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Clinical Neuroscience > Session 9: Dementia and Delirium > Flashcards

Session 9: Dementia and Delirium Flashcards

1
Q

Describe dementia.

A

A chronic progressive syndrome of insidious onset with cognitive decline due to disease of the brain.

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2
Q

Give general causes of confusion in elderly patients.

A

Delirium

Depression

Dementia

Drugs

Metabolic abnormalities

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3
Q

Give metabolic reasons for confusion.

A

Hypothyroidism

Hypercalcaemia

Vitamin B12 deficiency

Hydrocephalus

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4
Q

Give common drugs that can cause confusion.

A

Morphine

Cocaine

Alcohol

Zopiclone

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5
Q

What is dementia?

A

A decline in higher cortical function of a progressive nature.

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6
Q

How can dementia be divided?

A

Into early onset or late onset

Early = <65

Late = >65

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7
Q

Cognitive symptoms of dementia

A

Impaired memory (temporal)

Impaired orientation (temporal)

Impaired learning capacity (temporal)

Impaired judgment (frontal)

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8
Q

Non-cognitive symptoms.

A

Behavioural symptoms

Depression and anxiety

Psychotic features

Sleep symptoms such as insomnia or daytime drowsiness.

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9
Q

Give behavioural symptoms.

A

Agitation

Aggression

Wandering

Sexual disinhibition

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10
Q

Give psychotic features of dementia

A

Visual and auditory hallucinations

Persecutory delusions

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11
Q

How is a diagnosis of dementia made?

A

By exclusion of other causes of cognitive decline such as hypothyroidism, hypercalcaemia, B12 def, hydrocephalus or delirium.

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12
Q

Give types of dementia.

A

Alzheimer’s disease

Demntia with Lewy body

Vascular dementia

Fronto-temporal dementia

AIDS-Dementia Complex

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13
Q

Macroscopic features of AD.

A

Global atrophy of the brain.

Starts of temporal lobe and then also frontal and parietal. Not generally occipital.

Sulcus widening

Enlarged 3rd and 4th interventricular spaces as well as enlarged lateral ventricles.

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14
Q

Microscopic features of AD.

A

Senile amyloid plaques

Neurofibrillary tau tangles

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15
Q

What are the senile amyloid plaques made of?

A

Derived from proteolytic breakdown from beta-amyloid precursor protein.

This is found in normal aging brains as well but in much larger quantities in AD.

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16
Q

What are neurofibrillary tangles made of?

A

Tau protein (hyperphosphorylated)

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17
Q

Explain microscopic changes and neuronal death.

A

Since neurogenesis is limited in CNS neurons won’t be replaced and neuronal death is imminent.

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18
Q

What are the predominant neurones affected?

A

Cholinergic

Noradrenergic

Serotonergic

Somatostatic

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19
Q

Genetic test of AD.

A

Early-onset:

beta-amyloid precursor protein

Presenelin - 1

Presenelin - 2

Late-onset:

Apolipoprotein E gene

Genetic test is not common!

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20
Q

What are the usual presenting complaints of AD?

A

Bad memory

Bad spatial navigation

Difficulty in executive functions such as language, visuospatial functioning and calculation.

It also affets activities of daily living

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21
Q

Treatment of AD.

A

Acetyl Cholineesterase inhibitors such as donepezil, galantamine, rivastigmine.

Also can give Memantine which is a glutamate inhibitor.

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22
Q

Pathophysiology of dementia with lewy bodies.

A

Aggregation of alpha-synuclein protein which is spherical in shape.

They can be found in the cytoplasm.

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23
Q

Where do you usually see depositions of lewy bodies?

A

Substantia nigra

Temporal lobe

Frontal lobe

Cingulate gyrus

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24
Q

What are the three core clinical features of dementia with Lewy bodies?

A

Fluctuating cognition. Attention and alertness will vary.

Visual hallucinations

Features of Parkinsonism with a shuffling gait and flexed posture. (Usually no tremors etc…)

25
Q

How does Parkinson’s differ to dementia with Lewy bodies?

A

Parkinson has its parkinsonian features before its dementia.

Lewy body dementia has its parkinsonian features after its dementia.

26
Q

Why should you not give antipsychotics (dopamine antagonists) to a patient with Lewy bodies dementia?

A

It can cause neuroleptic malignant syndrome which is a psychiatric emergency of:

Fever

Encephalopathy

Tachycardia

Tachypnoea

Eleveated creatine phosphokinase

Rigidity

27
Q

Treatment of dementia with lewy bodies.

A

ACh esterase inhibitors as lewy bodies use up the ACh.

28
Q

2nd most common cause of early-onset dementia.

A

Fronto-temporal dementia (AD still no. 1)

29
Q

Peak onset of fronto-temporal dementia.

A

55-65 y/o

With an atrophy of frontal and temporal lobe

30
Q

Symptoms of FTD.

