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MRCPsych Part B - Al-Rashid Hospital > Old Age Psychiatry > Flashcards

Old Age Psychiatry Flashcards

1
Q

Changes in the worlds population from 2000-2050?

A

Worlds population >60 years will double from 11% to 22%

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2
Q

By how much is the absolute number of people >60 years of age expected to increase?

A

From 605 million to 2 billion from 2000-2050

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3
Q

How many people in the UK are >65?

A

One sixth of the population

10 million

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4
Q

How many people are expected to be >65 years of age in the UK in 2050?

A

19 million

1/4 of the population

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5
Q

How many people in the UK are over 80?

A

3 million

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6
Q

What does the national Service Framework for older people (2001) state?

A

Older people with MH problems should have access to specialist services

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7
Q

What does Everybodys Business (2005) state?

A

Older people’s MH problems require input from both health and social care, physical and MH services and mainstream and specialist services.

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8
Q

What does No Health Without Mental Health (2011) state?

A

Services should be age appropriate non discriminatory

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9
Q

Needs based criteria for Older Peoples MH Services for commissioners by RcPsych?

A

People of any age with primary dementia
People with MI and physical illness or frailty, which contribute or complicate management of their MI
People with psychosocial difficulties related to ageing process or EoL issues or who feel their needs may be best met by a service for older people

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10
Q

What % of carers suffer from depression at some stage?

A

30%

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11
Q

What are the 10 key points from JCPMH guidance for commissioners of older peoples MH services?

A

Older people will form a larger proportion of the population
Older peoples MH services benefit from an integrated approach with social care
Older peoples MH services need to work closely with primary care and community services
Services must be commissioned on basis of need and not age alone
Older peoples MH services must address needs of people with functional illness as well as dementia
Older people often have a combination of MI and physical illness
Older peoples MH services must be disciplinary
Older people with MH needs should have access to community CRHTTs
Older people with MH needs respond well to psychological input
Older people should have dedicated liaison services in acute hospitals

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12
Q

What domains need to be taken into account when assessing an older adult with MH problems?

A

Cognitive assessment
Functional abilities
Physical health issues and how these impact on MH
Role of imaging in dementia daignosis
Assessment of carer needs and holistic approach to care
Physical examination
Assessment of capacity issues

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13
Q

Why is medication regimen and timing so important in Parkinsons?

A

Failure can result in delirium, depression, slowed cognition and anxiety

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14
Q

How many patients with PD have depression?

A

2/3

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15
Q

How many patients with PD develop dementia?

A

40%

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16
Q

Common cognitive deficits in Parkinsons?

A 
Higher executive dysfunction
Attention
Memory
Visuomotor processing
Visual attention
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17
Q

How many patients with stroke have delirium?

A

30-40% after one week

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18
Q

Which diseases commonly result in Charles Bonnet?

A

Macular Degeneration
Cataracts
Diabetic retinopathy

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19
Q

Which diseases are associated with psychotic sx in the elderly?

A

Auditory impairment

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20
Q

How do metabolic changes during illness accentuate emotional response to it?

A 
Dehydration
Electrolyte imbalance
Endocrine changes
Infection
can all produce affective sx
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21
Q

How common is depression in people with chronic physical health problems?

A

2-3 times more common

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22
Q

How many patients with chronic physical illness will have depression?

A

20%

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23
Q

First line treatment for depression in chronic physical illness

A

SSRI - keep in mind interactions

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24
Q

Intracranial reversible causes of dementia

A

Normal pressure hydrocephalus
Subdural haematoma
Cerebral tumours
Tertiary syphilis

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25
Q

Systemic disorders which can cause reversible dementia

A 
Alcoholism
Anoxia
Low BM
Myxoedema
Vitamin deficiencies
Drug or chemical poisoning
Pseudodementia
Renal/hepatic disease
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26
Q

How many diagnosis of dementia are due to young onset of dementia?

A

12%

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27
Q

How can alcohol use lead to dementia?

A

Damage to limbic structures and frontal lobes leading to memory and executive impairments

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28
Q

Which impairment in alcohol-induced dementia can improve with abstinence?

A

Memory impairment

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29
Q

Which type of memory is affected in alcohol-induced dementia?

A

Autobiographical

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30
Q

What does neuroimaging show in alcohol-induced dementia?

