Cognitive Impairment and Confused States Flashcards
What is cognition?
the mental processes involved in making sense of and learning about the world around us, including:
- memory
- attention
- perception
- knowledge
- problem solving
- judgement
- language
Does cognition decline with age?
- Crystallised cognitive abilities are well
preserved hence will not decline (as much):
- cumulative skills and memories;
preserved on tests of general knowledge - Fluid cognitive abilities:
- processing new info to quickly solve
problems
- linear decline from the age of 20
When might young adults without health problems experience cognitive impairment?
- acute illnesses
- post-surgery
- sleep deprivation
- extreme exercise
- alcohol
- drugs
- depression
Delirium: Key Features (4):
- ***acute onset of confusion
- impairment of attention and awareness
- fluctuating
- often worse in the evening
Delirium: Causes:
- usually caused by systemic illness
Delirium: Clinical Features:
- impaired awareness, attention and
concentration - disorientation (person, time, place)
- memories may be preserved
- hallucinations, especially visual
- delusions (complex and distressing)
- anxious, low, labile mood
- Behaviour: hyperactive, hypoactive, mixed
Hyperactive Behaviour:
- agitation
- pacing
- aggression
Hypoactive Behaviour:
- reduced movement
- appetite
- withdrawn
- sleepy
Mixed Behaviour:
- fluctuates between hypo- and hyper-active
behaviours
Delirium affects what % of hospital inpatients?
> 20%
High prevalence of delirium in:
- up to half of elderly inpatients
- high prevalence in ITU patients
- if hospitalised with delirium, two fold
increased of mortality after - often don’t return to full cognition despite
being classed as reversible
Which of the following is not a risk factor for delirium?
- older age
- younger age
- multiple morbidities/frailties
- polypharmacy
- learning disabilities
- dementia
- sensory impairment
learning disabilties
How can delirium be prevented (7)?
- early detection and treatment of any
infection - orientation
- preventing dehydration and constipation
- maximise healthy sleep patterns
- encourage mobility where possible
- manage pain well
- ensure good nutrition (dentures)
Delirium: Management:
- treat underlying cause
- calm, quiet environment
- regular reorientation
- consistent routine
- promote healthy sleep pattern
- appropriate lighting
- aggression meds if needed
- MDT follow up
What is dementia?
- group of progressive, neurodegenerative
brain disorders - impairment in memory, thinking and
behaviour that interferes with a person’s
daily activities
Dementia Terminology:
Prevalence of dementia related with ages:
- 1 in 100 people (65-69yrs)
- 1 in 25 people (70-79yrs)
- 1 in 6 people (+80yrs)
What % of people living in care homes have dementia?
70%
Delirium is the main cause of disability later in life.
True or False?
False
Dementia is the main cause of disability later in life
Difference between delirium and dementia.
Main types of dementia:
Dementia: Pathology:
- misfolding of proteins: amyloid, tau, synuclein
Which misfolding of proteins occur in Alzheimer’s disease?
- amyloid
- tau
Which misfolding of proteins occur in Parkinson’s disease?
- synuclein
Which misfolding of proteins occur in Alzheimer’s disease?
- amyloid
- tau
Dementia: Assessment:
- no single diagnostic test
- clinical history
- physical examination (neuro)
- basic blood tests: FBC, U&E, LFTs, Thyroid, Ca2+,
Glucose, B12, folate, ESR - neuroimaging: CT, MRI, advanced imaging
- cognitive testing
- lumbar puncture sometimes (young onsert)
Alzheimer’s Disease:
- incidence
- survival from diagnosis
- most common form of dementia (62%)
- 4-20 years
Alzheimer’s: Pathophysiology:
- amyloid cascade hypothesis
- amyloid plaques are an insoluble protein that is
extracellulary deposits - Neurofibrillary Tangles (intracellular)
- Tau = normal intracellular proteins, binds to
microtubules, supports axonal transport,
maintenance of cytoskeleton
- abnormal phosphorylation: paired helixes,
neurofibrillary tangles - reduced cholinergic activity in cortex
Amyloid Cascade Hypothesis:
Beta-Amyloid is cleaved from a transmembrane protein called amyloid precursor protein (APP).
APP is usually broken down into non--amyloid peptides by what has been called the -secretase pathway.
The amyloid cascade hypothesis suggests that there is more breakdown of APP by other pathways (called - and -secretase pathways), leading to overproduction of -amyloid.
-Amyloid is insoluble and is normally cleared from the brain via several different mechanisms. Overproduction results in aggregation and plaque formation.
Alzheimer’s: Clinical Features:
- amnesia: short-term impairment, later affects
long-term memory - disorientation
- apraxia (loss of motor skills)
- agnosia (disturbances in recognition of objects
and faces) - difficulty in performing complex tasks: planning,
organisation, sequencing, abstraction - behavioural and psychological disturbances
Genetic Causes of Alzheimer’s Disease:
- complicated, generally different for young and
late onset - young onset clusters withing families are rare
- mutations in the amyloid precursor protein
(APP) genes and two presenillin genes (PSEN-1
and PSEN-2), autosomal dominant - late onset = more complex
- small but growing number of risk genes but are
NOT mutations
What is the largest known risk factor (genetic) of late onset alzheimer’s?
