Schizophrenia Flashcards

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1
Q

What is schizophrenia?

A

a severe mental disorder where contact with reality and insight are impaired

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2
Q

How are diagnosis and classification are interlinked?

A

in order to diagnose a specific disorder, u need to distinguish one disorder from another by identifying symptoms that occur together and classifying that as one disorder

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3
Q

What are the 2 major systems for the classification of of mental disorder ?

A

World health organisation international classification of disease (ICD-10)

American psychiatric association diagnostic and statistical manual diction 5 (DSM-5)

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4
Q

To diagnose schizophrenia:
a) what does the DSM-5 state
b) what does the ICD-10 state?

A

a) DSM-5: 1” positive symptom” must be present
b) ICD-10: 2 “negative symptoms” must be present

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5
Q

what are the positive symptoms of sz?

A

hallucinations
delusions

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6
Q

what are hallucinations?

A

unusual sensory experiences:
some are related to events in environment whereas others bear no relationship to what the senses are picking up from the environment
e.g voices heard either talking to or commenting on a person

can be experienced in relation to any sense
e.g person sees distorted facial expressions or occasionally people/animals that are not there

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7
Q

what are delusions?

A

(paranoia) irrational beliefs
common ones: being an important historical, political or religious figure, being persecuted e.g by government/aliens, having superpowers, may believe they are under external control

ppl w delusions more likely to be victims but some lead to aggression

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8
Q

what are negative symptoms of sz?

A

(involves loss of usual abilities)
speech poverty
avolition

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9
Q

what is speech poverty?

A

(Seen as a negative symptom bc of emphasis on reduction in the amount n quality of speech, somet8mes accompanied by a delay in persons verbal responses during convo )
more emphasis is now placed on SPPECH DISORGANISATION (speech becomes incoherent or speaker changes topic mid sentence)
classified as a positive symptom in DSM-5 but remains a negative symptom

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10
Q

what is avolition (apathy)?

A

described as finding it difficult to begin or keep up with a goal-directed activity
ppl w sz have sharply reduced motivation to carry out range of activities

andreasen (1982) identified 3 signs of avolition:
poor hygiene n grooming, lack of persistence in work/education, lack of energy

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11
Q

eval: how is it a a strength that the diagnosis of sz has good reliability?

A

reliability has now improved: osorio et al. (2019) reported excellent reliability for diagnosis in 180 individuals using DSM-5. pairs of interviewers achieved inter-rater reliability (when diff clinicians reach the same diagnosis for same individual) of +9.7 and test-retest reliability (when same clinician reaches same diagnosis for same individual on 2 occasions) of +9.2

means we can be reasonably sure that the diagnosis of sz is constantly applied

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12
Q

eval: how is it a limitation that the sz diagnosis has co-morbidity with other conditions?

A

if conditions occur together, questions the validity of diagnosis and classification as it may be a single condition
sz is common,y diagnosed w other conditions e.g depression/substance abuse

problem for classification s sz may not exist as a distinct condition
prom for diagnosis as at least some pp, w sz may have unusual cases if conditions e.g depression

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13
Q

eval: how is it a limitation that there is an existence of gender bias?

A

since 1980s men diagnosed more than woman ( 1.4:1 fischer n buchanan 2017)
possible explanation: women are less vulnerable than men bc of genetic factors
women under diagnosed as they have close relationships and get support (cotton et al. 2009) leading to women w sz functioning better than men

underdiagnosis = gender bias and means women may not be receiving treatment and services that might benefit them

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14
Q

eval: how is it a limitation that there is an existence of culture bias?

A

some symptoms of sz e.g hearing voices, have diff meaning in diff cultures (in Afro-caribbeans, may mean communication from ancestors)
culture bias as diagnosis if clients is done by psychiatrists from a diff cultural background, appears to lead to an over-interpretation if symptoms in black British people (Escobar 2012)

means Afro-Caribbean people may be discriminated against by a. Culturally-biased diagnostic system

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15
Q

eval: how is it a limitation that there is a symptom overlap with other conditions?

A

overlap between sz n other conditions e.g bipolar disorder : both involve positive symptoms e.g delusions and negative symptom e.g avolition
in terms of classification: suggests sz and BPD may be a variation of a single condition rather than 2 different ones
in terms of diagnosis it means sz is hard to distinguish from BPD

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16
Q

how have family studies confirmed the risk of sz increases in line w genetic similarity to a relative w sz?