A

Generalised cerebral atrophy with frontal preponderance

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31
Q

What happens in normal pressure hydrocephalus?

A

Dilatation of cerebral ventricles - usually 3rd ventricle, with normal CSF pressure at P.

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32
Q

Triad of sx of normal prssure hydrocephalus?

A

Dementia
Gait ataxia
Urinary incontinence

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33
Q

Population prevalence of NPH in the elderly

A

0.4%

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34
Q

Which sx precedes all others in NPH?

A

Mildly broad based, symmetrical short stepped gait

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35
Q

What type of dementia occurs in NPH?

A

Progressive slowing of cognitive and motor functioning consistent with pattern of subcortical dementia

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36
Q

What is the pattern of subcortical dementia?

A

Pronounced slowness of thought
Difficulties in sustaining, switching attention
Difficulties in planning

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37
Q

How many cases of NPH are idiopathic?

A

50%

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38
Q

What are 50% of NPH non-idiopathic cases due to?

A

Mechanical obstruction of CSF flow across meninges due to infection, trauma, SAH etc

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39
Q

Which sx is late sx of NPH?

A

Urinary incontinence

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40
Q

What does CT show in NPH?

A

Increased size of lateral ventricles and thinning of cortex

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41
Q

Treatment of NPH

A

Surgical placement of ventriculo-peritoneal shunt

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42
Q

Which sx is most likely to improve with treatment of NPH?

A

Gait impairment

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43
Q

What is related to good outcome of NPH?

A

Mild dementia

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44
Q

Why are subdural veins more vulnerable to tears in the elderly?

A

Cortical shrinking

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45
Q

When should subdural haematoma (SDH) be suspected?

A

Changing pattern in cognitive function with risk factors

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46
Q

Risk factors for SDH

A 
Post trauma - elderly after fall, HI
Cerebral atrophy
Alcoholism
Epilepsy
Clotting disorders
Predisposing drugs such as Warfarin, Aspirin
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47
Q

How many SDH cases have bilateral SDH?

A

30%

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48
Q

How many patients with SDH have a history of HI?

A

50%

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49
Q

Common features of SDH

A

Headache
Drowsiness
Altered consciousness
Confusion - fluctuating severity

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50
Q

What does CT show in SDH

A

Crescent shaped haematoma compressing sulci and midline shift

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51
Q

When might CT not show a SDH?

A

First 3 weeks as clot is isodense during early phase

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52
Q

Treatment of SDH

A

Surgical - burr holes

Conservative - steroids

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53
Q

Complications of surgical treatment of SDH

A

Seizures

Re-bleeding

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54
Q

Mortality of SDH

A

10%

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55
Q

Which patients with SDH have highest mortality?

A

Depressed consciousness level

Bilateral SDH

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56
Q

How does Huntingtons dementia present?

A

Frontal dementa

movement disorder

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57
Q

Prominent deficits in Huntingtons dementia?

A 
Attention
Semantic verbal fluency
Processing speed
Executive function
Recall more affected than recognition
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58
Q

Key diagnostic test for dementia in MS

A

MRI

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59
Q

Problem with MRI scan in elderly with MS

A

Distinguishing between demyelination and vascular damage can be difficult in the elderly

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60
Q

How is diagnosis of dementia in MS confirmed?

A

CSF and evoked potentations

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61
Q

Where is Prion protein coded?

A

PRNP gene on Chromosome 20

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62
Q

When does prion disease occur?

A

When protein undergoes changes which render it insoluble

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63
Q

Which diseases are caused by prions?

A

Spongiform encephalopathies - transmissible dementias

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64
Q

What are the four forms of prion dementia?

A

Kuru
CJD
Fatal familial insomnia
Gerstmann Straussler Syndrome

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65
Q

Worldwide prevalence of sporadic CJD

A

0.1 per 100,000

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66
Q

Which prion disease is most common?

A

CJD

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67
Q

What causes CJD?

A

Pathological form of prion protein PrPsc

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68
Q

What is the normal form of the prion protein?

A

PrPc

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69
Q

Difference between PrPc and PrPsc

A

PrPsc is resistant to proteases, thus leading to accumulation and rapid degenerative changes

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70
Q

Onset of CJD

A

After 5th decade but can occur at any age

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71
Q

Clinical picture of CJD

A 
Rapidly deteriorating dementia
Myoclonus
Cortical blindness
Cerebellar and EPSE
Death within one year
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72
Q

When do fulminant sx develop in CJD?

