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MRCPsych Part B - Al-Rashid Hospital > Liaison Psychiatry 1.2 > Flashcards

Liaison Psychiatry 1.2 Flashcards

1
Q

Risk factors for Depression in Parkinsons

A 
Female
Younger onset
Prominent right-sided lesions
Bradykinesia and gait-disturbance
Rapid disease progression
Poorer cognitive status and activities of daily living
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2
Q

What is apathy without depression linked to in Parkinsons?

A

Executive dysfunction

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3
Q

What is mania linked to in Parkinsons?

A

Levodopa

Dopamine agonists

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4
Q

When is risk of drug-induced mania increased in Parkinsons?

A

Pre-existing bipolar

FHx of bipolar

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5
Q

Side effects of Levodopa

A

Hypomania
Pathological gambling
Hypersexuality
Hallucinations

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6
Q

Rate of drug-induced hallucinatinos in Parkinsons

A

20% - mainly visual

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7
Q

Rate of drug-induced delusions in Parkinsons

A

3-30%

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8
Q

Treatment of drug-induced psychosis in Parkinsons

A

<100mg/day of Clozapine

Quetiapine

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9
Q

When does cognitive impairment suggest poor prognosis of Parkinsons?

A

If present at time of initial referral

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10
Q

Risk factors of cognitive impairment in Parkinsons?

A

Older age
Late onset
Low socio-economic status and education
Presence of EPSEs

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11
Q

Neurobiology of those with Parkinsons and cognitive impairment

A

Frontal executive dysfunction with subcortical pattern of dementia
Neuroleptic sensitivity

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12
Q

Treatment for cognitive impairment in Lewy Body Dementia?

A

Rivastigmine

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13
Q

Treatment for Parkinson related dementia>

A

No drugs licensed

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14
Q

What is Huntingtons Disease?

A

Progressive neurodegenerative disorder with chorea and dystonia, incoordination, cognitive decline and behavioural difficulties with AD high penetrance pattern of inheritance.

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15
Q

Onset of sx of Huntingtons

A

Middle age

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16
Q

Prevalence of psychiatric sx in Huntingtons at first presentation?

A

30%

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17
Q

Suicide rates in patients with Huntingtons

A

4x higher than general population

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18
Q

How many patients with Huntingtons first present with schizophreniform psychosis?

A

3-6%

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19
Q

When can OCD-like sx occur in Huntingtons?

A

If basal ganglia involvement

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20
Q

What is the mutant protein in Huntingtons?

A

Huntingtin

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21
Q

What results in Huntingtin mutation?

A

Expanded CAG repeat leading to polyglutamine strand of variable length at N terminus.

This tail confers toxic gain of function

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22
Q

Where is gene for Huntington Disease?

A

Short arm of chromosome 4, associated with expanded trinucleotide repeat.

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23
Q

When is Huntingtons fully penetrant?

A

CAG repeats reach 41 or more

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24
Q

When does Huntingtons show incomplete penetrance?

A

36-40 repeats

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25
Q

How many repeats is associated with no Huntingtons disorder?

A

35 or less

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26
Q

How much does number of CAG repeats account for variation in age of onset of Huntingtons?

A

60%

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27
Q

Penetrance of Huntingtons

A

95%

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28
Q

How many patients present with Wilsons disease via psychiatric presentations?

A

20%

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29
Q

How many patients with Wilsons disease will have psychiatric abnormalities at some point?

A

50%

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30
Q

Most common psychiatric sx of Wilsons?

A

Personality disturbance
Mood abnormalities
Cognitive dysfunction

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31
Q

Which form of Wilsons have psychiatric manifestations usually?

A

Neurological rather than hepatic

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32
Q

How many patients with Wilsons have cognitive impairment?

A

25%

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33
Q

What type of dementia occurs in Wilsons?

A

Frontosubcortial pattern of dementia

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34
Q

How many patients with Wilsons have depression?

A

30%

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35
Q

How many patients with Wilsons show suicidal behaviour?

A

4-16%

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36
Q

How many patients with Wilsons have psychosis?

A

2%

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37
Q

How many patients with Wilsons have Kayser-Fleischer rings

A

95% of those with neurological sx
50-60% of those without neurological sx
10% of asymptomatic siblings

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38
Q

What does MRI show in patients with Wilsons?

