Schizophrenia Flashcards
what are the two major systems for the classification of mental disorders for schizophrenia
ICD-11 (UK) and the DSM-5 (USA)
compare ICD-11 and DSM-5
For the ICD-11 2 or more negative symptoms for one month or longer can result in a diagnosis whereas in the DSM-5 only one negative symptom.
Also the ICD-11 recognizes subtypes of schiz such as paranoid schizophrenia (characterized by powerful hallucinations and delusions) or catonic (involves problems with patients movements) whereas in DSM-5 it does not categorise.
Positive symptoms
(additional experience)
Hallucinations- are sensory experiences such as auditory hallucinations (hearing voices that arent present) and visual hallucinations ( seeing things that arent there)
Delusions- irrational beliefs/false
such as delusions of prosecution which is a false belief that you are being harasses or delusions of control a false belief that you are being controlled by something external eg aliens.
Negative symptoms
(Loss of usual abilities)
Avolition- loss of motivation to carry out everyday tasks. Andreason identified three signs of avolition: poor hygiene, lack of persistence in work or education and lack of energy.
speech poverty- reduction in the amount and quality of speech, lack of fluency
Diagnosis
The identification of the nature of an illness or other problem by examination of the symptoms. (Labelled)
Classification
The action or process of classifying something: the classification of disease according to symptoms
Ao1 Reliability for diagnosis and classification
Reliability refers to consistency. This refers to whether we can gain consistent results when classifying and diagnosing Sz. Therefore, the extent to which different classification systems agree upon how schizophrenia should be classified and the extent to which two or more health professionals would agree on the same diagnosis, regardless of time period or culture, measured by inter-rater reliability.
Ao1 Validity for diagnosis and classification
Validity refers to accuracy, the extent to which we are measuring what we intend to measure (schizophrenia). For example, are the classification systems accurately outlining the signs and symptoms of schizophrenia and are health professionals’ accurately diagnosing schizophrenia?
Ao1 Cheniaux (2009) for diagnosis and classification
Cheniaux (2009) asked two psychiatrists to diagnose the same 100 patients using the DSM and ICD. One psychiatrist diagnosed 26 according to DSM and 44 according to ICD. The other diagnosed 13 according to DSM and 24 according to ICD. This shows poor inter-rater reliability as one psychiatrist diagnosed almost double the amount than the other psychiatrist. Moreover, it demonstrates poor reliability in the classification of schizophrenia as both psychiatrists diagnosed almost double the number of patients using the ICD than the DSM, which also calls in to question the validity of the diagnosis.
Symptom overlap
This is where two or more conditions share similar symptoms. For example, both schizophrenia and depression involve negative symptoms such as avolition.
Co-morbidity
This is where two illnesses/conditions occur at the same time. Schizophrenia is commonly diagnosed with other conditions such as depression and/or OCD as they share common symptoms i.e. lowered motivation/mood. This is a problem as it means that schizophrenia may not exist as a distinct condition which may lead to misdiagnosis.
Gender bias in diagnosing and classifying schizophrenia
Since the 1980s men have been diagnosed with schizophrenia more often than women. This may be because men are more genetically vulnerable to developing schizophrenia than women. However, it could be because females with schizophrenia typically function better than men, being more likely to work and have good family relationships
Culture bias in diagnosing and classifying schizophrenia
English people of African origin are much more likely to be diagnosed with schizophrenia in the UK. (rates in the West Indies and Africa are not high so this cannot be due to generic vulnerability). Higher diagnosis rates in the UK may be because some behaviours classed as positive symptoms of schizophrenia are normal in African cultures (e.g. hearing voices as part of ancestor communication)
A03 for Reliability and validity in diagnosis and classification of schizophrenia, including reference to co-morbidity, culture and gender bias and symptom overlap.
One problem of reliability and validity of the classification and diagnosis of schizophrenia is that there is often ‘Symptom overlap’. This is where two or more conditions share similar symptoms. For example, both schizophrenia and depression involve negative symptoms such as avolition. This questions the validity and reliability of the classification and diagnosis of schizophrenia because an individual may be diagnosed with the wrong disorder. This is an issue as doctors may not be diagnosing schizophrenia correctly, and therefore individuals may not receive appropriate treatment. This weakens the validity and reliability in the classification and diagnosis of schizophrenia as it negatively affects its accuracy and consistency.
