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
2
Q
What is apathy without depression linked to in Parkinsons?
A
Executive dysfunction
3
Q
What is mania linked to in Parkinsons?
A
Levodopa
Dopamine agonists
4
Q
When is risk of drug-induced mania increased in Parkinsons?
A
Pre-existing bipolar
FHx of bipolar
5
Q
Side effects of Levodopa
A
Hypomania
Pathological gambling
Hypersexuality
Hallucinations
6
Q
Rate of drug-induced hallucinatinos in Parkinsons
A
20% - mainly visual
7
Q
Rate of drug-induced delusions in Parkinsons
A
3-30%
8
Q
Treatment of drug-induced psychosis in Parkinsons
A
<100mg/day of Clozapine
Quetiapine
9
Q
When does cognitive impairment suggest poor prognosis of Parkinsons?
A
If present at time of initial referral
10
Q
Risk factors of cognitive impairment in Parkinsons?
A
Older age
Late onset
Low socio-economic status and education
Presence of EPSEs
11
Q
Neurobiology of those with Parkinsons and cognitive impairment
A
Frontal executive dysfunction with subcortical pattern of dementia
Neuroleptic sensitivity
12
Q
Treatment for cognitive impairment in Lewy Body Dementia?
A
Rivastigmine
13
Q
Treatment for Parkinson related dementia>
A
No drugs licensed
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.
15
Q
Onset of sx of Huntingtons
A
Middle age
16
Q
Prevalence of psychiatric sx in Huntingtons at first presentation?
A
30%
17
Q
Suicide rates in patients with Huntingtons
A
4x higher than general population
18
Q
How many patients with Huntingtons first present with schizophreniform psychosis?
A
3-6%
19
Q
When can OCD-like sx occur in Huntingtons?
A
If basal ganglia involvement
20
Q
What is the mutant protein in Huntingtons?
A
Huntingtin
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
22
Q
Where is gene for Huntington Disease?
A
Short arm of chromosome 4, associated with expanded trinucleotide repeat.
23
Q
When is Huntingtons fully penetrant?
A
CAG repeats reach 41 or more
24
Q
When does Huntingtons show incomplete penetrance?
A
36-40 repeats
25
How many repeats is associated with no Huntingtons disorder?
35 or less
26
How much does number of CAG repeats account for variation in age of onset of Huntingtons?
60%
27
Penetrance of Huntingtons
95%
28
How many patients present with Wilsons disease via psychiatric presentations?
20%
29
How many patients with Wilsons disease will have psychiatric abnormalities at some point?
50%
30
Most common psychiatric sx of Wilsons?
Personality disturbance
Mood abnormalities
Cognitive dysfunction
31
Which form of Wilsons have psychiatric manifestations usually?
Neurological rather than hepatic
32
How many patients with Wilsons have cognitive impairment?
25%
33
What type of dementia occurs in Wilsons?
Frontosubcortial pattern of dementia
34
How many patients with Wilsons have depression?
30%
35
How many patients with Wilsons show suicidal behaviour?
4-16%
36
How many patients with Wilsons have psychosis?
2%
37
How many patients with Wilsons have Kayser-Fleischer rings
95% of those with neurological sx
50-60% of those without neurological sx
10% of asymptomatic siblings
38
What does MRI show in patients with Wilsons?
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
39
Treatment of Wilsons
Copper chelating or depleting agents
40
What is essential for treatment of Wilsons?
Early diagnosis and initiation of treatment
41
Diagnostic criteria of transient global amnesia
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
42
Rate of transient global amnesia
5-10/100,000 per year
43
Rate of transient global amnesia in those >50 years of age
30/1000,000 per year
44
Aetiology of transient global amnesia
Hypoperfusion in temporal and parietotemporal regions, mainly left hemisphere
45
Characteristics of transient global amnesia
Abrupt onset of anterograde amnesia characterised by significant new learning deficit.
Mild confusion and lack of insight into problem but intact sensorium.
46
Episode length of transient global amnesia
6-24 hours
47
Recurrence rate of transient global amnesia
Most patients show complete improvement but recurrence is high
48
What happens in Fahrs disease?
Idiopathic progressive calcium deposition in basal ganglia
49
Onset of Fahrs disease
20-40 years
| 40-60 years
50
What is Fahrs disease at 20-40 years associated with
Schizophreniform psychoses
| Catatonic sx
51
What is Fahrs disease at 40-60 years associated with?
