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Schizophrenia Flashcards

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1
Q

defining characteristic

A

there is no single defining characteristic
is a collection of seemingly unrelated symptoms.
there are many misconceptions and exaggerations surrounding the nature of schizophrenia.

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2
Q

DSM 5 classification

A

one positive symptom must be present

delusions, hallucinations or speech disorganisation

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3
Q

ICD-10 classification

A

2 or more negative symptoms are sufficient for diagnosis

e.g avolition and speech poverty

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4
Q

positive symptoms

A

additional experiences beyond those of ordinary existence

  1. hallucinations
  2. delusions
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5
Q

hallucinations

A

+ve symptom
sensory experiences that have no basis in reality or distorted perceptions of real things. experienced in relation to any sense.
e.g hearing voices or seeing people who aren’t there

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6
Q

delusions

A

+ve symptom
beliefs that have no basis in reality. make a person with schizophrenia behave in ways that make sense to them but are bizarre to others.
delusions of importance or persecution are common.
e.g beliefs about being a very important person or the victim of a conspiracy.

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7
Q

negative symptoms

A

loss of usual abilities and experiences

  1. avolition
  2. speech poverty
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8
Q

avolition

A

-ve symptom
severe loss of motivation to carry out everyday tasks (e.g work, hobbies, personal care)
results in lowered activity levels and unwillingness to carry out goal directed behaviours

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9
Q

speech poverty

A

-ve symptom
a reduction in the amount and quality of speech.
may include a delay in verbal responses during conversation
DSM emphasises speech disorganisation and incoherence

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10
Q

key issues with diagnosis (6)

A
  1. reliability
  2. validity
  3. co-morbidity
  4. symptom overlap
  5. gender bias
  6. cultural bias
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11
Q

issues with diagnosis
reliability
(evaluation)

A

the extent to which the diagnosis of schizophrenia is consistent
Cheniaux et al
2 psychiatrists independently diagnose 100 patients using both DSM and ICD criteria.
inter rater reliability was poor. one psychiatrist diagnosed 26 with schizophrenia using DSM and 44 using ICD. second psych diagnosed 13 with DSM and 24 with ICD.
this consistency between mental health professionals and the different classification systems is a limitation.

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12
Q

issues with diagnosis
validity
(evaluation)

A

the extent to which the diagnosis and classification techniques measure what they are designed to measure, schizophrenia.
a standard way to assess validity of diagnosis is criterion validity, do different assessments systems arrive at the same diagnosis for the patients Cheniaux et al study shows that schizo is much more likely to be diagnosed using ICD than DSM. this suggests that schiz is either over diagnosed in ICD or under diagnosed in DSM. this is poor validity and a weakness of the diagnosis

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13
Q

issues with diagnosis
co-morbidity
(evaluation)

A

2 conditions or more occur together. if conditions occur together a lot of the time it might call into question whether they are actually a single condition.
Buckley et al (2009)
concluded that around half patients with diagnosis of schiz also have a diagnosis of depression (50%) or substance abuse (47%).
in terms of classification if very severe depression looks like schizophrenia and vice versa, it may be they are a single condition. this confusing picture is a limitation.

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14
Q

issues with diagnosis
symptom overlap
(evaluation)

A

when 2 or more conditions share symptoms, questioning the validity of the classification

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15
Q

issues with diagnosis
gender bias
(evaluation)

A

review studies of the prevalence of schizophrenia and concluded that since the 1980s men have been diagnosed more often than women.
another study found female patients typically function better than men. this may explain why some women escape diagnosis because their better interpersonal functioning may bias practitioners to under diagnose schizophrenia.
this is a problem because men and women with similar symptoms may experience differing diagnoses.

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16
Q

issues with diagnosis
cultural bias
(evaluation)

A

African Americans and English people of African origin are much more likely to be diagnosed with schiz in the UK. rates in the west, indies and Africa are not high, so this is not due to genetic vulnerability.
higher diagnosis rates in the UK may be because some behaviours classed as +ve symptoms of schiz are normal in African cultures (e.g hearing voices as part of ancestor communication).
this highlights an issue in the validity of diagnosis because it suggests that individuals from some cultural backgrounds are more likely to be diagnosed than others due to bias.

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17
Q

genetic bias

family research

A

strong relationships between genetic similarity of family members and likelihood of both developing schiz
Gottesman’s (1991) family study found MZ twins have a 48% shared risk of schiz. DZ twins have a 17% shared risk and siblings (about 50% genes shared) have a 9% shared risk.

