Schizophrenia

Classification of schizophrenia

• 1% of the population have schizophrenia. Onset of first symptoms is typically around 15 to 45 years of age. Men are more likely to get schizophrenia, typically having an earlier onset.

• The Diagnostic and Statistical Manual (DSM) is most often used to diagnose schizophrenia. However the ICD (International Classification of Disease) can also be used. DSM-5 and ICD-10 are two separate systems/criteria for diagnosis.

o DSM-5 requires one positive symptom.

o ICD-10 requires two negative symptoms.

Positive symptoms of schizophrenia, including hallucinations and

delusions

• Positive Symptoms: additional experiences that are beyond those of ordinary existence. Examples include hallucinations (additional sensory experiences such as seeing distortions in objects that look like faces, or hearing voices), and delusions (irrational beliefs about themselves or the world, such as feelings of persecution or grandeur).

Negative symptoms of schizophrenia, including speech poverty and avolition

• Negative symptoms are losses of normal experiences and abilities. Examples are Avolition (a lack of purposeful behaviour. No energy to socialise or look after hygiene. Generally apathetic) and Speech Poverty (Brief verbal communication style. Loss of quality and quantity of verbal responses. Can be classified as a positive symptom if speech is excessively disorganised with sufferers wandering off the point).

Reliability and validity in diagnosis and classification of schizophrenia, including reference to co-morbidity, culture and gender bias and symptom overlap

• Reliability is the extent to which a finding is consistent. It is the extent to which psychiatrists can agree on the same diagnosis when independently assessing patients (inter-rater reliability). In order for a classification system to be reliable, the same diagnosis should be made each time. Therefore different psychiatrists should reach the same decision when assessing a patient.

• Test-retest reliability is if the same thing measured under the same conditions yields the same results every time, i.e: the same doctor giving the same diagnosis over time for the same symptoms.

• Inter-rater reliability of schizophrenia diagnosis is often low. Beck (1963) found only a 54% concordance rate between doctors’ assessments of 153 patients.

• However Jakobsen et al. (2005) tested the reliability of the ICD-10 classification system in diagnosing schizophrenia. A hundred Danish patients with a history of psychosis were assessed using operational criteria, and a concordance rate of 98% was obtained. This demonstrates the high reliability of the clinical diagnosis of schizophrenia using up-to-date classification.

• Validity is the extent to which we are measuring what we are intending to measure. In the case of an illness like schizophrenia we have to consider the validity of the diagnostic tools; for example, do different assessment systems arrive at the same diagnosis for the same patient? Validity of schizophrenia is also the question as to whether or not it is a unique disorder or not, meaning that (if it is) it has its own unique characteristics and causes.

• One reason that the validity of schizophrenia as a condition is questioned is comorbidity. Comorbidity is when a person has more than one mental condition. Buckley (2009) found that 50% of schizophrenics are also diagnosed with depression, 47% with drug abuse, and 29% with PTSD, and 23% with OCD. So conditions like severe depression could be being misdiagnosed as schizophrenia. Or, as these diagnoses often happen together, perhaps they are not even separate disorders.

• Another issue with the validity of schizophrenia diagnosis is symptom overlap. Other disorders like bipolar disorder have hallucinations and delusions as positive symptoms as well. If two disorders are very similar then they may be the same disorder.

• Another issue with schizophrenia is gender bias. It may be that men are more likely to be diagnosed due to gender bias as women’s issues aren’t taken as seriously. Cotton et al (2009) suggests that women could just have better coping strategies and so don’t access treatment as often as men. On the contrary Lewin (1984) found that the number of female sufferers reduced when clearer diagnostic criteria were used, meaning that clinicians were overdiagnosing women.

• The next issue is predictive validity. If diagnosis leads to successful treatment, the diagnosis can be seen as valid. But in fact some Schizophrenics are successfully treated whereas others are not. Heather (1976) there is only a 50% chance of predicting what treatment a patient will receive based on diagnosis, suggesting that diagnosis is not valid.

• Then there is aetiological validity – for a diagnosis to be valid, all patients diagnosed as schizophrenic should have the same cause for their disorder. This is not the case with schizophrenia: The causes may be one of biological or psychological or both.

