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Semester 4 - Clinical Neuroscience > 12. Dementia, delirium and toxic insults > Flashcards

12. Dementia, delirium and toxic insults Flashcards

1
Q

define dementia

A

a syndrome characterised by deterioration in cognition resulting in behavioural problems and impairment in the activities of daily living. Decline in cognition is extensive, often affecting multiple
domains of intellectual functioning

A chronic, progressive syndrome of insidious onset

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2
Q

What are the causes of confusion in elderly patients?

A

Delirium, depression, dementia, drugs and metabolic (endocrine)

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3
Q

Define depression.

A

change in mood and feeling of self-worth

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4
Q

What drugs may cause confusion in the elderly?

A

morphine, coccaine, alcohol, zopiclone

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5
Q

What metabolic conditions may cause confusion in the elderly?

A

o Hypothyroidism
o Hypercalcaemia
o B12 deficiency
o Normal pressure hydrocephalus

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6
Q

what are the Cognitive symptoms of dementia

A
  • Impaired memory (temporal lobe involvement)
  • Impaired orientation (temporal lobe involvement)
  • Impaired learning capacity ((temporal lobe involvement)
  • Impaired judgement (frontal lobe involvement)
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7
Q

what are the non-Cognitive symptoms of dementia

A
  • Behavioural symptoms
  • Depression and anxiety
  • Psychotic features
  • Sleep symptoms
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8
Q

what are the Behavioural symptoms of dementia

A
  • Agitation
  • Aggression (frontal lobe involvement)
  • Wandering
  • Sexual disinhibition (frontal lobe involvement)
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9
Q

what are the Psychotic features of dementia

A
  • Visual and auditory hallucinations (hallucinations=false perceptions)
  • Persecutory delusions (delusions=false beliefs)
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10
Q

what are the Sleep symptoms of dementia

A
  • Insomnia

* Daytime drowsiness (decreased cortical activity)

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11
Q

how is dementia diagnosed?

A
  • By exclusion
    • Exclude organic causes of cognitive decline
    • Exclude delirium
  • Look for features of progressive cognitive decline, impairment of activities of daily living in a patient with a normal conscious level (cf. delirium where conscious level is diminished with acute cognitive decline)
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12
Q

symptoms of Normal pressure hydrocephalus

A

 Abnormal gait
 Incontinence
 Confusion

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13
Q

What are 5 different types of dementia?

A
  • Alzheimer’s Dementia
  • Dementia with Lewy body
  • Vascular Dementia
  • Fronto-Temporal Dementia
  • AIDS-Dementia Complex
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14
Q

What are 2 common tests used to test cognition?

A
  • mini mental state examination (MMSE)

- montreal cognitive assessment

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15
Q

What are the macroscoptic changes in alzheimers?

A

Causes global atrophy of brain lobes: Mostly frontal, parietal and temporal lobes. Less so for occipital lobes.
Also causes:
- Sulcus widening
- Enlarged ventricles (primarily lateral and third affected)

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16
Q

What are the microscoptic changes in alzheimers?

A

 Plaques
• Composed of amyloid beta
 Tangles
• Hyperphosphorylated tau

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17
Q

What is the pathophysiology in alzheimer’s?

A
  • senile amyloid plaques
  • neurofibrillary tau tangles
  • results in neuronal death
  • Since neurogenesis is limited in the CNS any neurones that die are unlikely to be replaced
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18
Q

what is the amyloid hypothesis for Alzheimer’s pathophysiology

A
  • Excess of interneuronal amyloid (Abeta) peptides, due to overproduction or diminished clearance of beta-amyloid
  • Formation of dense amyloid oligomers, which are deposited as diffuse plaques
  • Inflammatory process through microglial activation, cytokine formation, and activation of the complement cascade
  • Formation of neuritic plaques, causing synaptic and neuritic injury and cell death
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19
Q

what is the tau hypothesis for Alzheimer’s pathophysiology

A
  • abnormal aggregation of the tau protein
  • Tau accumulates into intraneuronal masses known as neurofibrillary tangles and as dystrophic neurites
  • The abundance of tangles is roughly proportional to the severity of clinical disease and cognitive decline
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20
Q

What is the normal function of beta amyloid and tau proteins?