A

Intense hyperintensity of midbrain with relative sparing of red nucleus, superior colliculus and part of pars reticulata of substantia nigra
Hypointensity of aqueduct - called Giant Panda sign

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39
Q

Treatment of Wilsons

A

Copper chelating or depleting agents

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40
Q

What is essential for treatment of Wilsons?

A

Early diagnosis and initiation of treatment

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41
Q

Diagnostic criteria of transient global amnesia

A

Witnessed attacks with information available from observer
Clear-cut anterograde amnesia during attack
Absence of clouding of consciousness & loss of personal identity
Cognitive impairment limited to amnesia only
No accompanying focal neurological symptoms during attack and no signs afterwards
Absence of epileptic features
Attack resolves within 24 hours
Exclusino of patients with HI or active epilepsy

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42
Q

Rate of transient global amnesia

A

5-10/100,000 per year

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43
Q

Rate of transient global amnesia in those >50 years of age

A

30/1000,000 per year

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44
Q

Aetiology of transient global amnesia

A

Hypoperfusion in temporal and parietotemporal regions, mainly left hemisphere

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45
Q

Characteristics of transient global amnesia

A

Abrupt onset of anterograde amnesia characterised by significant new learning deficit.
Mild confusion and lack of insight into problem but intact sensorium.

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46
Q

Episode length of transient global amnesia

A

6-24 hours

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47
Q

Recurrence rate of transient global amnesia

A

Most patients show complete improvement but recurrence is high

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48
Q

What happens in Fahrs disease?

A

Idiopathic progressive calcium deposition in basal ganglia

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49
Q

Onset of Fahrs disease

A

20-40 years

40-60 years

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50
Q

What is Fahrs disease at 20-40 years associated with

A

Schizophreniform psychoses

Catatonic sx

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51
Q

What is Fahrs disease at 40-60 years associated with?

A

Dementia

Choreoathetosis

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52
Q

How many patients with Fahrs disease have psychiatric sx?

A

50%

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53
Q

What do psychiatric sx correlate with in Fahrs disease?

A

More extensive calcification

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54
Q

Cognitive impairment in Fahrs disease?

A

Frontosubcortical type

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55
Q

Neurological sx of Fahrs disease

A 
Parkinsonism
Chorea
Dystonia
Tremor
Gait disturbance
Dysarthria
Seizures
Myoclonus
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56
Q

MRI sign of Fahrs disease

A

Hypointensity of striatum

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57
Q

Commonest cause of viral encephalitis?

A

Herpes simplex encephalitis

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58
Q

Commonest cause of limbic encephalitis

A

Herpes simplex encephalitis

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59
Q

What is affected in limbic encephalitis?

A

Temporal lobe

Limbic circuit

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60
Q

How many patients with Herpes Simplex Encephalitis have Herpes Simplex Type 1?

A

70%

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61
Q

What type of Herpes Simplex Encephalitis are immunocompromised patients likely to have?

A

Herpes Simplex Type 2

HHV 6 or 7

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62
Q

Sx of HSE?

A

Abrupt onset of confusion, memory impairment and seizures
Depression
Psychosis
Fever

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63
Q

How many patients with HSE show psychiatric disturbance?

A

70%

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64
Q

Neuroimaging results of HSE

A

Signal change and swelling within temporal lobes on MRI

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65
Q

What does CSF show in HSE

A

Lymphocytosis and raised protein

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66
Q

Gold standard test for HSE

A

CSF PCR for herpes viruses

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67
Q

Most sensitive investigation for detecting early lesions in HSE

A

MRI

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68
Q

Earlier signs in EEG of HSE

A

Non-specific slowing

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69
Q

Later signs in EEG of HSE

A

High voltage periodic lateralizing epileptiform discharges

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70
Q

Fatality of HSE is untreated

A

70%

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71
Q

Treatment of HSE

A

IV aciclovir

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72
Q

By how much does IV aciclovir reduce mortality of HSE?

A

To 20-30%

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73
Q

How long does treatment need to continue for HSE?

A

14 days.

Longer in immuno-compromised patients

74
Q

What is the most common cause of Kluver-Busy syndrome?