• Finally, there is cultural bias in the diagnosis of schizophrenia. Cochrane (1977) found that the rate of diagnosis of schizophrenia in the UK for afro-caribbean people was 7%, compared to 1% for the general Uk population and 1% for afro-caribbeans in the caribbean.This suggests that afro-caribbean people are overdiagnosed in the UK due to culture bias. Fernando (1998) suggests ‘category failure’, that is that western definitions applied to non-western cultures lead to a higher diagnosis rate in people from non-Western cultures. In addition, Copeland et al. (1971) gave a description of a patient to 134 US and 194 British psychiatrists. 69% of the US psychiatrists diagnosed schizophrenia but only 2% of the British gave the diagnosis of schizophrenia. No research has found any cause for this, so it suggests that the symptoms of ethnic minorities are misinterpreted. This calls into question the reliability of the diagnosis of schizophrenia as it suggests that patients can display the same symptoms but receive different diagnoses because of their ethnic background; i.e. a patient’s ethnicity makes it more or less likely that they will be diagnosed with schizophrenia.

A key study on the validity of psychiatric assessment is Rosenhan (1973): Being Sane in Insane places.

• Aim: To investigate how situational factors affect a diagnosis of schizophrenia. 

• Method: Sane confederates went into psychiatric hospitals and told medical health professionals they had a hallucination, and observed whether staff would realise that they were sane. If staff did not detect their sanity, it would have implications for methods of diagnosing mental illness and show that situational factors affect diagnosis. 8 confederates acted as pseudopatients, going to 12 different hospitals. The real participants were the hospital staff who did not know about the experiment. The pseudopatient called the hospital for an appointment. When they arrived they complained of hearing voices saying “empty”, “hollow” and “thud”. They said that the voices were unclear, unfamiliar and of the same sex as the pseudopatient. Pseudopatients gave false names, occupations and symptoms, but gave real life histories. Once on the ward, the pseudopatients stopped pretending symptoms, behaved normally and wrote observations. Pseudopatients were discharged only when they convinced staff that they were sane.

• Results: On admission, staff diagnosed 11 pseudopatients with schizophrenia, and one with manic-depression. Staff never detected their sanity. Nurses reported their behaviour as showing “no abnormal indications”, but did interpret their behaviour in the context of their diagnosis (see conclusion). The average hospital stay was 19 days. All pseudopatients were discharged with diagnosis of schizophrenia ‘in remission’. 35 real patients detected sanity (e.g., saying “You’re not crazy”).

• Conclusion: Doctors should not have diagnosed patients with schizophrenia as they only had one relatively mild symptom (this is type 1 error). Psychiatric staff cannot always distinguish sanity from insanity. Any diagnostic method that makes such errors cannot be very reliable or valid. However, physicians may not identify sanity because it is less risky to diagnose a healthy person as sick than vice versa. So therefore situational factors do affect diagnosis. Normal behaviour was interpreted in the context of illness (e.g., nursing records suggest writing is pathological). Staff reversed some diagnoses due to the situation (expecting pseudopatients). Staff may be more likely to reverse diagnoses when risks are high (e.g., loss of professional esteem). This suggests that once diagnosed the label of schizophrenia is difficult to remove. Essentially Rosenhan’s research showed that psychiatrists cannot reliably tell the difference between an insane and sane person, calling into question the reliability of a schizophrenia diagnosis. ‘Normal’ behaviour was misinterpreted as ‘abnormal’ to support their idea that the pseudopatients had a mental illness. This suggests the validity of psychiatric diagnoses was low and the DSM was flawed.

Biological explanations for schizophrenia: genetics, the dopamine hypothesis and neural correlates

Genetics

• If schizophrenia is genetic then the more closely related two people are, then if one person has the disorder the other is more likely to have the disorder. That measure of probability is called a concordance rate.

• Genetic concordance is shown via family studies, with siblings being more likely to both have the disorder than cousins. However, the more closely related two people are, the more likely they are to share the same environmental stimuli (education level, diet, family stresses ..etc).

• Schizophrenia is polygenic and aetiologically heterogeneous.

The existence of different candidate genes means:

1. Each gene confers a small increased risk of developing schizophrenia (polygenic)

2. Different combinations of the candidate genes can lead to schizophrenia (aetiologically heterogeneous)

Evaluation

• Ripke (2014) found 108 variations of genetic combinations associated with an increased risk of schizophrenia in 37,000 patients.

• For twin studies both twins often share the same home environment, but monozygotic (identical, 100% DNA shared) twins still tend to have a higher concordance rate than dizygotic (non-identical, around 50% DNA shared) twins, suggesting that this stronger concordance rate is likely down to genetic rather than environmental factors.

• Gottesman (1991) reviewed cases of schizophrenia and found concordance rates of 48% for identical twins and 17% for non-identical twins. This compares to a 1% chance of developing schizophrenia for the general population, suggesting a strong genetic basis for schizophrenia.

• However an issue with this is that both normal siblings and dizygotic twins share around 50% of their DNA, but normal siblings only have a 9% chance of also having schizophrenia compared the the dizygotic twins chance of 17%, and  there also isn’t a 100% concordance rate between identical twins even though they share all of their DNA, so something other than genetics must be affecting whether a person develops schizophrenia or not (i.e: the environment).