A

Within weeks

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73
Q

Which sign becomes prominent as CJD progresses?

A

Myoclonus

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74
Q

How many CJD cases are sporadic?

A

85%

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75
Q

How many CJD cases are genetic?

A

10%

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76
Q

How many cases of CJD result from iatrogenic transmission of transplant surgery?

A

5%

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77
Q

What types of transplant surgery can lead to CJD?

A

Transplant of dura, corneal grafts and pituitary growth home

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78
Q

What does CT show in CJD?

A

Atrophy of cortex, worse centrally

Atrophy of cerebellum

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79
Q

What does MRI show in CJD?

A

Non-specific basal ganglia hyperintensities

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80
Q

What does EEG show in CJD

A

Periodic bi or triphasic discharges against slight low voltage background

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81
Q

In which type of CJD is EEG change not seen?

A

Variant CJD

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82
Q

CSF findings in CJD

A

14-3-3 protein elevated.

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83
Q

What is 4-3-3?

A

Normal neuronal protein

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84
Q

Definitive diagnosis of CJD

A

Post-mortem microscopic exam:

spongiform neural degeneration and gliosis throughout cortical and subcortical grey matter, sparing white matter tracts

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85
Q

Treatment of CJD

A

Symptomatic; valproate and clonazepam to reduce movement disorder

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86
Q

What is vCJD?

A

Bovine Spongiform Encephalopathy

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87
Q

What is Bongine Spongiform Encephalopathy?

A

Prion disease of cows caused by cattle feeds that contained CNS material from infected material.

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88
Q

Incubation period between ingestion of contaminated meat and development of vCJD?

A

<20 years

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89
Q

Who does vCJD typically affect?

A

Men in 20s

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90
Q

Characteristics of vCJD?

A

Anxiety and depressive sx
Personality changes
Progressive dementia
Ataxia and myoclonus

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91
Q

Course of vCJD

A

1-2 years followed by death

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92
Q

What is diagnostic of vCJD?

A

Pulvinar sign; symmetric high-signal-intensity changes affecting pulvinar and medial areas of thalamus and tectal plate on FLAR sequence in MRI

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93
Q

How many patients with vCJD had pulvinar sign

A

> 70%

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94
Q

Does CSF in vCJD show 14-3-3 protein?

A

Yes

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95
Q

Aside from MRI, how else can vCJD be diagnosed?

A

Immunostaining from tonsillar biopsy

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96
Q

EEG in vCJD?

A

No distinctive changes, sometimes diffuse slow waves

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97
Q

Most common Dementia in the developed world?

A

Alzheimers

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98
Q

Onset of Alzheimers

A

40-90

Most often >65

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99
Q

Predicted risk of developing Alzheimers in first-degree relatives

A

15-19%

5% in controls

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100
Q

Relative risk of Alzheimers if you have a first-degree relative with the disease?

A

3-4 times relative to the risk in controls

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101
Q

Risk of Alzheimers at the age of 60

A

1%

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102
Q

Risk of Alzheimers at age of 65

A

5%

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103
Q

Risk of Alzheimers at age 85

A

40%

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104
Q

How does risk of Alzheimers correlate with age?

A

Doubles every 5 years

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105
Q

Risk of people >75 for Alzheimers vs Vascular Dementia

A

Risk is 6x greater for alzheimers than for Vascular DEmentia

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106
Q

In which group of patients is onset of Alzheimers earlier?

A

FHx of Alzheimers

107
Q

Proven risk factors of Alzheimers

A

Age
Downs
Apolipoprotein 4 allele

108
Q

Likely risk factors of Alzheimers

A

Female
HI
Postmenopausal oestrogen decline

109
Q

Possible risk factors of Alzheimers

A

FHx of Downs
FHx of Parkinsons
Vascular factors

110
Q

Proven protective factors of Alzheimers

A

Apolipoprotein 2 allele

111
Q

Possible protective factors of Alzheimers

A

Smoking
NSAIDs
Oestrogwn
Premorbid intelligence and education

112
Q

Which genes are associated with early onset Alzheimers?

