schizophrenia Flashcards

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1
Q

what is schizophrenia?

A

a severe psychotic disorder where contact with reality and insight are impaired.

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2
Q

two major classification systems for disorders

A
  1. The International Classification of Diseases 10 (ICD-10)
  2. The Diagnostic and Statistical Manual 5 (DSM-5)

The definitions in these manuals differ. This can lead to inconsistency and therefore unreliability however it can also be good since there is competition to be the “best most accurate manual”.

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3
Q

ICD classification of Schizophrenia

A
  • recognises sub-types
  • having a positive symptom is not necessary
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4
Q

DSM classification of Schizophrenia

A
  • does not recognise sub-types
  • one positive symptom must be present at the time of diagnosis
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5
Q

what are positive symptoms (give examples within schizophrenia)?

A
  • additional experiences to normal functioning
    eg. hallucinations
    eg. delusions aka paranoia
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6
Q

what are hallucinations?

A
  • unusual sensory experiences
  • can both be related and irrelated to the environment
  • such as voices (often critical) talking to or commenting on the sufferer
  • can be experienced in relation to any sense eg. distorted faces or people/animals that aren’t actually there
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7
Q

what are delusions?

A
  • irrational beliefs either of persecution (such as people following you) or of grandeur (such as believing you are a political figure)
  • mostly not aggressive and sufferers are more likely to be the victims than aggressors
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8
Q

what are negative symptoms (give an example from schizophrenia)?

A
  • the loss of usual functioning/experiences
    eg. avolition aka apathy
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9
Q

what is avolition (apathy)?

A
  • finding it difficult to begin or keep up with goal-directed activity, sharply reduced motivation
    > Andreason (1982) identified 3 identifying signs of avolition: poor hygiene and grooming, lack of persistence in work/education, lack of energy
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10
Q

what is speech poverty (compare ICD and DSM)?

A

In the ICD-10, speech poverty is considered a negative symptom of schizophrenia characterised by:
- changes in patterns of speech
- reduction in the amount and quality of speech
- sometimes accompanied by a delay in verbal responses during conversation

The DSM 5 places emphasis more on speech disorganisation in which the speech becomes incoherent or involves mid-sentence topic changes, this is classified as a positive symptom.

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11
Q

what were the subtypes of Schizophrenia?

A

Paranoid Schizophrenia - powerful delusions but relatively few other symptoms
Hebephrenic Schizophrenia - primarily negative symptoms present (also called disorganised)
Catatonic Schizophrenia - disturbance to movement leaving the sufferer immobile

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12
Q

what is classification?

A

the process of organising symptoms into categories based on which symptoms cluster together in sufferers. Psychologists use the DSM and ICD to diagnose patients with Schizophrenia

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13
Q

what is diagnosis?

A

the assigning of a label to a patient

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14
Q

reliability issues in the diagnosis/classification of schizophrenia

A
  • level of agreement on a diagnosis by different psychiatrists (inter-rater reliability)
  • stability of diagnosis overtime (when symptoms remain unchanged)
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15
Q

validity issues in the diagnosis/classification of schizophrenia

A
  • symptom overlap (especially with bipolar)
  • gender bias
  • culture bias
  • comorbidity (especially with depression, substance abuse, and PTSD)
  • criterion validity (both assessment systems arrive at the same diagnosis for the same patient)
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16
Q

Cheniauz et al. (2009) - schizophrenia diagnosis has low criterion and inter-rater reliability

A
  • two psychiatrists independently diagnose 100 patients using both DSM and ICD criteria.
  • one psychiatrist diagnosed 26 according to the DSM and 44 according to the ICD and the other diagnosing 13 according to the DSM and 24 according to the ICD - LOW INTER-RATER

> some patients may not receive a diagnosis when it is needed, inhibiting their ability to obtain treatment
low criterion validity (either over- or under- diagnosed using the ICD or DSM), may receive a diagnosis when they shouldn’t, perhaps leading to the use of unsuitable medications

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17
Q

Buckley et al. (2009) - comorbidity of Schizophrenia

A
  • 50% of patients with Schizophrenia are also diagnosed with depression, 47% are also diagnosed with substance abuse, 29% with PTSD, and 23% with OCD.
    > could be that practitioners are poor at telling the difference between conditions like depression and schizophrenia
    > if someone is incorrectly diagnosed with schizophrenia, this is difficult to change later and could result in the use of ineffective/inappropriate treatments which could worsen symptoms
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18
Q

