Paper 3- Schizophrenia

Question 1

What is schizophrenia

Answer 1

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.

Question 2

What are the two major systems for the classification of mental disorder of SZ

Answer 2

DSM-5 and ICD-10

Question 3

What is the classification of a mental disorder

Answer 3

The process of organising symptoms into categories based on which symptoms cluster together in sufferes

Question 4

What is the DSM-5

Answer 4

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

Question 5

What does the DSM-5 states much be present for a diagnosis of SZ

Answer 5

One of the so-called positive symptoms (delusions, hallucinations or speech disorganisation)

Question 6

What is the ICD-10

Answer 6

The most recent version of the International Classification of Diseases, published by the World Health Organisation

Question 7

What does the ICD-10 state is needed for a diagnosis of SZ

Answer 7

Two or more negative symptoms of schizophrenia (avolition and speech poverty)

Question 8

What is a positive symptom of SZ

Answer 8

Atypical symptoms experienced in addition to normal experiences. They include hallucinations and delusions

Question 9

What is a delusion

Answer 9

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.

Question 10

What are hallucinations

Answer 10

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.

Question 11

What are negative symptoms of SZ

Answer 11

Atypical experiences that represent the loss of a usual experience, such as clear thinking or ‘normal’ levels of motivation

Question 12

What is avolition

Answer 12

Involved the loss of motivation to carry out tasks and results in lowered activity levels

Question 13

What is speech poverty

Answer 13

Involves reduced frequency and quality of speech. This is sometimes accompanied by a delay in the verbal responses during conversation.

Question 14

What are the 4 issues in diagnosing SZ

Answer 14

Reliability
Validity
Co-morbidity
Symptom overlap

Question 15

What is reliability in the instance of it being an issue in diagnosing SZ

Answer 15

The extent to which the diagnosis of SZ is consistent

Question 16

What is validity in the instance of it being an issue in diagnosing SZ

Answer 16

The extent to which the diagnosis and classification techniques measure what they are designed to measure

Question 17

What is co-morbidity

Answer 17

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

Question 18

What is symptom overlap

Answer 18

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

Question 19

5 limitations of the diagnosis of SZ

Answer 19

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.

Question 20

What are the 3 biological explanations for SZ

Answer 20

The genetic basis.
The dopamine hypothesis.
Neural correlates of SZ.

Question 21

Why does SZ tend to run in families

Answer 21

There is a strong relationship between genetic similarity between family members and the likelihood of both family members developing SZ

Question 22

What did GOTTESMAN find

Answer 22

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

Question 23

What does the identification of different candidate genres for SZ indicate

Answer 23

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.

Question 24

What did RIPKE find

Answer 24

In 37,000 patients that 108 separate genetic variations were associated with increased risk; many codes for the functioning of the dopamine neurotransmitter

Question 25

What is dopamine

Answer 25

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

Question 26

What does the original dopamine hypothesis suggest

Answer 26

Hyperdopaminergia - high levels or activity of dopamine in the subcortex (central areas of the brain) may be associated with hallucinations and poverty of speech

Question 27

What is the subcortex

Answer 27

Parts of the frontal region of the brain that are not part of the cerebral cortex. They lie under the cortex.

Question 28

Example of hyperdopaminergia

Answer 28

An excess of dopamine receptors in Broca’s area

Question 29

What does a more recent dopamine hypothesis focus on

Answer 29

Hypodopaminaergia - low levels of dopamine in the prefrontal cortex - which is responsible for thinking and decision-making

Question 30

What is the prefrontal cortex

Answer 30

A region in the frontal lobe which is involved with the highest-order cognitive activities, such as working memory

Question 31

What are neural correlates

Answer 31

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

Question 32

What is the neural correlate of the negative symptom Avolition

Answer 32

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.

Question 33

What is the ventral striatum

Answer 33

Major portion of the basal ganglia and functions as part of the rewards system. It includes the nucleus accumbens.

Question 34

What did JUCKEL find

Answer 34

A negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms

Question 35

What is the neural correlate of the positive symptoms of hallucinations

Answer 35

ALLEN found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus

Question 36

What is the superior temporal gyrus

Answer 36

An area in the brain containing the primary auditory cortex, which is responsible for recording sounds

Question 37

What is the anterior cingulate gyrus

Answer 37

Frontal part of the cingulate cortex that resembles a ‘Collar’ surrounding the frontal part of the corpus callosum

Question 38

2 strengths of biological explnations of SZ

Answer 38

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.

Question 39

What is mutation

Answer 39

A genetic change which can then be inherited by any offspring

Question 40

3 limitations of the biological explanations for SZ

Answer 40

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.

Question 41

What are dopamine agonists

Answer 41

A drug that has the same effect as a naturally-produced neurotransmitter

Question 42

What is an antipsychotic drug

Answer 42

Drugs used to reduce the intensity of psychotic symptoms (in particular the positive symptoms) of illnesses like SZ

Question 43

What is the interactionist approach

Answer 43

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

Question 44

What are the two biological therapies for SZ

Answer 44

Typical antipsychotics

Atypical antipsychotics

Question 45

What are typical antipsychotics

Answer 45

The first generation of antipsychotic drugs, having been used since the 1950s. They work as dopamine antagonists and include the drug Chlorpromazine

Question 46

What is an antagonist

Answer 46

A drug that prevents the effects of a naturally-produced neurotransmitter

Question 47

What do dopamine antagonists aim to do

Answer 47

Reduce the action of dopamine

Question 48

How do dopamine antagonists work

Answer 48

By blocking dopamine receptors in the synapses in the brain, reducing the action of dopamine.

