Dementia Flashcards

1
Q

What is the most common cause of dementia?

A

Alzheimer’s disease - fatal neurodegenerative disorder characterised by progressive cognitive, social and functional impairment

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2
Q

Is there a cure or treatment?

A

No cure, treatment with acetylecholinesterase inhibitors having modest symptomatic benefit in the early stages

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3
Q

In what age group are rarer forms of dementia more prevalent?

A

Younger population = more prevalent rarer forms of dementia; for late onset dementia (i.e. >65) it is usually Alzheimer’s

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4
Q

Other than Alzheimer’s disease, what are some other types / causes of dementia?

A

Vascular dementia

Frontotemporal dementia

Dementia with Lewy bodies

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5
Q

What are some potentially reversible causes of dementia?

What are some rarer causes of dementia?

A

Potentially reversible = depression, alcohol related brain damage, endocrine (hypothyroidism, Addison’s, Cushing’s), B1/B12/B6 deficiency, benign tumours, infections etc.

Rare = progressive supranuclear palsy, multiple system atrophy, corticobasal degeneration, Huntington’s disease, etc.

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6
Q

How does cognitive function compare between dementia and aging?

A

Dementia - curve for cognitive function decreases much faster than in aging

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7
Q

Why is cognition difficult to assess clinically?

A

Dependent on: quality of sleep, UTIs, taking sleeping tablets, diet, infections etc.

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8
Q

Why is it difficult to accurately diagnose dementia in the clinic?

A

Disease follows heterogenous course
In old age, the disease presents with multiple co-morbidities
Mixed and uncertain pictures (of the brain)
Clinical history, function of the patient and how they change is most important for diagnosis

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9
Q

How is dementia diagnosed clinically?

A
Usually referral to memory clinic
Patient goes for clinical interview - take detailed history (most important)
Examination
Investigations 
Diagnosis 
Management
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10
Q

What is the checklist for the clinical interview for patients and their friend / partner / children etc.?

A
Memory
Language 
Numerical skills e.g. manage their finances
Executive skills
Visuospatial skills
Neglect phenomena 
Visual perception 
Route finding and landmark identification 
Personality and social conduct 
Sexual behaviour 
Eating 
Motivation / apathy
Anxiety / agitation
Delusions / hallucinations 
Activities of daily living
Ask about mood - may be depressed, so medications e.g. SSRIs can reverse the declining cognitive function
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11
Q

How can the speed of deterioration point to the type of dementia a patient might have?

A

Slow deterioration = most likely Alzheimer’s

Fast deterioration = rarer causes, maybe vascular dementia

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12
Q

Define dementia:

A

Severe loss of memory and other cognitive abilities which leads to impaired daily function (regardless of underlying cause)

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13
Q

What examination is usually taken from the patient?

A

Neurological tests:
e.g. test CNs, upper limbs and lower limbs (gait), focused tests (e.g. frontal lobe), perception and cognition tests, mental state tests etc.

MMSE - Mini mental state examination

ACE - Addenbrook’s Cognitive Assessment

Head turning sign - patient turns to partner / friend and waits for them to answer as they either don’t know or is unsure of the answer

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14
Q

What sort of investigations take place?

How may these investigations show cognitive impairment?

A
Neuropsychology
Bloods (look for cause of cognitive impairment- may be reversible) - full blood count, inflammatory markers, thyroid function, biochemistry and renal function, glucose, B12 and folate, clotting, syphilis serology, HIV, caeruloplasmin 

MRIs - as disease progresses, narrow gyri and widened sulci, venticles dilated and englarged, volume loss of medial temporal lobe esp. hippocampus (CSF fills the space instead) - look at coronal T1 MRIs

PET scans - contrast on PET scans show in vivo amyloid plaque in brain and they correspond with amyloid plaque presence post-mortem (the more amyloid, the more progressed the dementia)

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15
Q

What are the common possible diagnoses after taking patient history, examining the patient and conducting further investigations?

A
Alzheimer's 
Vascular
Lewy body
STD
Depression
Delirium
Nothing
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16
Q

What are some possible management options after the diagnosis?

A
Acetylcholinesterase inhibitors for alzheimer's 
Watch adn wait if unsure about diagnosis
Treating behavioural symptoms 
Anti-psychotics 
Anti-depressants
Refer to therapy
Occupational therapy
17
Q

How can conditions be ruled in or out? What are some common presentations?

Delirium - 
Depression - 
Alzheimer's - 
Vascular - 
Dementia with Lewy bodies - 
Frontotemporal - 
Rapidly progressing -
A

Delirium - usually acute, organic (physical) cause

Depression - mood

Alzheimer’s - subtle, insidious amnestic / non-amnestic presentation

Vascular - related to cerebrovascular diseases with step wise deterioration with or without multiple infarcts

Dementia with Lewy bodies - cognitive impairment within 1 year of Parkinsonian symptoms, visual hallucinations, fluctuating cognition

Frontotemporal - behaviour variant FTD, semantic dementia, progressive non-fluent aphasia

Rapidly progressing - dementia progresses fast

18
Q

How does Alzheimer’s present clinically?

A

Patient often feel’s there is nothing wrong, thinks they are aging
Short term memory loss - forggeting things they have done or watched, asking the same questions again and again
Forgetting medications
Forgetting common routes e.g. to shops, children’s homes, etc.
Episodic memory loss
Irritable

19
Q

What are the biomarker patterns in Alzheimer’s?

A

Amyloid plaques for first, then Tau mediated neuronal injury and dysfunction
This causes changes in brain structure leading to decrease in cognitive function

20
Q

How does B-amyloid in CSF fluid compare in normal people to Alzheimer’s patients?

How does CSF Tau compare in normal people to Alzheimer’s patients?

A

Significantly lower CSF Beta-amyloid in Alzheimer’s patients than in normal control group

Significantly higher CSF Tau in Alzheimer’s patients than in normal control group

21
Q

How does dementia with Lewy bodies normally present?

A

Associated with fluctuating cognition
Different cognitive profile to Alzheimer’s
Often visual hallucinations
REM sleep disorder - restless at night, shouting etc.
Development of symptoms associated with Parkinson’s
High risk of falls

22
Q

What is the biochemical cause for dementia with Lewy bodies?

A

Aggregation of alpha-Synuclein leading to deposition of lewy bodies and so symptoms

23
Q

How do MRIs and PET scans show differences between alzheimer’s and dementia with lewy bodies?

A

Alzheimer’s = medial temporal lobe and hippocampal atrophy

Dementia with lewy bodies = preserved hippocampal atrophy

24
Q

What is a DATscan, how is it conducted, and what are the differences in imaging between Alzheimer’s and dementia with lewy body patients?

A

DATscan = brain imaging
Uses 123-Iodine tracer = images dopamine transporter
Alzheimer’s = dopamine transporters in caudate putamen
Dementia with Lewy body = decreased dopamine transporter in caudate putamen

25
Q

How does frontotemporal dementia (FTD) present clinically?

A

Aphasia - using the wrong words, agrammatical
Significant anomia
Difficulty understanding speech
Angry, irritable, frustrated when misunderstood
Rude on number of occasions
Obsessive with routine
Lesser personal hygiene
Spontaneous conversation limited and dysfluent

26
Q

How does FTD show up on blood tests and MRIs?

A

Blood tests usually normal

MRIs often show significant volume loss in the temporal lobes and frontal opercula (more so on the right)