Longenecker et al. (2010) - prevalence in men vs women

A
  • reviewed studies on the prevalence of Schizophrenia and found that (since the 1980s) men have been diagnosed with schizophrenia more frequently than women.
    > could reflect genuine differences in prevalence or reflect the gender bias in the classification/diagnosis of Schizophrenia
    > lack of faith in the mental health field due to failure to diagnose when women seek out help
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19
Q

Cotton et al (2010) - characterisation in men vs women

A

found that female patients typically function better than men, being more likely to work and have good family relationships.
> so may go undiagnosed

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20
Q

Harrison et al. - culture bias

A
  • found that African Americans and English people of Afro-Caribbean origin are 8 times more likely to be diagnosed with schizophrenia than white people.
    > Escobar (2012) explained this by pointing out that psychiatrists (often white) tend to over-interpret symptoms and distrust the honesty of black people during diagnosis
    > some African cultures find hearing voices more acceptable due to cultural beliefs in talking to ancestors, this could mean that they are more likely to acknowledge and report these experiences
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21
Q

writing about issues with classification/diagnosis of schizophrenia

A
  • no AO1 paragraph at the start
  • in a 16 marker, at least 4 PEECs describing and evaluating each issue
  • in an 8 marker, at least 2, ideally 3 PEECs
  • for each paragraph:
    1. state the issue
    2. explain what the issue is
    3. bring in evidence of this issue
    4. explain why this is a problem
    5. detailed consequence of this issue
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22
Q

Rosenhan’s study: ‘On Being Sane in Insane Places’ (1973)

A

> testing stability of diagnosis over time (when symptoms change)
- 8 pseudopatients at different hospitals claimed to hear unfamiliar voices of the same sex as the pseudopatient saying ‘empty’, ‘hollow’, and ‘thud’
- 7 were diagnosed with schizophrenia and 1 with manic depression
- once admitted, they behaved normally and wrote down their observations of the institution
- staff never detected that they were ‘sane’ and interpreted ‘normal’ behaviours as abnormal eg. pathological writing

23
Q

conclusions based on Rosenhan’s research

A
  • so their symptoms changed but the diagnosis didn’t, suggesting that the diagnosis was not reliable over time
    > since then, the system has changed significantly and the study is also over forty years old

It is also very difficult to get a diagnosis removed, especially if it is one that invalidates your view of reality.

24
Q

what are the biological explanations for schizophrenia?

A

genetics and neural correlates

25
Q

genetic explanations for schizophrenia

A
  • investigated using family, adoption, and twin studies
  • schizophrenia has been found to run in families
  • a positive correlation has been found between genetic similarity and shared risk of developing schizophrenia
  • concordance rates are used to demonstrate the percentage risk of developing schizophrenia, eg. Gottesman (1991)
  • Schizophrenia is polygenic and aetiologically heterogeneous
  • 108 candidate genes for schizophrenia
26
Q

what are candidate genes?

A
  • individual genes believed to have an association with risk of inheritance, Schizophrenia appears to have a number of candidate genes so is polygenic
27
Q

candidate genes in Schizophrenia

A
  • according to Ripke et al. (2014), Schizophrenia has been associated with 108 separate genetic variations
  • since it appears to have a number of genes that give an increased risk, it is considered polygenic (requires a number of factors to work in combination)
28
Q

what does aetiologically heterogeneous mean?

A
  • different combinations of factors can lead to the condition
29
Q

evaluation of the genetic explanation

A

+ Gottesman as supporting the genetic explanation, as genetic similarity increased, so did concordance
- MZ twins do not have 100% concordance rate so there must also be environmental factors, siblings and DZ twins have different concordance rates but the same genetic similarity
- not useful, not direct causation from the 108 candidate genes
- diathesis stress model/interactionist approach may be a better alternative to genetics as a sole explanation
- dangerous to link genetics to characteristics/disorders, eg. eugenics policies

30
Q

what are neurotransmitters?

