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Neuroscience > 9.1 Dementia, Delerium and toxic insults > Flashcards

9.1 Dementia, Delerium and toxic insults Flashcards

1
Q

What is dementia ?

A

Dementia is a syndrome (usually progressive) characterised by an appreciable 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

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2
Q

Which dementia is the most common?

A

Alzheimer’s

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3
Q

What are the 5 types of dementia?

A 
Alzheimer’s
Vascular
Levy body
Frontotemporal 
AIDS-Dementia complex
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4
Q

Describe the changes seen in brain structure in alzheimers

A

Global atrophy of brain lobes, mostly frontal, parietal and temporal lobes
Sulcus widening
Enlarged 3rd and 4th interventricular spaces

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5
Q

What are the 2 different hypothesis for Alzheimer’s disease?

A

The amyloid hypothesis

Aggregation of tau protein

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6
Q

Describe the pathophysioogy of the amyloid hypothesis of alzheimers

A
  1. Excess of interneuronal amyloid peptide (overproduction/decreased clearance)
  2. Formation of dense amyloid oligomers, deposited as defuse plaques across the brain
  3. inflammatory process through micro glial activation, cytokines formation, and activation of the complement cascade
  4. Formation of neuritic plaques, causing synaptic and neuritic injury and cell death.
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7
Q

What are microglials?

A

Neuroglial cells in the CNS that migrate from the bone marrow. Act as phagocytes of waste products of the CNS

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8
Q

What is a neuritic plaque?

A

Spherical mass composed of amyloid fibrils and interwoven neuronal processes, seen in alzheimers

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9
Q

What is the pathophysiology of the tau protein theory of alzheimers?

A

abnormal aggregation of the tau protein, a microtubule- associated protein that stabilises microtubules in the cell:
• 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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10
Q

What are risk factors for alzheimers dementia?

A 
Older age 
Head injury
Increased serum cholesterol and homocysteine levels
Smoking
Midlife obesity
Diet high in saturated fats
Family history of Down’s syndrome
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11
Q

What are the symptoms and signs of AD?

A

Memory loss, most recent first
Disorientation to time and place (misplacing items and getting lost)
Nominal dysphasia (word retrieval failure)
Apathy
Decline in ADLs (activities of daily living)
Personality and mood changes

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12
Q

What is the management of AD?

A 
Carer Support
- OT/community services/ID bracelets
Pharmacological
- Cholinesterase inhibitors
- Antidepressants
- Antipsychotics (controversial)
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13
Q

Why is it controversial to prescribe antipsychotics to treat dementia?

A

Some studies show increases the risk of death. Also significant side effects to do with motor control - shaky hands and salivation. Can also cause confusion, thereby worsening the expression of the dementia.

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14
Q

What cholinesterase inhibitors are used to treat AD?

A

Newly diagnosed = donepezil, galantamine, rivastigmine

Severe = memantine

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15
Q

What is the pathophysiology of vascular dementia?

A

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.

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16
Q

What are the signs and symptoms of vascular dementia?

A 
History of stoke of anything that might cause a stroke
Difficulty solving problems
Apathy
Disinhibition
Slowed processing of information
Poor attention
Retrieved memory deficit
Risk factors similar to IHD (over 50yrs, high BP, hypercholesterolaemia, diabetes, sedentary lifestyle, genetics and obesity)
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17
Q

Why is the presentation of vascular dementia very variable?

A

As presentation depends on which cerebral artery is being affected and therefore which lobes of the brain are being affected.

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18
Q

What is the management of vascular dementia?

A

Basically reducing risk of further sclerotic/embolic effects
Antiplatelet therapy/Anticoagulation (aspirin + clopidogrel and warfarin)
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

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19
Q

What should cholinesterase inhibitors be considered to treat vascular dementia?

A

If they are suspected to have one of the following comorbidities:
Alzheimer’s dementia
Parkinson’s disease
Dementia with Lewy bodies

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20
Q

What is the pathophysiology of Lewy body dementia?

A

Accumulation of Lewy bodies in vulnerable sites of CNS
• Substantia Nigra
• Temporal Lobe
• Frontal Lobe
• Cingulate gyrus
The distribution and density of Lewy bodies are thought to be correlated with clinical symptoms. Co-existing AD pathology is common

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21
Q

What are Lewy bodies?

A

Lewy bodies are composed of the protein alpha-synuclein, a cytoplasmic protein associated with synaptic vesicles. Other proteins include neurofilament and ubiquitin

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22
Q

How does Lewy body dementia vary from Parkinson’s disease?

