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delirium and cognition Flashcards

1
Q

What is cognition

A

The mental processes involved in making sense of and learning about the world around us, including:
* Memory
* Attention
* Perception
* Knowledge
* Problem solving
* Judgement
* Language

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2
Q

When might young adults without health problems experience cognitive impairment?

A
  • Acute illness * Post-surgery * Sleep deprivation * Extreme exercise * Alcohol * Drugs * Depression
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3
Q

Does cognition decline with age?

A

“Crystallised” cognitive abilities are well-preserved
* Cumulative skills and memories from cognitive
processing that occurred in the past
* E.g. preserved on tests of general knowledge,
vocabulary, reading comprehension, maths,
science
“Fluid” cognitive abilities
* Processing new information to quickly solve
problems * Linear decline from age of 20

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4
Q

What is delirium?

A

“Acute brain failure”
Usually caused by systemic illness
Also referred to as “acute confusional state”

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5
Q

Key features of delirium?

A

Key features
* Acute onset
* Impairment of attention and awareness
* Fluctuating (hr(s) to hr)
* Often worse in evening

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6
Q

Delirium clinical features?

A
  • Impaired awareness, attention and concentration
  • Disorientated – person, time, place
  • Memory may be preserved
  • Hallucinations, especially visual
  • Delusions – often complex and distressing
  • Mood – often anxious, low, labile

Behaviour
* Hyperactive – agitation, pacing, aggression
* Hypoactive – reduced movement, appetite, withdrawn, sleepy (more dangerous)
* Mixed – fluctuates between hypo- and hyper-active

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7
Q

delirium is important because…
What three groups are more likely to develop delirium?

A

> 20% of hospital inpatients
* Up to half of elderly inpatients
* High prevalence in ITU patients

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8
Q

delirium is important because…
What risks increase after delirium?

A
  • If hospitalized, two-fold increased mortality risk year afterwards
  • Increased risk of dementia in the years following a delirium
  • Worse outcomes for longer period of delirium
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9
Q

Who is at greater risk of delirium?

A
  • Higher risk in older people and young children
  • Multiple medical problems/frailty
  • Polypharmacy
  • Pre-existing cognitive impairment (dementia)
  • Sensory impairment
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10
Q

List some common causes of delirium?

A

Systemic infection
post-surgery
pain
consiptaion
medication (sedatives/analgesics/polypharm)
MI
Hepatic/renal failure
CVA
Heart failure
Alcohol withdrawal, Drug intox/withdraw
Neuro inf. (meningitis/encephalitis)
Vitamin deficiencies (B12/folate)
Trauma/ head injury
Hypo or Electrolyte abnormality (esp. low Na)
Tumours/raised intracranial pressure
Epilepsy: post-ictal or status epilepticus

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11
Q

What can help prevent delirium?
Is this easy in hospital setting?

A

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 (includes looking after dentures)

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12
Q

How is delirium managed?
Is this easy in hospital setting?

A

Treat underlying cause
* Calm, quiet environment
* Regular reorientation
* Consistent routine
* Promote healthy sleep pattern * Appropriate lighting
* Medications for aggression are sometimes needed
* Follow-up in multidisciplinary clinic

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13
Q

What is dementia?

A

Dementia is an umbrella term for impaired cognition cause by a group of progressive, neurodegenerative brain disorders
* Impairment in memory, thinking and behaviour that interferes with a person’s normal activities of daily living
* Many different types of dementia
* Each with specific patterns of symptoms and cause

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14
Q

Why is dementia important?

A

There are currently about 850 000 people in UK with dementia,
set to rise to 1.6 million by 2040 * Financial cost of dementia in the UK is £34.7 billion per annum
* Prevalence increases with increasing age
* One in 100 people aged 65-69yrs
* One in 25 people aged 70-79yrs
* One in 6 people over 80yrs
* 70% of people living in care homes have dementia

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15
Q

What is young-onset dementia?

A

Dementia under 65y

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16
Q

What is dementia with onset late in life?

A

Dementia over 65y

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17
Q

Why is dementia important?

A
  • Dementia is one of the main causes of disability later in life ahead of cancer, cardiovascular disease and stroke.
  • UK spends much less on dementia than on these other
    conditions.
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18
Q

Delirium v Dementia…
Onset rapid v gradual?
Alertness and attention?
Hallucinations?

A

Dementia is gradual, delirium is rapid onset and action needs to be taken quickly
Delirium has an impact on attention alertness, dementia usually does not.
Most types of dementia do not include hallucinations (there are exceptions)

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19
Q

Name 4 subtypes of dementia
Which two are often comorbid?

A

Alzheimers disease and Vascular dementia (often comorbid)
Lewy body disorders
FTD

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20
Q

Subtypes of Lewy-body disorders…
——– with —- —–
and
———’s disease dementia

A

Dementia with Lewy bodies
Parkinson’s disease dementia

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21
Q

Pathology of dementia: Which proteins can be misfiled?