A

Presenilin 2 gene
Presenilin 1 gene
Beta amyloid precursor protein gene

113
Q

Which chromosome is Presenilin 2 gene on?

A

1

114
Q

Which chromosome is Presenilin 1 gene on?

A

14

115
Q

Which chromosome is beta amyloid precursor protein gene on?

A

21

116
Q

Where on chromosome 21 is beta amyloid precurser protein gene found?

A

Long arm

117
Q

What is the major constituent of senile plaques in Alzheimers?

A

Beta amyloid protein

118
Q

Describe structure of the beta amyloid protein

A

42 amino acid peptide that is a breakdown product of amyloid precursor protein

119
Q

What is the breakdown product of amyloid precursor protein?

A

Beta amyloid protein

120
Q

Why are people with Downs at increased risk of Alzheimers?

A

They have three copies of the amyloid precursor protein gene (found on long arm of chromosome 21)

121
Q

What can cause excessive deposition of beta amyloid protein?

A

Downs

Mutation on codon 717 in amyloid precursor protein gene

122
Q

What imaging can be used to confirm diagnosis of Alzheimers?

A

Amyloid PET scanning

123
Q

What increases risk of late onset Alzheimers?

A

Apolipoprotein allele 4

124
Q

Where can Apolipoprotein allele 4 be found?

A

Chromosome 19

125
Q

Risk of Alzheimers if you have one copy of the Apolipoprotein allele 4 gene?

A

3x

126
Q

Risk of Alzheimers if you have two copies of the Apolipoprotein allele 4 gene?

A

8x

127
Q

Criteria for diagnosis of probable Alzheimers

A

Clinical examination and documented by MMSE, Blessed Dementia scale or confirmed by neuropsychological tests.

128
Q

What features are required for a diagnosis of Alzheimers?

A

Deficits in 2 or more areas of cognition
Progressive worsening memory and other cognitive functions
No disturbance of consciousness
Absence of system disorders or other brain diseases that could account for progressive deficits

129
Q

What is CT used for in diagnosis of Alzheimers?

A

Exclude treatable causes

130
Q

CT findings in Alzheimers

A

Cortical atrophy; particularly over parietal and temporal lobes
Dilatation of third ventricles

131
Q

What CT findings correlate with cognitive impairment?

A

Dilatation of 3rd ventricles

132
Q

MRI findings in Alzheimers

A

Reduced grey matter, hippocampus, amygdala and temporal lobe volumes

133
Q

SPECT findings in Alzheimers

A

Reduction in blood flow in temporal and parietal regions

134
Q

PET findings in Alzheimers

A

Reduced blood flow and metabolism in temporal and parietal regions

135
Q

MRS findings in Alzheimers

A

Abnormal synthesis of membrane phospholipids early in disease

136
Q

Amyloid PET imaging findings in Alzheimers

A

Deposition of beta amyloid

137
Q

What type of memory loss is seen in Alzheimers?

A

Short-term memory initially, then long term memory deficit later
Amnesia universal, mainly for recent events

138
Q

What type of disorientation is seen in Alzheimers?

A

For time

139
Q

Language findings in Alzheimers?

A 
Expressive and receptive dysphasia
Lexical anomia (word finding difficulties)
140
Q

Other cognitive deficits in Alzheimers

A

Apraxia; inability to perform coordinated learnt motor tasks
Agnosia
Impaired visuospatial skills
Impaired exectutive function

141
Q

Psychiatric sx of Alzheimers

A

Delusions 15%
Hallucinations 10-15%
Depression 20%

142
Q

Most common psychiatric sx in Alzheimers

A 
Apathy - 59%
Depression - 58%
Irritability - 44%
anxiety - 44%
Agitation - 41%
143
Q

Most common behavioural sx of Alzheimers

A

Wandering

Aggressive outbursts

144
Q

Average survival expectation for patients with Alzheimers?

A

8 years

145
Q

Sx correlated with progression of Alzheimers?

A 
Increased agitation
Frequent emotional outbursts
Night pacing
Poor sleep
Wandering
146
Q

Sx in terminal phase of Alzheimers?

A

Profound disorientation
Amnesia
Incontinent of urine and faeces

147
Q

Areas of cognition tested in AMTS

A

Memory

Orientation

148
Q

Cut off for AMTS?