- apolipoprotein epsilon4
Alzheimer’s disease: Investigation:
- most important factor = history
- cognitive testing is helpful
- CT/MRI: global cortical atrophy, hippocampal
atrophy - lumbar puncture@ beta-amyloid ratios in csf,
other measures - amyloid PET
Vascular Dementia is caused by
cerebrovascular disease
Vascular Dementia: Clinical Features:
- diverse presentation
- classically stepwise progression: rarely seen,
gradual decline also possible, abrupt onset can
occur - focal neurology may be present
- patchy cognitive impairment
- slowing of gait and falls
Dementia with Lewy bodies & Parkinson’s Dementia:
- both conditions are cause by Lewy bodies:
- intracellular inclusions
- alpha-synuclein
- subcortical lewy bodies in parkinson’s
- cortical lewy bodies in dementia with lewy
bodies
- DLB diagnosed if congitive symptoms onset
before or about same time as movement
symptoms; not everyone develops movement
symptoms
Dementia with Lewy Bodies: Core Features:
- one or more of cardinal motor features of
Parkinson’s Disease - visual hallucinations
- marked fluctuations in cognition and alertness
- REM sleep behaviour disorder
Note for patients of dementia with Lewy Bodies:
- high sensitivity to antipsychotic medication
- risk of falls
Dementia with Lewy Bodies: Investigations:
- MRI/CT often normal, may atrophy
- SPECT imaging using a ligand for the dopamine
transported protein has high sensitivity and
specificity
What is Frontotemporal Dementia (FTD)?
- diverse group of conditions that are collectively
a common cause of young onset dementia - selective progressive atrophy involving the
frontal or temporal lobes or both - aka frontotemporal lobar degeneration
Frontotemporal Dementia (FTD): Pathology:
- three major pathogenic proteins:
- phosphorylated Tau
- Transactive response DNA-binding protein 43
(TDP-43) - Fused in sarcoma protein (FUS)
not needed knowledge
What is Pick’s disease?
type of FTD caused by Tau
Frontotemporal Dementia (FTD): Risk groups:
- 4-15 per 100,000 under 65 West
- onset typically 50s-60s but varies
Causes of Frontotemporal Dementia (FTD:)
- often genetic
- can be sporadic
Frontotemporal Dementia (FTD): Two Variants:
- behavioural variant (frontal lobe)
- language variant (temporal lobe)
Behavioural Frontotemporal Dementia: Clinical Features:
- frontal lobe affected
- affects personality or behaviour
- relative preservation of memory
- often misdiagnosed as psychiatric condition or
personality disorder
Language Frontotemporal Dementia (FTD): Clinical Features:
- temporal lobe affected
- affects language
- different subtypes affect language differently
Frontotemporal Dementia (FTD): Investigations:
- MRI/CT: frontal/temporal lobe atrophy
- amyloid-PET negative
- perfusion studies (FDG-PET): reduced perfusion
in frontal/temporal lobes - Lumbar Puncture: normal alzheimer’s
biomarkers, elevated neurofilament light - Genetics Testing: specific mutation identification
Dementia: Behavioural and Psychological Symptoms:
- cognitive impairment
- disturbed perception
- disturbed thought content
- disturbed mood
- disturbed behaviour
Dementia: Management:
- psychological and social support (particularly
isolation) - some meds: cholinesterase inhibitors,
memantine - mild-dementia do not need dementia-specific
services
Dementia: Practical and Social Interventions:
- care package
- OT assessments
- daycentres and clubs
- one to one support
- sitting services
- carer support
Dementia: Psychological Interventions:
- pre and post diagnostic support
- cognitive stimulation therapy
- individual and group work
Cognitive Stimulation Therapy:
- can improve cognition
- ## mainly evidenced for mild dementia
Dementia: Post-diagnosis support groups: How many sessions?
4-6 sessions
Medications for cognitive symptoms of dementia:
- symptomatic treatments to reduce rate of
decline, modest effects - Cholinesterase Inhibitors: block breakdown of
ach, helpful for mild to moderate dementia in
Alzheimer’s - Alzheimer’s leads to loss of cells and nerve
endings that produce ach, so there is less
available - Memantine: moderate to severe dementia in
Alzheimer’s disease- excess glutamate activates NMDA receptors
- increases Ca2+ influx
- leads to cell death
- memantine blocks receptors to reduce
glutamate mediated excitotoxicity
- excess glutamate activates NMDA receptors
What medications are licensed for use in dementia?
There are many medications that are effective in managing behavioural and psychological symptoms of dementia (BPSD).
True or False?
False
medications have a very small role to play
often furthers effects of polypharmacy
Dementia: Depression:
- antidepressants are not effective for treating
depression in dementia in most cases - may reduce impulsivity in frontotemporal
dementia - sometimes used for the bejvioural symptoms
Antipsychotic use in dementia treatment:
- massive initiative to reduce prescribing due to
risk of stroke and mortality - used in very specific situations
Sedative medication in dementia treatment:
- benzodiazepines
- generally avoided due to risk of adverse effects
What is shown below?
insert picture
Cortical atrophy of the temporal/frontal lobe
FTD
Young Onset Dementia:
- <65 year old onset
- atypical presentatons
- rare and genetic causes more frequent
- typically takes 4.4 years from symptom onset to
diagnosis compared to 2.2 in late onset
dementia - very few specialist service that can be used
Can we prevent dementia?
- may risk factors are modifiable:
- limited education
- hypertension
- obesity
- hearing loss
- smoking
- diabetes
- depression- social isolation
What is cognitive reserve?
- higher level of cognitive function reduces risk of
dementia - brain more able to compensate for pathological
changes - cognitive reserve linked to number of years of
education - cognitively stimulating activity as adults can
boost cognitive reserve