A

Amyloid
Tau
Synuclein

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22
Q

Which proteins are misfolded in Alzheimers?

A

Amyloid and tau

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23
Q

Which protein is misfolded in Parkinson’s disease dementia?

A

Synuclein

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24
Q

What is the difference b/ween Alzheimers and dementia?

A

Alzheimers is the name of an underlying disease with particular molecular mechanism, dementia would be the clinical presentation

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25
Q

Which protein misfolding causes FTD

A

Tau

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26
Q

What diseases can Tau misfolding causes?

A

Alzheimers and FTD

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27
Q

What disease can synuclein misfolding causes?

A

FTD

28
Q

What disease can amyloid misfolding causes?

A

Alzheimers

29
Q

What disease can amyloid misfolding causes?

A

Alzheimers

30
Q

Hos is dementia assessed?

A

No single diagnostic test
* Good clinical history of paramount importance (including
collateral)
* Physical examination, focus on neurological
* Basic blood tests
* FBC, U&Es, LFTs, Thyroid, Ca, Glucose, B12 and folate, ESR
* Neuroimaging
* CT, MRI, advanced imaging
* Cognitive testing
* Lumbar puncture in some cases, especially young onset

31
Q

what is Alzheimers disease?

A

Most common form of dementia (62%)
* German Neurologist, Alois Alzheimer, early 1900s
* Survival from diagnosis 4-20 years

32
Q

What is happening in the brains of people with Alzheimer’s disease

A

Amyloid plaques (Extracellular deposits)
* Insoluble protein
* Neurofibrillary tangles (Intracellular)
* Tau = normal intracellular protein, binds to microtubules and
supports axonal transport and maintenance of cytoskeleton * Abnormal phosphorylation
* Paired helixes * Neurofibrillary tangles
* Reduced cholinergic activity in cortex

33
Q

What happens in Alzheimers brains at a molecular level?

A

The amyloid cascade hypothesis
beta-Amyloid is cleaved from a transmembrane protein called amyloid precursor protein (APP). APP is usually broken down into non-beta-amyloid peptides by what has been called the alpha-secretase pathway. The amyloid cascade hypothesis suggests that there is more breakdown of APP by other pathways (called beta- and gamma-secretase pathways), leading to overproduction of beta-amyloid. beta-Amyloid is i

34
Q

What are the clinical features of Alzheimer’s disease?

A

Amnesia
Impairment of short- term memory
Later impairment of long-term memory
Disorientation
Loss of motor skills (apraxia)
Disturbances in recognition of objects and faces (agnosia)
Disturbances of speech (nominal dysphasia)
Difficulty in performing complex tasks
Planning, organization, sequencing, abstraction
Behavioural and psychological disturbances

35
Q

Are there genetic links to Alzheimers?

A

Complicated, generally different for young and late onset

36
Q

Young onset Alz D genetics?

A

Young onset clusters within families (rare) – mutations in amyloid precursor protein gene (APP) and two presenilin genes (PSEN-1 and PSEN-2)

37
Q

Late onset Alz d genetics?

A

Late onset is more complex - small but growing number of risk genes (not mutations)
Apolipoprotein ε4 (APOE ε4) largest known risk factor

38
Q

what Investigations in Alzheimer’s disease?

A

Most important factor in diagnosis is history

Cognitive testing helpful

CT/MRI: Global cortical atrophy, hippocampal atrophy

Lumbar puncture: beta-Amyloid ratios in csf, other measures

Amyloid PET (Positron emission tomography)

39
Q

what is vascular dementia?

A

caused by cerebrovascular disease

40
Q

who is at risk of vascular dementia?

A

Age
Vascular risk factors
(e.g. hypertension, hypercholesterolaemia, smoking, physical inactivity, diabetes)

Alzheimer’s disease and vascular dementia often co-exist
Share many risk factors

Dementia develops in 15-30% of people in 3 months after stroke (not fully understood)

41
Q

Clinical features of vascular dementia

A

Diverse presentation
Classically stepwise progression
(Rarely seen, gradual decline also possible)
Abrupt onset/decline may be associated with CVA (cerebral vascular accident/abnorm)
Focal neurology may be present
Patchy cognitive impairment
Slowing of gait and falls

42
Q

what is common to Dementia with Lewy bodies and Parkinson’s disease dementia

A

Both conditions are caused by Lewy bodies
Intracellular inclusions
a-synuclein
Subcortical Lewy bodies in Parkinson’s disease
Cortical Lewy bodies in Dementia with Lewy bodies (DLB)

Many people with Parkinson’s disease develop dementia
Increases with length of years lived with condition

43
Q

Does everyone with CLB (dementia Lewy bodies) develop movement diorsders?

A

DLB diagnosed if cognitive symptoms onset before or about same time as movement symptoms (as opposed to Parkinsons movement first)
Not everyone with DLB develops movement symptoms, but most do

44
Q

If cognitive symptoms present concurrently with movement symptoms, is Dementia with Lewy bodies more or less likely diagnosis than Parkinson’s?