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

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23
Q

What are the presenting signs and symptoms of a patient with Lewy body dementia?

A

Cognitive fluctuations
Hallucinations, typically visual and complex; up to 80% of patients
Motor symptoms → Parkinsonian features present in >85% of patients
Vivid dreams are accompanied by loss of associated atonia of REM sleep; ‘acting out’ dreams
Depression
Repeated falls/syncope
Urinary incontinence
Constipation

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24
Q

What are risk factors for Lewy body dementia?

A

AD

Old age

25
Q

What is the management of Lewy body dementia?

A 
Cholinesterase inhibitors (donepreail, galantamine, rivastigmine, memantine)
Antidepressants 
Synthetic dopamine - Carbidopa/levodopa if motor symptoms are present and severe.
26
Q

Why are synthetic dopamines prescribed during Lewy body dementia? Why must they be carefully prescribed?

A

As Lewy body dementia associated with parkinsonian features - if motor symptoms severe they will help.
Prescribed with caution as can worsen behavioural problems and hallucinations.

27
Q

What is frontotemporal dementia?

A

Focal neurodegeneration of the frontal or temporal lobes of the brain
Dutch epidemiological study reported a positive family history in 43% of cases

28
Q

What are the signs and symptoms of frontotemporal dementia?

A

3 behavioural presentations:
Apathetic, disinhibited, stereotypic
Primary progressive aphasia
Coarsening of personality, social behaviour, and habits
Progressive loss of language fluency or comprehension
Development of memory impairment, disorientation, or apraxias
Progressive self-neglect and abandonment of work, activities, and social contacts
Altered eating habits

29
Q

What are risk factors of frontotemporal dementia?

A

Over 50 yrs

Family history

30
Q

What is the management of frontotemporal dementia?

A

Standard dementia medications (cholinesterase inhibitors) not effective in FTD
Dependent on patient need:
Acute irritability, restlessness, agitation, or aggression → benzodiazapenes
Home-assistance, respite care
Compulsions → SSRIs
Sleeping disturbance → Mirtazapine 1st line
Distractibility → amantadine
Gluttony → topiramate

31
Q

why is the chance of developing AIDS associated dementia increasing?

A

As patients with HIV live linger now thanks to modern treatments

32
Q

what causes AIDs associated dementia?

A

HIV-infected macrophages enter the brain, causing indirect damage to neurones. Insidious onset, but rapid progression once established

33
Q

what are the clinical features of AIDs associated dementia?

A 
• Related to global damage but also some manifestations of cerebellar involvement:
• Cognitive impairment 
• Psychomotor retardation (slow thoughts and movements, also seen in
depression) 
• Tremor 
• Ataxia 
• Dysarthria 
• Incontinence
34
Q

what investigations are used for dementia?

A

• Mini-Mental State Exam
• Dementia screen:
- FBC → anaemia
- U&E → deranged sodium, calcium, glucose
- TSH → hyper/hypothyroidism
- Serum Vitamin B12
• Urine drug screen
• CT head
• MRI brain
• ECG in vascular dementia (arrhythmias)
• Routine syphilis testing is not necessary but should be done if a risk is identified in the history

35
Q

what 6 things are tested in a mini mental state examination?

A 
orientation
registration
attention and calculation
recall
language
copying
36
Q

what are the complications associated with delirium?

A

increased mortality
longer length of stay in hospital
higher risk of falls and pressure sores

37
Q

what is delirium?

A

Delirium (sometimes called ‘acute confusional state’) is an acute, fluctuating syndrome of disturbed consciousness, attention, cognition and perception

38
Q

how might a patient with delirium present?

A

sleepy / drowsy in the daytime
insomnia and hyperactivity in the nighttime
disorganised thinking
dilutions

39
Q

what are the 3 different types of delirium?

A

hyperactive - agitation, restlessness, wandering, inappropriate behaviour.
hypoactive - lethargy, reduced concentration
mixed

40
Q

what is done to investigate delirium

A

thorough history and examination- collateral history is very important
delirium assessment
investigations are tailored to the individual and the underlying cause

41
Q

what are the potential underlying causes for delirium?

A 
trauma (head injury, intracranial event) 
hypoxia
increasing age / frailty 
neck of femur fracture 
smoke or alcohol withdrawal 
drugs 
environment 
lack of sleep, reversal of sleep-wake cycle
imbalanced electrolytes
retention (urine/constipation)
infection/sepsis
uncontrolled pain 
medical conditions (dementia, parkinsons disease)
42
Q

how do we manage delirium?

