Lecture 2 - Psychosis and schizophrenia Flashcards

1
Q

What are the five main psychosis symptoms?

A
  • Delusions
  • Hallucinations
  • Disorganised thinking/ speech
  • Disorganised behaviour
  • Social/ emotional flatness
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2
Q

What are the two positive symptoms of psychosis?

A

Hallucinations and delusions

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3
Q

What is an example of a persecutory delusion?

A

e.g. they’re out to get me

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4
Q

What is an example of a grandiose delusion?

A

e.g. I am more powerful than any human

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5
Q

What is an example of a nihilistic delusion?

A

e.g. the end of the world is nigh

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6
Q

What is an example of an erotomaniac delusion?

A

e.g. Kim Kardashian is in love with me

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7
Q

What is an example of a somatic delusion?

A

e.g. my stomach acid is dissolving my other organs

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8
Q

What is an example of a referential delusion?

A

e.g. the TV presenter is sending me signals

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8
Q

What is thought broadcasting, insertion and withdrawal?

A

People doing things with your thoughts that you have no control over

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9
Q

What are examples of types of delusions that can be bizarre or non-bizarre? (seen in older literature)

A

Bizarre would be somatic
Non-bizarre would be persecutory

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10
Q

Does delusion content reflect socio-political themes of an era?

A

Yes
More oppressive political regime shows increases in persecution and self-reference delusions
The spread of radio in 20s and TV in 50s showed increases in delusions of outside influence and control and technical themes
Reduced religious content in delusions reflects Western declines in organised religion

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11
Q

What is the definition of a delusion?

A

False beliefs that remain fixed despite conflicting evidence

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12
Q

What is the definition of a hallucination?

A

Vivid, clear sensory perceptions experienced in the absence of external stimulation

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13
Q

What are the five types of hallucinations?

A
  • Auditory (most common)
    • Visual (second most common)
    • Tactile - tingling or burning of the skin
    • Somatic - feeling of insects inside you
    • Gustatory (tastes) or olfactory (smells)
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14
Q

What is the most common and second most common kind of hallucination?

A

Auditory - most
Visual - second most

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15
Q

Luhrmann et al (2015) found that the meaning of people’s voice hearing experiences differed between cultures. How was this different between people from USA, South India and West Africa?

A
  • USA = voices as intrusive, unreal thoughts
  • South India = voices as providing useful guidance, sometimes unwelcome
  • West Africa = voices as morally good and causally powerful
  • Different levels of distress
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16
Q

What is the definition of negative symptoms?

A

Flattening of usual responses, these often persist beyond positive symptoms

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17
Q

What are the five types of negative symptoms?

A
  • Diminished emotional expression in face, body, gestures
  • Avolition - decrease in motivated self-initiated purposeful activities
  • Anhedonia - reduced pleasure from things that previously evoked pleasure
  • Asociality - decreased interest in social interactions
  • Alogia - decreased speech
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18
Q

What are the three main types of disorganisation in psychosis?

A
  • Disorganised thinking/speech (thought disorder)
  • Disorganised behaviour - motor symptoms
  • Other cognitive symptoms
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19
Q

What is speech poverty in thought disorder (disorganised thinking/speech)?

A

Coherent but slow and vague speech

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20
Q

What is an example of derailment/ loose associations in thought disorder (disorganised thinking/speech)?

A

e.g. switching topics

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21
Q

What is an example of tangentiality in thought disorder (disorganised thinking/speech)?

A

e.g. unrelated answers to questions

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22
Q

What is perseveration in thought disorder (disorganised thinking/speech)?

A

Repetition of words or trains of thought

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23
Q

What is an example of clanging in thought disorder (disorganised thinking/speech)?

A

e.g. stringing together words that rhyme

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24
Q

What is flight of ideas in thought disorder (disorganised thinking/speech)?

A

Leaping from one idea to another rapidly, often with discernible but meaningless pattern of linking

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25
Q

What are seven motor symptoms of disorganised behaviour?
C, N, H, A, P, S, I

A

Catatonic behaviour - decrease in reactivity to the environment
Negativism - resisting instructions and requests
Holding rigid, inappropriate or bizarre posture
Absence of verbal or motor response
Purposeless or excessive motor activity
Stereotyped movements, staring, grimacing
Involuntary movements

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26
Q

What four cognitive impairments can be seen in disorganisation in psychosis?
E, F, W, VL&M

A

Executive functioning
Focusing or paying attention
Working memory
Verbal learning and memory

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27
Q

What cognitive deficit can be an early warning sign for schizophrenia onset in high risk individuals? What evidence supports this?

