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%
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
3
Q
How many people in the UK are >65?
A
One sixth of the population
10 million
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
5
Q
How many people in the UK are over 80?
A
3 million
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
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.
8
Q
What does No Health Without Mental Health (2011) state?
A
Services should be age appropriate non discriminatory
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
10
Q
What % of carers suffer from depression at some stage?
A
30%
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
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
13
Q
Why is medication regimen and timing so important in Parkinsons?
A
Failure can result in delirium, depression, slowed cognition and anxiety
14
Q
How many patients with PD have depression?
A
2/3
15
Q
How many patients with PD develop dementia?
A
40%
16
Q
Common cognitive deficits in Parkinsons?
A
Higher executive dysfunction Attention Memory Visuomotor processing Visual attention
17
Q
How many patients with stroke have delirium?
A
30-40% after one week
18
Q
Which diseases commonly result in Charles Bonnet?
A
Macular Degeneration
Cataracts
Diabetic retinopathy
19
Q
Which diseases are associated with psychotic sx in the elderly?
A
Auditory impairment
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
21
Q
How common is depression in people with chronic physical health problems?
A
2-3 times more common
22
Q
How many patients with chronic physical illness will have depression?
A
20%
23
Q
First line treatment for depression in chronic physical illness
A
SSRI - keep in mind interactions
24
Q
Intracranial reversible causes of dementia
A
Normal pressure hydrocephalus
Subdural haematoma
Cerebral tumours
Tertiary syphilis
25
Systemic disorders which can cause reversible dementia
```
Alcoholism
Anoxia
Low BM
Myxoedema
Vitamin deficiencies
Drug or chemical poisoning
Pseudodementia
Renal/hepatic disease
```
26
How many diagnosis of dementia are due to young onset of dementia?
12%
27
How can alcohol use lead to dementia?
Damage to limbic structures and frontal lobes leading to memory and executive impairments
28
Which impairment in alcohol-induced dementia can improve with abstinence?
Memory impairment
29
Which type of memory is affected in alcohol-induced dementia?
Autobiographical
30
What does neuroimaging show in alcohol-induced dementia?
Generalised cerebral atrophy with frontal preponderance
31
What happens in normal pressure hydrocephalus?
Dilatation of cerebral ventricles - usually 3rd ventricle, with normal CSF pressure at P.
32
Triad of sx of normal prssure hydrocephalus?
Dementia
Gait ataxia
Urinary incontinence
33
Population prevalence of NPH in the elderly
0.4%
34
Which sx precedes all others in NPH?
Mildly broad based, symmetrical short stepped gait
35
What type of dementia occurs in NPH?
Progressive slowing of cognitive and motor functioning consistent with pattern of subcortical dementia
36
What is the pattern of subcortical dementia?
Pronounced slowness of thought
Difficulties in sustaining, switching attention
Difficulties in planning
37
How many cases of NPH are idiopathic?
50%
38
What are 50% of NPH non-idiopathic cases due to?
Mechanical obstruction of CSF flow across meninges due to infection, trauma, SAH etc
39
Which sx is late sx of NPH?
Urinary incontinence
40
What does CT show in NPH?
Increased size of lateral ventricles and thinning of cortex
41
Treatment of NPH
Surgical placement of ventriculo-peritoneal shunt
42
Which sx is most likely to improve with treatment of NPH?
Gait impairment
43
What is related to good outcome of NPH?
Mild dementia
44
Why are subdural veins more vulnerable to tears in the elderly?
Cortical shrinking
45
When should subdural haematoma (SDH) be suspected?
Changing pattern in cognitive function with risk factors
46
Risk factors for SDH
```
Post trauma - elderly after fall, HI
Cerebral atrophy
Alcoholism
Epilepsy
Clotting disorders
Predisposing drugs such as Warfarin, Aspirin
```
47
How many SDH cases have bilateral SDH?
30%
48
How many patients with SDH have a history of HI?
50%
49
Common features of SDH
Headache
Drowsiness
Altered consciousness
Confusion - fluctuating severity
50
What does CT show in SDH
Crescent shaped haematoma compressing sulci and midline shift
51
When might CT not show a SDH?