• One strength of the genetic explanation is the role of mutations. It is possible for people to develop schizophrenia even in the absence of a family history of the disorder. This could be through mutation in the paternal DNA in the sperm because of mutagenic agents. Brown et al. (2002) found a relationship between paternal age (linked with increased risk of mutation) and the risk of developing schizophrenia. He found that in men under 25 the risk was 0.7% and men over 50 was 2%. This supports the theory of the genetic explanation.

Neurotransmitters

• One neurotransmitter is dopamine. The Dopamine Hypothesis states that the symptoms of schizophrenia result from an imbalance of dopamine across the brain.

• The exact mechanism is not certain, however too much dopamine in speech centres like Broca’s area may lead to the positive symptom of auditory hallucinations. Lower levels of dopamine in areas like the frontal cortex could lead to negative symptoms like avolition and speech poverty.

• This theory originated form the observation that dopamine releasing drugs like L-dopa can produce schizophrenic-like symptoms in healthy patients. Also, antipsychotic drugs like phenothiazine that decrease symptoms of schizophrenia also seem to reduce dopamine levels as their main effect.

• So dopamine is the main neurotransmitter that is implicated in schizophrenia, however glutamate and serotonin are also thought to play a role.

• Glutamate is an excitatory neurotransmitter involved in learning, attention, and memory. It is found in low quantities in schizophrenics. Its presence reduces dopamine levels.

• Clozapine is also used to effectively treat schizophrenia, but works primarily on the serotonin system, implying that serotonin is involved in schizophrenia.

Evaluation

• Leucht et al (2013) reviewed 212 studies in a meta-analysis on the effectiveness of biological antipsychotic treatments that work by normalising levels of dopamine. Leucht found that treatment of symptoms with drugs were found to be much more effective than the placebo. The effectiveness of these treatments suggest that dopamine is involved in the underlying mechanisms/cause of schizophrenia.

• One limitation is that there is mixed support for the for the dopamine hypothesis. Dopamine agonists (eg: amphetamines) that increase dopamine levels have been found to induce schizophrenia-like symptoms in the people who do not have the disorder. Likewise, antipsychotics (eg: chlorpromazine) that reduce the availability of dopamine receptors have been found to reduce the severity of the symptoms. This supports the role of dopamine in causing the symptoms of schizophrenia. However, challenging this is that some candidate genes that increase the risk of schizophrenia have been found to code for the neurotransmitter glutamate. This suggests dopamine does provide a full explanation for schizophrenia and that it may actually only be one of many major factors involved. This reduces the validity of the dopamine hypothesis as it may not be only dopamine that we are measuring as a cause.

Neural correlates

• Neural correlates are correlations between neuronal structures and positive or negative symptoms. 

• One neural correlate is ventricle size. The ventricles are internal brain cavities that contain and produce Cerebrospinal fluid. CSF provides a cushioning effect that protects the brain from damage when we receive knocks to the head.

Research and evaluation on neural correlates

• A strength is that the research into enlarged ventricles and neurotransmitter levels have high reliability. The reason for this is because the research is carried out in highly controlled environments, with specialist, high tech equipment such as MRI and PET scans. These machines take accurate readings of brain regions such as the frontal and prefrontal cortex, the basal ganglia, the hippocampus and the amygdala. This suggests that if this research was tested and re-tested the same results would be achieved.

• Supporting evidence for the brain structure explanation comes from further empirical support from Suddath et al. (1990). He used MRI (magnetic resonance imaging) to obtain pictures of the brain structure of MZ twins in which one twin was schizophrenic. The schizophrenic twin generally had more enlarged ventricles and a reduced anterior hypothalamus. The differences were so large the schizophrenic twins could be easily identified from the brain images in 12 out of 15 pairs. This suggests that there is wider academic credibility for enlarged ventricles determining the likelihood of schizophrenia developing.

• A weakness of the neuroanatomical explanations is that it is biologically deterministic. The reason for this is because if the individual does have large ventricles then does it really mean that they will develop schizophrenia? This suggests that biological explanations do not account for freewill.

Evaluation of the biological explanation of schizophrenia

• Explaining schizophrenia at the basic cellular and chemical level has the advantage of the scientific principle of parsimony (preferring the theory with fewer assumptions). However, this biologically reductionist approach fails to consider evidence for the range of psychological aspects of schizophrenia such as expressed emotion (see environmental explanations below) that seem to have a large influence on the development and relapse of the disorder. 