A
  • endogenous (internal) chemicals that enable neurotransmission
  • a type of chemical messenger which transmits signals across a chemical synapse
  • carry, boost, and balance signals between neurons, or nerve cells, and other cells in the body.
  • sent over synapses whereas hormones travel through the bloodstream.
31
Q

the dopamine hypothesis

A
  • the neurotransmitters of a schizophrenic patient seem to work differently to a non-schizophrenic individual (although the differences are not the same across all patients)
  • in particular, dopamine is believed to be involved in the disorder with excess or lack of the neurotransmitter in specific areas of the brain
  • dopamine is important in the functioning of several brain symptoms that may be implicated in the symptoms of schizophrenia
  • two types: hyperdopaminergia and hypodopaminergia
32
Q

hyperdopaminergia

A
  • the original dopamine hypothesis
  • high levels of dopamine in the subcortex (just below the outer edge of the forefront of the brain)
  • could be that messages from neurons fire too easily or too often leading to hallucinations and delusions, also individuals with schizophrenia are thought to have abnormally high numbers of D2 receptors on post-synaptic neurons, resulting in more dopamine binding and therefore more neurons firing
33
Q

example for hyperdopaminergia

A
  • eg. an excess of dopamine receptors in Broca’s area (responsible for speech production) may be association with poverty of speech in schizophrenics
34
Q

amphetamines evidence for hyperdopaminergia

A
  • amphetamine stimulates nerve cells containing dopamine causing the synapse to be flooded with dopamine, typically individuals exposed to large doses develop characteristic hallucinations and delusions of a schizophrenic episode, this generally disappears with abstinence from the drug
  • people who suffer from Parkinson’s who take the drug L-dopa to raise the levels of dopamine have also displayed schizophrenic symptoms
35
Q

Hypodopaminergia and example

A
  • the more recent version of the hypothesis
  • abnormal dopamine systems in the brain’s cortex
  • eg. Goldman-Rakic et al. (2004) have identified a role for low levels of dopamine in the prefrontal cortex (responsible for thinking and decision making) in the negative symptoms of schizophrenia eg. disordered thinking and avolition
36
Q

ventral striatum and schizophrenia (neural correlates)

A
  • responsible for motivation and the anticipation of reward > avolition
  • eg. Juckel et al. (2006) measured activity levels in the ventral striatum of people with schizophrenia and found much lower activity than in control groups
  • They also observed a negative correlation between activity levels in the ventral striatum and severity of negative symptoms
37
Q

superior temporal gyrus and anterior cingulate gyrus

A

eg. Allen et al. scanned the brains of patients experiencing auditory hallucinations and a control group whilst they identified pre-recorded speech as theirs or others, low activation levels in these areas were found in the hallucination group, they also made more errors

38
Q

evaluation of the dopamine hypothesis

A

+ amphetamine research
+ practical applications for helping people with schizophrenia (drug therapies to change the dopamine levels)
- correlation not causation - it may be that the symptoms are altering brain chemistry, so avolition leading to low levels of dopamine in the prefrontal cortex
- neglects environmental factors, too simplistic (eg. diathesis stress model)

39
Q

two types of drug given to treat schizophrenia

A
  1. Typical antipsychotics - 1st generation, developed in the 1950s, primarily used to combat the positive symptoms of schizophrenia
  2. Atypical antipsychotics - 2nd generation, combat positive symptoms but also have some benefit on negative symptoms
40
Q

typical antipsychotics

A
  • aim to reduce the effect of dopamine and so reduce the symptoms of schizophrenia
  • work by acting as antagonists in the dopamine system (bind to but do not stimulate dopamine receptors in the synapses of the brain therefore blocking their action and thus reducing the action of dopamine)
  • this dopamine antagonist effect normalises neurotransmission in key areas of the brain, reducing symptoms of hallucinations and delusions
    eg. Chlorpromazine (1950s)
41
Q

atypical antipsychotics

A
  • called ‘second generation’ because of their three main differences to typical antipsychotics:
    1. they carry a lower risk of extrapyramidal side effects (related to movement)
    2. have a beneficial effect on negative symptoms and cognitive impairment
    3. suitable for treatment-resistant patients
  • these drugs also act on the dopamine system but by temporarily blocking D2 receptors but then rapidly dissociate to allow normal dopamine transmission
42
Q

clozapine

A

(1970s - atypical antipsychotic) binds to dopamine receptors but it also acts as an agonist (increase) on serotonin and glutamate receptors believed to help improve mood and reduce depression, due to this, clozapine is sometimes prescribed when a patient is at particular risk of suicide

43
Q

risperidone

A

(1990s- atypitcal antipsychotic)
- an attempt to produce a drug as effective as Clozapine but without the serious side effects
- believed to bind to dopamine and serotonin receptors but binds to dopamine receptors much more strongly than Clozapine so it is effective in much smaller doses
- it is believed that because of this it produces less side effects.