A

gottesman’s (1991) large-scale family study found
e.g person w aunt w sz has a 2% chance of developing
increases to 9% if individual is a sibling and 48% if they are a twin

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17
Q

how is sz polygenic?

A

a number of different genes are involved (genes coding for neurotransmitters e.g dopamine)

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18
Q

what did the study conducted by ripke et al. (2014) show?

A

combined previous data from genome wide studies
genetic makeup of 37k people w diagnosis of sz were compared to that of 113k controls

found 108 separate genetic variations were associated w slightly increased risk of sz

shows sz is AETIOLOGICALLY HETEROGENEOUS (bc diff studies have identified diff candidate genes i.e diff combos of factors including genetic variation can lead to sz)

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19
Q

how can sz have genetic origin in the absence of a family history of the disorder?

A

explanataion: mutation in parental DNA caused by radiation, poison, viral infection

evidence for mutation comes from positive correlations between paternal age (associated w increased risk of sperm mutation) and risk of sz, increasing from 0.7% w fathers under 25 to over 2% in fathers over 50 (brown et al. 2002)

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20
Q

what was the original dopamine hypothesis?

A

based on discovery that drugs used to treat sz (antipsychotics which reduce dopamine) caused symptoms similar to those in people w parkinsons disease (associated w low dopamine levels)

therefore s must be result of high dopamine levels in subcortical parts of the brain

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21
Q

eval: how is it a strength that the genetic explanation has a strong evidence base?

A

gottssman: shows risk increases w genetic similarity

adoption studies e.g tienari et al. (2004): shows biologiczl children of parents w sz are at heightened risk even if they grow up in an adoptive family

shows people are more vulnerable to sz as a result of their genetic makeup

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22
Q

eval: how is it a limitation that there is evidence to show that environmental factors also increase the risk of developing sz?

A

environmental factors include biological (birth complications and smoking THC rich cannabis in teenage years) and psychological influences (childhood trauma, leaves ppl more vulnerable to mental health problems)

morkved et al. (2017) 67% of ppl w sz and related psychotic conditions reported at least one childhood trauma as opposed to 38% of a matched group w non-psychotic mental health problems

MEANS GENETIC FACTORS ALONE CANNOT PROVIDE A COMPLETE EXPLANATION FOR SZ

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23
Q

eval: how is it a strength that dopamine is involved in sz?

A
  1. amphetamines increase D and worsen symptoms in people w sz and induce symptoms in people without (curran et al. 2004)
  2. antipsychotic drug reduce D activity and reduce intensity of symptoms (tauscher et al. 2014)
  3. candidate genes act on production of D/D receptors

strongly suggests that D is involved in symptoms of sz

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24
Q

eval: how is it a limitation of the dopamine hypothesis that there is evidence for central role of glutamate?

A

post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in severl brain regions of people w sz (McCutcheon et al. 2020)

several candidate genes for sz are believed to be involved in glutamate production or processing

MEANS THAT AN EQUALLY STRONG CASE CAN BE MADE FOR A ROLE FOR OTHER NTS

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25
Q

what was the psychodynamic explanation for sz proposed fromm-reichmann (1948)

A

schizophrenogenic (sz causing) mother
(based off accounts of patients talking ab particular type of parent)

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26
Q

what are the characteristics of the schizophrenogenic mother?

A

cold, rejecting, controlling
tends to create family climax (characterised by tension n secrecy)

leading to distrust that later develops into paranoid delusions and ultimately sz

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27
Q

what is the double-bind theory proposed by bateson et al. (1972)?

A

agreed family climate is important in the development of sz but emphasised role of communication style within a family

developing child finds themselves trapped in situations where they fear doing the wrong thing and seek clarification ab mixed signals

child punished by withdrawal of love
(leaves them w disorganised thinking and paranoid delusions)

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28
Q

what are expressed emotions?

A

the level of emotion (particularly negative emotion) expressed towards a patient by their carers who are often family members

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29
Q

what are the elements of expressed emotions?

A
  1. verbal criticism of the patient occasionally accompanied by violence
  2. hostility towards the patient including anger and rejection
  3. emotional over involvement in the life of a patient including needles self sacrifice
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30
Q

what are the elements of expressed emotions?

A
  1. verbal criticism of the patient occasionally accompanied by violence
  2. hostility towards the patient including anger and rejection
  3. emotional over involvement in the life of a patient including needles self sacrifice
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31
Q

what are the cognitive explanations for sz?