First 3 weeks as clot is isodense during early phase
52
Treatment of SDH
Surgical - burr holes
| Conservative - steroids
53
Complications of surgical treatment of SDH
Seizures
| Re-bleeding
54
Mortality of SDH
10%
55
Which patients with SDH have highest mortality?
Depressed consciousness level
| Bilateral SDH
56
How does Huntingtons dementia present?
Frontal dementa
| movement disorder
57
Prominent deficits in Huntingtons dementia?
```
Attention
Semantic verbal fluency
Processing speed
Executive function
Recall more affected than recognition
```
58
Key diagnostic test for dementia in MS
MRI
59
Problem with MRI scan in elderly with MS
Distinguishing between demyelination and vascular damage can be difficult in the elderly
60
How is diagnosis of dementia in MS confirmed?
CSF and evoked potentations
61
Where is Prion protein coded?
PRNP gene on Chromosome 20
62
When does prion disease occur?
When protein undergoes changes which render it insoluble
63
Which diseases are caused by prions?
Spongiform encephalopathies - transmissible dementias
64
What are the four forms of prion dementia?
Kuru
CJD
Fatal familial insomnia
Gerstmann Straussler Syndrome
65
Worldwide prevalence of sporadic CJD
0.1 per 100,000
66
Which prion disease is most common?
CJD
67
What causes CJD?
Pathological form of prion protein PrPsc
68
What is the normal form of the prion protein?
PrPc
69
Difference between PrPc and PrPsc
PrPsc is resistant to proteases, thus leading to accumulation and rapid degenerative changes
70
Onset of CJD
After 5th decade but can occur at any age
71
Clinical picture of CJD
```
Rapidly deteriorating dementia
Myoclonus
Cortical blindness
Cerebellar and EPSE
Death within one year
```
72
When do fulminant sx develop in CJD?
Within weeks
73
Which sign becomes prominent as CJD progresses?
Myoclonus
74
How many CJD cases are sporadic?
85%
75
How many CJD cases are genetic?
10%
76
How many cases of CJD result from iatrogenic transmission of transplant surgery?
5%
77
What types of transplant surgery can lead to CJD?
Transplant of dura, corneal grafts and pituitary growth home
78
What does CT show in CJD?
Atrophy of cortex, worse centrally
| Atrophy of cerebellum
79
What does MRI show in CJD?
Non-specific basal ganglia hyperintensities
80
What does EEG show in CJD
Periodic bi or triphasic discharges against slight low voltage background
81
In which type of CJD is EEG change not seen?
Variant CJD
82
CSF findings in CJD
14-3-3 protein elevated.
83
What is 4-3-3?
Normal neuronal protein
84
Definitive diagnosis of CJD
Post-mortem microscopic exam:
| spongiform neural degeneration and gliosis throughout cortical and subcortical grey matter, sparing white matter tracts
85
Treatment of CJD
Symptomatic; valproate and clonazepam to reduce movement disorder
86
What is vCJD?
Bovine Spongiform Encephalopathy
87
What is Bongine Spongiform Encephalopathy?
Prion disease of cows caused by cattle feeds that contained CNS material from infected material.
88
Incubation period between ingestion of contaminated meat and development of vCJD?
<20 years
89
Who does vCJD typically affect?
Men in 20s
90
Characteristics of vCJD?
Anxiety and depressive sx
Personality changes
Progressive dementia
Ataxia and myoclonus
91
Course of vCJD
1-2 years followed by death
92
What is diagnostic of vCJD?
Pulvinar sign; symmetric high-signal-intensity changes affecting pulvinar and medial areas of thalamus and tectal plate on FLAR sequence in MRI
93
How many patients with vCJD had pulvinar sign
>70%
94
Does CSF in vCJD show 14-3-3 protein?
Yes
95
Aside from MRI, how else can vCJD be diagnosed?
Immunostaining from tonsillar biopsy
96
EEG in vCJD?
