Schizophrenia Flashcards
(96 cards)
1
Q
what is sz
A
a severe mental disorder that affects thought processes and ability to determine reality
roughly 1% of people worldwide suffer sz
most often diagnosed between 15 and 35
men and women are affected equally
many symptoms of the disorder and not everyone displays the same symptoms
2
Q
sz symptoms can be split into two categories
A
negative and positive symptoms
3
Q
what are positive symptoms
A
involve displaying of behaviours concerning loss of touch with reality
occur in short episodes with normal periods in between and respond well to medication
4
Q
types of positive symptoms
A
hallucination
delusions
disorganised speech
grossly disorganised
5
Q
positive symptoms - hallucinations
A
to do with senses, bizarre unreal perceptions of the environment that are usually auditory but may also be visual and tactile
6
Q
positive symptoms - delusions
A
to do with beliefs, bizarre beliefs that seem real to the person but are not real, sometimes can be paranoid in nature, delusions can involve inflated beliefs of persons grandeur, may also experience delusions of reference when events in environment seem related to them
7
Q
positive symptoms - disorganised speech
A
result of abnormal thought processes where individual struggles organising thoughts this shows in the speech, they might slip from one topic to another or their speech might sound like complete gibberish
8
Q
positive symptoms - grossly disorganised
A
catatonic behaviour - includes inability or motivation to initiate a task or to complete it once started individuals may act or dress bizarrely
catatonic behaviour are characterized by a reduced environment to immediate environment
9
Q
what are negative symptoms
A
appear to reflect a reduction or loss of normal functions occurring in chronic, longer lasting periods
tend to be resistant to medication
negative symptoms contribute to sufferers not being able to live normally
10
Q
types of negative symptoms
A
speech poverty
avolition
affective flattening
anhedonia
11
Q
negative symptoms - speech poverty
A
lessening of speech fluency and productivity reflecting slower thoughts, individual may produce fewer thoughts in a given time its not that they dont know them
12
Q
negative symptoms - avolition
A
reduction of interests and desires and inability to initiate and persist goal-directed behaviour, not having contact with friends family is not avolition, avolition is specified as a reduction in self initiated involvement
13
Q
negative symptoms - affective flattening
A
reduction in range and intensity of emotional expression includes facial expression, voice tone, eye contact, body language
patients may also show deficit in prosocial linguistic features such as interaction
14
Q
negative symptoms - anhedonia
A
a loss of interest and pleasure in almost all activities or a lack of reactivity to normally pleasurable stimuli, physical anhedonia - inability to experience physical pleasure, social anhedonia is inability to experience pleasure from interpersonal situations
15
Q
diagnosing
A
schizophrenia is diagnosed by using classification systems that include lots of mental disorders, grouped in terms of their common features
16
Q
diagnostic criteria for sz (DSM-V)
A
two or more of the following, present for a significant portion of time during a one-month period, at least one of the symptoms must be 1,2 or 3
1. delusions
2. hallucinations
3. disorganised speech
4. completely disorganised/ catatonic behaviour
5. negative symptoms
extra - level of functioning has been affected in a major area of life
17
Q
ICD and DSM differences
A
ICD requires only 2 or more negative symptoms
DSM requires at least one positive symptom and one other symptom
18
Q
reliability
A
can be replicated/ standardised
consistent over time, assuming symptoms dont change
different Dr’s diagnose same person with same thing, inter-rater reliability
19
Q
validity
A
you’ve diagnosed them with sz and they actually have it
20
Q
Rosenhan (1973) - highlights unreliability of diagnosis
A
normal people presented themselves to psychiatric hospitals in the US claiming they heard an unfamiliar voice in their head saying the words empty, hollow and thud
they were all diagnosed as having schizophrenia and admitted. throughout their stay none of the staff actually recognised they were normal, Rosenhan had to go and collect them himself
in a follow up study Rosenhan warned hospitals of his intention to send out more pseudo patients, this resulted in a 21% detection rate, although Rosenhan didnt actually send anyone
21
Q
reliability in diagnosis
A
diagnostic reliability means that a diagnosis of sz must be consistent and repeatable
a single clinician needs to be able to reach the same conclusion at two different points in time
different clinicians must reach the same conclusions as each other