A

dysfunctional thinking
metarepresentation dysfunction
central control dysfunction

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32
Q

what are the cognitive explanations for sz?

A

dysfunctional thinking
metarepresentation dysfunction
central control dysfunction

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33
Q

what are the cognitive explanations for sz?

A

dysfunctional thinking
metarepresentation dysfunction
central control dysfunction

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34
Q

what is dysfunctional thinking?

A

sz = characterised by disruption to normal thought processing:
reduced thought processing in the ventral striatum is associated w negative symptoms
reduced processing of info in the temporal and cingulate gyri are associated w hallucinations (simon et al 2015)

lower than usual level of info processing suggests cognition is likely to be impaired

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35
Q

what is metarepresentation?

A

1 of 2 discoveries made by frith et al:

= the cognitive ability to reflect on thoughts and behaviour
allows us insight into our own intentions and goals, interpret actions of others

dysfunction in metarepresentation would disrupt our ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else: explains hallucinations (of hearing voices etc)

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36
Q

what is central control dysfunction?

A

frith et al.: identified issues w cognitive ability to suppress automatic responses while we perform deliberate actions:
speech poverty and thought disorder could result from inability to suppress automatic thoughts and speech triggered by other thoughts

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37
Q

eval: how is a strength that there is evidence linking family dysfunction to schizophrenia?

A

indicators of family dysfunction include insecure attachment and exposure to childhood trauma esp abuse

read et al (2005) found adults w sz are disproportionately likely to have insecure attachment (type C or D) + reported that 69% women 59% men w sz have a history of physical and/or sexual abuse

strongly suggests family dysfunction makes ppl more vulnerable to sz

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38
Q

eval: how is it a limitation of family explanations that there is a poor evidence base?

A

there is no evidence to support the importance of traditional family based theories e.g schizophrenogenic mother/double bind

both theories are based off clinical observation of pts and informal assessment of personality of mothers of pts but no systematic evidence

means family explanations have not been able to account for the link between childhood trauma n sz

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39
Q

eval: how is it a strength of cognitive explanations that there is evidence for dysfunctional thought processing?

A

stirling et al. (2006) compared performance on a range of cognitive tasks in 30 ppl w sz and a cntrl of 30 wo sz
(tasks included stroop task - name font colour of colour words)

as predicted by central cntrl colour theory ppl w sz took longer to name font colours

MEANS COGNITIVE PROCESS OF PPL W SZ ARE IMPAIRED

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40
Q

eval: how is it a limitation of cognitive explanations that they only explain the PROXIMAL origins of symptoms?

A

cognitive explanations = proximal ones bc they explain what is happening now to produce symptoms - as distinct from distal explanation (genetic + family dysfunction) which focus on what caused the condition

unclear how genetic variation or childhood trauma might lead to problems w metarepresentation or central control

means that cognitive theories on their own only provide partial explanations for sz

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41
Q

What are anti psychotics?

A

Drugs used to reduce the intensity of the symptoms of sz

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42
Q

What are typical antipsychotics?
use an example.

A

Around since 1950s,
taken as tablets /syrup / injection
Maximum dosage of 1000mg
initial dose is 400-800mg

CHLORPROMAZINE

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43
Q

how do typical antagonists work?

A

acts as antagonists (chemicals that reduce action of a neurotransmitter): block dopamine receptors in synapses of the brain REDUCING THE ACTION OF DOPAMINE (reduces symptoms like hallucinations etc)

44
Q

how is chlorpromazine work as a sedative?

A

believed to be related to its effect on histamine receptors (not fully understood how it leads to sedation)
used to calm pts w sz and other conditions e.g done when patients are admitted to hospitals and are anxious

45
Q

what are atypical antipsychotics?
give examples

A

used since 1970s
aimed to maintain/improve upon the effectiveness of drugs in suppressing the symptoms of psychosis and minimise side effects

CLOPAZINE
RISPERIDONE

46
Q

what is the dosage of clozapine?

A

300-450mg a day

47
Q

how does clozapine work?

A

binds to dopamine receptors in the same way that chlorpromazine does but also acts on SEROTONIN and GLUTAMATE receptors (believed to improve mood and reduce depression + anxiety and may improve cognitive functioning)

prescribed when individual is considered high risk of suicide (30-50% of ppl w sz attempt everyday)

48
Q

why do pts taking clozapine have to have regular blood tests?