No distinctive changes, sometimes diffuse slow waves
97
Most common Dementia in the developed world?
Alzheimers
98
Onset of Alzheimers
40-90
| Most often >65
99
Predicted risk of developing Alzheimers in first-degree relatives
15-19%
| 5% in controls
100
Relative risk of Alzheimers if you have a first-degree relative with the disease?
3-4 times relative to the risk in controls
101
Risk of Alzheimers at the age of 60
1%
102
Risk of Alzheimers at age of 65
5%
103
Risk of Alzheimers at age 85
40%
104
How does risk of Alzheimers correlate with age?
Doubles every 5 years
105
Risk of people >75 for Alzheimers vs Vascular Dementia
Risk is 6x greater for alzheimers than for Vascular DEmentia
106
In which group of patients is onset of Alzheimers earlier?
FHx of Alzheimers
107
Proven risk factors of Alzheimers
Age
Downs
Apolipoprotein 4 allele
108
Likely risk factors of Alzheimers
Female
HI
Postmenopausal oestrogen decline
109
Possible risk factors of Alzheimers
FHx of Downs
FHx of Parkinsons
Vascular factors
110
Proven protective factors of Alzheimers
Apolipoprotein 2 allele
111
Possible protective factors of Alzheimers
Smoking
NSAIDs
Oestrogwn
Premorbid intelligence and education
112
Which genes are associated with early onset Alzheimers?
Presenilin 2 gene
Presenilin 1 gene
Beta amyloid precursor protein gene
113
Which chromosome is Presenilin 2 gene on?
1
114
Which chromosome is Presenilin 1 gene on?
14
115
Which chromosome is beta amyloid precursor protein gene on?
21
116
Where on chromosome 21 is beta amyloid precurser protein gene found?
Long arm
117
What is the major constituent of senile plaques in Alzheimers?
Beta amyloid protein
118
Describe structure of the beta amyloid protein
42 amino acid peptide that is a breakdown product of amyloid precursor protein
119
What is the breakdown product of amyloid precursor protein?
Beta amyloid protein
120
Why are people with Downs at increased risk of Alzheimers?
They have three copies of the amyloid precursor protein gene (found on long arm of chromosome 21)
121
What can cause excessive deposition of beta amyloid protein?
Downs
| Mutation on codon 717 in amyloid precursor protein gene
122
What imaging can be used to confirm diagnosis of Alzheimers?
Amyloid PET scanning
123
What increases risk of late onset Alzheimers?
Apolipoprotein allele 4
124
Where can Apolipoprotein allele 4 be found?
Chromosome 19
125
Risk of Alzheimers if you have one copy of the Apolipoprotein allele 4 gene?
3x
126
Risk of Alzheimers if you have two copies of the Apolipoprotein allele 4 gene?
8x
127
Criteria for diagnosis of probable Alzheimers
Clinical examination and documented by MMSE, Blessed Dementia scale or confirmed by neuropsychological tests.
128
What features are required for a diagnosis of Alzheimers?
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
What is CT used for in diagnosis of Alzheimers?
Exclude treatable causes
130
CT findings in Alzheimers
Cortical atrophy; particularly over parietal and temporal lobes
Dilatation of third ventricles
131
What CT findings correlate with cognitive impairment?
Dilatation of 3rd ventricles
132
MRI findings in Alzheimers
Reduced grey matter, hippocampus, amygdala and temporal lobe volumes
133
SPECT findings in Alzheimers
Reduction in blood flow in temporal and parietal regions
134
PET findings in Alzheimers
Reduced blood flow and metabolism in temporal and parietal regions
135
MRS findings in Alzheimers
Abnormal synthesis of membrane phospholipids early in disease
136
Amyloid PET imaging findings in Alzheimers
Deposition of beta amyloid
137
What type of memory loss is seen in Alzheimers?
Short-term memory initially, then long term memory deficit later
Amnesia universal, mainly for recent events
138
What type of disorientation is seen in Alzheimers?
For time
139
Language findings in Alzheimers?