A further problem with the reliability and validity of the diagnosis and classification of schizophrenia is ‘Co-morbidity’. This is where two illnesses/conditions occur at the same time. For example, Buckley et al (2009) concluded that 50% of patients diagnosed with schizophrenia also have a diagnosis of depression and 23% of patients diagnosed with schizophrenia are diagnosed with OCD. This questions the validity and reliability of classification and diagnosis of schizophrenia, because the two conditions may be better seen as one and doctors may diagnose the wrong condition.
Moreover, another issue with the validity of the diagnosis and classification of schizophrenia is Gender bias in diagnosis. Since the 1980s men have been diagnosed with schizophrenia more often than women. This may be because men are more genetically vulnerable to developing schizophrenia than women. However, it could be because females with schizophrenia typically function better than men, being more likely to work and have good family relationships therefore their symptoms may be masked by good interpersonal skills (Cotton et al). This questions the validity and reliability of the classification and diagnosis of schizophrenia as women who share similar symptoms as men may not receive the same diagnosis as their symptoms seem mild.
Biological explanations for Schizophrenia: genetics Ao1 + Ao3
The genetic explanation states that schizophrenia is hereditary and passed on from one generation to the next through genes. Therefore, a person is born with a genetic predisposition (likelihood) to schizophrenia. It is believed that several maladaptive ‘candidate’ genes such as PCM1, are involved (polygenic) which increases an individual’s vulnerability to developing schizophrenia. Studies have shown that 108 separate genetic variations are associated in the risk of developing schizophrenia.
a03- Gottesman (1991) studied 40 twins and found that the concordance rate for monozygotic twins was 48% and only 17% for dizygotic twins. Therefore, the closer the genetic link to somebody with schizophrenia, the more chance of developing schizophrenia.
neural correlates: Brain Structure or Function – AO1+ Ao3
One neural correlate of schizophrenia is enlarged ventricles. A meta-analysis by Raz and Raz found that over half of individuals tested, with schizophrenia had increased ventricle size compared to a control group. Enlarged ventricles are associated with damage to central brain areas and the pre-frontal cortex, this damage is associated with negative symptoms of schizophrenia.
Research to support the role of neural correlates as an explanation for schizophrenia comes from Suddath et al. (1990). He used MRI scans to investigate the brain structure of MZ twins in which one twin was schizophrenic. They found that the schizophrenic twin generally had more enlarged ventricles. This suggests enlarged ventricles do play a role in determining the likelihood of schizophrenia developing.
Neural Correlates: Dopamine Hypothesis – AO1
The brains chemical messengers (neurotransmitters) appear to work differently in the brain of a patient with schizophrenia. In particular, Dopamine (DA) is widely believed to be involved as individuals with sz may release too much dopamine or have a large amount of D2 receptors on the post synaptic neuron.
Hyperdopaminergia in the subcortex:
High dopamine activity in the central areas of the brain such as Broca’s area (responsible for speech production) may be associated with auditory hallucinations.
Hypodopaminergia in the cortex:
Low dopamine activity in the prefrontal cortex (thinking and decision making) have been associated with the negative symptoms of schizophrenia such as avolition.
Overall - Biological explanation of schizophrenia - AO3
A strength of the biological explanation of schizophrenia is that it uses scientific methods. This is because the theory is based on objective and empirical techniques such as gene mapping studies and brain scans such as FMRI which are used to identify specific genes (PCM1) or areas of the brain linked to schizophrenia (enlarged ventricles). Therefore, this increases the overall internal validity of the biological explanation of schizophrenia, thus, raising Psychology’s scientific status.
However, the biological explanation of schizophrenia can be criticised for biological determinism, this is because the theory states that an individual is controlled by internal factors such as high dopamine activity (hyperdopaminergia) in the subcortex which inevitably causes auditory hallucinations. Therefore, it neglects the role of free will, and choice that individuals have; this could leave victims feeling like they have no control over their schizophrenic behaviour. THINK FURTHER. Furthermore, it be seen as unethical as it can leave victims’ families feeling guilty as they have passed on a gene that has affected their children and it cannot be stopped. Therefore, this limits the biological explanation of schizophrenia.