Dementia
| Choreoathetosis
52
How many patients with Fahrs disease have psychiatric sx?
50%
53
What do psychiatric sx correlate with in Fahrs disease?
More extensive calcification
54
Cognitive impairment in Fahrs disease?
Frontosubcortical type
55
Neurological sx of Fahrs disease
```
Parkinsonism
Chorea
Dystonia
Tremor
Gait disturbance
Dysarthria
Seizures
Myoclonus
```
56
MRI sign of Fahrs disease
Hypointensity of striatum
57
Commonest cause of viral encephalitis?
Herpes simplex encephalitis
58
Commonest cause of limbic encephalitis
Herpes simplex encephalitis
59
What is affected in limbic encephalitis?
Temporal lobe
| Limbic circuit
60
How many patients with Herpes Simplex Encephalitis have Herpes Simplex Type 1?
70%
61
What type of Herpes Simplex Encephalitis are immunocompromised patients likely to have?
Herpes Simplex Type 2
| HHV 6 or 7
62
Sx of HSE?
Abrupt onset of confusion, memory impairment and seizures
Depression
Psychosis
Fever
63
How many patients with HSE show psychiatric disturbance?
70%
64
Neuroimaging results of HSE
Signal change and swelling within temporal lobes on MRI
65
What does CSF show in HSE
Lymphocytosis and raised protein
66
Gold standard test for HSE
CSF PCR for herpes viruses
67
Most sensitive investigation for detecting early lesions in HSE
MRI
68
Earlier signs in EEG of HSE
Non-specific slowing
69
Later signs in EEG of HSE
High voltage periodic lateralizing epileptiform discharges
70
Fatality of HSE is untreated
70%
71
Treatment of HSE
IV aciclovir
72
By how much does IV aciclovir reduce mortality of HSE?
To 20-30%
73
How long does treatment need to continue for HSE?
14 days.
| Longer in immuno-compromised patients
74
What is the most common cause of Kluver-Busy syndrome?
HSE
75
Sx of Kluver-Bucy syndrome?
Emotional blunting
Hyperphagia
Visual agnosia
Inappropriate sexual behaviour
76
What causes sx of Kluver-Bucy Syndrome?
Bilateral temporal lobe damage
77
What can be used to control sx in Kluver-Bucy Syndrome?
Carbamazepine
78
Who described Meige Syndrome?
Henri Meidge in 1904
79
What characterisis Meige syndrome?
Repetitive blinking, chin thrusting, lip pursing or tongue movements.
80
What causes secondary Meige's syndrome?
Antipsychotics
Levodopa
Lewy Body Dementia
81
Which patients are more likely to get Meige Syndrome?
Female
| Middle Age
82
When do symptoms of Meige syndrome disappear?
During sleep
83
What can help lessen symptoms of Meige syndrome?
Chewing gum
Whistling
Touching face
84
Peak incidence of HI
15-24 years
85
What does concussion cause?
Transient coma for hours followed by complete clinical recovery
86
What can contusion cause?
Prolonged coma
Focal Signs
Lasting brain damage
87
Mechanism of traumatic brain injury
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
What types of amnesia occur after HI?
Post-traumatic
| Retrograde
89
What is post-traumatic amnesia?
Amnesia for period of injury and period following injury until normal memory resumes. Usually anterograde
90
What is retrograde amnesia post-HI?
Dense amnesia for period between last clearly recalled memory prior to injury to the injury itself.
91
Usual duration of post-HI retrograde amnesia?
Minutes
| Reduces with time
92
Poor prognostic factors of psychiatric morbidity following traumatic HI?
```
Long duration of LOC
Long PTA
Elderly
Chronic alcohol use
Diffuse brain damage
New onset seizures
Focal damage to dominant lobe
```
93
What is used to assess severity of HI?
GCS after 24 hours
Length of coma
PTA
Abbreviated Injury Scale
94
What is used to predict functional outcome after HI?
Length of coma
| PTA
95
What is used to predict survival after HI?
