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Clinical neuroscience > Lecture 14- Dementia and delirium > Flashcards

Lecture 14- Dementia and delirium Flashcards

1
Q

Dementia summary

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

  • Alzheimer’s most common (50-70%)
    • Women>men
  • Vascular dementia (25%)
  • Lewy body (15%_
  • Frontotemporal dementia
  • AIDS-dementia complex
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2
Q

pathophysiology of alzheimers dementia

A
  • Global atrophy of brain lobes
    • Mostly frontal, parietal and temporal lobes
  • Sulcus widening
  • Enlarged 3rd and 4th interventricular space
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3
Q

2 theories for AD

A

amyloid hypothesis

abnormal aggregation of Tau protein

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4
Q

The amyloid hypothesis – 1st theory

A
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5
Q

Abnormal aggregation of the Tau protein- 2nd theory

A
  • Tau is a microtubule associated protein that stabilises microtubules in the cell
  • Tau accumulates into intraneuronal masses known as neurofibrillary tangles and as dystrophic neurites
  • Abundance of tangles roughly proportion to the severity of clinical disease and cognitive decline
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6
Q

AD RF

A
  • Head injury
  • High serum cholesterol and fats
  • Lifestyle factors: smoking, midlife obesity and diet high in sat fats
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7
Q

AD history: questions to ask

A
  • Ask RF (inc family history of down syndrome)
  • Memory loss –> loss of recent first
  • Disorientation to time and place (misplacing items/getting lost)
  • Nominal dysphasia à proper name sand low-frequency words decline first
  • Apathy
  • Decline in ADLs
  • Personality/ mood change
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8
Q

Management of AD

A
  • Carer support (OT, community services, ID bracelets)
  • Pharmacological
    • Cholinesterase inhibitors
    • Antidepressants
    • Antipsychotics (controversial)
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9
Q

Vascular dementia pathophysiology

A
  • Common endpoint of many vascular pathologies intracranially
    • Infarction
    • Leukaoraisois –> 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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10
Q

vascualt dementia : history questions to ask

A
  • History of stroke
  • Difficulty solving problems
  • Apathy
  • Disinhibition
  • Slow processing
  • Poor attention
  • Retrieval memory deficit
  • Risk factors similar to IHD
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11
Q

Management of VD

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 concomitant AD
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12
Q

Lewy body dementia pathophysiology

*

A
  • Accumulation of lewy bodies in vulnerable sites of the CNS
    • substantia nigra
    • temorpal lobe
    • frontal lobe
    • cingulate gyrus
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13
Q

what are lewy bodies

A
  • Lewy bodies are composed of protein alpha-synuclein, a cytoplasmic protein associated with synaptic vesicles. Other proteins include neurofilament and ubiquitin
  • The distribution and density of Lewy bodies are thought to be correlated with clinical syndromes
  • Co-existing AD pathology is common
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14
Q

Parkinson’s or Lewy body dementia?

A
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15
Q

lewy body dementia history taking

A

History

  • Risk factor = old age
  • 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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16
Q

management of lewy body dementia

A
17
Q

Frontotemporal dementia

Aetiology

A
  • Focal neurodegeneration of the frontal or temporal lobes of the brain
  • Strong family history
18
Q
A
19
Q

frontotemporal dementia pathophysiology

A

Pathophysiology

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. Specific accumulations found:

  • FTD-tau
  • FTD-U (ubiquitin)
20
Q

classification of FTD

A

3 behavioural presentations of FTD

  • Apathetic
  • Disinhibited
  • Stereotypic

Can be overlapping

Distinction between behavioural FTD vs Primary progressive aphasia

21
Q

History FTD

A
  • 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
  • Age at onset peak in mid-50s
  • FHx
  • Altered eating habits
22
Q

Management of FTD

A

*not standard dementia medication*

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
23
Q

AIDs dementia complex pathophysiology

A
  • As patients with HIV infection live longer thanks to modern treatments, their chance of developing AIDS associated dementia is increasing
  • HIV-infected macrophages enter the brain, causing indirect damage to neurones
  • Insidious onset, but rapid progression once established
24
Q

Clinical features of AIDs dementia complex

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
25
Q

Prognosis of dementia

A
26
Q

dementia investigations

A
  • Mini-mental state exam
  • dementia screen
    • FBC (anaemia)
    • U&E (deranged sodium, calcium, glucose)
    • TSH –> hyper/hypothryodisms
    • serum vitamin B12
  • 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
27
Q
  • Mini-Mental State Exam
A
28
Q

define delirium

A
29
Q

why is delirium important to recognise

A

Patients who develop delirium also have longer length of stay and more likely to develop hospital acquire complications such as falls and pressure sores

  • Increased mortality
30
Q

Types of delirium

A
  • Hyperactive – easier to spot
    • Agitated
    • Restless
    • Inappropriate behaviour
  • Hypoactive
    • Lethargy
    • Reduced conc
    • Increased appetite
  • Mixed- hyperactive and hypoactive
31
Q

Screening for delirium

A
32
Q

delirium assessment- what is the underlying cause

A
  • history and examiantion
  • collateral history is very important
  • investgiations tailored to individual
33
Q

Potential underlying causes

A

THINK

  • Trauma (head injury, intracranial event)
  • Hypoxia (PE< CCF, MI, COPD, pneumonia)
  • Increasing age/frailty
  • Neck of femur fracture
  • SmoKer or alcohol withdrawal

DELIRIUM

  • Drugs (new stopped /started, side effects, drug interactions)
  • Environment- especially ward moves
  • Lack of sleep
  • Imbalanced electrolytes (renal failure, Na+, Ca2+, glucose, liver function)
  • Retention (urinary and constipation)
  • Infection/sepsis
  • Uncontrolled pain
  • Medial conditions (Dementia, Parkinson’s disease)
34
Q

Management of delirium

A
  • Minimise/treat precipitating factors
  • Encourage normal day/nigh cycle
  • Allow wandering if safe
  • Consider DOLs (deprivation of liberties safeguard)
  • Involve family/loved ones
  • For challenging behaviour
    • Distraction techniques
    • Medications last resort
35
Q

Prognosis of delirium

A

‘Reversible cause of confusion’

36
Q

compare dementia and delirium

A

Clinical neuroscience (30 decks)

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