A

DLB
DLB is diagnosed if cognitive symptoms onset before or about same time as movement symptoms (as opposed to Parkinsons movement first)

45
Q

What is “DLB”

A

Dementia with Lewy bodies

46
Q

what are the core features of dementia with Lewy bodies

A

One of more of cardinal motor features of Parkinson’s disease
Visual hallucinations
Marked fluctuations in cognition and alertness
REM sleep behaviour disorder

Also note:
High sensitivity to antipsychotic medication
Risk of falls

DLB can be difficult to differentiate from delirium – the speed of onset and presence of parkinsonism can be helpful

47
Q

can you prescribe antipsychotics to DLB pt?

A

not recommended due to high sensitivity to antipsychotic medication

48
Q

what is REM sleep behaviour disorder?

A

thrashing in sleep

49
Q

what is REM sleep behaviour disorder?

A

thrashing in sleep
a sleep disorder in which you physically act out vivid, often unpleasant dreams with vocal sounds and sudden, often violent arm and leg movements during REM sleep — sometimes called dream-enacting behavior.

50
Q

Investigations in dementia with Lewy bodies?

A

MRI/CT often normal, may show atrophy

SPECT imaging using a ligand for the dopamine transporter protein has high sensitivity and specificity

51
Q

Investigations in dementia with Lewy bodies?

A

MRI/CT often normal, may show atrophy

SPECT imaging using a ligand for the dopamine transporter protein has high sensitivity and specificity

52
Q

What is SPECT?

A

SPECT = single photon emission computed tomography – relies on a radiolabelled ligand attaching to the target protein after being injected peripherally (e.g. in SPECT scan for DLB, the radiolabelled ligand is injected into a vein in the arm, and the scan is taken several hours later)

53
Q

What does this image show?

A

This image shows MRI (top row) and FP-CIT SPECT (bottom row) scans in Alzheimer’s disease (AD), dementia with Lewy bodies (DLB) and normal control (NC). The MRI scan in Alzheimer’s disease shows marked global and hippocampal atrophy, which is not the case in the DLB and NC scans. The FPCIT SPECT scan shows normal upate of the dopamine trasporter protein ligand across both the caudate and putamen (“comma” in AD and NC, and severely reduced uptake in DLB, limited to the caudate.

Image from: McKeith, I.G. et al (2017) ”Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB consortium” Neurology 89: 88-100 (creative commons licence)

54
Q

what is notable in this image?

A

FTD - atrophy

55
Q

What is frontotemporal dementia (FTD)?

A

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

Also referred to as frontotemporal lobar degeneration (FTLD)

complex range of underlying mechanisms

56
Q

what three main pathologies cause FTD/FTLD? (molecular)

A

Three major pathogenic proteins responsible for different types of FTD

Phosphorylated tau

Transactive response DNA-binding protein 43 (TDP-43)

Fused in sarcoma protein (FUS) protein

57
Q

What is pick’s disease?

A

Pick’s disease is a type of FTD caused by Tau

58
Q

what disease is caused by problems with these proteins?

Phosphorylated tau

Transactive response DNA-binding protein 43 (TDP-43)

Fused in sarcoma protein (FUS) protein

A

FTD/FTLD

59
Q

FTD population prevalence of _______ per 100 000 under ____ years in European and US epidemiological studies?

A

Population prevalence of 4-15 per 100 000 under 65 years in European and US epidemiological studies

60
Q

Typical FTD onset

A

50s/60s, but can be younger and not well supported socially financially. Takes a while to diagnose as unexpected

61
Q

FTD pathology always genetic or not?

A

Often genetic, although many cases sporadic

62
Q

What are the clinical features of FTD?

A

Noticable behavioural disinhibition

Behavioural variant (frontal lobe)
Affects personality/behaviour
Relative preservation of memory
Often misdiagnosed as psychiatric condition or personality disorder

Language variant (temporal lobe)
Affects language
Different subtypes affect language differently

63
Q

Investigations in frontotemporal dementia

A

MRI/CT: Frontal and/or temporal lobe atrophy
Amyloid-PET negative
Perfusion studies (FDG-PET): Reduced perfusion in frontal/temporal lobes
Lumbar puncture:
Normal Alzheimer’s disease biomarkers
Elevated neurofilament light
Genetics: Testing may identify specific mutation

64
Q

Behavioural and psychological symptoms of dementia

A

Multiple brain processes are disrupted in dementia
Cognitive impairment is a central feature
Dementia also results in a range of neuropsychiatric symptoms

65
Q

What is BPSD?

A

“behavioural and psychological symptoms of dementia”

range of dementia associated neuropsychiatric symptoms-

Referred to as BPSD
Includes symptoms of disturbed:
Perception
Thought content
Mood
Behaviour

66
Q

What is good support for ppl with dementia?

A

Person-centred

Services designed to meet needs of people living with dementia

Many people with mild dementia do not need dementia-specific services

67
Q

slide 53 onwards

A

slide 53

NSB (10 decks)

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