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Neurology > 8. Dementia - Alzheimer's, Frontotemporal, Lewy Body and Vascular > Flashcards

8. Dementia - Alzheimer's, Frontotemporal, Lewy Body and Vascular Flashcards

1
Q

Define dementia.

A

An umbrella term for a syndrome characterised by a set of symptoms that may include memory loss and difficulties with thinking, problem solving or language, resulting in impairment in ADL (activities of daily living).

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2
Q

Describe the epidemiology of dementia.

A

10% of people over 65 and 20% of people over 80 have dementia.

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3
Q

Give 3 causes of dementia.

A
  1. Alzheimer’s disease (65%).
  2. Fronto-temporal.
  3. Vascular.
  4. Lewy bodies.
  5. Vitamin deficiency e.g. B12.
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4
Q

What is the most common type of dementia?

A

Alzheimer’s disease.

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5
Q

What is Alzheimer’s disease (AD)?

A

A chronic neurodegenerative disease with an insidious onset and progressive but slow decline.

  • It is the most common type of dementia.
  • Occurs more commonly in women.
  • Deterioration is over 8-10 years.
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6
Q

Give 3 risk factors for Alzheimer’s disease.

A
  1. 1st degree relative with AD.
  2. Down’s syndrome.
  3. Homozygous for apolipoprotein e (ApoE) 4 allele
  4. Vascular risk factors
  5. Decreased physical/cognitive activity
  6. Depression
  7. Loneliness
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7
Q

Describe the pathophysiology behind Alzheimer’s disease.

A

2 major factors:
1. Amyloid plaques
2. Neurofibrillary tangles

Accumulation of beta-amyloid plaques -> progressive neuronal damage -> neurofibrillary tangles -> raised numbers of amyloid plaques and loss of ACh.

As neurones die, there are large structural changes to the brain:
- The brain atrophies and shrink
- Gyri get narrower
- Sulci between gyri get wider
- Ventricles get larger

Neuronal loss is selective:
- Hippocampus
- Amygdala
- Temporal neocortex
- Subcortical nuclei

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8
Q

What are pathological features of Alzheimer’s? (histology etc)

A
  1. Beta amyloid plaques (degradation product of APP- amyloid precursor protein)
  2. Tau proteins - containing neurofibrillary tangles
  3. Synaptic degradation / neuronal reduction
  4. Atrophy of the centre of the brain
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9
Q

What lobe of the brain is affected in Alzheimer’s disease?

A

Temporal lobe.

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10
Q

Give 3 functions of the temporal lobe.

A
  1. Hearing.
  2. Language comprehension.
  3. Memory.
  4. Emotion.
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11
Q

What are the 2 main categories of Alzheimer’s disease?

A
  1. Familial
  2. Sporadic
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12
Q

What is often the first cognitive marker of AD?

A

Short term memory impairment.

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13
Q

Give 5 symptoms of Alzheimer’s disease.

A
  1. Memory loss
    - short-term
  2. Selective attention
  3. Language impairments
    - difficulty in understanding or finding words
    - difficulty naming objects + people (dysphasia)
  4. Apraxia
    - impaired ability to carry out skilled motor tasks
  5. Disorientation
    - in time and place
  6. Behavioural + psychological issues - personality change
    - apathy, agitation, aggression, psychosis
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14
Q

25% of all patients with AD will develop what?

A

Parkinsonism.

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15
Q

What condition is highly associated with Alzheimer’s?

A

Down’s syndrome

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16
Q

Investigations for Alzheimer’s disease.

A
  1. History
    - to assess cognitive functions by asking various questions
  2. CT/MRI of the brain
    - should show generalised atrophy with media temporal lobe and later parietal predominance
  3. Cognitive Assessment tool:
    (1) Mini Mental State Examination (MMSE)
    - Commonly used to screen for cognitive function (out of 30)
    - Score of 25 or above = normal
    - Score of 18-24 = mild/moderate impairment
    - Score of 17 or below = serious impairment
    (2) 6CIT
    - The 6-item cognitive impairment test
  4. To rule out other causes: - blood tests
    - FBC = rule out anaemia
    - Metabolic panel = rule out abnormal Na+, Ca2+ and glucose
    - U&E
    - ESR & CRP
    - Liver biochemistry
    - Thyroid tests
    - Vitamin B12 + folate = rule out vitamin B12 deficiency-induced dementia
    - Urine drug screen = rule out recreational drug use

Exclusion of rare treatable causes of dementia (substance abuse, vitamin B12 deficiency, hypothyroidism) should be considered.

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17
Q

What questions are asked in 6CIT?

A
  1. What year is it?
  2. What month is it?
    (Give an address).
  3. Count backwards from 20.
  4. Say the months of the year in reverse.
  5. Repeat the address.
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18
Q

Name the staging system that classifies the degree of pathology in AD.

A

Braak staging.

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19
Q

Describe Braak staging.