Question 49

How does Chlopromazine work

Answer 49

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.

Question 50

Besides treating SZ, what else is chlorpromazine used for

Answer 50

Calming anxious patients when they are first admitted to hospital

Question 51

What are atypical antipsychotics

Answer 51

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

Question 52

What is the aim of atypical antipsychotics

Answer 52

To maintain or improve upon the effectiveness of drugs in suppressing psychoses such as SZ and also minimums the side effects.

Question 53

Typically, what neurotransmitters do atypical antipsychotics target

Answer 53

Dopamine and serotonin

Question 54

How does Clozapine work

Answer 54

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.

Question 55

What does Clozapine do

Answer 55

Improved mood and reduces depression and anxiety in patients as well as improving cognitive functioning

Question 56

What is glutamate

Answer 56

The principle excitatory neurotransmitter in the brain, involved in most aspects of normal brain function, including cognition, memory and learning

Question 57

Why was risperidone developed

Answer 57

Because Clozapine was involved in the deaths of some patients from a blood condition called agranulocytosis

Question 58

Why does risperidone need a small dose than most antipsychotics

Answer 58

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

Question 59

Strength of biological therapies for SZ

Answer 59

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

Question 60

4 weaknesses of biological therapies for SZ

Answer 60

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

Question 61

What is NICE

Answer 61

The National Institute for Health and Clinical Excellence

Question 62

What are the two psychological explanations for SZ

Answer 62

Family dysfunction

Cognitive explanations

Question 63

What are the three parts of family dysfunction

Answer 63

Schizophrenogenic mother
Double-bind theory
Expressed emotion

Question 64

What did FROMM-REICHMANN propose

Answer 64

A psychodynamic explanation based on her patients childhood experiences of what she termed ‘schizophrenogenic mothers’

Question 65

What is a schizoprenogenic neither

Answer 65

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

Question 66

What is family dysfunction

Answer 66

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

Question 67

Who emphases the role of communication in the family as a risk factor in the redevelopment of SZ (double bind)

Answer 67

BATESON

Question 68

What is double-bind theory

Answer 68

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

Question 69

What is expressed emotion

Answer 69

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

Question 70

What 3 things does expressed emotion include

Answer 70

Verbal criticism of the patient.
Hostility towards the patient.
Emotional over-involvement in the life of the patient.

Question 71

What does high levels of EE cause

Answer 71

Stress in the patient and a it is a primary explanation for relapse in patients with SZ

Question 72

What do cognitive explanations of SZ focus on

Answer 72

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

Question 73

What did FRITH identify

Answer 73

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.

Question 74

What is dysfunctional thought processing

Answer 74

A general term meaning information processing that is not functioning normally and produces undesirable consequences

Question 75

What is metarepresentation

Answer 75

The cognitive ability to reflect on thoughts and behaviours

Question 76

How would dysfunctional thought processes in metarepresentation lead to positive symptoms

Answer 76

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)

Question 77

What is central control

Answer 77

The cognitive ability to suppress automatic responses while we perform deliberate actions instead

Question 78

How would dysfunctional thought processes in central control lead to SZ

Answer 78

People with SZ tend to experience derailment or thoughts and spoken sentences because each word triggers automatic associations that they cannot surpress

Question 79

Strength of the psychological explanations for SZ

Answer 79

Support for different information processing in people with SZ.

Question 80

Strength for cognitive explanations for SZ

Answer 80

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.

Question 81

What is a proximal cause

Answer 81

The cause of the symptoms

Question 82

What is the underlying distal cause

Answer 82

The origins of the disorder

Question 83

Limitation of the cognitive explanation for SZ

Answer 83

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.

Question 84

2 limitations of family dysfunction explanation for SZ

Answer 84

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.

Question 85

Limitation of psychological explanations for SZ

Answer 85

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.

Question 86

What are the three psychological therapies for SZ

Answer 86

CBT
family therapy
Token economies

Question 87

What is the aim of CBT

Answer 87

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

Question 88

How does CBT help treat SZ

Answer 88

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.

Question 89

What is the aim of family therapy

Answer 89

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.

Question 90

What is CBT

Answer 90

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

Question 91

Who identitied a range of strategies family therapists can use

Answer 91

PHAROH

Question 92

What 4 strategies did PHAROH identity that family therapists can use

Answer 92

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.

Question 93

What is family therapy likely to reduce

Answer 93

The chance of relapse and readmission to hospitals

Question 94

What are token economies

Answer 94

Reward systems (operant conditioning) used to manage the behaviour of patients with SZ who spend long periods in psychiatric hospitals.

Question 95

How do token economies work

Answer 95

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)

Question 96

How are tokens secondary reinforcers

Answer 96

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

Question 97

5 limitations of psychological therapies for SZ

Answer 97

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.

Question 98

What is the diathesis-stress model

Answer 98

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.

Question 99

Who created the original diathesis stress model

Answer 99

MEEHL

Question 100

What did the original diathesis stress model state

Answer 100

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

Question 101

What is one way in which our understanding of diathesis has developed

Answer 101

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

Question 102

What is the HPA system

Answer 102

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

Question 103

What is a modern definition of stress (in relation to diathesis-stress)

Answer 103

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

Question 104

What is the treatment for SZ according to the interactionist model

Answer 104

Combining antipsychotic medication and CBT

Question 105

What did TURKINGTON suggest

Answer 105

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

Question 106

Why is there a slower adoption of the interactionist approach in the US compared to the UK

Answer 106

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

Question 107

2 strengths of the interactionist approach

Answer 107

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.

Question 108

3 limitations of the interactionist approach to SZ

Answer 108

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.