A

HSE

75
Q

Sx of Kluver-Bucy syndrome?

A

Emotional blunting
Hyperphagia
Visual agnosia
Inappropriate sexual behaviour

76
Q

What causes sx of Kluver-Bucy Syndrome?

A

Bilateral temporal lobe damage

77
Q

What can be used to control sx in Kluver-Bucy Syndrome?

A

Carbamazepine

78
Q

Who described Meige Syndrome?

A

Henri Meidge in 1904

79
Q

What characterisis Meige syndrome?

A

Repetitive blinking, chin thrusting, lip pursing or tongue movements.

80
Q

What causes secondary Meige’s syndrome?

A

Antipsychotics
Levodopa
Lewy Body Dementia

81
Q

Which patients are more likely to get Meige Syndrome?

A

Female

Middle Age

82
Q

When do symptoms of Meige syndrome disappear?

A

During sleep

83
Q

What can help lessen symptoms of Meige syndrome?

A

Chewing gum
Whistling
Touching face

84
Q

Peak incidence of HI

A

15-24 years

85
Q

What does concussion cause?

A

Transient coma for hours followed by complete clinical recovery

86
Q

What can contusion cause?

A

Prolonged coma
Focal Signs
Lasting brain damage

87
Q

Mechanism of traumatic brain injury

A

Axonal and neuronal damage from shearing and rotational stresses of decelerating brain, often at sites of opposite impact (contrecoup effect)
Damage from direct trauma
Brain oedema and raised ICP
Brain hypoxia and ischaemia

88
Q

What types of amnesia occur after HI?

A

Post-traumatic

Retrograde

89
Q

What is post-traumatic amnesia?

A

Amnesia for period of injury and period following injury until normal memory resumes. Usually anterograde

90
Q

What is retrograde amnesia post-HI?

A

Dense amnesia for period between last clearly recalled memory prior to injury to the injury itself.

91
Q

Usual duration of post-HI retrograde amnesia?

A

Minutes

Reduces with time

92
Q

Poor prognostic factors of psychiatric morbidity following traumatic HI?

A 
Long duration of LOC
Long PTA
Elderly
Chronic alcohol use
Diffuse brain damage
New onset seizures
Focal damage to dominant lobe
93
Q

What is used to assess severity of HI?

A

GCS after 24 hours
Length of coma
PTA
Abbreviated Injury Scale

94
Q

What is used to predict functional outcome after HI?

A

Length of coma

PTA

95
Q

What is used to predict survival after HI?

A

Abbreviated Injury Scale

96
Q

Classification of mild HI

A

PTA <60 minutes

97
Q

Classification of moderate HI

A

PTA between 1-24 hours

98
Q

Classification of severe HI

A

PTA 1-7 days

99
Q

Classification of very severe HI

A

PTA >7 days

100
Q

Functional outcome for mild HI

A

Return to work in <1 month

101
Q

Functional outcome in moderate HI

A

Return to work in 2 months

102
Q

Functional outcome for severe HI

A

Return to work in 4 months

103
Q

Functional outcome in very severe HI

A

May require >1 year for return to work

104
Q

In which type of HI is cognitive impairment common

A

After closed HI with PTA >24 hours

105
Q

In which type of HI is personality change common?

A

HI to orbitofrontal lobe or anterior temporal lobe

106
Q

How many patients with

A

25%

107
Q

What predicts depression in patients with HI?

A

Proximity of lesion to left frontal lobe

108
Q

In which type of HI might there by schizophrenia-like psychosis with prominent paranoia?

A

Left temporal injury

109
Q

In which type of HI might there by affective psychoses?

A

Right temporal or orbitofrontal injury

110
Q

Prevalence of schizophrenia in HI

A

2-5%

111
Q

Post-traumatic epilepsy in HI

A

5% in closed

30% in open

112
Q

When does concussion syndrome occur?

A

Following mild-moderate HI

113
Q

Sx of post-concussion sx

A 
Headache
Dizziness
Fatigue
Poor memory and concentration
Irritability
Depression
Sleep disturbance
Restlessness
Sensitivity to noise
Blurred/double vision
Nausea
Photophobia
Tinnitus
114
Q

How many patients with post-concussion recover?