A

developed in 1960s but withdrawn in 1970s due to pt deaths from agranulocytosis (blood condition)
so to make sure theyre not developing agranulocytosis

49
Q

why was risperidone developed?

A

developed in 1990s
developed in an attempt to produce a drug without serious side effect
taken in form of injection tablets or syrup 4-8mg

50
Q

how does risperidone work?

A

believed to bind to dopamine receptors and serotonin receptors
binds MORE STRONGLY to dopamine receptors than clozapine there is much more effective in much smaller doses than most antipsychotics

51
Q

eval: how is it a strength of antipsychotics that there is evidence to support their effectiveness?

A

typical: thornley et al. (2003) reviewed studies comparing effects of chlorpromazine and control conditions:
13 trails w 1121 ppts showed chlorpromazine was associated w better functioning and reduced symptom severity compared to placebo

atypical: meltzer (2012) concluded that clozapine is more effective than a/typical antipsychotics and is effective in 30-50% of treatment-resistant cases where T antipsychotics have failed

therefore antipsychotics work!

52
Q

eval: what is the counterpoint to the strength about effectiveness?

A

healy (2012) suggested flaws w evidence for effectiveness:
studies are of short term effects only
some successful trails have had data published multiple times exaggerating effects
easy to say they have positive effect not the same as they really reduce the severity of psychosis

meaning evidence base is less impressive

53
Q

eval: how is it a limitation that there are serious side effects?

A

T antipsychotics associated w effects e.g
dizziness, agitation, sleepiness, stiff jaw, weight gain, itchy skin

long term can cause tardive dyskinesia ( caused by dopamine supersensitivity) + causes involuntary facial movements e.g blinking lipsmacking grimacing

CAUSES NMS (NEUROLEPTIC MALIGNANT SYNDROME)
(caused when drug blocks dopamine action in the hypothalamus) -> results in high temp, delirium n coma and can be fatal

shows it can also do harm as well as good and treatments may be ineffective if individuals experience these symptoms

54
Q

eval: how is it a limitation that the mechanism is unclear for antipsychotics?

A

our understanding is strongly tied w original dopamine hypothesis 9idea symptoms are linked to high levels of dopamine activity) however it is not a full explanation and D levels are too low rather than too high (if this is true than antipsychotics shouldn’t work) -> adds to argument they are ineffective

means antipsychotics may not be the best treatment to opt for

55
Q

what is cognitive behavioural therapy? (CBT)

A

method for treating mental disorders based on both cognitive and behavioural techniques

56
Q

what is the aim of CBT?

A

aims to deal w both thoughts and behvaiour
used to treat ppl w sz (takes place over 5-20 sessions) either in groups or individual basis

57
Q

how does CBT help a client make sense of how their irrational cognitions impact their feelings and behaviour?

A

e.g auditory hallucinations

client hears voices and believes it represents demonic forces, therapist can convince them voice comes from malfunctioning speech centre in their brain and cannot hurt them, it becomes less frightening
(doesn’t eliminate symptoms but helps them to cope)

leads to REDUCED STRESS and IMPROVES ABILITY TO FUNCTION CORRECTLY

58
Q

what is normalisation in terms of CBT with clients hearing voices?

A

clients experiencing auditory hallucinations can be taught voice-hearing is an extension of the ordinary experience of thinking in words

59
Q

how does CBT challenge delusions?

A

e.g by a process of reality testing in which person w sz and therapist jointly examine the likelihood that beliefs are true

(can be used to tackle anxiety and depression of person w sz)

60
Q

what is a case example of CBT (turkington et al. 2004)

A

paranoid client: the mafia are observing me to decide how to kill me
therapist: you are obviously very frightened… there must be a good reason for this.
PC: do you think its the mafia?
T: It’s a possibility, but there could be other explanations. How do you know it’s the mafia?

61
Q

What is family therapy?

A

Therapy carried out with all/ some of a members family with the aim of improving the communications within the family and reducing stress of living

62
Q

(Identified by pharaoh et al. 2010) how does family therapy help reduce negative emotions?

A

Aims to reduce levels of expressed emotion (negative emotions anger + stress) reducing stress is important to reduce likelihood of relapse

63
Q

(Identified by pharaoh et al. 2010) how does family therapy improve the family’s ability to help?

A

therapist encourages family members to form a therapeutic alliance where they all agree on aims of therapy

also tries to improve families’ beliefs ab the behaviour towards sz

64
Q

what is a further aim of family therapy?