22
Q
inter-rater reliability
A
this is measured using a kappa score, a score of 1 means perfect inter-rater reliability, a zero indicates zero agreement
a kappa score of 0.8 or above is generally considered good
in the 2013 DSM field trials the diagnosis of sz had a kappa score of 0.43 which is low inter-rater reliability
23
Q
cultural differences in diagnosis - us and uk
A
the reliability of diagnosis in sz is further challenged by the finding that there is a massive variation between countries
Copeland (1971) gave 134 US and 194 British psychiatrists a description of a patient, 69% of the US psychiatrists diagnosed sz but only 2% of the British psychiatrists gave the same diagnosis this study doesnt have temporal validity though
24
Q
A03 - reliability - cultural and racial differences
A
research has established cultural and racial differences in the diagnosis of sz
research suggests there is a significant variation between countries when it comes to diagnosing sz e.g. Harrison et al (1984) research suggested that those of Afro-Caribbean origin were over-diagnosed with sz, by white doctors in Bristol because of their ethnic background, positive symptoms like hallucinations are more acceptable in African cultures because of cultural beliefs in communication with ancestors, and therefore people are also more ready to talk about these experiences
25
A03 - reliability - lack of inter-rater reliability
despite revisions to the DSM still little to suggest reliability of diagnosis has improved, Whaley (2001), inter-rater reliability correlations as low as 0.11
26
A03 - reliability - Cheniaux (2009)
had two psychiatrists independently diagnose 100 patients using both DSM and ICD criteria, inter-rater reliability was poor, with one diagnosing 26 according to the DSM and 44 according to the ICD, the other psychiatrist diagnosing 13 with the DSM and 24 with the ICD
27
criterion validity
does the criteria/ measure actually describe sz
28
concurrent validity
do the findings of a new measure match findings of established measure
29
example of poor criterion and concurrent validity
looking at the figures in cheniaux (2009), sz is more likely to be diagnosed with the ICD than the DSM, so it is either over-diagnosed with the ICD or under-diagnosed with the DSM, either way this is poor criterion and concurrent validity
30
A03 - validity - gender bias
Loring and Powell (1988) - 290 male and female psychiatrists read nameless patient notes, asked to offer diagnosis based on standard criteria
when described as males or no gender information given, 56% of clinicians gave sz diagnosis, when described as females, 20% of clinicians gave sz diagnosis
gender bias not evident in female clinicians
so gender of patients and gender of clinicians important
31
A03 - validity - co-morbidity
common in patients with sz
comorbidity describes people who suffer from two or more mental illnesses, at one time
for example sz and depression are often found together, this makes it more difficult to confidently diagnose sz, comorbidity occurs because the symptoms of different disorders overlap
for example, major depression and sz both involve very low levels of motivation, this creates problems of motivation, this also creates problems of validity
32
A03 - validity - differences in prognosis
prognosis tells us if something is curable, what is it what the treatment will be, what are the next steps
no evidence that patients share the same outcomes post diagnosis
20% recover to previous level of functioning
10% significant and lasting improvement with intermittent relapses
this is a problem because it means that our definition of sz might be wrong and our classification of sz might also be wrong
33
biological explanations of sz
neural correlates, genetic factors
34
neural correlates - enlarged ventricles - Johnstone et al (1976)
used ct scans to study MZ twins and saw a clear size difference in the cerebral ventricles of the sz twin compared to the non-sz twin
the cerebral ventricles provide supporting fluid of the brain and keep everything in place by creating internal pressure. if there is damage to the brain and parts of it die then the ventricles will enlarge to fill the space left, so ventricular enlargement is often a good indicator of brain damage
35
neural correlates - ventral striatum, low activity - Juckel et al (2006)
measured activity levels in the ventral striatum in sz and found significantly lower levels of activity than observed in healthy controls, moreover they observed a negative correlation between activity levels in the ventral striatum and the severity of the negative symptoms
the ventral striatum is believed to be involved with the anticipation of a reward this anticipation is linked to feelings of motivation and avolition
36