A
  • Stage 5/6 - high likelihood of AD.
  • Stage 3/4 - intermediate likelihood.
  • Stage 1/2 - low likelihood.
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20
Q

How is AD diagnosed?

A

When criteria (Braak staging) for intermediate or high likelihood AD are met AND the patient has a clinical history of dementia.

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21
Q

What is the treatment for Alzheimer’s disease?

A

Supportive care.
AChE inhibitors e.g. galantamine.

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22
Q

How might you treat Alzheimer’s disease?

A

No cure

  1. Supportive therapy - first line
    - Socially active - talking to family and friends
    - Cognitively active - cognitive stimulation programmes, board games etc.
    - Specialist memory service
  2. Medications
    (1) Acetylcholinesterase inhibitors (rivastagmine, donezepil, galantamine).
    (2) Antiglutamatergic treatment (memantine) -> for advanced stages
    (3) Folic acid and vitamin B
23
Q

Differential diagnoses of AD.

A

Delirium.
Depression.
Substance abuse.
Hypothyroidism.
Space-occupying intracranial lesions.
Huntington’s.

24
Q

Complications of AD.

A
  • Pneumonia
  • Institutionalisation
    (the state of being placed or kept in a residential institution)
  • UTI
  • Falls
  • Weight loss
25
Q

What is frontotemporal dementia (FTD)?

A

A primary neurodegenerative disease causing specific atrophy + degradation of the frontal and temporal lobes of the brain.

  • Often recognised in patients under 65 years old
    (average age of onset between 45 and 65 years)
  • Manifests primarily as disruption in personality and social conduct or as a primary language disorder
  • Almost 50% of affected people have some form of Parkinsonism
26
Q

Who is frontotemporal dementia more common in?

A

Under 65s

27
Q

How is frontotemporal dementia inherited?

A

Dominant

28
Q

Explain the pathophysiology of frontotemporal dementia.

A

Characterised by the presence of PICK BODIES:
-> Pick bodies = a tangle of abnormal tau proteins.
(FTD = a tauopathy).

Tau proteins:
1. Function:
- Make sure microtubules don’t break down
2. 6 isoforms
3. In FTD: 3R isoform of tau protein is hyperphosphorylated and becomes non-functional.
4. Tau protein isoforms clump together to form tangles.
5. As tau proteins clump, neurones undergo apoptosis and the brain atrophies, gyri get narrower, sulci get wider, ventricles expand.

29
Q

Give 3 symptoms for FTD - frontal lobe damage.

A
  1. Behaviour variants: personality and behavioural change
  2. Lower disinhibition
    - Inability to withhold a prepotent response or suppress an inappropriate or unwanted behavior
  3. Impaired social conduct - social withdrawal
  4. Impulsivity - making rash decisions
  5. Difficulty planning
30
Q

Give 3 symptoms for FTD - temporal lobe damage.

A
  1. Progressive Aphasia - difficulty forming language
  2. Memory loss
    - preservation of episodic memory
  3. Semantic dementia - loss of vocabulary + problem understanding
  4. Difficulty in concentrating
  5. Inability to learn new things
31
Q

Which disease is fronto-temporal dementia often associated with?

A

Motor neurone disease.

32
Q

Investigations for FTD.

A
  1. MRI - GOLD STANDARD:
    - Shows frontal and temporal lobe atrophy
  2. Cognitive testing - MMSE
  3. Blood tests - to rule out other causes:
    - FBC, Vitamin B12, TFT, U&E
  4. Brain biopsy:
    - Presence of Pick’s bodies
    - The only real definitive diagnosis method, but it is not recommended = typically obtained at the end of life
33
Q

Treatment of FTD.

A
  1. Supportive therapy - first line
    - Socially active - talking to family and friends
    - Cognitively active - cognitive stimulation programmes, board games etc.
    - Help with ADLs
    - Speech and language therapy
  2. Antidepressants - SSRIs
    - to help with behavioural symptoms
34
Q

What is Lewy body dementia (LBD)?

A

A neurodegenerative disease with the presence of Lewy bodies

35
Q

What is a Lewy body?

A

Collection of alpha synuclein
- an eosinophyllic intracytoplasmic neuronal inclusion body

Present in Lewy body dementia and also sometimes Parkinson’s.

36
Q

Briefly explain the pathophysiology of LBD.

A
  1. Misfolded alpha synuclein protein within the neurones.
  2. Protein aggregates to form Lewy bodies that deposit inside the neurones.
  3. Deposit particularly in the brainstem & neocortex in the substantia nigra
    = dark eosinophilic inclusions inside affected neurones.
  4. Disease progression - more Lewy bodies accumulate in more neurones
37
Q

Give 3 early symptoms of Lewy body dementia (LBD).

A

Early symptoms are often cognitive (similar to AD).

  1. Progressive, fluctuating cognitive function impairment:
    - Attention
    - Difficulty focusing
    - Poor memory
    - Disorganised speech
  2. Visual hallucinations
  3. Depression
38
Q

Give 3 late symptoms of Lewy body dementia (LBD).