On the other hand, it could be argued that a deterministic stance is a strength as a cause for behaviour can be established, and this can lead to treatments being created, therefore…
A strength of the biological explanation of schizophrenia is that it has practical applications. This is because the principles of the theory, that schizophrenia is caused by an imbalance of dopamine has led to the treatment of drug therapies such as typical and atypical antipsychotics. These drugs are effective in treating schizophrenia by balancing levels of dopamine in the patient’s brain and therefore reducing symptoms of schizophrenia such as hallucinations and delusions. Therefore the biological explanation of schizophrenia is an important part of applied psychology as it helps to treat people in the real world.
However, there are alternative treatments for schizophrenia and therefore there are also…
An alternative explanation for the development of schizophrenia is family dysfunction. This would argue that schizophrenia is due to faulty communication patterns within a family such as schizophrenogenic mother, whereby the mother is cold and creates a family climate characterised by tension and secrecy. This leads to distrust that later develops into paranoid delusions, rather than delusions being due to levels of dopamine/genes/neural correlates. Therefore, the biological explanation of schizophrenia is not the only explanation that needs to be considered.
Family dysfunction AO1
Family dysfunction is the idea that an individual develops schizophrenia because they have been raised in a dysfunctional family environment. The family is dysfunctional in the way that they communicate with each other as they have high levels of tension and arguments. This results in creating risk factors for the development and maintenance of schizophrenia.
Schizophrenogenic mother (N)
(E) The idea that schizophrenia is caused by the patient’s early experience of a schizophrenogenic mother (Frieda Fromm-Reichman, 1948).
(E) A schizophrenogenic mother is cold, controlling, rejecting, emotionally unresponsive and builds a family climate characterised by tension and secrecy. (F) This leads to distrust that later develops into paranoid delusions (S positive symptom) in schizophrenia.
The father in such families is often passive.
Double Bind communication (N)
(E) Bateson et al (1956) argues that schizophrenia is due to the faulty communication patterns that exist within families. This communication type is double bind communication; this occurs when the parent communicates a verbal message which is not matched with their non-verbal message, so the child receives mixed messages.
For example, a father may be verbally loving but emotionally rejecting, for example, becoming rigid when the child tries to show affection.
(F) These conflicting, confusing forms of communication can contribute or cause schizophrenia. The child feels they cannot do the right thing and becomes increasingly anxious, leading to them withdrawing and avoiding social contact – signs of avolition (S negative symptoms) and the mixed messages result in disorganised thinking and paranoid delusions.
1c) Expressed Emotion (N)
This is the level of emotion, in particular negative emotion, expressed towards a patient by their family members.
(E) High levels of expressed emotion such as,
* Verbal criticism and occasional violence towards the patient
* Hostility towards the patient, including anger and rejection
* Emotional over-involvement in their life.
(F) The development of schizophrenia: This can cause stress in the patient and the constant harassment from the family can trigger onset schizophrenia.
The maintenance of schizophrenia: The stress caused is a primary explanation for relapse in patients with schizophrenia. (Kavanagh, 1992). This is because when a patient with SZ is placed back into the stressful environment, there is a resurgence of positive and negative symptoms (S)
Family dysfunction - AO3
Research to support the schizophrenogenic mother theory comes from Mednick et al (1984). They researched 207 children (high risk for developing SZ) who were raised in dysfunctional families where the mothers were cold, rejecting and emotionally unresponsive to their children’s needs. It was found that 10 years later, 17 children of this high-risk group were diagnosed with schizophrenia, this is 8%, compared to 1% of the general population and thus supporting the theory that family dysfunction can lead to schizophrenia.
A-A* Discussion: This research can be praised as it is based on prospective data (a sample, followed for a long period of time), therefore does not have the confounding variable of patients with schizophrenia having to look back to their childhood and recall information that may be incorrect due to the passing of time. This increases the internal validity of the research into family dysfunction as an explanation for schizophrenia.
😊 Research to support double bind communication was conducted by Berger (1965). When asked about the interactions with their parents in childhood, it was found that schizophrenics could remember more instances of double bind communication from their mother than non-schizophrenics. This provides clear support for mixed communication in schizophrenics’ childhood and therefore supports family dysfunction as an explanation of schizophrenia. Discussion: However, this research is based on retrospective data as the patient has to think back to childhood. Therefore, this could mean that there are inaccuracies in recall as a long period of time has passed. This reduces the internal validity of the research to support the family dysfunction as an explanation of schizophrenia.