A

Behavioural disinhibition

Personality changes

Social conduct impairment

Disinhibited social features and apathy (without depression)

Broca’s aphasia

Wernicke’s aphasia

Primitive reflexes such as grasp reflex or palmomental reflex.

Short/long-term memory impairment

This disorder can early on mimic depression.

31
Q

What is vascular dementia?

A

Occurs due to cerebrovascular disease whether it is ischaemic or haemorrhagic.

Multiple lacuna strokes e.g.

32
Q

Risk factors of vascular dementia.

A

Hypertension

Smoking

Diabetes

Vascular disease

Alcohol

33
Q

How does the decline in cognition differ between AD compared to vascular dementia.

A

A step-wise fashion in vascular induced by a cerebrovascular event. The symptoms are usually focal.

AD has a more gradual progressive decline.

34
Q

Treatment of vascular dementia.

A

Manage risk factors.

Do not give ACh esterase inhibitor unless you suspect co-morbidity of e.g. AD, Parkinson’s or Lewy bodies.

35
Q

Pathophysiology of AIDS-Dementia Complex (ADC)

A

An increasing prevalence as people with HIV live to be much older now.

It is due to HIV-infected macrophages will enter the brain and cause indirect damage to neurones.

It is non-specific and global.

36
Q

Explain the progression of ADC.

A

Insidious (slow) onset but once it has been established it has a rapid progression.

37
Q

Presenting complaints of ADC.

A

Cognitive impairment

Psychomotor retardation

Tremors

Ataxia

Dysarthria

Incontinence

Note the cerebellar impairments which is indicative of the dementia being global.

38
Q

Treatment of ADC

A

Anti-virals

39
Q

What tests need to be done within six months of recording a new diagnosis of dementia.

A

FBC

U&Es

ESR or CRP

TFT (thyroid)

LFTs

Random blood sugar

Vitamin B12 and folate

Syphilis only if history suggest it.

40
Q

What is memantine?

A

An NMDA antagonist

Given late in dementia (AD or Lewy body)

AChe’s are given in mild to moderate AD.

41
Q

Explain the bio-psycho-social approach to dementia.

A

Mobility problems that can arise

Driving

Talk about problems that will arise.

Explain results

Discuss finance and wills

Discuss day care and possible residential/nursing home placements

42
Q

Effects on carers and self in dementia.

A

Physical stress

Emotional stress

Psychological stress

Socio-economic stress

43
Q

What is delirium?

A

An acute onset of altered mental status and fluctuating course

Inattention

Disorganised thinking and confusion

An altered level of consciousness

44
Q

How is delirium assessed?

A

Confusion Assessment Method (CAM)

45
Q

Give general causes of delirium

A

Drugs toxicity - e.g. withdrawal like alcohol, benzodiazepine, cocaine or coffee. Also use of anti-cholinergics.

Endocrine

Liver failure

Intracranial

Renal failure

Infections

Urinary retention/ constipation

Metabolic

46
Q

Give endocrine causes of delirium.

A

Hyper/hypothyroidism

Addison’s

Cushing’s

47
Q

Intracranial causes of delirium.

A

Stroke

Haemorrhage

Cerebral abscess

Epilepsy

48
Q

Common infections causing delirium.

A

Pneumonia

UTI

Sepsis

Meningitis

Infections are by far the most common cause of delirium

49
Q

Metabolic causes of delirium

A

Electrolyte imbalance (sodium, calcium, magnesium, phosphate, glucose)

Hypoxia

50
Q

Pathophysiology of delirium

A

Possibly cholinergic-dopaminergic imbalance

51
Q

Ix of delirium

A

Blood tests such as FBC, UEs, CRP, TFTs, LFTs, glucose, blood culture.

Urine dipstick

O2 sats

CXR

Drug history

52
Q

Treatment of delirium

A

Treat underlying cuase

Calm environment

Rehydration

Haloperidol only if essential

53
Q

How does delirium differ from dementia?

A

Acute onset which is often reversible.

Clouded consciousness

Fluctuating course with possible visual hallucinations (in dementia hallucinations are rare)

Can be aggressive

The symptoms are often worse at start and end of day. (May be related to cortisol levels)

54
Q

Types of delirium

A

Hypoactive

Hyperactive

55
Q

CP of hypoactive delirium

A

Withdrawn

Quiet

Sleepy

(often confused with something else)

56
Q

CP of hyperactive delirium

A

Restless

Agitated

Aggressive

57
Q

How to assess a patient who is unconscious.

A

1 - Breathing + pulse

2 - Lie them on their left side

3 - Call for help

4 - Sternal rub, trapezius squeeze, fingernails pressure test

5 - Ensure that patient is stable

6 - GCS

58
Q

Prognosis of delirium.

A

Increases risk of dementia

Associated with mortality

Patients often have lenghthy hospital stays and high risk of re-admissions.

Clinical Neuroscience (22 decks)

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