A

Later symptoms are often motor (similar to mild PD).

  1. Resting tremors
  2. Stiff and slow movement
  3. Reduced facial expressions
39
Q

Investigations for LBD.

A
  1. Clinical diagnosis
    - Based on pattern of symptoms
  2. Brain autopsy
    - Fully confirms diagosis showing Lewy bodies in neurones
  3. Bloods - to exclude other causes:
    - FBC, B12, TFTs, U&Es
  4. Cognitive tests:
    - MMS
    - 6-item cognitive impairment test
  5. Single-photon emission computer tomography (SPECT)
    - Known commercially as a DaTscan
    - ~ 90% sensitivity + 100% specificity for LBD diagnosis
    = Shows low basal ganglia dopamine transporter uptake
40
Q

How is LBD diagnosed?

A

Dementia + 2 of:
- Fluctuating concentration
- Visual hallucinations
- Spontaneous Parkinsonism
- SPECT/PET scan shows low DA transmission

41
Q

Management of LBD.

A
  1. Supportive therapy - first line
    - Socially active - talking to family and friends
    - Cognitively active - cognitive stimulation programmes, board games etc.
    - Help with ADLs
    - Exercise programmes
  2. Refer to specialist
  3. Symptomatic relief
    - Choliesterase inhibitors
    - e.g. rivastigmine suggested to treat cognitive decline

Note: Avoid use of neuroleptic drugs, e.g. haloperidol, as they can produce severe sensitivity reactions.

42
Q

What is vascular dementia?

A

A chronic progressive, heterogenous impairment of cognitive function, resulting from multiple cerebrovascular events / chronic ischaemia.

  • Men are more likely to develop
  • Incidence increased with age
43
Q

Explain how vascular dementia arises.

A

Cumulative effects of many small strokes.

Sudden onset, with stepwise deterioration.

44
Q

What is the pattern of onset in vascular dementia?

A

Stepwise.
Stable symptoms with a sudden increase, which you do not recover from.

45
Q

Give 4 risk factors for vascular dementia.

A
  1. Smoking
  2. Hypertension
  3. Diabetes
  4. Insulin resistance
  5. Hyperlipidaemia
46
Q

Give 3 causes of vascular dementia.

A
  1. Cerebral artery atherosclerosis
  2. Carotid artery / heart embolism
  3. Vasculitis
  4. Chronic hypertension -> cerebral arterioles sclerosis
47
Q

Give 4 symptoms for vascular dementia.

A

Progressive, stepwise cognitive function impairment
-> dependent on which part of the brain is affects + where the infarcts are.

  1. Focal motor signs e.g. visual disturbance, sensory or motor problems
  2. Gait disturbance
  3. Difficulty with attention and concentration
  4. Seizures
  5. Memory disturbance (especially retrieval of memory)
  6. Frontal release reflexes (grasp, glabella tap, jaw-jerk)
  7. Speech disturbance
  8. Emotional disturbance
  9. Urinary frequency / incontinence
48
Q

Investigations for vascular dementia.

A
  1. Clincal diagnosis including comprehensive history and physical examination
    - Make sure to note any previous stroke or TIA!
  2. Congitive impairment screen
    - Assess the orientation, attention, language function, visuospatial functions, motor control
  3. Bloods - to exclude other causes:
    - FBC, ESR, Blood glucose, LFTs, B12, TFTs
  4. Medication review
    -> to exclude medication causes of cognitive decline
  5. CT or MRI
    - to look for previous infarcts and cerebrovascular lesions
  6. ECG - to check for AF
    -> AF increases risk of embolic cerebral ischaemia
49
Q

Management of vascular dementia.

A
  1. Supportive therapy - 1st line
  2. Antiplatelet therapy - 1st line
    -> Monotherapy of either Aspirin or Clopidogrel
  3. SSRIs or Anti-psychotics to control symptoms
    -> e.g. Lorazepam
  4. Antihypertensive - BP control
    -> To reduce further vascular damage
    - e.g. ACEi - RAMIPRIL
50
Q

Which dementia is associated with hallucinations & recurrent falls / syncope?

A

Lewy body dementia

51
Q

Frontal lobe atrophy is seen on an MRI. What kind of dementia is this patient likely to have?

A

Fronto-temporal.

52
Q

What is functional memory dysfunction?

A

Acquired dysfunction of memory that significantly affects a person’s professional/private life in the absence of an organic cause.

53
Q

How could you determine whether someone has functional memory dysfunction or a degenerative disease?

A

When asked the question ‘when was the last time your memory let you down?’, someone with functional memory dysfunction would give a good detailed answer whereas someone with degenerative disease would struggle to answer.

54
Q

Give 5 ways in which dementia can be prevented.

A
  1. Stop smoking.
  2. Healthy diet.
  3. Regular exercise.
  4. Healthy weight.
  5. Low alcohol intake.

Neurology (20 decks)

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