```
Expressive and receptive dysphasia
Lexical anomia (word finding difficulties)
```
140
Other cognitive deficits in Alzheimers
Apraxia; inability to perform coordinated learnt motor tasks
Agnosia
Impaired visuospatial skills
Impaired exectutive function
141
Psychiatric sx of Alzheimers
Delusions 15%
Hallucinations 10-15%
Depression 20%
142
Most common psychiatric sx in Alzheimers
```
Apathy - 59%
Depression - 58%
Irritability - 44%
anxiety - 44%
Agitation - 41%
```
143
Most common behavioural sx of Alzheimers
Wandering
| Aggressive outbursts
144
Average survival expectation for patients with Alzheimers?
8 years
145
Sx correlated with progression of Alzheimers?
```
Increased agitation
Frequent emotional outbursts
Night pacing
Poor sleep
Wandering
```
146
Sx in terminal phase of Alzheimers?
Profound disorientation
Amnesia
Incontinent of urine and faeces
147
Areas of cognition tested in AMTS
Memory
| Orientation
148
Cut off for AMTS?
<8/10
149
Areas of cognition tested with MMSE
```
Orientation
Memory
Concentration
Language
Praxis
Gnosis
```
150
Cut-off for MMSE?
24/30
151
Most widely used cognitive test in Old age Psychiatry?
MMSE
152
What test is best for screening global cognitive dysfunction?
MMSE
153
What types of variations is MMSE subject to?
Age
Socio-economic status
Educational achievement
154
What is MMSE heavily weighted towards?
Verbal performance
155
What does CAPE stand for?
Comprehensive Clifton Assessment for the Elderly
156
What does CAPE assess?
Level of disability and estimate need for care
157
What is the DRS?
Clinical Dementia Rating Scale
158
Areas of cognition assessed by DRS?
```
Memory
Orientation
Judgement & Problem solving
Community Affairs
Homes and Hobbies
Personal Care
```
159
What scale is commonly used to assess severity and stage of Alzheimers?
DRS
160
Cognitive areas of assessment of Addenbrookes
```
Orientation
Registration
Recognition
Recall
Perceptual abilities
Language
Verbal fluency
```
161
Cognitive areas of assessment of NPI
```
Delusions
Hallucinations
Agitation
Depression
Anxiety
Euphoria
Apathy
Disinhibition
Irritability
Aberrant
```
162
What does NPI do?
Rates frequency and severity of a range of neuropsychiatric sx.
163
What does NPI-NH measure?
Rates of occupational disruptiveness, a measure of caregiver distress.
164
How long does CAMCOG take to complete?
40 minutes
165
What does CAMCOG give a score out of?
104
166
Cognitive areas of assessment tested by CAMCOG?
```
Orientation
Comprehension
Perception
Memory
Abstract Thinking
```
167
What does Clock drawing test .. test?
Praxis
| Higher executive function
168
What drugs are used to treat mild to moderate cognitive impairment in Alzheimers?
Cholinesterase inhibitors
169
Give some examples of cholinesterase inhibitors used in the treatment of mild Alzheimers
Donepezil
Rivastigmine
Galantamine
170
How do cholinesterase inhibitors work in Alzheimers?
Reduce inactivation of Acetylcholine and thus potentiate cholinergic neurotransmitter, which in turn produces a most improvement in memory and goal-directed thought
171
Plasma half-life of Donepezil
70 hours
172
Plasma protein binding of Donepezil
Almost 100%
173
How does Donepezil work?
Highly selective reversible inhibition of acetylcholine.
174
Side effects of Donepezil
```
Mainly GI:
Nausea/vomiting
Diarrhoea
Anorexia
Headache/dizziness
Syncope
Muscle cramps
```
175
Which Alzheimers drugs cause more neuropsychiatric adverse effects?
Rivastigmine
| Galantamine
176
How does Galantamine work?
Direct nicotinic stimulatory action
| Cholinesterase inhibitor
177
Which drug improves sx of dementia in Parkinsons?
Rivastigmine
178
Which sx of Parkinsons does Rivastigmine improve?