Despite this criticism,
😊 A strength of Family dysfunction as an explanation of schizophrenia is that it has practical applications. This is because the principles of the explanation, that schizophrenia is caused by faulty family communication has led to the treatment of family therapy. This is effective in treating schizophrenia by a therapist meeting with the patient and their family in order to try and alter relationship and communication patterns. This reduces stress levels and expressed emotion and can help prevent relapse of schizophrenia (Leff et al, 1985), therefore family dysfunction as an explanation of schizophrenia is an important part of applied psychology as it helps to treat people in the real world.
However, there are alternative treatments for schizophrenia and therefore there are also…
☹ An alternative explanation for schizophrenia is the biological explanation. This would suggest that schizophrenia is due to hyperdopaminergia, high levels of dopamine in central areas of the brain, that are associated with symptoms of schizophrenia. For example, auditory hallucinations have been associated with high levels of dopamine around the Broca’s area rather than dysfunction within family communications, such as having a schizophrenogenic mother. Therefore, this weakens family dysfunction as an explanation of schizophrenia as it is not the sole explanation that should be considered.
Cognitive explanations, including dysfunctional thought processing - Metarepresentation
Metarepresentation is the cognitive ability to reflect on thoughts and behaviour. This allows us to understand our actions and the actions of others. Dysfunction in metarepresentation would disrupt our ability to recognise our own actions and thoughts as being carried out by ourselves or others.
This could explain Auditory hallucinations (positive symptom) as an individual may not understand that a voice in their head is their own voice and not somebody else’s. Therefore, causing distress in the individual.
For example, believing that the voice telling you that your friends hate you is a different person rather than yourself
Cognitive explanations, including dysfunctional thought processing - Central control
Central control is the cognitive ability to suppress automatic responses whilst performing a deliberate action instead.
Dysfunction in central control could explain Speech poverty and thought disorder as the individual is not able to suppress automatic thoughts and speech triggered by other thoughts/words spoken.
can experience disrupted spoken sentences, known as derailment. This is where the individual’s speech is disrupted as the spoken words trigger other associations and the person cannot suppress the action.
Cognitive explanations, including dysfunctional thought processing - Ao3
Research to support dysfunctional thought processing (central control) was conducted by Stirling et al (2006). They compared 30 patients with schizophrenia with 18 non-patient controls on a range of cognitive tasks such as the Stroop Test. Participants had to accurately name the ink colour of the colour word printed. Schizophrenia patients took over twice as long to complete the task as the control group, as they could not supress their automatic response of saying the word rather than the colour. Thus, supporting Frith’s theory of central control dysfunction as an explanation of schizophrenia.
An alternative explanation for schizophrenia is the biological explanation or Family Dsyfunction. This would suggest that schizophrenia is due to hyperdopaminergia, where high levels of dopamine in central areas of the brain are associated with auditory hallucinations rather than a dysfunction in thought processing, such as a lack of metarepresentation. Therefore, weakening the cognitive explanation for schizophrenia as it is not the only explanation of schizophrenia that should be considered.
A strength of the cognitive explanation of schizophrenia has practical applications. This is because the principles of the theory, that schizophrenia is caused by delusional thoughts has led to the treatment of cognitive behavioural therapy. This is effective in treating schizophrenia as, patients are helped to identify and challenge their delusional thoughts. This can reduce positive symptoms of schizophrenia such as delusions of control, therefore the cognitive explanation of schizophrenia is an important part of applied psychology as it helps to treat people in the real world.
Drug therapy antisychotics: typical (first gen) - Chlorpromazine
Chlorpromazine are dopamine antagonists; they reduce levels of dopamine activity in the brain. Chlorpromazine works by binding to the D2 receptors on post synaptic neurons in the brain, reducing the action of dopamine. This reduces dopamine activity levels and results in a reduction of positive symptoms of schizophrenia, such as hallucinations.
Drug therapy antisychotics: atypical (sec gen)- Clozapine
act upon neurotransmitters dopamine AND serotonin. Clozapine also binds to D2 dopamine receptor sites on the post synaptic neuron, reducing positive symptoms such as hallucinations. They also act as agonists upon serotonin receptor sites (2A and 2C) to increase levels of serotonin. It is believed that this action reduces negative symptoms of schizophrenia such as a lack of emotions as it helps improve mood and reduce depression and anxiety in patients
Outline the difference between typical and Atypical antipsychotics
-Atypical antipsychotics (clozapine) can be used to treat both positive and negative symptoms of schizophrenia as they act upon both dopamine and serotonin whereas typical antipsychotics (chlorpromazine) only treat the positive symptoms as they only act upon dopamine.