A

to ensure family members achieve a balance between caring for the individual w sz and maintaining their own lives

65
Q

what is the model of practice proposed by burbach (2018)?

A

model for families dealing w sz: begins w sharing basic info and providing emotional + practical support and develops through deeper levels

66
Q

what are is phase 2 of burbach’s (2018) model of practice?

A

2: identifying resources including what diff family members can/cant offer

67
Q

what are is phase 3 of burbach’s (2018) model of practice?

A

3: aims to encourage mutual understanding ( creates safe space for all family members to express their feelings

68
Q

what are is phase 4 of burbach’s (2018) model of practice?

A

4: identifying unhelpful patterns of interaction

69
Q

what are is phase 5 of burbach’s (2018) model of practice?

A

5: skills training such as learning stress management techniques

70
Q

what are is phase 6 of burbach’s (2018) model of practice?

A

6: relapse prevention planning

71
Q

what are is phase 7 of burbach’s (2018) model of practice?

A

7: planning for the future

72
Q

eval: how is it a strength that there is evidence for CBT’s effectiveness?

A

jauher et al (2014): reviewed 34 studies of using CBT w sz concluding there is clear evidence for small but significant effects on both positive and negavtive symptoms

pontillo et al. (2016) found reductions in frequency n severity of auditory hallucinations

clinical advice from NICE (2019) (national institute for health and care excellence) recommends CBT for sz

SHOWS BOTH RESEARCH AND CLINICAL EXPERIENCE SUPPORTS BENEFITS OF CBT FOR SZ

73
Q

eval: how is it a limitation for CBT that there is a wide range of techniques and symptoms included in studies?

A

CBT techniques and sz symptoms vary widely for each case:

thomas (2015) points out that diff studies have involved the use of diff CBT techniques and ppl w diff combos of + and + symptoms

overall modest benefits of CBT for sz probably coneal a wide variety of effects of diff CBT techniques on diff symptoms

MAKES IT HARD TO SAY HOW EFFECTIVE CBT WILL BE FOR A PARTICULAR PERSON W SZ

74
Q

eval: how is it a strength for family therapy that there is evidence of its effectiveness?

A

Mcfarlane (2016) concluded that family therapy was one of the most consistently effective treatments available for sz: relapse rates were reduced (by 50-60%)

clinical advice from NICE recommends family therapy for everyone w diagnosis of sz

MEANS FAMILY THERAPY IS LIKELY TO BE OF BENEFIT TO PPL W EARLY AND ‘FULL_BLOWN’ SZ

75
Q

eval: how is it a strength of family therapy that it benefits all family members?

A

Lobban n barrowclough (2016) concluded allthese effects are important bc families provide bulk of care for ppl w sz
by strengthening functioning of family, family therapy lessens the negative impact of sz on other family members and strengthens ability to support person w sz

MEANS FT HAS WIDER BENEFITS BEYOND OBVIOUS + IMPACT ON IDENITFIED PATIENT

76
Q

what are token economies?

A

form of behavioural modification where desirable behaviours are encouraged by the use of selective reinforcement where ppl are given tokens to exchange for rewards when they engage in socially desirable behaviours

77
Q

how was a token economy trailed by ayllon and azrin (1968)?

A

trialled in a ward of women w sz: every time ppt carried out task (e.g making bed), given plastic token to swap for ward privileges (e.g watching a film)
number of tasks carried out increased significantly

78
Q

how does institutionalisation develop under circumstances of prolonged hospitalisation?

A

people develop bad habits e.g they might cease to maintain good hygiene or stop socialising with others
(an understandable response to living without the kind of routine and small pleasures we experience in everyday life)

79
Q

what were the 3 categories of institutional behaviour commonly tackled by the means of token economies identified by matson et al. (2016) ?

A

personal care
condition related behaviours e.g apathy
social behaviour

80
Q

(although it doesn’t cure sz) what are the 2 major benefits of modifying these behaviour?

A
  1. improves the persons quality of life within the hospital setting
    e.g make up for someone who usually takes in a lot of pride in their appearance or social interaction for a usually sociable person
  2. normalises behaviour and this makes it easier for people who have spent a time in hospital to adapt back into life in the community
    e.g getting dressed in the morning or making their bed
81
Q

what are involved in a token economy?