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18
Q

what does the existence of different candidate genes indicate?

A
  • schiz is polygenetic. each individual gene confers a small increased risk of schiz
  • Aetiologically heterogeneous. different combinations can lead to schiz.
    Ripke et al (2014) studied 37,000 patients and found 108 separate genetic variation associated with increased risk; many coded for the dopamine neurotransmitter.
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19
Q

dopamine hypothesis

role of dopamine

A

dopamine (DA) is widely believed to be involved in schiz because it is featured in the functioning of brain systems related to the symptoms of schizophrenia.

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20
Q

dopamine hypothesis

hyperdopaminergia linked to subcortex

A

high dopamine activity in subcortex (central areas of the brain) associated with hallucinations and poverty of speech.
(e.g excess of dopamine receptors in Broca’s area)

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21
Q

dopamine hypothesis

hypodopaminergia linked to prefrontal cortex

A

more recent versions of the hypothesis have focused on low levels of dopamine in the prefrontal cortex.
(responsible for thinking and decision making)

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22
Q

neural correlates

A

neural correlates are measurements of the structure or function of the brain that correlate with +ve or -ve symptoms of schizophrenia.

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23
Q

neural correlates

avolition + ventral striatum

A

ventral striatum is involved in anticipation of reward (relation to motivation)
loss of motivation (avolition) in schiz may be explained by low activity levels here.
Juckel et al (2006) found a -ve correlation between ventral striatum activity and overall negative symptoms.

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24
Q

neural correlates

hallucinations + superior temporal gyrus

A

Allen et al (200&) found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cinglulate gyrus

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25
Q

evaluation of biological explanations

strengths

A
  1. evidence for genetic vulnerability to schiz. Gottesman family study clearly shows how genetic similarity and shared risk are closely related. adoption studies show children of people with schiz are still at heightened risk of schiz if adopted into families without a history. overwhelming evidence that genetic factors make some people more vulnerable.
  2. role of mutations support genetic. schiz can take place in absence of family history (e.g through mutation of paternal DNA in sperm cells caused by radiation, poison or viral infection). Brown found link between paternal age and risk of schiz increasing from 0.7% in fathers under 25 to 2% in fathers over 50. this evidence supports importance of genetic factors.
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26
Q

evaluation of biological explanations

limitations

A
  1. mixed support for dopamine. dopamine agonists that increase dopamine induce schiz like symptoms in people without. anti-psychotic drugs that lower dopamine can be effective reducing symptoms however, some candidate genes code for production of other neurotransmitters. suggests that dopamine cannot provide complete explanation.
  2. correlation -causation problem
    whether unusual activity in brain causes the symptoms or other explanations. -ve correlation may suggest low activity in the ventral striatum causes avolition. but it could be that avolition means that less info passes through the striatum resulting in low activity. neural correlates tell us little about the causes.
  3. clear environmental involvement. after all the probability of developing schiz of MZ twins is only 50%. evidence environmental factors also play a role in development. suggests schiz may be result of combination of bio and psych approaches. interactionist.
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27
Q

family dysfunction

schizophrenogenic mother

A

Fromm-Reichmann’s (1948) psychodynamic explanation based on patients early experiences of schizophrenogenic mothers’ (mothers who cause schiz)
these mothers are cold rejecting and controlling and create a family climate of tension and secrecy. this leads to distrust and paranoid delusions and schiz.

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28
Q

family dysfunction

double bind theory

A

Bateson et al (1972) described how a child may be regularly trapped in situations where they fear doing the wrong thing, but receive conflicting messages about what counts as wrong. they cannot express their feeling about the unfairness of the situation.
when they get it wrong (often) the child is punished by withdrawal of love, they learn the world is confusing and dangerous, leading to disorganised thinking and delusions.

29
Q

family dysfunction

expressed emotion

A

expressed emotion (EE) is the level of emotion (mainly negative) expressed towards the schizophrenic patient and includes:
- verbal criticism of the patient
- hostility towards them
- emotional over-involvement in their lives
high levels of EE cause stress in the patient, a primary explanation for relapse in patients with schiz.

