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Clinical Neuroscience > Dementia > Flashcards

Dementia Flashcards

1
Q

What is dementia?

A

a progressive irreversible decline in cognitive function over several months

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2
Q

Types of dementia

A
  • Alzheimer disease
  • Vascular dementia
  • Lewy body dementia
  • Frontotemproal
  • Parkinson’s disease with dementia
  • Aids related
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3
Q

Cognitive symptoms of dementia
What lobe is involved?

A
  • impaired memory - temporal
  • impaired orientation - temporal
  • impaired learning capacity - temporal
  • impaired judgement - frontal
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4
Q

Non cognitive symptoms of dementia

A
  • behavioural symptoms - agitation, aggression, sexual disinhibition
  • depression + anxiety
  • insomnia
  • daytime drowsiness
  • visual + auditory hallucinations
  • persecutor delusions
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5
Q

How is dementia diagnosed?

A

By exclusion:
- exclude delirium
- exclude organic causes of cognitive decline:
- hypothyroidism
- hypercalcaemia
- B12 deficiency
.
Look for features of progressive cognitive decline, impairment of daily living in patients with a normal conscious level

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6
Q

What must be excluded when making a diagnosis of dementia?

A
  • exclude delirium
  • exclude organic causes of cognitive decline:
  • hypothyroidism
  • hypercalcaemia
  • B12 deficiency
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7
Q

Diagnosis of Alzheimer’s dementia

A

Clinically but hippocampal atrophy on imaging is supportive

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8
Q

Macroscopic pathological features of Alzheimer disease

A
  • hippocampal atrophy
  • Global cortical atrophy
  • Sulcal widening
  • Gyri narrowing
  • Enlarged ventricles (primarily lateral + 3rd)
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9
Q

Microscopic pathological features of Alzheimer disease

A

Plaques
Tangles

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10
Q

What are Alzheimer plaques composed of?

A

Amyloid beta

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11
Q

What is amyloid precursor protein?
How is it normally broken down?
What pathology can occur?

A
  • A protein involved in repairing neurones after damage
  • Normally it is replaced + chopped up into soluble parts by a + gamma secretases
  • In Alzheimer disease, B secretase causes insoluble breakdown > formation of B amyloid plaques
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12
Q

How are plaques formed in Alzheimer disease?

A

Amyloid precursor protein is broken down by B secretase into insoluble parts > forming B amyloid plaques

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13
Q

Outline Alzheimer disease in relation to Tau tangle formation

A
  • B amyloid plaque induce pathological response in neuron > hyperphosphrylation of Tau proteins
  • change in shape of Tau proteins
  • reduced support of cytoskeleton
  • neuron death
  • aggregate into tangles
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14
Q

Function ofTau proteins

A

Play a role in stabilising microtubules within neuronal cytoskeleton

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15
Q

Types of Alzheimer disease

A

Sporadic (most common)
Familial

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16
Q

Outline sporadic Alzheimer disease

A
  • 90-95%
  • causes are poorly understood
  • increasing prevalence with age
17
Q

Outline familial Alzheimer disease

A
  • 5-10%
  • early onset dementia
  • PSEN1/2 genes implicated > mutation of gamma secretase
18
Q

Relationship between Down syndrome and Alzheimer disease

A

Disease can present as early as 40 years old

19
Q

Symptoms of Alzheimer disease

A
  • initially symptoms hard to detect
  • short term memory loss initially
  • motor and language skills affected
  • long term memory loss
  • disorientation
20
Q

What is used to assess severity of dementia?

A

Mental state examination

21
Q

Treatment of Alzheimer disease

A
  • Acetyl cholinesterase inhibitors pyridostigmine
  • Memantine (glutamate receptor antagonist) for advanced cases
22
Q

Early symptoms of Lewy body dementia

A

Cognitive symptoms:
- distressing hallucination
- depression
- REM sleep disorders - sleep walking/talking

23
Q

Outline Lewy body dementia

A
  • dementia features early then Parkinsonian features
  • caused by misfolding of alpha synuclein
  • misfolded aggregate into Lewy bodies
  • deposition into cortex (dementia type symptoms) + substantia nigra (Parkinsonian features)
24
Q

Late symptoms of Lewy body dementia

A

Parkinsonian symptoms:
- bradykinesia
- resting tremor
- stiffness

25
Q

Treatment of Lewy body dementia

A

Symptom based
Levodopa

26
Q

What is frontotemporal lobe dementia?

A

Frontal + temporal lobe atrophy
Umbrella term for heterogeneous group of disease that can be characterised on the type of glial + neuronal proteinaceous inclusions or underlying genetic mutation

27
Q

How does frontotemporal lobe dementia occur?

A
  • aggregate proteins
  • Tau protein hyperphosphorylation (Pick’s disease)
  • frontal + temporal lobe atrophy
28
Q

Symptoms of frontotemporal lobe dementia

A
  • behavioural + emotional changes
  • inappropriate social behaviour
  • loss of motivation without depression
  • broca type aphasia
29
Q

How does AIDs dementia occur?

A
  • occurs when CD4+ count falls below threshold
  • entry of HIV infected macrophages into brain > inflammation + neuron damage
30
Q

Clinical features of AIDs dementia

A
  • congitive impairment
  • psychomotor retardation
  • tremor
  • ataxia
  • dysarthria
  • Incontience
31
Q

Outline vascular dementia

A

Cognitive impairment caused by cerebrovascular disease (multiple small strokes)

32
Q

Risk factors for vascular dementia

A
  • previous stroke or MI
  • hypertension
  • hypercholesteroaemia
  • diabetes
  • smoking
33
Q

Difference between Parkinson’s disease + Lewy body dementia

A
  • Parkinson’s disease: movement disorder followed by dementia
  • Lewy body dementia: dementia followed by movement disorder (Parkinsonism)
34
Q

Why should you not give anti-psychotics e.g. haloperidol in Lewy body dementia?

A

It can cause neuroleptic malignant syndrome

35
Q

Features of neuroleptic malignant syndrome

A

Fever
Confusion
Tachycardia
Tachypnoea
Fluctuating BP
Elevated creatine phosphokinase
Rigidity

Clinical Neuroscience (22 decks)

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