A

Amyloid: essential role in neural growth and repair
Tau: stability of microtubules

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21
Q

risk factors for Alzheimer’s

A
  • head injury
  • increased serum cholesterol and homocysteine levels
  • Lifestyle factors including smoking, midlife obesity, and a diet high in saturated fats
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22
Q

What genes are associated with alzheimer’s?

A 
Early-onset :
- β-amyloid precursor protein (β-APP)
- Presenilin 1
- Presenilin 2.
Late-onset :
- Apolipoprotein E gene
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23
Q

What is the clinical presentation of alzheimer’s

A
  • Memory loss → loss of recent first
  • Disorientation to time and place
  • misplacing items/getting lost
  • Nominal dysphasia → Proper names and low-frequency words decline first
  • Apathy
  • Decline in ADLs
  • Personality/mood change
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24
Q

What are the pharmacological options alzheimers?

A
  • AcetylCholinesterase inhibitors (+ memantine)
  • Antidepressants
  • Antipsychotics (controversial)`
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25
Q

non pharmacological interventions for Alzheimer’s

A
  • Carer support
  • OT
  • Community services
  • ID bracelets
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26
Q

Give examples of AChE inhibitors.

A

Donepezil, galantamine, rivastigmine

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27
Q

What is memantine and how best prescribed?

A

NMDA receptor antagonist
- blocks glutamate

  • best when combined with AChE inhibitors but can be given as monotherapy in severe cases
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28
Q

what are the Predominant neurones affected in Alzheimer’s

A

o Cholinergic (treatments target this)
o Noradrenergic
o Serotonergic
o Those expressing somatostatin

29
Q

What is the pathophysiology of vascular dementia?

A

Cognitive impairment caused by cerebrovascular disease (multiple small strokes)

Common endpoint of many vascular pathologies intracranially:
• Infarction
• Leukoaraiosis → a disease of white matter also called subcortical leukoencephalopathy
• Haemorrhage
• Alzheimer’s disease → although not classified as a vascular pathology, AD has a strong vascular risk-factor spectrum

30
Q

What are the risk factors for vascular dementia?

A 
Risk factors same as for any vascular disease (and indeed same as for Alzheimer's)
o Previous stroke / MI etc
o Hypertension
o Hypercholesterolaemia
o Diabetes
o Smoking
31
Q

WHat is the clinical presentation of vascular dementia?

A

Step-wise deterioration of cognitive function with focal neurological symptoms

32
Q

typical history of vascular dementia

A
  • History of stroke
  • Difficulty solving problems
  • Apathy
  • Disinhibition
  • Slowed processing of information
  • Poor attention
  • Retrieval memory deficit
  • Risk factors similar to IHD
33
Q

What is the treatment for vascular dementia?

A

Basically reducing risk of further sclerotic/embolic effects
• Antiplatelet therapy/Anticoagulation
• Lifestyle modification
• BP control if HTN
• Statin therapy if elevated LDL cholesterol
• Optimisation of glycaemic control if diabetic
• Carotid endarterectomy if carotid stenosis >70%
• Cholinesterase inhibitors or memantine if concominant AD

34
Q

What is the pathophysiology in Lewy body dementia?

A
  • Accumulation of Lewy bodies in vulnerable sites of CNS
  • Lewy bodies are composed of the protein alpha-synuclein.
  • Forms spherical intracytoplasmic inclusions
  • Other proteins include neurofilament and ubiquitin
35
Q

Where are the main deposits of lewy bodies?

A
  • Substantia nigra
  • Temporal lobe
  • Frontal lobe
  • Cingulate gyrus
36
Q

What is thought to be correlated with clinical symptoms of Lewy body dementia?