A

tokens are given immediately to individuals when they have carried out a desirable behaviour: target behaviours are decided in individual basis n it is important to know the person in order to identify the most appropriate target behaviours for them (cooper et al. 2007)

tokens have no value in themselves but are swapped for rewards
given immediately bc delayed rewards = less effective

82
Q

what are examples of rewards in a hospital setting?

A

objects like sweets/magazines
access to activities e.g film, walk outside, appointment w social worker to plan for life after hospitalisation

83
Q

How are token economies an example of behaviour modification?

A

behaviour modification = behavioural therapy based on operant conditioning

tokens = secondary reinforcers -> only have value once the person receiving has learned they can be used to obtain meaningful rewards (primary reinforcers)

the tokens that can be exchanged for a range of different primary reinforcers are powerful secondary reinforcers -> called generalised reinforcers

in order for tokens to become secondary reinforcers they are paired with primary reinforces so at the start of a token economy programme tokens and primary reinforces are administered together

84
Q

eval: how is it a strength of token economies that there is evidence for its effectiveness?

A

glowacki et al. (2016) identified 7 high quality studies published between 1999-2013 that examined the effectiveness of token economies for people w chronic mental issues e.g sz and involved pts living in the hospital settings

all studies showed a reduction in negative symptoms and a decline in frequency of unwanted behaviours, supporting the value of token economies

85
Q

eval: what is the counterpoint to the strength of evidence of effectiveness?

A

7 studies = small evidence base
issue = file drawer problem: leads to bias towards positive published findings bc undesirable results have been ‘filed away’
this is a particular problem in reviews that only include a small number of studies

means that there is a serious question over the evidence for the effectiveness if token economies

86
Q

eval: how is it a limitation of the use of token economies that there are ethical issues?

A

gives professionals considerable power to control the behaviour of ppl in the role of the pt: involves imposing ones persons norms onto others (problematic if target behaviours are not identified sensitively)
(e.g someone who likes to look scruffy and get up late have these personal freedoms curtailed)

restricting the availability of pleasures to ppl who don’t behaviour as desired means that seriously ill ppl (who are already experiencing distressing symptoms) have an even worse time

legal actions by families who see their relative in this position has been a major factor in the decline of the use of token economies

MEANS THAT BENEFITS OF TOKEN ECONOMIES MAY BE OUTWEIGHED BY THEIR IMPACT OF PERSONAL FREEDOM N SHORT TERM REDUCTION IN QUALITY OF LIFE

87
Q

eval: how is it a limitation if token economies that there is the existence of more pleasant and ethical alternatives?

A

other approaches that do not raise the same ethical issues:
chiang et al. (2019) concluded that art therapy is a good alternative:
(evidence based is regularly small and has methodological limitations) but shows art therapy is a high gain low risk approach to managing sz

although benefits = modest, this is generally true for all approaches to treatment and management of sz but art therapy is a pleasant experience without major risks of side effects or ethical abuses (NICE guidelines recommend art therapy)

means art therapy might be a good alternative to token economies

88
Q

what is the interactionist approach?

A

approach that acknowledges that there are biological, psychological and social factors in development of sz

biological factors: genetic vulnerability, neurochemical + neurological abnormality

psychological factors: stress (resulting from life events and daily hassles)

socia factors: e.g poor quality interactions in the family

89
Q

how does the diathesis-stress model present an interactionist approach?

A

diathesis = vulnerability
stress = negative experience

D-S model says that both a vulnerability to sz and a stress trigger re necessary in order to develop the condition

one of more underlying factors make a person more vulnerable to developing sz (but onset of condition is triggered by stress)

90
Q

what is meehl’s model?

A

meehl 1962: original diathesis-stress model

diathesis = entirely genetic -> result of a single ‘schizogene’

led to idea of a biologically based schizotypic personality (one characteristic of which is sensitive to stress)

91
Q

according to meehl, if a person does not have the schizogene then…?

A

no amount of stress would lead to sz

92
Q

however within the carriers of this gene, how could it result in the development of sz?

A

chronic stress through childhood/adolescence (particularly in the prescence of a schizophrenogenic mother)

93
Q

what is the modern understanding of diathesis?

A

it is now clear how many genes each appear to increase egentic vulnerability slightly

no single ‘schizogene’ (ripke et al.2014)

includes a range of factors beyond the genetic, including psychological trauma (ingram and luxton 2005)

94
Q

modern understanding of diathesis: what was the neurodevelopmental model proposed by read et al. ?