A

Early difficulties with language/cognition can be very early warnings for schizophrenia onset in high risk individuals
- High risk adolescents’ deficits in verbal reasoning and verbal learning, and working memory, attention and processing speed predicted subsequent onset of schizophrenia, there was an abrupt not prolonged decline in preceding months

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28
Q

What has to happen for a diagnosis of brief psychotic disorder to turn into a schizophrenia diagnosis?

A

Episodes have to be recurrent (6 months of symptoms)

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29
Q

What is the DSM 5 diagnostic criteria for schizophrenia?

A

Must have either delusions, hallucinations or thought disorder
Must have one other symptom from the previous three OR abnormal motor behaviour OR negative symptoms
Symptoms occuring for at least 6 months
Have to rule out schizoaffective disorder and depressive/bipolar disorder with psychotic features, as well as substance use disorder

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30
Q

How long do symptoms have to occur for a schizophrenia diagnosis?

A

6 months

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31
Q

What is schizoaffective disorder?

A

Features of schizophrenia and severe mood disorder

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32
Q

What is schizophreniform disorder?

A

Schizophrenia-like psychoses lasting at least 1 month but less than 6 months

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33
Q

What is delusional disorder?

A

Delusional beliefs with otherwise normal behaviour

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34
Q

What is brief psychotic disorder?

A

Sudden onset of psychotic symptoms or disorganised speech or catatonic behaviour

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35
Q

What is the lifetime prevalence of schizophrenia? (per 100 people)

A

0.48 per 100 people

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36
Q

For every 7 men that develop schizophrenia, how many women develop it?

37
Q

What is the risk of dying when you have schizophrenia compared to when you do not have it?

A

Two or threefold risk when someone has schizophrenia

38
Q

What is the age peak of schizophrenia onset for men?

A

Late adolescence/ early adulthood

39
Q

Is there age-related prevalence of schizophrenia for women?

A

Slightly higher prevalence for schizophrenia after the menopause, otherwise not age-related

40
Q

What is the prodromal phase of schizophrenia? (Examples)

A
  • Gradual emergence of psychotic symptoms (sudden onset is rare)
  • Subtle changes e.g. unusual thoughts, abnormal perceptions, lack of interest in usual activities, impaired cognitive function
41
Q

What are key signs of a prodromal phase?

A
  • Early sign = lack of attention to personal care e.g., bathes / changes clothes less regularly
  • Behaviours increasingly unusual, speech affected
42
Q

Why is there a risk of symptoms worsening during the prodromal phase?

A
  • Often seen as just a phase by friends and family
  • Self-isolation during early symptoms makes symptoms worse
  • Critical period for intervention - this is why early intervention is so important
43
Q

Is schizophrenia a neurodevelopmental condition?

A

Not necessarily

While people with schizophrenia show differences in brain structure and function, schizophrenia is not purely caused by innate brain differences, as early life exposures shape the brain and behaviour inseparably

44
Q

What is the progression to schizophrenia as explained by the diathesis-stress model?
G P&P, NV, D&S OR P -> SZ

A

Genetic factors and prenatal and perinatal events ->
Neurological vulnerability ->
Developmental maturation process and stress factors (e.g. trauma, immune events, family) OR protective factors (e.g. nurturing family, low life stress, coping) -> Schizophrenia-spectrum disorder

45
Q

What is the dopamine hypothesis?

A
  • 50 years old - phenothiazines block dopamine receptors and reduce agitated symptoms, and amphetamines increase dopamine and cause symptoms mimicking schizophrenia
  • Theory - high levels of postsynaptic dopamine D2 receptor binding results in functional dopamine excess
46
Q

Is the dopamine hypothesis likely to be correct?

A

There is no evidence for higher levels of D2 receptors in drug-naïve people with schizophrenia
It could be increased dopamine synthesis instead, as well as other neurotransmitters

47
Q

What are the dopamine pathways and how are these different in people with schizophrenia?