30
Q

what are the 3 family dysfunction explanations

A
  1. schizophrenogenic mothers
  2. double bind theory
  3. expressed emotion
31
Q

evaluation of family dysfunction explanation

A
  1. limitation evidence is retrospective. read et al reviewed 42 studies and concluded that 69% of all adult female inpatients with schiz (and 59% of men) had a history of physical and or sexual abuse. but most of evidence based on info about childhood gathered after the diagnosis. the symptoms may have distorted patients recall. validity problem.
  2. evidence is weak. poor childhood experience may be associated but there is little evidence to support. theories are based on clinical observations of patients (open to interpretation) they have also historically led to blaming of suffering parents. issues undermine appropriateness and credibility of family based explanation.
  3. biological factors overlooked. hard to reconcile. perhaps both bio and psych factors can separately produce the same symptoms this raises the question of whether both outcomes are schiz. alternatively diathesis stress model.
32
Q

cognitive explanations (3)

A
  1. dysfunctional thought processing
  2. meta representation leads to hallucinations
  3. dysfunction of central control leads to speech poverty.
33
Q

cognitive explanations

dysfunctional though processing

A

lower levels of information processing in some areas of the brain suggests cognition is impaired.
e.g reduced processing in the ventral striatum is associated with -ve symptoms

34
Q

cognitive explanation

metarepresentation leads to hallucinations

A

metarepresentation is the cognitive ability to reflect on thoughts and behaviours (Frith et al)
this dysfunction disrupts our ability to recognise our thoughts as our own, could lead to the sensation of hearing voices (hallucinations) and having thoughts placed in the mind by others (delusions)

35
Q

cognitive explanation

dysfunction of central control leads to speech poverty

A

Frith et al (1992) also identified dysfunction of central control as a way to explain speech poverty, central control being the cognitive ability to suppress automatic responses while performing deliberate actions.
people with schiz experience derailment of thoughts and spoken sentences because each word triggers automatic associations they they cannot suppress.

36
Q

evaluation of the cognitive explanation

A
  1. support for different info processing. Stirling et al compared 30 patients with 18 control on cognitive tasks (e.g Stroop test colour and coloured words). patients took twice as ling as the control group to suppress impulse to read the word and to name the ink colour instead this supports Frith theory of central control dysfunction. however it is not clear whether these faulty cognition are merely the proximal cause or the underlying distal cause.
  2. biological factors overlooked. hard to reconcile. perhaps both bio and psych factors can separately produce the same symptoms this raises the question of whether both outcomes are schiz. alternatively diathesis stress model.
  3. direction of causality. remains unclear whether cognitive factors are a cause or a result of the neural correlates and abnormal neurotransmitter levels. e.g does dysfunctional metarepresentation reduce levels of dopamine in the superior temporal gyrus or vice versa. this questions the validity of the approach in explaining underlying origins.
37
Q

typical antipsychotics

A

have been around since the 1950s

38
Q

dopamine antagonists

A

typical antipsychotics
they work by acting as antagonists in the dopamine system and aim to reduce the action of dopamine, they are strongly associated with the dopamine hypothesis

39
Q

how do dopamine antagonists work?

A
  • dopamine antagonists work by blocking dopamine receptors in the synapses in the brain, reducing the action of dopamine
    initially dopamine levels build up after taking chlorpromazine, but then production is reduced.
    this normalises neurotransmitter in key areas of the brain, which in turn reduces symptoms like hallucinations
40
Q

chlorpromazine

A

is a typical antipsychotic. dopamine antagonist.
word like a dopamine antagonists
but is also has an effect on histamine receptors which appears to lead to a sedation effect.
therefore it is also used to calm anxious patients when they re first admitted to hospital.

41
Q

atypical antipsychotics

A

have been used since the 1970s
target dopamine and serotonin
the aim of these drugs was to improve effectiveness of drugs in suppressing psychoses such as schiz and also minimise the side effects

42
Q

clozapine

A

atypical antipsychotic
acts on dopamine, glutamate and serotonin
clozapine binds to dopamine receptors as chlorpromazine does but also acts on serotonin and glutamate receptors.
this drug was more effective than typical antispychotics.
clozapine reduces depression and anxiety in patients as well as improving cognitive functioning
it also improves mood, which is important as up to 50% of people suffering from schiz attempt suicide.

43
Q

risperidone

A

atypical antipsychotic
developed because clozapone was involved in the deaths of some patients from a blood condition called agranulocytosis
risperidone like clozapine binds to dopamine and serotonin receptors
but risperidone binds more strongly to dopamine receptors and is therefore more effective in smaller doses than most antipsychotics and has fewer side effects.