Cognition
| ADLs
179
Most common SEs of Rivastigmine?
Nausea/vomiting
| Anorexia
180
What does Rivastigmine work on?
Acetylcholinesterase
| Butyrylcholinesterase
181
How can Rivastigmine be taken?
PO
| Transdermal patch OD
182
What augmentation is beneficial in Alzheimers?
Memantine and Donepezil
183
What does Memantine do?
Protects neurons from excessive glutamate which may be neurotoxic
184
What can Memantine be used for?
DAT
Vascular
Mixed dementia
185
How does Memantine work?
Non-competitive, PCP-site NMDA antagonist
186
Most common SEs of Memantine?
```
Dizziness
Headache
Fatigue
Diarrhoea
Gstric pain
```
187
Which drug is used in treatment of moderate to severe Alzheimers?
Memantine
188
Which patients with mild Alzheimers is Memantine used in?
When cholinesterase inhibitors are contraindicated i.e. severe cardiac conduction defects, severe asthma
189
Why is Tacrine not used for Alzheimers?
Potential for hepatotoxicity
190
Starting dose of Donepezil for Alzheimers?
5mg OD
191
Treatment dose of Donepezil for Alzheimers?
10mg OD
192
Starting dose of Rivastigmine for Alzheimers?
1.5mg BD
193
Treatment dose of Rivastigmine for Alzheimers?
6mg BD
194
Starting dose of Galantamine for Alzheimers?
4mg BD
195
Treatment dose of Galantamine for alzheimers?
12mg BD
196
Starting dose of Memantine for Alzheimers?
5mg OD
197
Treatment dose of Memantine for Alzheimers?
10mg OD
198
Recommendations from Committee on Safety of Medicines re use of Olanzapine and Risperidone for Dementia?
Each associated with 2x increase in risk of stroke and therefore should not be used
199
Poor prognostic factors in Alzheimers
```
Male
Onset <65
Prominent behavioural problems
Parietal lobe damage
Depression
Severe cognitive deficits
Absence of misidentification syndrome
```
200
Prevalence of psychosis in people with Alzheimers?
30-50%
201
Which type of psychosis is more common in Alzheimers?
Delusions
202
Common delusions in Alzheimers
```
Capgras
Phantom boarder
Mirror sign
TV sign
Magazine sign
```
203
What is phantom boarder?
False belief that guests are living in a persons home
204
What is the mirror sign?
Individual identifies his or her own image as someone elses
205
What is the TV sign?
Misidentification of TV images as real
206
What is the magazine sign?
Misidentification of magazine images as real and existing in 3D
207
What is the second most common cause of dementia?
Vascular
208
How many cases of dementia are vascular?
20%
209
What is the NINCDS-AIREN criteria for vascular dementia?
Evidence of CVD both on examination and brain imaging
| Relationship between onset of dementia and CVD
210
How can one show a relationship between onset of dementia and CVD?
Either dementia occurring within 3 months of a stroke or
| Abrupt deterioration in cognitive function or fluctuating stepwise course
211
Most prevalent neurological sx in Vascular Dementia
Reflex asymmetry
212
What sx are associated with measures of small vessel disease?
```
Dysarthria
Dysphagia
Parkinsonian gait disorder
Rigidity
Hypokinesia
```
213
What sx were more likely observed in vascular dementia in the presence of a cerebral infarct?
```
Aphasia
Reflex asymmetry
Hemianopia
Hemimotor dysfunction
Hemisensory dysfunction
Hemiplegic gait
```
214
What are the three subtypes of Vascular dementia>
Cognitive deficits following single stroke
Multi-infarct dementia
Progressive smell vessel disease - Binswanger's disease
215
When are cognitive deficits following stroke often seen?
Following midbrain or thalamic strokes
216
What happens in multi-infarct dementia>
Multiple strokes leads to stepwise deterioration.
| Follows a number of minor ischaemic events
217
What type of dementia is Binswangers disease?
Subcortical
218
Characteristics of Binswangers disease?
```
Slow intellectual decline
Slowness of thought
Decreased STM
Disorientation
Motor problems; gait, dysarthria
```
219
What happens in Binswangers disease?