A

<8/10

149
Q

Areas of cognition tested with MMSE

A 
Orientation
Memory
Concentration
Language
Praxis
Gnosis
150
Q

Cut-off for MMSE?

A

24/30

151
Q

Most widely used cognitive test in Old age Psychiatry?

A

MMSE

152
Q

What test is best for screening global cognitive dysfunction?

A

MMSE

153
Q

What types of variations is MMSE subject to?

A

Age
Socio-economic status
Educational achievement

154
Q

What is MMSE heavily weighted towards?

A

Verbal performance

155
Q

What does CAPE stand for?

A

Comprehensive Clifton Assessment for the Elderly

156
Q

What does CAPE assess?

A

Level of disability and estimate need for care

157
Q

What is the DRS?

A

Clinical Dementia Rating Scale

158
Q

Areas of cognition assessed by DRS?

A 
Memory
Orientation
Judgement & Problem solving
Community Affairs
Homes and Hobbies
Personal Care
159
Q

What scale is commonly used to assess severity and stage of Alzheimers?

A

DRS

160
Q

Cognitive areas of assessment of Addenbrookes

A 
Orientation
Registration
Recognition
Recall
Perceptual abilities
Language
Verbal fluency
161
Q

Cognitive areas of assessment of NPI

A 
Delusions
Hallucinations
Agitation
Depression
Anxiety
Euphoria
Apathy
Disinhibition
Irritability
Aberrant
162
Q

What does NPI do?

A

Rates frequency and severity of a range of neuropsychiatric sx.

163
Q

What does NPI-NH measure?

A

Rates of occupational disruptiveness, a measure of caregiver distress.

164
Q

How long does CAMCOG take to complete?

A

40 minutes

165
Q

What does CAMCOG give a score out of?

A

104

166
Q

Cognitive areas of assessment tested by CAMCOG?

A 
Orientation
Comprehension
Perception
Memory
Abstract Thinking
167
Q

What does Clock drawing test .. test?

A

Praxis

Higher executive function

168
Q

What drugs are used to treat mild to moderate cognitive impairment in Alzheimers?

A

Cholinesterase inhibitors

169
Q

Give some examples of cholinesterase inhibitors used in the treatment of mild Alzheimers

A

Donepezil
Rivastigmine
Galantamine

170
Q

How do cholinesterase inhibitors work in Alzheimers?

A

Reduce inactivation of Acetylcholine and thus potentiate cholinergic neurotransmitter, which in turn produces a most improvement in memory and goal-directed thought

171
Q

Plasma half-life of Donepezil

A

70 hours

172
Q

Plasma protein binding of Donepezil

A

Almost 100%

173
Q

How does Donepezil work?

A

Highly selective reversible inhibition of acetylcholine.

174
Q

Side effects of Donepezil

A 
Mainly GI:
Nausea/vomiting
Diarrhoea
Anorexia
Headache/dizziness
Syncope
Muscle cramps
175
Q

Which Alzheimers drugs cause more neuropsychiatric adverse effects?

A

Rivastigmine

Galantamine

176
Q

How does Galantamine work?

A

Direct nicotinic stimulatory action

Cholinesterase inhibitor

177
Q

Which drug improves sx of dementia in Parkinsons?

A

Rivastigmine

178
Q

Which sx of Parkinsons does Rivastigmine improve?

A

Cognition

ADLs

179
Q

Most common SEs of Rivastigmine?

A

Nausea/vomiting

Anorexia

180
Q

What does Rivastigmine work on?

A

Acetylcholinesterase

Butyrylcholinesterase

181
Q

How can Rivastigmine be taken?

A

PO

Transdermal patch OD

182
Q

What augmentation is beneficial in Alzheimers?

A

Memantine and Donepezil

183
Q

What does Memantine do?

A

Protects neurons from excessive glutamate which may be neurotoxic

184
Q

What can Memantine be used for?

A

DAT
Vascular
Mixed dementia

185
Q

How does Memantine work?

A

Non-competitive, PCP-site NMDA antagonist

186
Q

Most common SEs of Memantine?

A 
Dizziness
Headache
Fatigue
Diarrhoea
Gstric pain
187
Q

Which drug is used in treatment of moderate to severe Alzheimers?

A

Memantine

188
Q

Which patients with mild Alzheimers is Memantine used in?