A

shows how early trauma alters the developing brain

early + sevre enough trauma (e.g child abuse) can seriously affcect many aspects of brain development

e.g HPA system (hypothalamic-pituitary-adrenal) can become overactive, making a person much more vulnerable to later stress

95
Q

what is the modern understanding of stress?

A

(og d-s model says stress seen as psychological in nature, more related to parenting)
modern definition of stress: includes anything that risks triggering sz (houston et al. (2008)

96
Q

why is the concern surrounding cannabis use (factor that risks triggering sz)?

A

cannabis = stressor -> increases risk of sz yp to 7x according to dose

may be bc cannabis interferes w dopamine system (however most ppl do not develop sz after smoking cannabis as they lack the requisite vulnerability factors)

97
Q

what is treatment for sz according to the interactionist model?

A

model is associated w combining antipsychotic medication n psychological therapies, most commonly CBT

98
Q

what did turkington et al. (2006) say about treatment of sz according to the interactionist model?

A

it is possible to believe in biological causes of sz and still practice CBT to relieve psychological symptoms

(requires adopting an interaction model - not possible to adopt purely biological approach, tell ppl w sz their condition is purely biological anf there is no psychological significance in symptoms then treat them w CBT)

99
Q

what is the difference between the UK and US w treatment of sz?

A

Uk - increasingly standard practice to treat ppl w sz w a combination of antipsychotic drugs n CBT

US - history of conflict between psychological n biological models of sz -> led to slower adoption of an interactionist approach

MEDICATION WO AN ACCOMPANYING PSYCHOLOGICAL TREATMENT IS MORE COMMON IN US THAN UK

100
Q

eval: how is it a strength for the interactionist approach that there is evidence supporting the role of vulnerability and triggers?

A

tienari et al. (2004) investigated the impact of both genetic vulnerability and psychological trigger (dysfunctional parenting) :

followed 19000 finnish children who had mothers w sz (high genetic risk), compared to a control group of adoptees w a low genetic risk

adoptive parents were assessed for child-rearing style:found that high levels of criticism, hositility and low levels of empathy were strongly associated w development of sz (ONLY IN HIGH GENETIC RISK GROUP)

SHOWS A COMBINATION OF GENETIC VULNERABLITY AND FAMILY STRESS CAN LEAD TO INCREASED RISK OF SZ

101
Q

eval: how is it a limitation of the og diathesis-stress model that it is oversimplified?

A

og model portrayed diathesis as single schizogene and stress as schizophrenogenic parenting = simplistic

multiple genes in multiple combinations influence diathesis, stress comes in many forms (including but not limited to dysfunctional parenting)

102
Q

how does the study by houston et al. (2008) shows diathesis can be influenced by psychological factors n stress can be biological asw as psychological?

what does this mean?

A

shows childhood sexual abuse emerged as the major influence on underlying vulnerability to sz and cannabis use as a major trigger

means that there are multiple factors (both biological n psychological) affecting both diathesis and stress, supporting the modern understanding of both diathesis and stress

103
Q

eval: how is it a strength that the interactionist approach has real world application?

A

combination of biological and psychological treatments enhances their effectiveness:

tarrier et al. (2004) RANDOMLY ALLOCATED 315 ppts to
1 (medication + CBT)
2 (medication + counselling)
3 (control group (med only))

ppts in 2 combination group showed lower symptoms following the trial than the med only group (no difference in hospital readmission though)

MEANS THAT THERE IS A CLEAR PRACTICAL ADVANTAGE TO ADOPTING AN INTERACTIONIST APPROACH TO SZ IN TERMS OF SUPERIOR TREATMENT OUTCOMES

104
Q

what is the counterpoint to the strength of real world application for the interactionist approach?

A

jarvis and okami (2019) pointed out saying that a successful treatment for mental disorder justifies a particular explanation is the logical equivalent of saying that because alcohol reduces shyness, shyness is caused by lack of alcohol

error = treatment-causation fallacy

THEREFORE WE CANNOT AUTOMATICALLY ASSUME THAT THE SUCCESS OF COMBINED THERAPIES MEANS INTERACTIONIST EXPLANATIONS ARE CORRECT

105
Q

evaluation extra: urbanisation

A

sz more commonly diagnosed in urban than rural areas: statistic used to justify the interactionist position as it assumes that urban living is more stressful than rural and living in the city acts like a trigger

may be simply that sz is more likely to be diagnosed in cities or ppl w a diathesis for sz tend to migrate to cities