A

The distribution and density of Lewy bodies

37
Q

difference between Parkinson’s disease and lewy body dementia?

A

Essentially the same disease as Parkinson’s. If
movement disorder followed by dementia then we call
this Parkinson’s disease. If dementia precedes
movement disorder we call it dementia with Lewy bodies

38
Q

What are the 3 core clinical features of Lewy body dementia?

A

o Fluctuating cognition and alertness
o Vivid visual hallucinations
o Parkinsonian features - shuffling gait, flexed posture.

39
Q

typical features of lewy body dementia

A
  • Risk factor = old age
  • Cognitive fluctuations
  • Hallucinations
  • Motor symptoms → Parkinsonian
  • Vivid dreams are accompanied by loss of associated atonia of REM sleep; ‘acting out’ dreams
  • Depression
  • Repeated falls/syncope
  • Urinary incontinence
  • Constipation
40
Q

What are the pharmacological options of Lewy body dementia?

A

AChE inhibitors and memantine

Carbidopa/levodopa if motor symptoms present and severe

41
Q

WHat is the pathophysiology of frontotemporal dementia?

A

Atrophy of frontal and temporal lobes.

Definitive diagnosis depends on the pathological examination of brain tissue, and identification of patterns of neuronal injury and characteristic intra neuronal and glial cell inclusions

  • FTD-tau
  • FTD-U (ubiquitin)
42
Q

What is the clinical presentation of frontotemporal dementia?

A

Symptoms mostly related to frontal lobe dysfunction
o Behavioural disinhibition
o Inappropriate social behaviour
o Loss of motivation without depression (caused by
damage to anterior cingulate cortex)
o Repetitive/ritualistic behaviours
o Non fluent (Broca type) aphasia

43
Q

what are the 3 classic behaviours of frontotemporal dementia?

A
  • Apathetic
  • Disinhibited
  • Stereotypic
44
Q

Treatment for frontotemporal dementia?

A

do not give Cholinesterase inhibitors or memantine

Dependent on patient need:
• Acute irritability, restlessness, agitation, or aggression → benzos
• Home-assistance, respite care
• Compulsions → SSRIs
• Sleeping disturbance → Mirtazapine 1st line
• Distractibility → amantadine
• Gluttony → topiramate

45
Q

why should antipsychotics (dopamine antagonists) not be given to patients with lewy body dementia?

A

can cause neuroleptic malignant syndrome, a psychiatric emergency

46
Q

features if neuroleptic malignant syndrome

A

 Fever
 Encephalopathy (confusion)
 Vital signs instability (tachycardia, tachypnoea (v.sensitive sign), fluctuating BP)
 Elevated creatine phosphokinase
 Rigidity (caused by dopamine antagonism)

47
Q

What is the pathophysiology of AIDS dementia complex (ADC)?

A
  • HIV-infected macrophages will enter the brain and cause indirect damage to neurones.
  • Insidious onset but once established - rapid progression.
48
Q

What is the pathophysiology of AIDS dementia complex (ADC)?

A
  • HIV-infected macrophages will enter the brain and cause indirect damage to neurones.
  • Insidious onset but once established - rapid progression.
49
Q

What are the clinical features of ADC?

A
  • Cognitive Impairment
  • Psychomotor retardation
  • Tremor
  • Ataxia
  • Dysarthria
  • Incontinence
50
Q

What is the treatment for ADC?

A

Anti-virals

51
Q

WHat are the common investigations for all suspected dementia cases/

A
  • Mini-Mental State Exam
  • Dementia screen
  • Urine drug screen
  • CT head
  • MRI brain
  • ECG in vascular dementia
  • Routine syphilis testing is not necessary but should be done if a risk is identified in the history
52
Q

what does dementia screen involve?

A
  • FBC → anaemia
  • U&E → deranged sodium, calcium, glucose
  • TSH → hyper/hypothyroidism
  • Serum Vitamin B12
53
Q

what 6 things are tested in Mini-Mental State Exam

A
  1. Orientation
  2. Registration
  3. Attention and Calculation
  4. Recall
  5. Language
  6. Copying
54
Q

What is the common management plan for all cases of dementia?