neural correlates - dopamine hypothesis
excess of dopamine causes sz
original version of the hypothesis focused on possible role of high dopamine levels (hyperdopaminergia) in central areas of the brain like Broca's area associated with speech poverty and hallucinations
in 1991 revised hypothesis says hypodopaminergic in the cortex (particularly pre-frontal cortex), recent version focused on abnormal dopamine systems in the brain subcortex, study found low levels of dopamine in the pre frontal cortex this links to negative symptoms of sz
both explanations are important
37
strength of dopamine hypothesis - amphetamines
amphetamines this is a dopamine agonist, this stimulates nerves cells containing dopamine causing the synapses to be flooded - large doses of the drug can cause hallucinations and delusion of a schizophrenic episode
increasing dopamine in some people increases hallucinations and delusion therefore bringing sz symptoms in non-sz patients
38
limitation of dopamine hypothesis
Noll (2009) claims there is strong evidence against both the original and revised dopamine hypothesis
he argues that antipsychotic drugs do not alleviate hallucinations and delusions in about 1/3 of people experiencing these symptoms, Noll also points out that, in some people, hallucinations and delusions are present despite levels of dopamine being normal
so there must be another factor causing the hallucinations and delusions
39
strength of new and old dopamine hypothesis- antipsychotic drugs
antipsychotic drugs (dopamine antagonists) which block the activty of dopamine in the brain, by reducing the stimulation of the dopamine system, eliminates hallucinations and delusions, by alleviating many of the symptoms of sz, antipsychotic drugs strengthen the case for dopamine being a significant contributing factor
however antipsychotics treat the symptoms not the cause, aetiology uncertain.
40
hypodopaminergia
in the cortex, with D1 receptors and leads to negative symptoms, high dopamine levels
41
hyperdopaminergia
in the sub-cortex, with D2 receptors and leads to positive symptoms, low dopamine levels
42
genetic factors - ripke et al (2014)
candidate genes = individual genes are believed to have been associated with risk of inheritance
Ripke et al carried out a huge study combining all previous data from genome wide studies (these looking at the entire genome and not particular genes) of schizophrenia. The genetic make-up of 37,000 patients was compared to that of 113,000 controls
108 separated genetic variations were associated with increased risk of schizophrenia
genes associated with increased risk included those coding for neurotransmitter function: including dopamine
43
A03 - genetic factors - adoption studies
tienari et al (2000) - conducted a study in Finland, of the 164 adopted children whose biological mothers had been diagnosed with sz 11 also received a diagnosis of sz, compared to just 4 of the 97 control adoptees
nature - nurture separated, raised in different environments from sz mother
being adopted is a traumatic process, trauma of adoption could lead to schizophrenia
no control over when children were adopted so don't know how long they spent with birth parent or in foster or with adoptive parent
44
A03 - genetic factors - family studies
Gottesman (1991) children with two schizophrenic parents had a concordance rate of 46%, children with one sz parent a rate of 13% and siblings a rate of 9%
family studies suggests that genetics do play a role in it but not a 100% role
not 100% shared DNA
isolating role of learning, sz parents could create a stressful environment for child leading to schizophrenia
45
A03 - genetic factors - metanalysis of twin studies
Joseph (2004) calculated that the pooled data for all schizophrenia twin studies carried out prior to 2001 showed a concordance rate for MZ twins of 40.4% and 7.4% for DZ twins
supports that genetic factors can cause sz as mz twins showed 40.4% to 7.4% for dz twins
large sample size allows for impact of anomalous results to be minimised
cant separate nurture vs nature, mz twins are more likely to be called twins and be treated the same whereas dz twins more likely to be viewed as separate individuals
46
A03 - genetic factors - biological determinism limitation
if you have the gene you will have sz the label could lead to a self fulfilling prophecy, it is also a negative label which could affect person with the gene because of social stigma
47
A03 - genetic factors - biological determinism strength
creating treatments + prevention is possible if you know who is most at risk
48
A03 - genetic factors - reductionist
sz is very complex behaviour with a huge variety of symptoms (positive, negative etc) and the genetic explanation reduces down the complexity of this disorder to just genetic, this ignores many contributing factors and ignores how unique different peoples experience with sz are