A

When cholinesterase inhibitors are contraindicated i.e. severe cardiac conduction defects, severe asthma

189
Q

Why is Tacrine not used for Alzheimers?

A

Potential for hepatotoxicity

190
Q

Starting dose of Donepezil for Alzheimers?

A

5mg OD

191
Q

Treatment dose of Donepezil for Alzheimers?

A

10mg OD

192
Q

Starting dose of Rivastigmine for Alzheimers?

A

1.5mg BD

193
Q

Treatment dose of Rivastigmine for Alzheimers?

A

6mg BD

194
Q

Starting dose of Galantamine for Alzheimers?

A

4mg BD

195
Q

Treatment dose of Galantamine for alzheimers?

A

12mg BD

196
Q

Starting dose of Memantine for Alzheimers?

A

5mg OD

197
Q

Treatment dose of Memantine for Alzheimers?

A

10mg OD

198
Q

Recommendations from Committee on Safety of Medicines re use of Olanzapine and Risperidone for Dementia?

A

Each associated with 2x increase in risk of stroke and therefore should not be used

199
Q

Poor prognostic factors in Alzheimers

A 
Male
Onset <65
Prominent behavioural problems
Parietal lobe damage
Depression
Severe cognitive deficits
Absence of misidentification syndrome
200
Q

Prevalence of psychosis in people with Alzheimers?

A

30-50%

201
Q

Which type of psychosis is more common in Alzheimers?

A

Delusions

202
Q

Common delusions in Alzheimers

A 
Capgras
Phantom boarder
Mirror sign
TV sign
Magazine sign
203
Q

What is phantom boarder?

A

False belief that guests are living in a persons home

204
Q

What is the mirror sign?

A

Individual identifies his or her own image as someone elses

205
Q

What is the TV sign?

A

Misidentification of TV images as real

206
Q

What is the magazine sign?

A

Misidentification of magazine images as real and existing in 3D

207
Q

What is the second most common cause of dementia?

A

Vascular

208
Q

How many cases of dementia are vascular?

A

20%

209
Q

What is the NINCDS-AIREN criteria for vascular dementia?

A

Evidence of CVD both on examination and brain imaging

Relationship between onset of dementia and CVD

210
Q

How can one show a relationship between onset of dementia and CVD?

A

Either dementia occurring within 3 months of a stroke or

Abrupt deterioration in cognitive function or fluctuating stepwise course

211
Q

Most prevalent neurological sx in Vascular Dementia

A

Reflex asymmetry

212
Q

What sx are associated with measures of small vessel disease?

A 
Dysarthria
Dysphagia
Parkinsonian gait disorder
Rigidity
Hypokinesia
213
Q

What sx were more likely observed in vascular dementia in the presence of a cerebral infarct?

A 
Aphasia
Reflex asymmetry
Hemianopia
Hemimotor dysfunction
Hemisensory dysfunction
Hemiplegic gait
214
Q

What are the three subtypes of Vascular dementia>

A

Cognitive deficits following single stroke
Multi-infarct dementia
Progressive smell vessel disease - Binswanger’s disease

215
Q

When are cognitive deficits following stroke often seen?

A

Following midbrain or thalamic strokes

216
Q

What happens in multi-infarct dementia>

A

Multiple strokes leads to stepwise deterioration.

Follows a number of minor ischaemic events

217
Q

What type of dementia is Binswangers disease?

A

Subcortical

218
Q

Characteristics of Binswangers disease?

A 
Slow intellectual decline
Slowness of thought
Decreased STM
Disorientation
Motor problems; gait, dysarthria
219
Q

What happens in Binswangers disease?

A

Multiple microvascular infarcts of perforating vessels lead to progressive lacunae formation

220
Q

What does MRI show in Binswangers disease?

A

Small distinct infarcts (lacunae) or more generalised white matter hyperintensities (leukoariasis)

221
Q

Risk factors of Vascular Dementia

A 
Old age
HTN
IHD
Smoking
EtOH
High lipid levels
AF
FHx
Valvular disease
Atrial myxoma
Carotid artery disease
APOE4 allele
Polycythaemia
Sickle cell anaemia
Coagulopathies
222
Q

What is Haschinski Ischemic score index?

A

Allows quantification of likelihood of patient having vascular rather than degenerative dementia

223
Q

Which dementia is more common in males?