A
  • Overactivity of the mesolimbic pathway (nucleus accumbens and ventral tegmental area) - positive symptoms
  • Mesocortical pathway dysfunction (ventral tegmental area and cortex) - negative and cognitive symptoms
48
Q

What were Stahl’s (2018) criticisms of the dopamine hypothesis?

A
  • Doesn’t adequately explain the cognitive/negative symptoms
  • 1/3 of patients don’t respond to dopamine focused treatments
  • Antipsychotics block dopamine rapidly but symptom relief takes weeks - something else must be going on too
  • Roles of glutamate and serotonin are increasingly recognised as important, and neurotransmitters are likely to interact in causing symptoms
49
Q

How enlarged are ventricles in schizophrenia?

A

25% bigger

50
Q

How reduced is brain volume in schizophrenia, what kind of matter and where in particular?

A

2% smaller
Mostly grey matter (neuronal cell bodies and synpases) (some white matter loss also found)
Mostly in the frontal lobe

51
Q

What might structural differences in the brain in schizophrenia be related to?

A

Possibly related to problems in development before or at birth

52
Q

What unusual patterns of brain activation are seen in schizophrenia?

A

Unusual patterns of activation for prefrontal cortex observed: underactive or overactive
Frontal cortex associated with planning, inhibition, goal setting i.e. cognitive symptoms of schizophrenia

53
Q

What issue is there in activation of the frontal cortex in people with schizophrenia?

A

Hypothesis: frontal cortex fails to appropriately deactivate, causing simultaneous findings of under- and over- activation (empirically supported)

54
Q

What are concordance rates for sz for MZ and DZ twins?

A

monozygotic = 48% dizygotic = 17%

55
Q

Is sz a polygenic condition?

A

Yes - multiple genes involved

  • Genes expressed in the brain and involved in brain development
  • Genes expressed in tissues with important roles in immunity
56
Q

What other conditions share genetic risk factors with those for sz?

A
  • There are shared genetic risk factors for schizophrenia spectrum and bipolar disorders - fits with observed symptom overlap between the conditions, notably delusions, low mood/negative symptoms, mania and hallucinations
  • Individual genes involved in schizophrenia are linked to other neurodevelopmental conditions
57
Q

How does the gene-environment interaction go both ways?

A
  • The environment can ‘activate’ pre-existing genetic risk for an individual;
  • Genetic features help determine how we shape and select our environments i.e. how we behave.
58
Q

Is risk of schizophrenia higher for men?

59
Q

Is risk of schizophrenia higher for people living in rural environments?

A

No
Higher for people living in urban environments (although there is mixed evidence)

60
Q

Is risk of schizophrenia higher for migrants?

61
Q

Is risk of schizophrenia higher for people who have experienced social adversity in infancy, childhood and adolescence?

62
Q

Is risk of schizophrenia higher for non-cannabis users?

A

No
Higher for cannabis users, especially if this is in adolescence or early adulthood

63
Q

Is risk of schizophrenia higher for people who sustain a serious head injury?

64
Q

Is risk of schizophrenia higher for people with immune disorders?

65
Q

Risk factors for sz: What are three obstetric risk factors?

A
  • Pregnancy complications (e.g., pre-eclampsia);
  • Abnormal foetal growth / development
  • Delivery complications

Oxygen deprivation during obstetric emergencies also impacts brain development in the neonatal period.

66
Q

Risk factors for sz: What are four antenatal factors?

A
  • Maternal stress / bereavement
  • Maternal poor nutrition
  • Maternal viral exposure
  • Metabolic, endocrine, and oxygen-related alterations to the uterine environment alter foetal development.
67
Q

How and why does sz incidence vary around the world for people born at certain times of the year?

A
  • Schizophrenia incidence may be higher for people born at certain times of year:
  • In the Northern Hemisphere, rates highest in people born between Jan - March.
  • This varies around the world: seasonal viruses may explain the effect
68
Q

How do viruses affect schizophrenia incidence?

A
  • Exposure to viruses in general may have an effect:
  • Levels of c-reactive protein (immune marker of infection) in amniotic fluid predict later schizophrenia in offspring.
69
Q

A history of trauma is common for psychotic symptoms, which symptom in particular?

A

Hallucinations

70
Q

What traumatic events are common risk factors to sz?

A
  • Abuse, other forms of violence/ victimisation, bereavement, and neglect
    Often chronic exposures i.e., long-term, inescapable

These can trigger the onset of psychotic episodes as well

71
Q

How does dissociation from reality as a trauma response lead to sz?