Abbreviated Injury Scale
96
Classification of mild HI
PTA <60 minutes
97
Classification of moderate HI
PTA between 1-24 hours
98
Classification of severe HI
PTA 1-7 days
99
Classification of very severe HI
PTA >7 days
100
Functional outcome for mild HI
Return to work in <1 month
101
Functional outcome in moderate HI
Return to work in 2 months
102
Functional outcome for severe HI
Return to work in 4 months
103
Functional outcome in very severe HI
May require >1 year for return to work
104
In which type of HI is cognitive impairment common
After closed HI with PTA >24 hours
105
In which type of HI is personality change common?
HI to orbitofrontal lobe or anterior temporal lobe
106
How many patients with
25%
107
What predicts depression in patients with HI?
Proximity of lesion to left frontal lobe
108
In which type of HI might there by schizophrenia-like psychosis with prominent paranoia?
Left temporal injury
109
In which type of HI might there by affective psychoses?
Right temporal or orbitofrontal injury
110
Prevalence of schizophrenia in HI
2-5%
111
Post-traumatic epilepsy in HI
5% in closed
| 30% in open
112
When does concussion syndrome occur?
Following mild-moderate HI
113
Sx of post-concussion sx
```
Headache
Dizziness
Fatigue
Poor memory and concentration
Irritability
Depression
Sleep disturbance
Restlessness
Sensitivity to noise
Blurred/double vision
Nausea
Photophobia
Tinnitus
```
114
How many patients with post-concussion recover?
50% recover within 3 months
115
Aetiology of post-concussion
Diffuse microscopic anxonal head injury
| Macroscopic brain lesions in 8-10% of people, mainly in frontal, temporal and deep white matter
116
In which patients with post-concussion is there slower recovery?
```
Age >40 years
Previous HI
Alcohol/substance misuse
Psychological factors
Females
```
117
What is severity of sx of post-concussion correlated with?
Severity of neuropsychological impairment in speed of information processing
118
Which psychosocial factors is post-concussion associated with?
Anxiety & depression
Stress
Time off work
Seeking compensation
119
What has been shown to reduce sx of post-concussion?
Early interventino in first few weeks
Single hour-long assessment and treatment session
Education & reassurance
120
What are dyssomnias?
Primary sleep disorders which cause either difficulty getting off to sleep or remaining asleep or excessive sleepiness during the day.
121
What are dyssomnias divided into?
```
Primar insomnia
Primary hypersomnia
Circadian sleep disorders
Narcolepsy
Breathing related sleep disorders
Sleep state misperception
```
122
What are parasomnias?
Disorders which intrude into the sleep process
123
What are parasomnias divided into?
```
Arousal disorders (NREM sleep)
Sleep-wake transition
REM sleep parasomnias
Sleep bruxism
Sleep enuresis
```
124
What disorders come under arousal disorders?
Confusional arousals
Sleepwalking
Sleep terrors
125
What disorders come under sleep-wake transition?
Sleep starts
| Sleep talking
126
What disorders come under REM sleep parasomnias?
REM behavioural disorder
Nightmares
Sleep paralysis
127
What comes under Sleep-related movement disorders?
Restless leg syndrome
Periodic limb movement disorder
Sleep-related bruxism
128
What comes under sleep disorders in ICD 10?
```
Nonorganic insomnia
Nonorganic hypersomnia
Nonorganic disorder of the sleep-wake schedule
Sleepwalking (somnambulism)
Sleep terrors
Nightmares
```
129
What is the most common circadian sleep disorder?
Delayed sleep phase syndrome
130
What happens in delayed sleep phase syndrome?
Patient is unable to fall asleep until very early morning.
131
Prevalence of narcolepsy
0.025%
132
Symptoms of narcolepsy
```
Excessive daytime sleepiness
Sudden sleep attacks (narcolepsy) - sleep is refreshing (REM)
Cataplexy
Sleep paralysis
Hypnagogic hallucinations
```
133
How many patients with narcolepsy have cataplexy?
75%
134
How many patients with narcolepsy have sleep paralysis?
30%
135
How many patients with narcolepsy have all 4 sx: narcolepsy, cataplexy, sleep paralysis and hypnagogic hallucinations?
10%
136
How many patients with narcolepsy have automatic behaviours?
33%
137
Is sleep duration increased in narcolepsy?
No - reduced and fragmented nocturnal sleep
138
What is strongly associated with narcolepsy?
HLA-DQB1*0602
| Low concentration of hypocretin-1 in CSF
139
What does sleep polysomnogram show in narcolepsy?