44
Q

evaluation of drug therapies

strengths

A
  • evidence shows moderately effective
    review of data from 13 trials found that chlorpromazine was associated with better functioning and reduced symptoms severity compared with placebo. support for the benefits of atypical antipsychotics. clozapine more effective than typical and that it is 30-50% more effective in treatment resistant cases. reasonably effective
45
Q

evaluation of drug therapies

limitations

A
  • side effects. typical- dizziness, agitation, sleepiness, weight gain etc. long term use- lip smacking and grimacing due to dopamine super sensitivity. neuroleptic malignant syndrome (NMS) caused by blocking dopamine in hypothalamus disruption to body regulation. atypical developed to reduce side effects but some still exist.
  • theoretical objection. strongly tied with dopamine hypothesis. evidence that dopamine levels lower in other levels of the brain. undermined faith of +ve effects
  • doubts about true effectiveness. data from successful trials published multiple times exaggerating +ve effects. short term effects. powerful calming effect but might not be effective in reducing psychosis. overestimated by empirical research
  • chemical cosh. used in hospitals to calm patients make them easier for staff to work with rather than to the patients benefit. short term use to calm patients is recommended by NICE. human right abuse. raises ethical issues in the use.
46
Q

cognitive behaviour therapy

irrational thought

A

to help patients identify irrational thoughts and try to change them
this may involve discussion of how likely a patient’s beliefs are to be true, and consideration of less threatening possibilities.

47
Q

cognitive behaviour therapy

understand symptoms

A

patients are helped to make sens of how their delusions and hallucinations impact on their feelings and behaviour.
e.g a patient may hear voices and believe they are demons so they will be afraid
offering explanations for these symptoms reduces anxiety and helps the patients realise their beliefs are not based on reality

48
Q

family therapy

what are the 2 aims

A
  • reduce expressed emotion

- improve family function

49
Q

family therapy

reduce expressed emotion

A

family therapy is with families rather than individual patients, aiming to improve communication and interaction in the family.
family therapists try to reduce stress within the family that may contribute to patient’s risk of relapse

50
Q

family therapy
improve family function
researcher name
(4 techniques)

A

pharaoh et al (2010) identified a range of strategies family therapists use to reduce the likelihood of relapse and readmission to hospital. for example

  1. reduce stress of caring for a relative with schiz
  2. improve ability of family to anticipate and solve problems
  3. reduce guilt and anger in family members
  4. improve beliefs about and behaviour towards schiz
51
Q

token economies use a type of conditioning

A

operant conditioning
token economies are reward systems used to manage the behaviours of patients with schiz who spend long period sin psychiatric hospital
tokens are given to patients who carry out desirable behaviours.
this reward reinforces the desirable behaviour and because it is given immediately prevents delay discounting (reduced effect of a delayed reward.

52
Q

token economies

why are tokens secondary reinforcers

A

because the tokens have no value themselves but can be swapped later for tangible reward
they are secondary reinforces because they only have value due to the learned association (classical conditioning) with innate primary reinforcers.

53
Q

evaluation of psychological therapies

A
  1. research shows limited benefits. CBT had a significant but small effect on +ve and -ve symptoms. found only 1 out of 3 studies of token that used random allocation showed improvement. reviewed effectiveness of family therapy moderate evidence for reduction of hospital readmission. evidence inconsistent. only modest support.
  2. help but not cure. CBT helps patients make sense of symptoms. family therapy reduces stress. token economies makes behaviour more socially acceptable. does not cure schiz. although bio don’t cure they do reduce severity of symptoms.
  3. ethical issues. token economy severely ill patients cannot get privileges because they are less able to comply than moderately ill. suffer discrimination. CBT challenge person’s paranoia but might interfere with their freedom of thought. modifying politics.
  4. low quality of some evidence. small scale studies that compare patients before and after found +ve result but lack control or random allocation. include interviews effectiveness overstated.
  5. alternatives under researched. NICE recommends art therapy. these therapies are not well research unclear how effective. should they be made available to patients?
54
Q

diathesis stress model

A

diathesis means vulnerability
stress in this context refers to -ve psychological experiences.
both a vulnerability and a stress trigger are needed to develop schiz.

55
Q

Meehl’s model of diathesis stress

A

the original diathesis stress mode.
diathesis was entirely the result of a single schizogene
Meehl argued that someone without this gene should never develop schiz no matter how much stress they were exposed to.
but a person who does have the gene is vulnerable to the effects of chronic stress (e.g a schizophrenogenic mother)
the schizogene is necessary but no sufficient for the development of schizophrenia.