A
  • Dissociation from reality a self-protective mechanism BUT may predispose to other reality-dissociated experience such as hallucinations and delusions.
72
Q

Is trauma a risk factor specific to sz?

A

No

Trauma is also a risk factor for a wide range of other mental health conditions

73
Q

How do cognitive differences in sz help explain hallucinations?

A
  • Patients with schizophrenia have an impaired ability to distinguish internal from external events / inputs and are much poorer at judging the original source of material to be external (someone else) vs internal (self-generated)
  • May help explain perception of hallucinations as coming ‘from outside’
    Has been functionally linked to the prefrontal cortex
74
Q

What happened to the Genain quadruplets in terms of their presentations of sz?

A

All developed schizophrenia-spectrum disorders by the age of 24, but the presentation – and level of functioning – varied between individuals.
Pre-existing genetic risk as well as family environment.
Some of the quadruplets were treated more favourably than the others i.e. there were shared and non-shared environmental aspects that influenced the presenting phenotype.

75
Q

Are hallucinations inherently bad?

A
  • People in the healthy population experience hallucinations on a regular basis, without the other features of schizophrenia
76
Q

What do first generation antipsychotics do?

A

Phenothiazines
Block dopamine receptors to reduce obvious symptoms including hallucinations and delusions
Effectiveness shown in double-blind placebo controlled studies

77
Q

What type of anti-psychotic medication has led to extra-pyramidal side effects?

A

1st generation antipsychotics
Extra-pyramidal side effects common to start with, but usually fade
BUT
Tardive dyskinesia (TD) can result from long term use
Involuntary chewing and eye movements, facial grimacing, involuntary movements
Irreversible

78
Q

What % of patients do not respond to 1st generation antipsychotics?

79
Q

What are 2nd generation/ atypical antipsychotics?

A

Largely replaced first gen, equally effective but fewer extra-pyramidal side effects
Include clozapine, risperidone, olanzapine
Act on serotonin receptors as well as dopamine receptors
Some effectiveness against negative as well as positive symptoms

80
Q

What side effects are associated with atypical antipsychotics?

A

Clozapine associated with neutropenia requiring regular blood checks
Side effects: weight gain; metabolic disorders linked to heart disease & stroke

81
Q

Wat other disorder are atypical antipsychotics also used to treat?

A

Bipolar disorder

82
Q

Are antipsychotics a cure to sz?

A

No

Antipsychotics help to control symptoms but do not = cure
- Do not significantly improve quality of life or negative symptoms so often supplemented with psychological treatment
- Maintenance doses needed and relapse possible even when on antipsychotics

83
Q

What is the lifetime remission rate after one episode of sz?

A

About 20% lifetime remission rate after one episode of schizophrenia

84
Q

What is the greatest risk factor for sz relapse?

A

Greatest risk of relapse for patients who stop taking antipsychotics

85
Q

Why are talking therapies useful for sz patients?

A

Increasing use of talking therapies to help patients find meaning in their symptoms, spot triggers - aim to empower and de-stigmatise

86
Q

Why would people with sz choose not to take medication?

A

Many people with schizophrenia choose not to take medication, often due to side effects or experienced ineffectiveness.

87
Q

Is CBT effective treatment for sz?

A

Not really

The evidence base for CBT in schizophrenia is mixed, with several high-quality trials finding null effects.
Effectiveness has typically been found in meta-analyses of several trials at once (increased power). However, effect sizes are small.
NICE recommends the option of CBT for schizophrenia, but in practice medication is overwhelmingly relied on in NHS settings.
Whether CBT is the ‘correct’ talking therapy for schizophrenia needs to be explored in further research …

88
Q

What is avatar therapy? Is it successful?

A

Patient claims control, voice is embodied and less scary
- Creates a face and voice for an auditory hallucination
- Patient has opportunity to talk back to voice and have control over it, tell it to go away
- Throughout 10 minute session, avatar gradually concedes and listens to person telling it to go away
- Avatar therapy very successful in clinical trial

89
Q

What is the original dopamine hypothesis and is it correct?

A

Based on the fact that amphetamine drugs that temporarily increase dopamine can induce schizophrenia-like symptom
Hypthesised that people with schizophrenia have more D2 receptors
However, THEY DO NOT.