-Atypical antipsychotics are seratonin agonists and dopamine antagonist as it works to increase levels of seratonin and reduces dopamine treating both neg and pos symptoms whereas typical antisychotics (chlorpromazine) are just dopamine antagonists as they reduce dopamine activity reducing the positive symptoms only.
Drug Therapy: typical and atypical antipsychotics- Ao3
A strength of antipsychotics as a treatment for Schizophrenia is that there is evidence to support their effectiveness. There is a large body of research to support the effectiveness of typical and atypical antipsychotics. Thornley et al (2003) found that a meta-analysis of 13 studies with a total of 1121 participants investigating Chlorpromazine (typical) against a placebo, that the typical antipsychotic was associated with better overall functioning and reduced symptom severity. Furthermore, Meltzer (2012) concluded that Clozapine (atypical) was more effective than typical antipsychotics and is effective in 30-50% of treatment resistant cases. Therefore, supporting that antipsychotics are an effective treatment for positive and negative symptoms of Schizophrenia.
A strength of drug therapy as a treatment for SZ, is that typical and atypical antipsychotics require little motivation from the patient. As the patient only has to take a tablet in order to reduce the symptoms of schizophrenia. This is unlike CBT which requires motivation from patients as they have to attend sessions and engage in them in order to identify and challenge irrational thoughts such as delusions. This may be difficult for a person with schizophrenia as they may not have an accurate perception of reality. Also, it is beneficial for those with negative symptoms such as Avolition who struggle with keeping up with everyday tasks as they receive immediate positive effects on their symptoms. Therefore, drug therapy may be more appropriate than CBT in treating schizophrenia BECAUSE it is a more accessible treatment across the symptoms.
A weakness of using drug therapy to treat Schizophrenia is that they can cause negative side effects. Typical antipsychotics such as chlorpromazine can produce movement side effects such as parkinsonism (Parkinson-like symptoms), moreover atypical antipsychotics carry the risk of a life-threatening illness, agranulocytosis (reduced white blood cell count). Unlike CBT, as this involves a person identifying and challenging their irrational thoughts (delusions), without the use of drugs so there are no negative and potentially life-threatening side effects. Therefore, drug therapy may not be appropriate for all patients as the side effects reduce the effectiveness of drug therapy as a treatment of schizophrenia as some people may stop taking them resulting in relapse of symptoms.
CBT - treating schizophrenia
-5-10 sessions
The aim of CBT is to help patients identify irrational/delusional thoughts and change them into more rational ones via disputing (making them less threatening)
Once the irrational thoughts have been identified, for example, a paranoid delusion that aliens were trying to abduct them, the psychiatrist would challenge the patient’s irrational thoughts in order to encourage patients to come up with a more plausible/less threatening explanation:
The therapist could use empirical disputing, in which the therapist would ask the patient where is the evidence of their delusion/hallucination? For example ‘Where is the evidence that aliens exist? Has anybody else seen these aliens?
This disputing helps patients to understand the delusions/hallucinations are not real and the therapist could explain that it is just a symptom of their schizophrenia. Offering more plausible explanations for these symptoms can reduce anxiety/distress and helps the patient realise their beliefs (e.g. delusions) are not based in reality and that their thoughts are less threatening.
positive self talk
for example, if an individual hears negative voices, they can say positive statements that challenge the auditory hallucinations.
self distraction stratedgies
The therapist could also teach the patient self-distraction strategies, for example listening to music to drown out voices when they occur.
cognitive Behaviour Therapy – AO3
Research into the effectiveness of CBT was carried out by Jauhar et al. They reviewed the results of 34 studies of CBT as a treatment for schizophrenia. They concluded that CBT has a significant but small effect on both positive and negative symptoms. Demonstrating that CBT is fairly effective in treating schizophrenia and that by challenging patients irrational thoughts it can reduce symptoms of depression. However, it is worth noting that out of the 34 studies, CBT only had a small impact on SZ symptoms. Therefore placing doubt on the effectiveness of cognitive behavioural therapy as a treatment for schizophrenia.