A

Vascular

224
Q

Which dementia is more common in females?

A

Alzheimers

225
Q

Which dementia has focal neurological signs?

A

Vascular

226
Q

Which dementia has loss of insight?

A

Alzheimers

227
Q

Which dementia has mood sx?

A

Alzheimers

228
Q

Which dementia has somatic complaints?

A

Vascular

229
Q

What is CADASIL?

A

Form of vascular dementia

230
Q

What does CADASIL stand for?

A

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy

231
Q

How is CADASIL transmitted?

A

AD trait with high penetrance

232
Q

Where is CADASIL gene?

A

Long arm of chromosome 19

233
Q

How do patients with CADASIL gene present?

A

Recurrent stroke at age of 40-50

Hx of migraine

234
Q

What do patients with CADSIL later develop?

A

Subcortical dementia

Pseudobulbar palsy

235
Q

What does MRI show in CADSIL?

A

Widespread white matter changes

236
Q

What does CT show in vascular dementia?

A

Increased number of infarcts

237
Q

What does MRI show in vascular dementia?

A

White matter lesions more numerous and severe than Alzheimers

238
Q

What does SPECT show in vascular dementia?

A

Irregular perfusion deficits

239
Q

What does PET show in vascular dementia?

A

Cerebral blood flow and metabolism reduced and uncoupled

240
Q

What does MRS show in vascular dementia?

A

Absence of phospholipid changes

241
Q

How many cases of dementia are lewy body dementia (LBD)?

A

15-20%

242
Q

How does LBD present?

A

Progressive dementia with parkinsonism and fluctuation in level of attention and severity of cognitive impairment

243
Q

What are Lewy bodies?

A

Eosinophilic intracytoplasmic neuronal inclusion bodies

244
Q

What are lewy bodies made of?

A

Abnormally phosphorylated neurofilament proteins which are aggregated with ubiquitin and alpha-synuclein

245
Q

Where can lewy bodies be found?

A

Brainstem
Subcortical nuclei
Limbic cortex - cingulate, entorhinal, amygdala
Neocortex - frontal, temporal, parietal lobes

246
Q

Central feature required for diagnosis of LBD?

A

Progressive cognitive decline of sufficient magnitude to interfere with normal social or occupational function

247
Q

Core features of LBD

A

2 for probable, 1 for possible diagnosis:
Fluctuating cognition with profound variatinos in attention and alertness
Recurrent visual hallucinations - well-formed and detailed
Spontaneous motor features of parkinsonism

248
Q

How many patients with LBD have motor features of Parkinsonism?

A

70%

249
Q

Supportive features for LBD

A 
Repeated falls due to autonomic dysfunction
Syncope
Transient disturbances in consciousness
Neuroleptic sensitivity
Systematized delusions
Hallucinations
250
Q

Describe visual hallucinations in LBD

A

Well formed and detailed

251
Q

Prevalence rate of delusions in LBD

A

65%

252
Q

Prevalence rate of auditory hallucinations in LBD

A

20%

253
Q

Prevalence rates of visual hallucinations in LBD

A

60-80%

254
Q

LBD and antipsychotics

A

Patients with LBD are very sensitive to antipsychotics; these can lead to worsening of parkinsonian sx

255
Q

How many patients with LBD experience life threatening adverse effects to antipsychotics?

A

50%

256
Q

Decline rate per year of worsening parkinsonism in LBD?

A

10% decline per year

257
Q

Which allele is seen in LBD?

A

Increased frequency of e4 allele (APOE)

258
Q

Which memory is spared in LBD?

A

Short term

259
Q

Which aspects of cognition are affected in LBD?

A

Attention
Frontal subcortical skills
Visuospatial ability

260
Q

CT/MRI findings of LBD

A

Relative sparing of medial temporal lobe

261
Q

Associated features of LBD pathologically

A 
Lewy-related neuritis
Plaques
Neurofibrillary tangles
Regional neuronal-loss in brainstem
Synapse loss
Microvacuolation
262
Q

Where is regional neuronal loss common in LBS?

A

Brainstem - locus cereleus and substantia nigra

Nucleus basalis of Meynert

263
Q

Which drugs improve cognition, delusions and hallucinations in LBD?

A

Cholinesterase inhibitors

MRCPsych Part B - Al-Rashid Hospital (64 decks)

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