A

50% recover within 3 months

115
Q

Aetiology of post-concussion

A

Diffuse microscopic anxonal head injury

Macroscopic brain lesions in 8-10% of people, mainly in frontal, temporal and deep white matter

116
Q

In which patients with post-concussion is there slower recovery?

A 
Age >40 years
Previous HI
Alcohol/substance misuse
Psychological factors
Females
117
Q

What is severity of sx of post-concussion correlated with?

A

Severity of neuropsychological impairment in speed of information processing

118
Q

Which psychosocial factors is post-concussion associated with?

A

Anxiety & depression
Stress
Time off work
Seeking compensation

119
Q

What has been shown to reduce sx of post-concussion?

A

Early interventino in first few weeks
Single hour-long assessment and treatment session
Education & reassurance

120
Q

What are dyssomnias?

A

Primary sleep disorders which cause either difficulty getting off to sleep or remaining asleep or excessive sleepiness during the day.

121
Q

What are dyssomnias divided into?

A 
Primar insomnia
Primary hypersomnia
Circadian sleep disorders
Narcolepsy
Breathing related sleep disorders
Sleep state misperception
122
Q

What are parasomnias?

A

Disorders which intrude into the sleep process

123
Q

What are parasomnias divided into?

A 
Arousal disorders (NREM sleep)
Sleep-wake transition
REM sleep parasomnias
Sleep bruxism
Sleep enuresis
124
Q

What disorders come under arousal disorders?

A

Confusional arousals
Sleepwalking
Sleep terrors

125
Q

What disorders come under sleep-wake transition?

A

Sleep starts

Sleep talking

126
Q

What disorders come under REM sleep parasomnias?

A

REM behavioural disorder
Nightmares
Sleep paralysis

127
Q

What comes under Sleep-related movement disorders?

A

Restless leg syndrome
Periodic limb movement disorder
Sleep-related bruxism

128
Q

What comes under sleep disorders in ICD 10?

A 
Nonorganic insomnia
Nonorganic hypersomnia
Nonorganic disorder of the sleep-wake schedule
Sleepwalking (somnambulism)
Sleep terrors
Nightmares
129
Q

What is the most common circadian sleep disorder?

A

Delayed sleep phase syndrome

130
Q

What happens in delayed sleep phase syndrome?

A

Patient is unable to fall asleep until very early morning.

131
Q

Prevalence of narcolepsy

A

0.025%

132
Q

Symptoms of narcolepsy

A 
Excessive daytime sleepiness
Sudden sleep attacks (narcolepsy) - sleep is refreshing (REM)
Cataplexy
Sleep paralysis
Hypnagogic hallucinations
133
Q

How many patients with narcolepsy have cataplexy?

A

75%

134
Q

How many patients with narcolepsy have sleep paralysis?

A

30%

135
Q

How many patients with narcolepsy have all 4 sx: narcolepsy, cataplexy, sleep paralysis and hypnagogic hallucinations?

A

10%

136
Q

How many patients with narcolepsy have automatic behaviours?

A

33%

137
Q

Is sleep duration increased in narcolepsy?

A

No - reduced and fragmented nocturnal sleep

138
Q

What is strongly associated with narcolepsy?

A

HLA-DQB1*0602

Low concentration of hypocretin-1 in CSF

139
Q

What does sleep polysomnogram show in narcolepsy?

A

Sleep latency <10 minute

Sleep-onset REM periods

140
Q

Treatment for narcolepsy

A

Methylphenidate

Modafinil

141
Q

Treatment for Cataplexy

A

Imipramine

142
Q

Prevalence of OSA

A

Men 4%

Women 2.5%

143
Q

Sx of OSA

A 
Loud snoring
Breathing pauses
Mouth breathing
Restless sleep
Increased perspiration at night
Excessive daytime sleepiness
Morning headaches
Behavioural changes
144
Q

What might occur in untreated OSA?

A

Right-sided cardiac failure

145
Q

What is sleepwalking?

A

Partial arousal during slow-wave stages 3 and 4.

146
Q

When is sleepwalking most common?

A

During initial third sate of sleep

147
Q

What are night terrors?

A

Recurrent episodes of abrupt awakening from sleep characterised by panicky scream with intense fear and autonomic arousal.
Individual has no recollection of evens and is unresponsive during episodes.