49
A03 - genetic factors - body of evidence
very reliable and big
50
what are antipsychotics
a general term for any drug that reduces psychotic (losing touch with reality) illnesses
the most common treatment for sz and almost always tried first to reduce symptoms bring them back to earth so that they can engage in other forms of therapy
taken as tablets or syrup
some are available as injections every 2 to 4 weeks
some people can take a short course of antipsychotics without their symptoms ever returning
others may require them for life
51
typical antipsychotic drugs e.g. chlorpromazine
original antipsychotics (since 1950s)
treat mostly positive symptoms (hallucinations/ thought disturbances)
work by reducing the amount of dopamine
52
atypical antipsychotic drugs e.g. clozapine, rispiridone
newer create in 1970s to improve symptom reduction
also treat negative symptoms in addition to positive symptoms
work on dopamine and serotonin
suitable for treatment resistant patients
53
how to do typical antipsychotics work
they work by binding to dopamine receptors, particularly d2 receptors, and thus blocking their action, not stimulating them
by reducing the stimulation of the dopamine system the neuron is less likely to fire thus reducing positive symptoms such as hallucinations
estimated that 60-75% of receptors in dopamine pathways need to be blocked so that the drugs are effective
to block this many d2 receptors in the brain must also be blocked
not all dopamine pathways are involved in sz some are involved in movement, however typical antipsychotics block all pathways
therefore when other pathways are blocked there are side effects like tardive dyskenesia
54
how to do atypical antipsychotics work
also block d2 receptors , but only loosely and temporarily, before rapidly dissociating, this rapid dissociation means that the dopamine pathways that aren't involved in sz are less affected leading to less side effects
atypical antipsychotics also bind to serotonin receptors, it is believed that this acts as a serotonin agonist and increases serotonin action and therefore helps symptoms such as flat affect and treats comorbid depression
this makes them very useful for high risk/ suicidal patients (extremely useful since 30-50% of sz patients attempt suicide at some point)
however the actual mechanisms a d how serotonin and dopamine interact are not actually well understood
55
some side effects of typical antipsychotics
dizziness, agitation, sleepiness, stiff jaw, weight gain, itchy skin
long term use can result in tardive dyskinesia which is caused by dopamine supersensitvity and manifests as involuntary facial movements such as grimacing, blinking and lip smacking
neuroleptic malignant syndrome is a very serious side effect and is believed to be caused because the drug blocks dopamine action in the hypothalamus affects 0.1% to 2% of people
atypical antipsychotics were created to reduce side effects, patients have regular blood tests to alert doctors to early signs of agranulocytosis
56
A03 - antipsychotics - evidence for effectiveness
large body of evidence
Ben thornley et al (2003) reviewed studies comparing the effects of chlorpromazine to placebo, so identical experience except for actual medicine taken, data from 13 trials with a total of 1121 ppts showed that the chlorpromazine was associated with a better overall functioning and reduced symptom severity, data from 3 trails with 512 ppts showed that the relapse rate was also lower
57
A03 - antipsychotics - problems with evidence for effectiveness
challenges to the usefulness, david healy (2012) has suggested that some successful trials have had their data published more than once, exaggerating the evidence for positive effects, healy also suggests that because antipsychotics have powerful calming effects, it is easy to demonstrate that they have the same positive effect on patients, this is not the same as saying they reduce the severity of psychosis
also most published studies asses the short term rather than the long term benefits and compare patients that continue taking antipsychotics compared to those who have just stopped taking them
58
A03 - antipsychotics - antipsychotics are unethical
antipsychotics used in hospital to make patients easier to deal with
rather than helping the patients this helps the staff, could be seen as human rights abuse, critics compared antipsychotics to straight jackets
there are also problems associated with antipsychotics medication recently in the us a tardive dyskinesia sufferer was awarded a huge out of court settlement
on the basis of the human rights act 'that no one shall be subjected to inhuman or degrading treatment or punishment'
59
A03 - antipsychotics - atypical better than typical ?
crossely et al (2010), meta-analysis of 15 studies to see efficacy, they found no significant differences between atypical and typical drugs in terms of their effects on symptoms
60
psychological explanations of sz
family dysfunction
cognitive explanations
61
family dysfunction
the schizophrenogenic mother
double-bind theory
expressed emotion
62
the schizophrenogenic mother
Fromm-Reichmann (1948) proposed a psychodynamic explanation based on accounts she heard from her patients and their childhood
many patients spoke of a particular type of parents, called the schizophrenogenic mother, this parents is cold, rejecting, controlling and creates a environment of tension and secrecy leading to distrust and develops into paranoid delusions
63
double-bind theory
Bateson et al (1977) suggsets children who receive contradictory messages go on to develop sz
for example if a mother tells her son she loves him and then turns her head away in disgust, this gives mixed messages
those interactions prevent the development of an internally coherent construction of reality
64
expressed emotion
expressed emotion is the level of emotion, particularly negative emotion, expressed towards the patient by their families
EE can be characterised by family members being highly critical, hostile or behave in a manner that indicates emotional over involvement or over concern for the patient
high levels of EE are more likely to lead to relapse rates, a patient returning to a high EE family is four times more likely to relapse
65
cognitive explanations
cognitive explanations of sz emphasise the role of dysfunctional thought processing particularly evident in those displaying positive symptoms
Frith (1992) identified two kinds of dysfunctional thought processing that could underline some symptoms
faulty meta representation
faulty central control
66
faulty meta representation
is the cognitive ability to reflect on though and behaviour, this allows us to interpret the actions of others and insight into our own goals
dysfunction in this would disrupt the ability to recognise our own thoughts and actions as being carried out by ourself as opposed to someone else
67
faulty central control
cognitive ability to suppress automatic responses while we perform deliberate actions instead, disorganised speech and thought disorder could result from the inability to supress automatic speech and thought triggered by other thoughts
Stroop test is how you measure central control, word colours in different colours, sz's do badly
68
A03 - psychological explanations - family dysfunction - interactionist approach better?
Tienari et al (1994) - Finnish adoption study
adopted children with sz parents more likely to develop sz than those with non-sz parents, but only seen in adopted families who were rated as disturbed (communication style)
this suggests that the illness only manifests under the appropriate environmental conditions, genetic vulnerability alone was not sufficient
this is a strength and a limitation because it only happened in disturbed families but the interactionist approach may be more appropriate
69
A03 - psychological explanations - family dysfunction - retrospective no control groups
early studies which demonstrated links between schizophrenia and dysfunctional families were mainly retrospective and made little use of control groups
therefore don't have control groups to compare results to and they may not remember accurately or they may lie + they are sz patients and may not be objective
therefore there are extraneous variables and cant establish cause and effect
70
A03 - psychological explanations - family dysfunction - double bind theory
Berger (1965) sz ppts reported a higher number of double bind statements by their mothers than non sz (its good that there was a control group)
however it does rely on recall and everyone remembers differently, and our memory has been known to be faulty
however Liem (1974) measured patterns of parental communication in families with a sz child and found no difference in comparison to typical families suggests no difference between sz families and non-sz families
71
A03 - psychological explanations - family dysfunction - relapse
many studies have demonstrated higher levels of relapse in families with disturbed communication, those who live in high EE environments are more likely to relapse than those in low EE settings
there are other factors which are important here like: external environment outside of home, treatment method, family support
72
A03 - psychological explanations - cognitive - can explain positive symptoms
sarin and wallin (2014) found supporting evidence for the claim that positive symptoms have their origins in faulty cognition e.g. delusional patients were found to jump to conclusions and show bias in their informative processing
those with hallucinations are more likely to experience own thoughts as voices
therefore psychological explanation can explain positive symptoms
supports faulty meta representation in sz
73
A03 - psychological explanations - cognitive - faulty central control
Stirling et al (2006) - compared 30 patients with a diagnosis of sz with 18 non-patients controls on a range of cognitive tasks including the stroop test, patients took twice as long to name the ink colours as the control group
supports faulty central control
74
A03 - psychological explanations - cognitive - explanation is valid
is the therapy is based on the explanation and the therapy works, this suggests that the explanation is valid the CBT asks patients to do homework and play an active role in their own treatment
75
psychological treatments of sz
CBT
token economies
family therapy
76
CBT
cognitive behavioural therapy
takes 5 to 20 sessions, either in group or individual basis. CBT involves helping patients identify irrational thoughts and help change them, cognitive restructuring, change reaction to thoughts and destructive thought patterns
this may involve argument or discussion about the trueness of beliefs and consideration of other less threatening possibilities
use homework between sessions + keeping a diary of thoughts to discuss, therapists might ask for evidence of thoughts
this helps patients to make sense of impact of their delusions and understanding where their symptoms come from
77
token economies
tokens given to patient when they carry out a desirable behaviour e.g. getting dressed in the morning, tokens themselves are arbitrary and have no value they are meaningless but they can be exchanged for a reward. reward can include taking a walk out of hospital, cigarettes, sweets
token - secondary reinforcer
reward - primary reinforcer
78
family therapy
close family must go e.g. people who live in house
at family therapy they use strategies like forming a therapeutic alliance with family members reducing stress of caring for a relative with sz
improving ability of family to anticipate and solve problems, reduction of anger and guilt in family members, improving family beliefs and behaviour towards sz family member
while decreasing levels of stress and expressed emotion, whilst increasing chance of patients complying with medication, reduced chance of relapse
79
A03 - CBT - evidence for effectiveness
Jauhar et al (2014) reviewed 34 studies for sz, they concluded CBT had a small but significant effect on both positive and negative symptoms
NICE review (2014) of sz treatments found consistent evidence that when compared with standard care (just antipsychotics) CBT was effective in reducing rehospitalisation rates up to 18 months after treatment
80
A03 - CBT - lack of availability
despite being recommended as a treatment for sz, it is estimated that in the uk only 1/10 of those who could benefit from the treatment can get access to it, waitlists on the NHS can be up to a year
private healthcare systems: insurance may not cover mental health and so CBT can cost hundreds of pounds per session, antipsychotics very cheap to make and buy in comparison
81
A03 - CBT - extra
motivation, requires engagement
82
A03 - family therapy - evidence for effectiveness
Pharaoh et al (2010) reviewed 53 studies to investigate the effectiveness of family intervention, the studies were from europe, north america, asia they concluded that there is moderate evidence to show family therapy reduces hospital readmission and improves quality of life
however they note that the results of different studies were inconsistent with the quality of some of the work therefore evidence is weak
83
A03 - family therapy - economic and family impact
NICE review of family therapy says that this therapy is associated with cost savings when offered to patients in addition with medication, due to a reduction in hospital costs due to fewer relapse rates
family therapy not only beneficial for sz patient but for family members as well
Lobban et al (2013) analysed 50 families studies that had included an intervention to support relatives, 60% reported a positive impact on at least one outcome category for relatives
84
A03 - family therapy - motivation + money
needs whole family to be motivated
money - therapists are expensive
85
A03 - token economies - evidence for effectiveness
McMonagle and Sultana (2009) reviewed 3 studies with a total of 110 patients who had token economies as part of their treatment, only one study of the three showed an improvement in symptoms and none provided useful information about behaviour change
could only find 3 studies on token economy which used random allocation
86
A03 - token economies - ethical issues
th use of token economies to treat patients with sz is controversial, the major issue is that the rewards become more available to patients with milder symptoms those with more severe symptoms might not be able to comply
therefore more ill patients have been discriminated against and some families have challenged the legality of this, this has reduced the use of token economies in psychiatric systems
luxuries being taken away to be given back is like we are infantilising adults
87
A03 - token economies - extra
cheaper, not cheaper than antipsychotics but much cheaper than therapy
there must be motivation for rewards
doesn't do something important like curing sz, is a very temporary solution
88
Meehls model
in the original model (1962), diathesis was entirely genetic, the result of a single schizogene, this led to the development of a biologically based schizotypic personality, one characteristic of which is sensitivity to stress
according to meehl, if a person doesnt have a schizogene then no amount of stress would lead to sz, however in carriers of the gene, chronic stress through childhood and adolescence particularly a schizophrenogenic mother could result in sz
89
modern understanding of diathesis
now clear that many genes increase genetic vulnerability, there is no single schizogene, modern views of diathesis also include a range of factors beyond the genetic, including psychological trauma - trauma becomes the diathesis rather than the stressor
Read (2001) proposed a neurodevelopmental model in which early development trauma alters the developing brain e.g. the hypothalamic-pituitary-adrenal system becomes over active and the person is more vulnerable to later stress
90
modern understanding of stress
originally stress was seen as psychological in nature, in particular related to parenting, psychological stress is still seen as important, a modern definition of stress includes anything that risks triggering sz e.g. cannabis. cannabis is a stressor because it increases the risk of sz up to 7 times as it interferes with the dopamine system, other stressors are grief, academia, increased family conflict
however most don't develop sz after smoking cannabis so there must be other vulnerability factors
91
treatment according to the interactionist model
this approach acknowledges both biological and psychological factors and is compatible with both types of treatment, the model suggests a combination of antipsychotics with psychological therapies such as CBT. standard practice in the UK is to combine two and it is unusual to treat using psychological therapies alone
92
A03 - interactionist approach - support for diathesis-stress
tienari et al (2004) investigated combination of genetic vulnerability and parenting style (the trigger), children adopted from 19,000, Finnish mothers with sz between 1960-79 followed up
adoptive parents were assessed for child rearing style and rates of sz were compared those in control group of adoptees with no risk
a child rearing style of increased criticism and conflict and decrease empathy was implicated in development of sz but only for the children with high genetic risk
suggests that both genetic vulnerability and family stress are important in development of sz and genetically vulnerable children are more sensitive to parenting behaviour
93
A03 - interactionist approach - issues with the original model
idea of single schizogene and schizophrenic parenting style as major source of stress is too simple
multiples genes increase vulnerability not just one single gene
stress can also come in many form not just dysfunctional parenting style
vulnerability can be caused by early trauma as well as genetics and stress can come in many forms including biological
Houston found that childhood sexual trauma emerged as a vulnerability factor whilst cannabis was a trigger showing that old model was too simple
94
A03 - interactionist approach - we dont know how diathesis-stress works
strong evidence to suggest some sort of underlying vulnerability coupled with stress can lead to sz
also have well informed suggestions for how vulnerabilities and stress might lead to symptoms
however do not fully understand mechanisms by which the symptoms of sz appear and how both vulnerability and stress produce them
therefore low predictive ability
95
A03 - interactionist approach - support for combination treatment
Tarrier (2004) 315 patients were randomly allocated to a medication + CBT group or medication + counselling group or the control group
patients in 2 combinations groups showed lower symptom levels than control, although there was no difference in hospital readmission rates
this shows clear advantage of adopting interactionist approach
96
diathesis
biological predisposition