A limitation of CBT as a treatment for schizophrenia is that it requires motivation and commitment from patients to attend sessions, this is something that individuals suffering from negative symptoms of schizophrenia, such as avolition, often lack. THINK FURTHER… CBT also requires a patient to engage with the therapy, however, somebody with positive symptoms of schizophrenia (delusions) may have a lack of awareness and an inaccurate perception of reality. Therefore, in some cases of schizophrenia, CBT is only effective when combined with antipsychotics. This is because the drugs help the patient to motivate themselves to attend the sessions/increase the patients awareness. Therefore, CBT alone may not be an effective treatment for all cases of schizophrenia.
Some may prefer this therapy as it avoids the chemical dependence. This is because CBT encourages individuals to identify and challenge their irrational/delusional thoughts independently, giving them control over their own behaviour. This is unlike drug therapy, which imposes the chemical straitjacket as the drug controls activity of neurotransmitters in the brain such as dopamine to reduce the symptoms of schizophrenia, which could cause dependence. Due to this, some may prefer CBT as a more appropriate treatment for schizophrenia.
family Therapy – AO1
Family therapy is based on the idea that as family dysfunction can play a role in the development of schizophrenia, altering relationship and communication patterns within dysfunctional families.. It also works by reducing Expressed emotion and stress levels within the family which may contribute to a patient’s risk of relapse.
The main aim of family therapy is to reduce levels of expressed emotions/stress by:
1) Improving families’ beliefs about and behaviour towards schizophrenia
2) Reducing the stress of caring for a relative with schizophrenia
3) Decreasing feelings of guilt and anger in family members.
4) Helping family members achieve a balance between caring for the individual with schizophrenia and maintaining their own lives.
Therapist meet w patients and family regurarily, 9months-1yr and encouraged t be open and talk abt patients symptoms, behavior and progress.
Family Therapy AO3
Research to support family therapy as a treatment for schizophrenia was conducted by Leff et al (1985). They compared family therapy with routine outpatient care for schizophrenics and found that in the first 9 months of treatment 50% of those receiving routine care relapsed, compared with only 8% of those receiving family therapy. This suggests that family therapy is an effective therapy for treating schizophrenics.
A limitation of family therapy as a treatment of schizophrenia is that it does not get to the root cause (aetiology) of schizophrenia. It works by helping to reduce the stress of living with schizophrenia in a family, for both the patient and family members, this does not eliminate the symptoms completely. This questions the appropriateness and effectiveness of the therapy as when the therapy stops patients could relapse, which is what Hogarty et al (1986) found in a follow up study of patients who had received family therapy.
Moreover, In family therapy emphasis is placed on ‘openness’, this can sometimes be an issue as it may cause or reopen family tensions. Some family members may also be reluctant to talk about, or even admit, their problems, lowering the effectiveness of family therapy as a treatment for schizophrenia.
or alternative- art therapy
Token economies as used in the management of schizophrenia AO1
Token economies are a behaviourist approach to manage the behaviour of patients with schizophrenia. It is mainly used with patients who have spent a long time in hospital and therefore who have developed maladaptive behaviour (institutionalised) such as bad hygiene or lack of communication with others.
Aim: The aim of token economies is to change a patient’s behaviour so that they are easier to manage, will have a better quality of life and thus enabling them to live outside of a hospital setting.
The technique uses Skinner’s operant conditioning principles, whereby patients receive reinforcements (rewards) in the form of tokens, such as coloured discs, immediately after producing a desired behaviour such as self-care or social interaction. The tokens can then be later exchanged for goods or privileges such as hours watching tv, magazines, a walk outside or sweets.
The tokens are secondary reinforcers, these are not rewarding by themselves (they don’t see the token as the reward). However, the patients learn to associate them with meaningful rewards such as going for a walk, sweets or watching a film (primary reinforcers).
In order for the token to become secondary reinforcers, they need to be paired with the primary reinforcers, so at the start of a token economy programme the tokens and primary reinforcers (e.g. sweets) are administered together
Token economies as used in the management of schizophrenia – A03
Research to support the use of token economy as a management technique for SZ was conducted by Dickerson et al (2005). A meta-analysis reviewing 13 studies of token economies found the technique was useful in increasing the adaptive behaviour of patients, such as self-hygiene. Studies also showed that there were significant increases when CBT was combined with drug therapies as the severity of the symptoms was reduced with the drug therapy and CBT challenged the irrational thought processes. This suggest that token economies is an effective management technique and it increases the credibility of the use of token economies in the management of schizophrenia.
However, one issue with using a meta-analysis is that there is a risk of publication bias as researchers have control over the studies they wish to report. A meta-analysis would review published research, and research studies that have significant results are more likely to be published than studies with non-significant results. This limits the support the meta-analysis research by Dickerson provides for the effectiveness of token economies in the management of schizophrenia as an accurate view of its effectiveness is skewed by bias.
Another issue with token economies is that they do not get to the root cause of schizophrenia. The aim is to make schizophrenia more manageable and improve patients’ quality of life; it helps by making patients’ behaviour more socially acceptable so that they can better integrate into society. Whilst this is important, the therapy does not treat schizophrenia. Further to this, Token economies is mainly effective in an institutionalised setting and when patients are sent back home, they lose the structure they had to help manage their behaviour i.e., they don’t have someone to give them a token for completing the desired behaviour. This questions the appropriateness and effectiveness of the therapy in managing schizophrenia, as there is high chance of relapse when patients are given independence.
Diathesis
Vulnerability (at risk)
Stress
A negative psychological experience eg childhood trauma
Interactionist approach- Diathesis-stress model
-In Meehl’s original diathesis stress model, diathesis (vulnerability) was entirely genetic. It was down to a single ‘schizo-gene’, which made somebody sensitive to stress.
-Meehl suggested that if a person does not have this schizo-gene then no amount of stress would lead to schizophrenia. However, if you have the gene, stress through childhood, such as having a schizophrenogenic mother could lead to schizophrenia.
-However, it is now believed that there is no single schizo-gene, but that it is many genes that increase generic vulnerability to schizophrenia (polygenic).
-factors other than genes can be a diathesis such as psychological trauma. Early and severe enough trauma, such as child abuse can seriously affect aspects of brain development and can make a person more vulnerable to later stress.
modern definition of stress (trigger) includes anything that risks triggering schizophrenia, not just parenting. Much of the recent research has concerned cannabis use. In terms of the diathesis-stress model cannabis is the stressor because it increases the risk of schizophrenia by up to seven times according to the dose. Probably due to its interference with the dopamine system. However, not everyone develops schizophrenia after smoking cannabis suggesting there must also be one or more vulnerability factors.
schizophrenia: The Diathesis-Stress model
As the interactionist model considers both biological and psychological factors in the development of schizophrenia, it is therefore compatible with both biological and psychological treatments for schizophrenia- combination of antipsychotic medication and psychological therapies, most commonly CBT.
Turkington et al (2006) argue that it is possible to believe in biological causes of schizophrenia and still practise CBT to relieve psychological symptoms. However, this requires adopting an interactionist model. It is not possible to adopt a purely biological approach and tell the patient their condition is purely biological and that there is no psychological significance to symptoms, and then to treat them with CBT.
In the UK, treatments such as CBT, family therapy and drug therapy are often combined.
AO3: The importance of an interactionist approach in explaining and treating schizophrenia; the diathesis-stress model
Research to support the interactionist approach in explaining schizophrenia comes from Tienari et al (2004). They followed up 19,000 adopted children in Finland whose mothers had schizophrenia and compared them to a control group of adopted children without any genetic risk. The child rearing styles of the adoptive parents were observed. Those children who were brought up in families with a lot of conflict and low empathy (family dysfunction) were much more likely to develop schizophrenia but only in the children who had a genetic vulnerability, not the control group. This suggests that both genetic vulnerability and family related stress are important in the development of schizophrenia.
However, one limitation of the interactionist approach to explaining schizophrenia is that there are individual differences, for example two people may have the same vulnerability and stressor but one may not develop schizophrenia. This means that we do not have a full understanding of the interactionist approach to explaining schizophrenia and more research may need to be conducted.
Research to support the interactionist approach in treating schziphrenia was conducted by Tarrier et al (2004). 315 patients were randomly allocated to treatment conditions. They found that patients given a combined therapy of medication and CBT/counselling had lower symptom levels than a control group with just one treatment (medication). This therefore suggests by adopting an interactionist approach and using both biological and psychological therapies, patient’s schizophrenic symptoms will be treated more effectively.