A

• Minimise/treat
precipitating factors
• Encourage normal day/night cycle
• Allow wandering if safe
• Consider DOLS (deprivation of liberty safeguard)
• Involve family/loved ones
• For challenging behaviours – distraction techniques, medications last resort

43
Q

what is the difference between dementia and delirium?

A

onset = dementia is chronic (months to years) whereas delirium is acute (hours to days)
course =dementia has a progressive decline, delirium is fluctuating
reversibility = dementia is irreversible whereas delirium is reversible
consciousness = can be normal in dementia, altered in delirium
attention = can be normal in dementia, altered in delirium
memory = is recent and remote impaired in dementia, is recent and immediate recall impaired.

44
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)
45
Q

what are the non-cognitive symptoms of dementia?

A
  • Behavioural symptoms (Agitation, Aggression (frontal lobe involvement), Wandering, Sexual disinhibition (frontal lobe involvement))
  • Depression and anxiety
  • Psychotic features (Visual and auditory hallucinations (hallucinations=false
    perceptions) , Persecutory delusions (delusions=false beliefs))
  • Sleep symptoms (Insomnia, Daytime drowsiness (decreased cortical activity))
46
Q

how is dementia diagnosed?

A

by exclusion of organic causes of cognitive decline

  • Hypothyroidism
  • Hypercalcaemia
  • B12 deficiency
  • Normal pressure hydrocephalus (Abnormal gait, Incontinence, Confusion)
  • 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)

47
Q

what are the macroscopic pathological features of alzheimers disease?

A
  • Global cortical atrophy
  • Sulcal widening
  • Enlarged ventricles (primarily lateral and third affected)
48
Q

what are the microscopic pathological features of alzheimers disease?

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

It is believed that plaques and tangles kill neurones. Since neurogenesis is limited in the CNS any neurones that die are unlikely to be replaced

49
Q

what neurones are predominantly affected in alzheimers disease?

A
  • Cholinergic (treatments target this)
  • Noradrenergic
  • Serotonergic
  • Those expressing somatostatin
50
Q

what is the presentation of vascular dementia?

A

Stepwise, maybe with focal neurological features

51
Q

what is the pathology of dementia with lewy bodies?

A

Aggregation of alpha synuclein

  • Forms spherical intracytoplasmic inclusions
  • Main deposits found across the brain in Substantia nigra, Temporal lobe, Frontal lobe, Cingulate gyrus (found just above the corpus callosum)
  • Can label alpha synuclein in the brain using advanced imaging techniques
52
Q

what is the presentation of dementia with lewy bodies?

A
  • Fluctuating cognition and alertness
  • Vivid visual hallucinations
  • Parkinsonian features
  • May cause repeated falls
  • Do not give antipsychotics (dopamine antagonists)
    as can cause neuroleptic malignant syndrome, a psychiatric emergency
53
Q

what is neuroleptic malignant syndrome?

A

Neuroleptic malignant syndrome (NMS) is a life-threatening idiosyncratic reaction to antipsychotic drugs characterized by

  • altered mental status
  • autonomic dysfunction.
  • Fever
  • Encephalopathy (confusion)
  • Vital signs instability (tachycardia, tachypnoea (v.sensitive sign), fluctuating BP)
  • Elevated creatine phosphokinase
  • Rigidity (caused by dopamine antagonism)
54
Q

what are the symptoms of frontotemporal dementia?

A

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

55
Q

what are the clinical features of AIDS associated dementia?

A

Clinical features (related to global damage but also some
manifestations of cerebellar involvement)
- Cognitive impairment
- Psychomotor retardation (slow thoughts and movements, also seen in depression)
- Tremor
- Ataxia
- Dysarthria
- Incontinence

56
Q

what are the biological managements of dementis?

A

Acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine, galantamine) - Modest efficacy for mild to moderate AD

NMDA antagonists (e.g. memantine). Useful for treating agitation

57
Q

what are the social managements of dementia?

A

• Mainstay of management

  • Explain the diagnosis sensitively
  • Talk about problems that will arise and how they will be managed
  • Give results of any special investigations (e.g. scans)
  • Driving – often a difficult topic to deal with as patients frequently desperate to retain their independence
  • Finances (Will, Power of attorney)
  • Day care and respite care (mainly to allow carers to rest and provide supportive environment for patients)
  • Residential/nursing home placement
58
Q

what is the 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

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