Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MRCPsych Part B > 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is apathy without depression linked to in Parkinsons?

A

Executive dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is mania linked to in Parkinsons?

A

Levodopa
Dopamine agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

Pre-existing bipolar
FHx of bipolar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Side effects of Levodopa

A

Hypomania
Pathological gambling
Hypersexuality
Hallucinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Rate of drug-induced hallucinatinos in Parkinsons

A

20% - mainly visual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Rate of drug-induced delusions in Parkinsons

A

3-30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Treatment of drug-induced psychosis in Parkinsons

A

<100mg/day of Clozapine
Quetiapine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When does cognitive impairment suggest poor prognosis of Parkinsons?

A

If present at time of initial referral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Risk factors of cognitive impairment in Parkinsons?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Neurobiology of those with Parkinsons and cognitive impairment

A

Frontal executive dysfunction with subcortical pattern of dementia
Neuroleptic sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment for cognitive impairment in Lewy Body Dementia?

A

Rivastigmine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment for Parkinson related dementia>

A

No drugs licensed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Onset of sx of Huntingtons

A

Middle age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Prevalence of psychiatric sx in Huntingtons at first presentation?

A

30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Suicide rates in patients with Huntingtons

A

4x higher than general population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How many patients with Huntingtons first present with schizophreniform psychosis?

A

3-6%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

When can OCD-like sx occur in Huntingtons?

A

If basal ganglia involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the mutant protein in Huntingtons?

A

Huntingtin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where is gene for Huntington Disease?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

When is Huntingtons fully penetrant?

A

CAG repeats reach 41 or more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When does Huntingtons show incomplete penetrance?

A

36-40 repeats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How many repeats is associated with no Huntingtons disorder?

A

35 or less

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

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

A

60%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Penetrance of Huntingtons

A

95%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How many patients present with Wilsons disease via psychiatric presentations?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

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

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Most common psychiatric sx of Wilsons?

A

Personality disturbance
Mood abnormalities
Cognitive dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which form of Wilsons have psychiatric manifestations usually?

A

Neurological rather than hepatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How many patients with Wilsons have cognitive impairment?

A

25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What type of dementia occurs in Wilsons?

A

Frontosubcortial pattern of dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How many patients with Wilsons have depression?

A

30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How many patients with Wilsons show suicidal behaviour?

A

4-16%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How many patients with Wilsons have psychosis?

A

2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Treatment of Wilsons

A

Copper chelating or depleting agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is essential for treatment of Wilsons?

A

Early diagnosis and initiation of treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Rate of transient global amnesia

A

5-10/100,000 per year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

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

A

30/1000,000 per year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Aetiology of transient global amnesia

A

Hypoperfusion in temporal and parietotemporal regions, mainly left hemisphere

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Episode length of transient global amnesia

A

6-24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Recurrence rate of transient global amnesia

A

Most patients show complete improvement but recurrence is high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What happens in Fahrs disease?

A

Idiopathic progressive calcium deposition in basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Onset of Fahrs disease

A

20-40 years
40-60 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is Fahrs disease at 20-40 years associated with

A

Schizophreniform psychoses
Catatonic sx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

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

A

Dementia
Choreoathetosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How many patients with Fahrs disease have psychiatric sx?

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What do psychiatric sx correlate with in Fahrs disease?

A

More extensive calcification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Cognitive impairment in Fahrs disease?

A

Frontosubcortical type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Neurological sx of Fahrs disease

A

Parkinsonism
Chorea
Dystonia
Tremor
Gait disturbance
Dysarthria
Seizures
Myoclonus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

MRI sign of Fahrs disease

A

Hypointensity of striatum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Commonest cause of viral encephalitis?

A

Herpes simplex encephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Commonest cause of limbic encephalitis

A

Herpes simplex encephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is affected in limbic encephalitis?

A

Temporal lobe
Limbic circuit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

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

A

70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

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

A

Herpes Simplex Type 2
HHV 6 or 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Sx of HSE?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

How many patients with HSE show psychiatric disturbance?

A

70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Neuroimaging results of HSE

A

Signal change and swelling within temporal lobes on MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What does CSF show in HSE

A

Lymphocytosis and raised protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Gold standard test for HSE

A

CSF PCR for herpes viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Most sensitive investigation for detecting early lesions in HSE

A

MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Earlier signs in EEG of HSE

A

Non-specific slowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Later signs in EEG of HSE

A

High voltage periodic lateralizing epileptiform discharges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Fatality of HSE is untreated

A

70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Treatment of HSE

A

IV aciclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

By how much does IV aciclovir reduce mortality of HSE?

A

To 20-30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 (64 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions