Paper 3- Schizophrenia Flashcards
(108 cards)
1
Q
What is schizophrenia
A
It does not have a single defining characteristic. It is a cluster of symptoms that seem to be unrelated. But it can be roughly defined as a severe mental illness where contact with reality and insight are impaired; an example of psychosis.
2
Q
What are the two major systems for the classification of mental disorder of SZ
A
DSM-5 and ICD-10
3
Q
What is the classification of a mental disorder
A
The process of organising symptoms into categories based on which symptoms cluster together in sufferes
4
Q
What is the DSM-5
A
The Diagnostic and Statistical Manual of Mental Disorders is a classification system of mental disorders published by the American Psychiatric Association. It contains typical symptoms of each disorder and guidelines for clinicians to make a diagnosis
5
Q
What does the DSM-5 states much be present for a diagnosis of SZ
A
One of the so-called positive symptoms (delusions, hallucinations or speech disorganisation)
6
Q
What is the ICD-10
A
The most recent version of the International Classification of Diseases, published by the World Health Organisation
7
Q
What does the ICD-10 state is needed for a diagnosis of SZ
A
Two or more negative symptoms of schizophrenia (avolition and speech poverty)
8
Q
What is a positive symptom of SZ
A
Atypical symptoms experienced in addition to normal experiences. They include hallucinations and delusions
9
Q
What is a delusion
A
Involve beliefs that have no basis in reality, for example, that the sufferer is someone else or that they are the victim of a conspiracy.
Delusions can make a sufferer behave in ways that make sense to the sufferer but are bizarre to others.
10
Q
What are hallucinations
A
Sensory experiences of stimuli that have either no basis in reality or are distorted perceptions of things that they are e.g hearing voices.
They can be experienced in relation to any sense.
11
Q
What are negative symptoms of SZ
A
Atypical experiences that represent the loss of a usual experience, such as clear thinking or ‘normal’ levels of motivation
12
Q
What is avolition
A
Involved the loss of motivation to carry out tasks and results in lowered activity levels
13
Q
What is speech poverty
A
Involves reduced frequency and quality of speech. This is sometimes accompanied by a delay in the verbal responses during conversation.
14
Q
What are the 4 issues in diagnosing SZ
A
Reliability
Validity
Co-morbidity
Symptom overlap
15
Q
What is reliability in the instance of it being an issue in diagnosing SZ
A
The extent to which the diagnosis of SZ is consistent
16
Q
What is validity in the instance of it being an issue in diagnosing SZ
A
The extent to which the diagnosis and classification techniques measure what they are designed to measure
17
Q
What is co-morbidity
A
The occurrence of two illnesses or conditions together, for example a person who have both SZ and a personality disorder. When two conditions are frequently diagnosed together, it calls into question the validity of classifying the two disorders separately
18
Q
What is symptom overlap
A
Occurs when two or more conditions share symptoms. Where conditions share many symptoms this calls into question the validity of classifying the two disorders separately
19
Q
5 limitations of the diagnosis of SZ
A
Low reliability. CHENIAUX has two psychiatrists independently diagnose 100 patients using both DSM and ICD. Inter-rater reliability was poor, with one diagnosing 26 with SZ according to DSM and 44 according to ICD, and the other diagnosing 13 according to DSM and 24 according to ICD. This inconsistency between professionals and the different classification systems is a limitation.
Validity. One standard way to assess validity of a diagnosis is criterion validity; do different assessment systems arrive at the same diagnosis for the same patient?. CHENIAUXs study shows SZ is more likely to be diagnosed using ICD. Suggests SZ is ether over-diagnosed or under-diagnosed using DSM. Shows poor validity.
Co-morbidity. If conditions occur together a lot then it might call into question whether they are actually a single condition. Around half of patients with a diagnosis of SZ have a diagnosis of depression or substance abuse (47%). In terms of classification, it may be that if very severe depression looks like SZ and vice versa, then they might be seen as a single condition. This can be confusing.
Gender bias in the diagnosis. LONGENECKER reviewed the studies of prevalence of SZ and concluded that, since the 1980s, men have been diagnosed more than woman. COTTON found that woman typically function better than men. This high functioning may explain why some women especially diagnosis because their better interpersonal functioning may bias practitioners to under-diagnosis SZ. Problem bc men and women with similar symptoms may experience different diagnosis.
Cultural bias. African Americans and English people of African origin are several times more likely to be diagnosed with SZ. Given that rates in the West Indies and Africa are not high, that is almost certainly not due to a genetic vulnerability. One factor that may be at work here is that positive symptoms, such as hearing voices, are more acceptable in Africa cultures due to communication with ancestors. 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.
20
Q
What are the 3 biological explanations for SZ
A
The genetic basis.
The dopamine hypothesis.
Neural correlates of SZ.
21
Q
Why does SZ tend to run in families
A
There is a strong relationship between genetic similarity between family members and the likelihood of both family members developing SZ
22
Q
What did GOTTESMAN find
A
He did a large-scale family study and found that identical twins (who share 100% of their genes) had a 48% shared risk of developing SZ. Siblings (who share 50% of their genes) have a 9% risk, and first cousins only have a 2% risk
23
Q
What does the identification of different candidate genres for SZ indicate
A
Sz is polygenic - Each individual gene confers a small increased risk of SZ.
SZ is aetiologically heterogenous - different combinations of factors can lead to SZ.
24
Q
What did RIPKE find
A
In 37,000 patients that 108 separate genetic variations were associated with increased risk; many codes for the functioning of the dopamine neurotransmitter
25
What is dopamine
A neurotransmitter that generally has an excitatory effect and is associated with the sensation of pleasure. Unusually high levels are associated with SZ as it’s important in the functioning of several brain systems involved with SZ and unusually low levels are associated with Parkinson’s disease
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What does the original dopamine hypothesis suggest
Hyperdopaminergia - high levels or activity of dopamine in the subcortex (central areas of the brain) may be associated with hallucinations and poverty of speech
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What is the subcortex
Parts of the frontal region of the brain that are not part of the cerebral cortex. They lie under the cortex.
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Example of hyperdopaminergia
An excess of dopamine receptors in Broca’s area
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What does a more recent dopamine hypothesis focus on
Hypodopaminaergia - low levels of dopamine in the prefrontal cortex - which is responsible for thinking and decision-making
30
What is the prefrontal cortex
A region in the frontal lobe which is involved with the highest-order cognitive activities, such as working memory
31
What are neural correlates
Patterns of structure or activity in the brain that occur in conjunction with an experience and may be implicated in the origins of that experience - in terms of SZ it’s where the positive or negative symptoms of SZ correlate with a structure in the brain
32
What is the neural correlate of the negative symptom Avolition
The ventral striatum is believed to be particularly involved in the anticipation of reward which is related to motivation. This loss of motivation (avolition) in some SZ patients may be explained by low activity levels in this area.
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What is the ventral striatum
Major portion of the basal ganglia and functions as part of the rewards system. It includes the nucleus accumbens.
34
What did JUCKEL find
A negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms
35
What is the neural correlate of the positive symptoms of hallucinations
ALLEN found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus
36
What is the superior temporal gyrus
An area in the brain containing the primary auditory cortex, which is responsible for recording sounds
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What is the anterior cingulate gyrus
Frontal part of the cingulate cortex that resembles a ‘Collar’ surrounding the frontal part of the corpus callosum
38
2 strengths of biological explnations of SZ
Research on the role of mutation in SZ supports the genetic explanation. Can take place in the absence of family history of the disorder, for example through mutation of paternal DNA in sperm cells caused by radiation, poison or viral infection. BROWN found a positive correlation between paternal age (associated with increased risks of mutation) and risk of SZ, increasing from 0.7% with fathers under 25 to 2% in fathers over 50. Supports the importance of genetic factors in the development of SZ.
Very strong evidence for genetic vulnerability to SZ. GOTTESMAN family study shows how genetic similarity and shared risk of SZ are closely related. Adoption studies such as TIENARI clearly show that children of SZ are still at a heightened risk of SZ if adopted into families without a history of SZ. Means that, while not entirely genetic, there is overwhelming evidence for the idea of genetic factors making people more vulnerable.
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What is mutation
A genetic change which can then be inherited by any offspring
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3 limitations of the biological explanations for SZ
Mixed support for the dopamine hypothesis. Dopamine agonists (e.g amphetamines) increase the levels of dopamine and can induce schizophrenic-like symptoms in people without the illness. In addition, antipsychotic drugs that lower dopamine activity have been effective in reducing symptoms. However, some of the candidate genes incentivised code for the production of other neurotransmitters such as glutamate. Suggests dopamine can not provide a complete explanation for SZ.
Correlation-causation problems in the neural correlate explanations. Question remains whether unusual activity in the brain causes symptoms or whether there are other possible explanations. E.g the negative correlation between activity in the ventral striatum May suggest that low activity causes avolition. Alternatively, it could be that negative symptoms mean that less information passes through the striatum resulting in the low activity. While they exist, neural correlates tell us relatively little about the causes of SZ.
Clear environment is involved. The probability of developing SZ even if your identical twin has it is less than 50%. There is evidence that environmental factors, such as family functioning, during childhood can also play a role in the development of SZ. Suggest SZ may be the result of a combination of biological and psychological factors which is acknowledged by the interactionist approach.
41
What are dopamine agonists
A drug that has the same effect as a naturally-produced neurotransmitter
42
What is an antipsychotic drug
Drugs used to reduce the intensity of psychotic symptoms (in particular the positive symptoms) of illnesses like SZ
43
What is the interactionist approach
A broad approach to explaining behaviour, which acknowledges that a range of factors, including biological and psychological factors, are involved in the development of behaviour
44
What are the two biological therapies for SZ
Typical antipsychotics
| Atypical antipsychotics
45
What are typical antipsychotics
The first generation of antipsychotic drugs, having been used since the 1950s. They work as dopamine antagonists and include the drug Chlorpromazine
46
What is an antagonist
A drug that prevents the effects of a naturally-produced neurotransmitter
47
What do dopamine antagonists aim to do
Reduce the action of dopamine
48
How do dopamine antagonists work
By blocking dopamine receptors in the synapses in the brain, reducing the action of dopamine.
49
How does Chlopromazine work
Initially, dopamine levels build up after taking Chlopromazine, but then production is reduced. This normalises neurotransmission in key areas of the brain which, in turn, reduces symptoms like hallucinations.
It also has an effect on histamine receptors which appears to lead to a deflation effect.
50
Besides treating SZ, what else is chlorpromazine used for
Calming anxious patients when they are first admitted to hospital
51
What are atypical antipsychotics
Drugs for SZ developed after typical antipsychotics in the 1970s. They typically target a range of neurotransmitters, such as dopamine and serotonin, and include the drug Clozapine
52
What is the aim of atypical antipsychotics
To maintain or improve upon the effectiveness of drugs in suppressing psychoses such as SZ and also minimums the side effects.
53
Typically, what neurotransmitters do atypical antipsychotics target
Dopamine and serotonin
54
How does Clozapine work
It binds to dopamine receptors in the same way that Chlorpromazine does but, in addition, acts on serotonin and glutamate receptors. This drug was was effective than typical antipsychotics.
55
What does Clozapine do
Improved mood and reduces depression and anxiety in patients as well as improving cognitive functioning
56
What is glutamate
The principle excitatory neurotransmitter in the brain, involved in most aspects of normal brain function, including cognition, memory and learning
57
Why was risperidone developed
Because Clozapine was involved in the deaths of some patients from a blood condition called agranulocytosis
58
Why does risperidone need a small dose than most antipsychotics
It binds to dopamine and serotonin receptors like Clozapine but it binds more strongly to dopamine receptors and is therefore more effective in smaller doses and has fewer side effects
59
Strength of biological therapies for SZ
Large body of evidence that shows antipsychotics are moderately effective. THORNLEY reviewed studies comparing Chlorpromazine and placebo control conditions. Data from 13 trails, with a total of 1121 participants, found that Chlopromazine was associated with better functioning and reduced symptom severity. Support for atypical ones as well. MELTZER concluded that Clozapine is more effective than typical antipsychotics, and it 30-50% more effective in treatment-resistant cases. Therefore, the evidence suggests the treatments are relatively effective
60
4 weaknesses of biological therapies for SZ
Liklihood if side effects (mild serious and fatal). Typical antipsychotics are associated with dizziness, agitation, sleepiness and weight gain. Long term use can lead to grimacing and lip smacking as a result of dopamine supersensitivty. The most serious effect of atypical antipsychotics if NMS caused by blocking dopamine action in the hypothalamus. This can be fatal due to disruption of the regulation of several body systems. Serious limitation of anti-psychotic drug therapies.
The theoretical objection to the use of drugs. The use of these drugs is strongly tied with the dopamine hypothesis and the idea that there are higher than usual levels of dopamine activity in the subcortex in the brain. However, there is evidence to show that this may not be correct and that in fact dopamine levels in other parts of the brain are too low rather than too high. If that’s true, then antipsychotics shouldn’t work. This has undermined the faith of some people that antipsychotics do in fact work.
They may simply be a ‘chemical cosh’. It is widely believed that antipsychotics have been used in hospitals to calm patients and make them easier to deal with, rather than to benefit the patients themselves. NICE recommend the short term use of antipsychotics to calm agitated patients, but the practice is seen by some as a human rights abuse. This raises ethical issues.
Doubts about true effectiveness. HEALY suggested that some successful trails have had their data published multiple times, exaggerating the evidence for produce effects. In addition, most studies only review the short term effects. Also suggested that because antipsychotics have a powerful calming effect, it is easy to demonstrate that they had a positive effect on a patient despite the fact the may not be effective in reducing psychosis. Suggests the effectiveness of antipsychotics may be overestimated by much of the empirical research
61
What is NICE
The National Institute for Health and Clinical Excellence
62
What are the two psychological explanations for SZ
Family dysfunction
| Cognitive explanations
63
What are the three parts of family dysfunction
Schizophrenogenic mother
Double-bind theory
Expressed emotion
64
What did FROMM-REICHMANN propose
A psychodynamic explanation based on her patients childhood experiences of what she termed ‘schizophrenogenic mothers’
65
What is a schizoprenogenic neither
A mother who is cold and rejecting, and overprotective and domineering, and tend to create a family climate characterised by tensions and secrecy. This leads to distrust that layer develops into paranoid delusions and schizophrenia
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What is family dysfunction
Abnormal processes within a family, such as poor family communication, cold parenting and high levels of expressed emotion. These may be risk factors for both the development and maintenance of SZ
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Who emphases the role of communication in the family as a risk factor in the redevelopment of SZ (double bind)
BATESON
68
What is double-bind theory
The developing child regularly finds themselves trapped in situations where they fear doing the wrong thing, but receives conflicting messages about what counts as wrong, and feel unable to express themselves about the unfairness of the situation. When they ‘get it wrong’ (which is often) the child is punished by withdrawal of love. This leaves them with an understanding that the world is confusing and dangerous which leads to disorganised thinking and delusions
69
What is expressed emotion
A measure of the family environment related to the extent had family members express critical, hostile and emotionally over-involved attitudes towards a family member with a disorder
70
What 3 things does expressed emotion include
Verbal criticism of the patient.
Hostility towards the patient.
Emotional over-involvement in the life of the patient.
71
What does high levels of EE cause
Stress in the patient and a it is a primary explanation for relapse in patients with SZ
72
What do cognitive explanations of SZ focus on
Abnormal information processing as the root cause of SZ. Lower levels of information processing in some areas in the brain suggests that cognition is impaired
73
What did FRITH identify
Dysfunctional thought processing in metarepresentation as a possible explanation of hallucinations and delusions.
Dysfunctional thought processing in central control as an explanation of speech poverty.
74
What is dysfunctional thought processing
A general term meaning information processing that is not functioning normally and produces undesirable consequences
75
What is metarepresentation
The cognitive ability to reflect on thoughts and behaviours
76
How would dysfunctional thought processes in metarepresentation lead to positive symptoms
Dysfunction in this ability would disrupt our ability to recognise our own thoughts as our own ; this could lead to the sensation of hearing voices (hallucinations) and having thoughts placed in the mind by others (delusions)
77
What is central control
The cognitive ability to suppress automatic responses while we perform deliberate actions instead
78
How would dysfunctional thought processes in central control lead to SZ
People with SZ tend to experience derailment or thoughts and spoken sentences because each word triggers automatic associations that they cannot surpress
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Strength of the psychological explanations for SZ
Support for different information processing in people with SZ.
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Strength for cognitive explanations for SZ
Support for different information processing in people with SZ. STIRLING compared 30 patients with SZ with 18 non-patient controls on cognitive tasks. For example, in the Stroop test participants had to name the ink colour of coloured words. In line with Friths theory of central control dysfunction, patterns took over twice as long as controls to suppress the impulse to read to word and to name the ink colour instead. It shows that processing is different in those with SZ. Unknown if the fault continuations are proximal cause or underlining distal cause.
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What is a proximal cause
The cause of the symptoms
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What is the underlying distal cause
The origins of the disorder
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Limitation of the cognitive explanation for SZ
Direction of causality. Mass of evidence about abnormal biological in SZ but it remains unclear whether cognitive factors are a cause or a result of the neural corrrelates and abnormal neurotransmitter levels seen in SZ. E.g does dysfunctional metarepresentation somehow reduce levels of dopamine in the superior temporal gyrus or is the direction of causality the other way around. Questions the validity of the cognitive approach in explaining the underlying origins of the condition.
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2 limitations of family dysfunction explanation for SZ
Evidence is often retrospective. READ reviewed 46 studies and concluded that 69% of all adult female inpatients with SZ and 59% of males had history of physical and/or sexual abuse in childhood. However most of the evidence is based on information about childhood experiences gathered after the diagnosis of SZ. As such the symptoms may have distorted the patients recall of their childhood experiences. Creates a problem with validity.
Evidence for family-based explanations is weak. Plenty of evidence supporting the principle that poor childhood experiences are associated with schizophrenia, there is little evidence to support the important of schizophrenic mothers, expressed emotion or double bind. These theories are mainly based on clinical observations of patients, which are open to interpretation and subjectivity. Furthermore, the dysfunctional family explanations have historically led to parent-blaming. Parents, already suffering through their child’s symptoms, underwent trauma by being blamed for their conditions. These issues undermine the appropriateness and credibility of the family-based explanation.
85
Limitation of psychological explanations for SZ
Biological factors are not always adequately considered. In their pure forms, psychological explanations for SZ (particularly family dysfunction) can be hard to reconcile with biological explanations (e.g genetic explanations, dopamine hypothesis); it could be that both biological and psychological factors can separately produce the same symptoms which raises the question of whether both outcomes are really SZ. Alternatively we can view this in terms of the diathesis-stress model where the diathesis may be biological or psychological.
86
What are the three psychological therapies for SZ
CBT
family therapy
Token economies
87
What is the aim of CBT
Involved helping patients identity irrational thoughts and trying to change them. This may involve argument or a discussion of how likely a patient beliefs are to be true, and a consideration of a less threatening possibility
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How does CBT help treat SZ
It can help patients make sense of how their delusions and hallucinations impact on their feelings and behaviour. If, for example, a patient hears voices and believes the voices are demons they will naturally be afraid. Offering psychological explanations for the existence of these symptoms can reduce this anxiety and help the patient realise their beliefs are not based on reality.
89
What is the aim of family therapy
It takes place with families rather than individual patients, it aims to improve the quality of communication and interaction between family members. Therapists are concerned with reducing stress within the family that might contribute to the patients risk of relapse. In particular, reducing levels of expressed emotion.
90
What is CBT
A method for treating disorders, including addictions, based on both cognitive and behavioural techniques. From the cognitive view point the therapy aims to deal with thinking, such as challenging negative thoughts. The therapy also includes behavioural techniques
91
Who identitied a range of strategies family therapists can use
PHAROH
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What 4 strategies did PHAROH identity that family therapists can use
Reducing the stress of caring for a relative with SZ.
Improving the ability of the family to anticipate and solve problems.
Reduction of guilt and anger in family members.
Improving families beliefs about and behaviour towards SZ.
93
What is family therapy likely to reduce
The chance of relapse and readmission to hospitals
94
What are token economies
Reward systems (operant conditioning) used to manage the behaviour of patients with SZ who spend long periods in psychiatric hospitals.
95
How do token economies work
Tokens (e.g coloured discs) are given to patients who carry out desirable behaviours, such as getting dressed in the morning, making a bed, etc. This reward reinforces the behaviour and, because it is given immediately, prevents ‘delay discounting’ (the reduced effect of a delay reward). They can be derailed later for tangible rewards (primary reinforcers like food or privileges)
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How are tokens secondary reinforcers
Because they only have value once the patient has learned they can be used to obtain rewards such as sweets, magazines or a walk outside
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5 limitations of psychological therapies for SZ
Research shows limited benefits. JAUHAR reviewer the results of 34 studies of CBT for SZ and found t has a significant but fairly small effect on both positive and negative symptoms. SULTANA conducted a similar review of token economies but found only one of three studies that used random allocation shower improvement in symptoms. PHAROH reviewed effectiveness of family therapy and concluded moderate evidence for the reduction of hospital readmissions over one year and some improvement to quality of life. However, the evidence was inconsistent. Over there is only modest support for psychological therapies.
They appear to help, but not cure. All therapies aim to make it more manageable and improve quality of life. CBT helps patients make sense of their symptoms, family therapy reduces the stress of living with SZ, token economies helps make patients behaviour more socially acceptable. These things are all worth doing, but should not be confused with curing SZ. Biological therapies don’t cure SZ either but they do reduce the severity of symptoms and this may be more desirable.
Ethical issues. Token economy systems have been controversial. Privileges become more available to patients with mild symptoms compared to those with more severe symptoms who are less able to comply with desirable behaviours. Means the most severely ill patients suffer discrimination. CBT also raises ethical issues bc it involves challenging a persons paranoia but at what point does that interfere with an individuals freedom of thought. E.g their politics can be modified. Ethical issues like this makes psychological therapies controversial.
Alternative psychological therapies are under-research. E.g NICE recommends art therapy, providing a qualified art therapist who has experience working with SZ patientsz however, these less well known therapies are not well researched so it is unclear how effective these therapies are. This questions whether under researched therapies should be made available to patients.
Issue with quality of some evidence. Many small scale studies in which mental health professionals have compared patients before and after psychological therapies have found positive results. However these studies often have a lack of a control group or patients are not randomly allocated to treatment and control conditions. Yet, these studies are included in reviews and conclusions. This may mean that the effectiveness of psychological therapies is overestimated by the evidence.
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What is the diathesis-stress model
An interactionist approach to explaining behaviour. E.g SZ is explained as the result of both an underlying vulnerability (diathesis) and a trigger, both of which are necessary for the onset of SZ.
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Who created the original diathesis stress model
MEEHL
100
What did the original diathesis stress model state
That diathesis was entirely genetic, the result of a single ‘schizogene’. When an individual possesses this gene, they are vulnerable to the effects of chronic stress - most notably a schizophrogenic mother could result in the development of the condition. The schizogene is necessary but not sufficient for the development of SZ
101
What is one way in which our understanding of diathesis has developed
It is now clear that many genes each appear to increase genetic vulnerability slightly; there is no ‘schizogene’.
It also does not have to be genetic. It can also include early psychological trauma which seriously affects brain development. For example, child abuse affecting the hypothalamic-pituitary-adrenal system (HPA) system can be over-active, making them vulnerable to stress
102
What is the HPA system
Hypothalamic-pituitary-adrenal system.
This controls how the body responds to a chronic stressor. The hypothalamus triggers the pituitary gland to release the hormone ACTH which, in turn, stimulates release of cortisol
103
What is a modern definition of stress (in relation to diathesis-stress)
Includes anything that risks triggering SZ. Much of the recent research has concerned cannabis use which can increase the risk of SZ up to seven times according to the dose. This is probably because it interferes with the dopamine system
104
What is the treatment for SZ according to the interactionist model
Combining antipsychotic medication and CBT
105
What did TURKINGTON suggest
That it is possible to believe in biological causes of SZ and still practise CBT to relive psychological symptoms. However, this requires adopting an interactionist model. It is not possible to adopt a purely biological approach, tell patients that their condition is purely biological (that there is no psychological significance to their symptoms), and then treat them with CBT
106
Why is there a slower adoption of the interactionist approach in the US compared to the UK
There is more of a conflict between psychological and biological models of schizophrenia, whereas in Britain it is increasingly standard practice to treat patients with a combination of drugs of CBT
107
2 strengths of the interactionist approach
Evidence to support the dual role of vulnerability and stress in the development of SZ. TIENARI investigated children adopted by 19,000 Finnish mothers with SZ between 1960-1979. Their adoptive parents were assessed for parenting style and compared those in a control group of adoptees without any genetic risk. A child-rearing style characterised by high levels of criticism and conflict and low levels of empathy was implicated in the development of SZ but only for children with a high genetic risk. Very strong support for the idea of genetic vulnerability and family related stress combining in the development of SZ.
Usefulness of adopting an interactionist approach in treatment. Studies show an advantage to combinations of treatment for SZ. TARRIER randomly allocated 315 patients to either: a medication and CBT group, a medication and supportive counselling group or a control group (just medication). Patients in the two combination groups showed lower symptom levels that those in the control although there was no difference in rates of hospital readmission. Studies like this show there is a clear practical advantage to adopting an interactionist approach in the form of superior treatment outcomes.
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3 limitations of the interactionist approach to SZ
Original diathesis stress is too simplistic. Now known that multiple genes increase vulnerability to SZ, each having a small effect on its own; there is no single schizogene. Also dress can come in many forms, including - but not limited to - dysfunctional parenting. In fact it is now believed that stress can also include biological factors such as the combination of childhood sexual trauma and cannabis use. Shows that the old idea of diathesis as biological and areas as psychological has turned out to be overly simple.
We don’t know exactly how diathesis and stress work. There is strong evidence to suggest that some sort of underlying vulnerability coupled with stress can lead to SZ. However, we do not yet fully understand the mechanisms by which the symptoms of SZ appear and how both vulnerability and stress produce them. This does not undermine the evidence supporting the approach, but it does mean that it presents us with an incomplete understanding of the actual mechanism.
Treatment-causation fallacy. TURKINGTON argued that there is a good logical fit between the interactionist approach and combining therapies. However, the fact that combined biological and psychological therapies are more effective than either on their own does not necessarily mean the interactionist approach to SZ is correct. Similarly, the fact that drugs help does not mean that SZ is biological in origin. This error of logic is called the treatment-causation fallacy. It means that the superior outcomes of combined therapies should not be over-interpreted in terms of evidence in support of the interactionist approach.