56
Q

modern understanding of diathesis

A

it is now believed that diathesis is not due to a single schizogene.
instead it is thought that many genes increase vulnerability.
also, diathesis doesn’t have to be genetic.
It could be early psychological trauma affecting brain development.
e.g, child abuse affects the hypothalamic- piturity- adrenal (HPA) system, making a child vulnerable to stress.

57
Q

modern understanding of stress

A

a modern definition of stress (in relation to diathesis-stress) includes anything that risks triggering schiz (including psychological stress)
e.g cannabis use can increase the risk of schiz up to 7 times depending on dose, probably because it interferes with the dopamine system

58
Q

treatments according to the interactionist approach

A

antipsychotic medication and CBT.
Turkington et al suggested it is possible to believe in biological causes of schiz and still practise CBT to relieve psychological symptoms
but this requires adopting an interactionist mode.
it is not possible to adopt purely biological approach tell patients that their condition is purely biological (no psychological significance to their symptoms) and then treat them with CBT

59
Q

UK approach to treating schiz

A

in Britain it is increasingly standard practice to treat patients with a combination of drugs and CBT

60
Q

US approach to treating schiz

A

there is more conflict between psychological and biological models of schiz and this may have led to slower adoption of the interactionist approach.

61
Q

evaluation of the interactionist approach

strengths

A
  1. support for dual role. studied children adopted away from schizophrenic mothers. the adoptive parents’ parenting styles were assessed and compared with a control. child rearing style with high levels of criticism and conflicts and low levels of empathy was implicated in development of schiz but only for children with high genetic risk. very strong direct support.
  2. usefulness in treatment. randomly allocated 315 patients (1) medication+ CBT (2) medication + supportive counselling (3) control. patients in the 2 combination groups showed lower symptom levels than thos in the control group. no difference in hospital readmission. clear practical advantage.
62
Q

evaluation of the interactionist approach

limitations

A
  1. original model too simplistic. multiple genes increase vulnerability each with a small effect there is no schizogene. stress comes in many forms. researchers now believe stress can also include biological factors. child sexual trauma was a diathesis and cannabis use trigger. old idea was too simplistic.
  2. don’t know how it works. strong evidence of diathesis stress, but don’t understand the mechanisms by which symptoms of schiz appear and how both produce them. does not undermine support but does mean its incomplete.
  3. treatment-causation fallacy. fact that combined biological and psychological therapies are more effective than either on their own does not necessarily mean interactionist is correct. similarity the fact that drugs help does not mean its biological. error of logic. superior outcomes of combined therapies should not be over interpreted in terms of evidence to support.
63
Q

quick evaluation of diagnosis and classification of schiz

A
  1. -ve diagnosis has low reliability
  2. -ve diagnosis lacks validity
  3. -ve co-morbidity
  4. -ve gender bias
  5. -ve cultural bias
64
Q

quick evaluation of biological explanations

A
  1. +ve strong evidence for genetic vulnerability
  2. -ve mixed support for the dopamine hypothesis
  3. -ve correlation-causation problem
  4. +ve role of mutation supports genetic explanations
  5. -ve clear environment also involved
65
Q

quick evaluation of psychological explanations

A
  1. -ve evidence for family relationships retrospective
  2. -ve evidence for family based explanations weak
  3. +ve support for different information processing
  4. -ve biological factors are sometimes overlooked
  5. -ve direction of causality in cognitive explanation
66
Q

quick evaluation of drug therapies

A
  1. +ve evidence shows antipsychotics are moderately effective
  2. -ve side effects
  3. -ve theoretical objection to the use
  4. -ve doubts about the true effectiveness
  5. -ve antipsychotic drugs are chemical cosh
67
Q

quick evaluation of psychological therapies

A
  1. -ve research shows limited benefits
  2. -ve help but not cure
  3. -ve ethical issues
  4. -ve quality of some evidence
  5. -ve alternative therapies under researched
68
Q

quick evaluation of interactionist approach

A
  1. +ve support for the dual role of vulnerability and stress
  2. -ve original model too simplistic
  3. +ve usefulness of interactionist approach in treatment
  4. -ve don’t know how diathesis and stress work
  5. -ve treatment causation fallacy

Psychology A level (15 decks)

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