cognitive decline and the specificity
- score out of 28
- score of 8-9 means mild cognitive impairment
- score of 10+ is severe and needs to be referred to a memory clinic
what is asked in the 6 item cognitive exam?
- what is the year?
- what is the month?
Give the patient something to remember - what is the time?
- count backwards from 20-1
- say the months in reverse
- repeat the phrase
Who is in the MDT and what are the benefits?
- made of specialist doctors, nurses, dietricians, occupationa l therapists, physiotherapists, carers, social workers which use their combined expertise to ensure the well-being and care of the patient. The dynamic ensures the patient has the best healthcare journey
What makes up the limbic system and describe the key functions?
-cingulate gyrus
- amygdala,
- hippocampus
- mamillary body
THE CINGULATE GYRUS IS CONNECTED TO THE TEMPORAL LOBE BY A BUNDLE OF NEURONES, THE CINGULUM
posterior cingular cortex - orientation (time, place and memory)
hippocampus - short term memory
anterior thalamus - concerned with attention
what is Lewy Body dementia?
- LBD is associated with aberrant deposits of alpha-synuclein protein within the primary motor cortex
- progressive symptoms over time
- symptoms include hallucinations, sleep problems and memory loss
- Parkinsons like features due to impaired movement
- treatment involves acetylcholinesterase inhibitors
What is fronto temporal dementia? What causes it?
NEURONAL ATROPHY of the frontal and temporal loves due to abnormal proteins, phosphorylated tau
autosomal dominant inheritance pattern in 1/3 cases
chronic and progressive disease, although the onset can occur more rapidly than other forms
what are the symptoms of frontotemporal dementia?
- frontal lobes are affected so speech, emotional problems, behavioural changes and disinhibition lead to inappropriate behaviour
- lack of interest in normal hygiene
- obsessions leading to unusual beliefs, interests
- diet changes
vascular dementia
associated with reduced blood supply to the brain due to diseased vessels, multiple infarcts within the minor blood vessels leading to stepwise progression with deterioriation in cognitive abilities over many years
- slower thinking
- personality changes
- movement problems
- bladder issues
alzheimer disease and symptoms
a chronic neurodegenerative disease with progressive and an insiduous onset. Memory impairment is prominent and the disease progresses changes include language deficits, impaired visuospatial skills,loss of judgement and an inability to conduct daily activities
symptoms of Alzheimer’s dementia
- amnesia
- anomia (cannot name things)
- apraxia (loss of dexerity)
-agnosia (cannot recognise things) - aphasia (cannot talk)
- misplacing items, forgetting recent events, faces, names, becomig increasingly repetitive
Alzheimer’s pathophysiology
- amyloid precursor protein (APP) is a transmembrane protein cleaved by alpha secretase typically
- however, beta and gamma secretase aberrantly cleave APP, leading to surplus of amyloid beta which form oligomers and fibrils outside the cell. This accumulation of extracellular amyloid beta forms amyloid plaques
what is meant by intracellular neurofibrillary tangles?
- TAU proteins are important for the assembly of microtubules
TAU hyperphosphorylation undergoes oligomerisation and forms NFTs - filamentous neuro-fibrillary tangles - which deposit into the hippocampus, medial temporal lobe, frontal cortices and the lateral parietotemporal regions
AMYLOID BETA PLAQUES TRIGGERS PHOSPHORYLATION OF TAU, DISSOCIATING FROM THE MICROTUBULES AND FORMING NFTs