Sleep latency <10 minute
| Sleep-onset REM periods
140
Treatment for narcolepsy
Methylphenidate
| Modafinil
141
Treatment for Cataplexy
Imipramine
142
Prevalence of OSA
Men 4%
| Women 2.5%
143
Sx of OSA
```
Loud snoring
Breathing pauses
Mouth breathing
Restless sleep
Increased perspiration at night
Excessive daytime sleepiness
Morning headaches
Behavioural changes
```
144
What might occur in untreated OSA?
Right-sided cardiac failure
145
What is sleepwalking?
Partial arousal during slow-wave stages 3 and 4.
146
When is sleepwalking most common?
During initial third sate of sleep
147
What are night terrors?
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
When do night terrors occur?
During first third of night
| During stages 3-4 of NREM sleep
149
How does REM sleep behavioural disorder occur?
No loss of muscle tone in REM sleep so dreams are acted as complex behaviours.
150
When do REM sleep behavioural episodes occur?
Middle to latter third of night during REM sleep
151
Which disorders is REM sleep behavioural disorder associated with?
Parkinsons
Diffuse lewy body disease
MSA
GBS
152
What can REM behavioural disorder be prodrome of?
Diffuse Lewy body disease
Parkinsons
Precede diagnosis of movement disorder by years
153
What type of lesions is REM behavioural sleep disorder associated with?
Lesions in brainstem
154
Treatment of REM behavioural sleep disorder?
Clonazepam
| Make sleeping environment safe
155
Diagnostic criteria for REM behavioural sleep disorder?
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
Diagnostic criteria for restless leg syndrome in patients >12 y/o
Akathisia usually accompanied by paresthesia (core feature)
Motor restlessness
Sx worse at rest
Sx worse at night
157
What characterises restless leg syndrome
Unpleasant sensation in legs that preclude smooth transition from wakefulness to sleep.
158
How many patients with restless leg syndrome have periodic movements during sleep?
80-90%
159
Prevalence of restless leg syndrome
3-15%
160
M:F ratio of restless leg syndrome
1:2
161
How many patients with restless leg syndrome show a familial pattern?
>50%
162
Predisposing factors to restless leg syndrome?
```
Iron deficiency
Peripheral neuropathy
Sedating antihistamines
Centrally acting dopamine receptor antagonists - metoclopramide, prochlorperazine
Antipsychotics
Caffiene
Antidepressants
```
163
Treatment of restless leg syndrome
```
Sleep hygiene
Relaxation techniques
Dopaminergic agents
Anticonvulsants
Opiods
Clonazepam
```
164
First licensed drug for restless leg syndrome
Ropinirole
165
Which dopaminergic agents can be used for restless legs?
Nonergot D2 agonists: ropinrole, pramipexole
| Bromocriptine and dopaminergic precursors: levodopa/carbidopa
166
Which anticonvulsants can be used for restless legs?
Gabapentin
| CBZ
167
Which opioids can be used for restless legs?
Oxycodone
| Propoxyphene
168
What is Periodic Limb Movement Disorder?
Periodic episodes of repetitive and stereotyped limb movements during sleep.
Can cause clinical sleep disturbance.
169
What is required for diagnosis of Periodic Limb Movement Disorder?
Polysomnographic documentation of increased number of episodes in association with significant disruption fo sleep architecture and symptomatolgy.
170
What are polysomnographic diagnostric critera for PLMS based on?
EMG of right and left anterior tibialis muscles.
171
What does rate of PLMS increase with?
Age
172
How many patients with PLMS also have Narcolepsy?
45-65%
173
How many patients with PLMS also have REM sleep behavioural disorder?
70%
174
What pathology has been linked to PLMS?
Dopaminergic impairment
| Fe deficiency
175
Treatment for PLMD
Sleep hygeine
176
When is medication warranted for PLMD?
If sleep disruption
177
Medication treatment for PLMD?
Similar to restless legs
178
What is bruxism considered to be?
Stereotyped movement disorder or rhythmic disorder
179
When is bruxism more frequent?
Early part of sleep
May be related to stress/anxiety
May be related to dentition abnormalities/stimulant use
180
What type of disorders is related to initial insomnia?
Anxiety
181
What type of disorders are related to middle insomnia?
Medical illness
Pain syndromes
Depression
182
What type of disorders are related to Terminal insomnia?
Depression