148
Q

When do night terrors occur?

A

During first third of night

During stages 3-4 of NREM sleep

149
Q

How does REM sleep behavioural disorder occur?

A

No loss of muscle tone in REM sleep so dreams are acted as complex behaviours.

150
Q

When do REM sleep behavioural episodes occur?

A

Middle to latter third of night during REM sleep

151
Q

Which disorders is REM sleep behavioural disorder associated with?

A

Parkinsons
Diffuse lewy body disease
MSA
GBS

152
Q

What can REM behavioural disorder be prodrome of?

A

Diffuse Lewy body disease
Parkinsons
Precede diagnosis of movement disorder by years

153
Q

What type of lesions is REM behavioural sleep disorder associated with?

A

Lesions in brainstem

154
Q

Treatment of REM behavioural sleep disorder?

A

Clonazepam

Make sleeping environment safe

155
Q

Diagnostic criteria for REM behavioural sleep disorder?

A

Movements of body or limbs associated with dreams and at least one of:
potentially harmful sleep behaviour
Dreams that appear to be acted out
Sleep behaviour that disrupts sleep continuity

156
Q

Diagnostic criteria for restless leg syndrome in patients >12 y/o

A

Akathisia usually accompanied by paresthesia (core feature)
Motor restlessness
Sx worse at rest
Sx worse at night

157
Q

What characterises restless leg syndrome

A

Unpleasant sensation in legs that preclude smooth transition from wakefulness to sleep.

158
Q

How many patients with restless leg syndrome have periodic movements during sleep?

A

80-90%

159
Q

Prevalence of restless leg syndrome

A

3-15%

160
Q

M:F ratio of restless leg syndrome

A

1:2

161
Q

How many patients with restless leg syndrome show a familial pattern?

A

> 50%

162
Q

Predisposing factors to restless leg syndrome?

A 
Iron deficiency
Peripheral neuropathy
Sedating antihistamines
Centrally acting dopamine receptor antagonists - metoclopramide, prochlorperazine
Antipsychotics
Caffiene
Antidepressants
163
Q

Treatment of restless leg syndrome

A 
Sleep hygiene
Relaxation techniques
Dopaminergic agents
Anticonvulsants
Opiods
Clonazepam
164
Q

First licensed drug for restless leg syndrome

A

Ropinirole

165
Q

Which dopaminergic agents can be used for restless legs?

A

Nonergot D2 agonists: ropinrole, pramipexole

Bromocriptine and dopaminergic precursors: levodopa/carbidopa

166
Q

Which anticonvulsants can be used for restless legs?

A

Gabapentin

CBZ

167
Q

Which opioids can be used for restless legs?

A

Oxycodone

Propoxyphene

168
Q

What is Periodic Limb Movement Disorder?

A

Periodic episodes of repetitive and stereotyped limb movements during sleep.
Can cause clinical sleep disturbance.

169
Q

What is required for diagnosis of Periodic Limb Movement Disorder?

A

Polysomnographic documentation of increased number of episodes in association with significant disruption fo sleep architecture and symptomatolgy.

170
Q

What are polysomnographic diagnostric critera for PLMS based on?

A

EMG of right and left anterior tibialis muscles.

171
Q

What does rate of PLMS increase with?

A

Age

172
Q

How many patients with PLMS also have Narcolepsy?

A

45-65%

173
Q

How many patients with PLMS also have REM sleep behavioural disorder?

A

70%

174
Q

What pathology has been linked to PLMS?

A

Dopaminergic impairment

Fe deficiency

175
Q

Treatment for PLMD

A

Sleep hygeine

176
Q

When is medication warranted for PLMD?

A

If sleep disruption

177
Q

Medication treatment for PLMD?

A

Similar to restless legs

178
Q

What is bruxism considered to be?

A

Stereotyped movement disorder or rhythmic disorder

179
Q

When is bruxism more frequent?

A

Early part of sleep
May be related to stress/anxiety
May be related to dentition abnormalities/stimulant use

180
Q

What type of disorders is related to initial insomnia?

A

Anxiety

181
Q

What type of disorders are related to middle insomnia?

A

Medical illness
Pain syndromes
Depression

182
Q

What type of disorders are related to Terminal insomnia?

A

Depression

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

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