A

Bio-Pscyho-Social Model

55
Q

what does the bio part of Bio-Pscyho-Social Model include?

A

• Acetylcholinesterase inhibitors (e.g. donepezil,
rivastigmine, galantamine)
- Modest efficacy for mild to moderate Alzheimer’s disease
• NMDA antagonists (e.g. memantine)
- Useful for treating agitation

56
Q

what does the psycho part of Bio-Pscyho-Social Model include?

A

Few psychological treatments are available for dementia due to its progressive nature

57
Q

what does the social part of Bio-Pscyho-Social Model include?

A 
o Explain the diagnosis sensitively
o Talk about problems that will arise and how they
will be managed
o Give results of any special investigations (e.g.
scans)
o Driving
o Finances
- Will
- Power of attorney
o Day care and respite care 
o Residential/nursing home placement
58
Q

Define delirium

A

Delirium (sometimes called ‘acute confusional state’) is
an acute, fluctuating syndrome of disturbed
consciousness, attention, cognition and perception
- often reversible due to organic cause

59
Q

What are the features of delirium?

A
  • Rapid onset of confusion
  • Clouded consciousness (may be drowsy)
  • Fluctuating course
  • Maybe transient visual hallucinations
  • Often exaggerated emotional responses (e.g. aggression)
60
Q

what is delirium associated with?

A

o Associated with a variety of insults to the brain which may cause neuronal damage and inflammation
o Dementia can predispose to episodes of delirium

61
Q

What are 2 types of delirium?

A

hyperactive and hypoactive

62
Q

What are the features of hypoactive delirium?

A
  • Withdrawn
  • Quiet
  • Sleepy
  • Consequently more likely to be missed / confused with something else
63
Q

What are the features of hyperactive delirium?

A
  • Restless
  • Agitated
  • Aggressive
64
Q

features of mixed delirium

A

 Mood may rapidly fluctuate
 Persecutory delusions (narrative of elusion often not coherent)
 Symptoms worse at start and end of day

65
Q

What are the causes of delirium?

A 
THINK DELIRIUM:
T - trauma
H - hypoxia
I - Increasing age
N - neck of femur fracture
smoKer or alcohol withdrawal

D- Drugs, (vitamin)deficiencies, discomfort (pain)

E- Electrolytes, endocrine(thyroid, pancreas), environment

L- Lungs (hypoxia), liver, lack of sleep, long ED stay

I- Infection(UTI, pneumonia), iatrogenic events, infarction (cardiac, cerebral), intracranial (Strokes, TIAs, epilepsy, infection etc)

R- Restraints, restricted movement/mobility, renal failure

I- Injury, impaired sensory input, intoxication (alcohol)

U- UTI, unfamiliar environment

M- Metabolic abnormalities ( Hypoxia, Renal, Hepatic), metastasis (brain), medications

66
Q

What is the treatment for delirium?

A

-Treat underlying cause!
-Encourage normal day/night cycle
- Calm environment.
- Rehydration.
- Allow wandering if safe
- Consider DOLS
- Involve family/loved ones
- For challenging behaviours – distraction
techniques, medications last resort - Haloperidol (antipsychotic) (ONLY IF ESSENTIAL).

67
Q

prognosis of delirium

A

• Increases risk of dementia
• Associated with mortality
• These patients often have lengthy hospital stays and
have a high risk of re-admission

68
Q

compare delirium to dementia

A

Dementia Delirium
Onset Chronic – months Acute – Hours
to years to days
Course Progressive decline Fluctuating
Reversible? Irreversible Reversible –
days/weeks
Consciousness Can be normal Altered
Attention Can be normal Altered
Memory Recent and remote Recent and
impaired Immediate
recall impaired

Semester 4 - Clinical Neuroscience (19 decks)

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