44
Q

evaluation of biological therapies for schizophrenia

A

+ supporting evidence eg. Thornley et al. compared the effects of chloropromazine to control conditions in which patients recieved a placebo, 1121 participants showed that the drug produced better overall functioning and reduced symptom severity, relapse rate was also lower
> David Healey suggested that studies are exaggerating the evidence for positive effects eg. powerful calming effects of antipsychotics may have been confused with positive results, the drug treatments are not actually reducing severity of psychosis, many studies also fail to assess long-term effects and significant withdrawal symptoms
> still improving quality of life?
- in response to criticisms around the severe side effects which raise ethical issues, eg. coma, death, tardive dyskenesia (involuntary facial movements), atypical antipsychotics have significantly reduced side effects in comparison to typical antipsychotics
- medication may not be an appropriate treatment for patients dealing with less severe hallucinations/questioning reality, they may refuse to take tablets so talking therapy may be more useful to deal with symptoms so that they will engage with medication, therapy is also useful for dealing with family dysfunction which can be an underlying cause

45
Q

psychological explanations of schizophrenia

A
  1. family dysfunction (double bind theory, expressed emotion, schizophrenogenic mother)
  2. cognitive explanations (for hallucinations and for delusions)
46
Q

double-bind theory

A
  • Bateson’s (1956)
  • suggests that the developing child regularly finds themselves in situations where they feel they are doing the wrong thing but they repeatedly receive mixed messages about what this is
  • when the child ‘gets it wrong’ they are punished with withdrawal of love
  • this leaves them with the belief that the world is confusing and dangerous, causing them to develop a false concept of reality and an inability to communicate effectively
  • this is reflected in the symptoms of schizophrenia (disorganised thinking, paranoid delusions)
  • Bateson was clear that his double-bind theory was a risk factor for developing schizophrenia not the only factor
47
Q

flow chart of the double-bind theory

A

child receives mixed messages about right and wrong —> gets it wrong —> withdrawal of love from parent –> false concept of reality and cannot communicate effectively —> disorganised thinking and paranoia

48
Q

expressed emotion

A
  • originally based on work by Brown (1972) which suggested that patients with Schizophrenia are 4x more likely t o relapse if they returned to homes characterised by high levels of expressed emotions eg. hostility, criticism, and over-concern
  • high levels of expressed emotion are a serious source of stress for the patient beyond their already impaired coping mechanisms thus triggering a schizophrenic episode
49
Q

how is expressed emotion measured?

A

measured by taping an interview with a relative of someone with schizophrenia and rating the following:
- hostility
- critical comments
- over-concern and over-involvement

50
Q

issues with the method of measuring expressed emotion

A
  • subjective and open to bias
  • only a snapshot in time, they may not act in the same way around the person - they are under a lot of stress and pressure (an opportunity to vent and be honest)
  • social desirability bias
  • hard to differentiate between categories (especially critical comments and hostility)
  • given the situation, a loved one who has schizophrenia and may have put themselves in danger before, over-concern may not be unreasonable
51
Q

schizophrenogenic mother

A

(schizophrenia-causing)
- Fromm-Reichmann (1948) proposed a psychodynamic explanation for schizophrenia based on the accounts she heard from her patients about their childhoods
> retrospective studies like this are often inaccurate due to memory
> reality-distortion

52
Q

the schiziphrenogenic mother is… how does this lead to schizophrenia?

A
  • cold
  • rejecting
  • controlling
  • creates a family climate characterised by tension and secrecy
    These characteristics lead to distrust that then later develops into paranoid delusions and, ultimately, schizophrenia.
53
Q

evaluation of family dysfunction as an explanation of schizophrenia

A

+ Bateson recognises that DBT is a risk factor which allows for and encourages further research
- retrospective data-collection which is inaccurate (schizophrenogenic mother and double-bind)
- subjective methods of investigation
- ethical implications: could lead to blame (eg. “schizophrenogenic mother”) for families who are already likely to be struggling

54
Q
A