Multiple microvascular infarcts of perforating vessels lead to progressive lacunae formation
220
What does MRI show in Binswangers disease?
Small distinct infarcts (lacunae) or more generalised white matter hyperintensities (leukoariasis)
221
Risk factors of Vascular Dementia
```
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
What is Haschinski Ischemic score index?
Allows quantification of likelihood of patient having vascular rather than degenerative dementia
223
Which dementia is more common in males?
Vascular
224
Which dementia is more common in females?
Alzheimers
225
Which dementia has focal neurological signs?
Vascular
226
Which dementia has loss of insight?
Alzheimers
227
Which dementia has mood sx?
Alzheimers
228
Which dementia has somatic complaints?
Vascular
229
What is CADASIL?
Form of vascular dementia
230
What does CADASIL stand for?
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy
231
How is CADASIL transmitted?
AD trait with high penetrance
232
Where is CADASIL gene?
Long arm of chromosome 19
233
How do patients with CADASIL gene present?
Recurrent stroke at age of 40-50
| Hx of migraine
234
What do patients with CADSIL later develop?
Subcortical dementia
| Pseudobulbar palsy
235
What does MRI show in CADSIL?
Widespread white matter changes
236
What does CT show in vascular dementia?
Increased number of infarcts
237
What does MRI show in vascular dementia?
White matter lesions more numerous and severe than Alzheimers
238
What does SPECT show in vascular dementia?
Irregular perfusion deficits
239
What does PET show in vascular dementia?
Cerebral blood flow and metabolism reduced and uncoupled
240
What does MRS show in vascular dementia?
Absence of phospholipid changes
241
How many cases of dementia are lewy body dementia (LBD)?
15-20%
242
How does LBD present?
Progressive dementia with parkinsonism and fluctuation in level of attention and severity of cognitive impairment
243
What are Lewy bodies?
Eosinophilic intracytoplasmic neuronal inclusion bodies
244
What are lewy bodies made of?
Abnormally phosphorylated neurofilament proteins which are aggregated with ubiquitin and alpha-synuclein
245
Where can lewy bodies be found?
Brainstem
Subcortical nuclei
Limbic cortex - cingulate, entorhinal, amygdala
Neocortex - frontal, temporal, parietal lobes
246
Central feature required for diagnosis of LBD?
Progressive cognitive decline of sufficient magnitude to interfere with normal social or occupational function
247
Core features of LBD
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
How many patients with LBD have motor features of Parkinsonism?
70%
249
Supportive features for LBD
```
Repeated falls due to autonomic dysfunction
Syncope
Transient disturbances in consciousness
Neuroleptic sensitivity
Systematized delusions
Hallucinations
```
250
Describe visual hallucinations in LBD
Well formed and detailed
251
Prevalence rate of delusions in LBD
65%
252
Prevalence rate of auditory hallucinations in LBD
20%
253
Prevalence rates of visual hallucinations in LBD
60-80%
254
LBD and antipsychotics
Patients with LBD are very sensitive to antipsychotics; these can lead to worsening of parkinsonian sx
255
How many patients with LBD experience life threatening adverse effects to antipsychotics?
50%
256
Decline rate per year of worsening parkinsonism in LBD?
10% decline per year
257
Which allele is seen in LBD?
Increased frequency of e4 allele (APOE)
258
Which memory is spared in LBD?
Short term
259
Which aspects of cognition are affected in LBD?
Attention
Frontal subcortical skills
Visuospatial ability
260
CT/MRI findings of LBD
Relative sparing of medial temporal lobe
261
Associated features of LBD pathologically
```
Lewy-related neuritis
Plaques
Neurofibrillary tangles
Regional neuronal-loss in brainstem
Synapse loss
Microvacuolation
```
262
Where is regional neuronal loss common in LBS?
Brainstem - locus cereleus and substantia nigra
| Nucleus basalis of Meynert
263
Which drugs improve cognition, delusions and hallucinations in LBD?
Cholinesterase inhibitors