• Tienari (2004) studied biological children of schizophrenic mothers who had been adopted. 5.8% of those adopted into healthy families developed schizophrenia, compared to 36.8% of those raised in dysfunctional families.This suggests a biological aspect as 5.8% is much higher than the average (1%) in the general population. However it also shows the importance of the psychological effects of family dysfunction in the development of schizophrenia as those in dysfunctional families were over six times more likely to develop it than those in healthy families.

• The very process of being adopted is a stressful situation, so this may explain the increased incidence in the sample of schizophrenics

• A biological explanation of schizophrenia, such as a genetic basis, assumes that schizophrenia is inevitable, or biologically determined. Other more psychological approaches such as the cognitive approach (see below) may accept biological causes, but their soft determinist perspective would suggest that mental processes can be altered or managed via free will to control the disorder.

• A full, holistic explanation of schizophrenia would consider the diathesis stress approach in which the root cause of the disorder is biological/genetic weakness (diathesis, see below), with an environmental stressor such as poverty or family dysfunction triggering the disorder.

Psychological explanations for schizophrenia: family dysfunction and cognitive explanations, including dysfunctional thought processing

Family dysfunction

• Family dysfunction is a psychological explanation thought to contribute to an individual’s risk of developing schizophrenia.

• The earliest explanation in terms of family dysfunction was the Schizophrenogenic mother. This is a psychodynamic theory that suggests that people with schizophrenia get their delusions as a result of the influence of a cold, rejecting, controlling mother and a passive father. The mother creates an atmosphere of stress, tension, and secrecy in the family. This atmosphere triggers psychotic thinking.

• Another, similar theory is the double bind theory. This theory suggests that in a family where a child gets mixed messages from parents, the child feels unable to do their own thing. An example of mixed messages would be telling a child that they need to be more independent and then being overprotective and critical of their attempts to be independent. Bateson (1972) suggests that this upbringing results in disorganised thinking and paranoia.

• A third theory in terms of dysfunctional families is Expressed Emotion (how emotion is conveyed by the carers/family of the sufferer)- Butzlaff and Hooley (1998) showed via meta-analysis of 27 studies that relapse back into schizophrenia was twice as likely in families that had high expressed emotion. Examples of behaviours shown by family/carers with high expressed emotion are; exaggerated involvement (families that indicate the sufferer to be a burden via self sacrifice, i.e: by reminding the sufferer what an inconvenience they are all the time), excessive criticism & control of the sufferer’s behaviour (criticising the sufferer in order to control what they do) and general hostility towards the sufferer (physical, mental, verbal or emotional that suggests rejection).

Evaluation

• Bateson (1972), Butzlaff and Hooley (1998) 

• Tienari (2004) shows a strong link between the development of schizophrenia and the level of dysfunction in a family. While there may be a biological link as 5.8% is much higher than the 1% risk for the general population, the rise to 36.8% is entirely down to environmental effects as the biological heritability can be assumed to be the same in both groups.

• It is ethically difficult to suggest that schizophrenia is caused by the family, as they are already dealing with the difficulty of their relative’s behaviour without the additional stress and anxiety of thinking they are responsible and experiencing greater social stigma/judgement from others.

• There is a significant amount of research suggesting that schizophrenia has a biological cause such as genetics (Gottesman), neurotransmitters (Leucht), and neural structures like ventricles (Suddath). Therefore family dysfunction may be a trigger for schizophrenia, but the basic cause is biological.

• Dysfunctional families as a cause of schizophrenia results in useful finding applications that can help schizophrenics, such as family therapy (see below).

• Family therapy has been demonstrated to reduce expressed emotion in families and to be an effective intervention for reducing relapse rates, thus supporting the argument that family dysfunction causes schizophrenia.

• Family dysfunction has not been the subject of significant systematic research. Much of the research that has been done has been case studies, and these have idiographic problems. 

• Family studies can’t be ethically controlled (can’t tell some families to be high expressed emotion as causes harm), so hard to demonstrate direct cause and effect.

• It could be that the schizophrenia of the child causes the family dysfunction, not the family dysfunction leading to the schizophrenia.

Cognitive explanations of schizophrenia

• The cognitive explanation sees schizophrenia as being caused by disorganised thinking.

• Firth’s (1979) “Attention-deficit theory” suggests that schizophrenia is due to a faulty attention system unable to filter preconscious thoughts and gives too much significance to information that would usually be filtered out, thus overloading the mind. This accounts for positive symptoms such as hallucinations and delusions.

• Firth also suggests that the ability to suppress and override automatic actions and speech and make deliberate actions to achieve goals (Central Control) is sometimes faulty in schizophrenic patients. For example, when you see a door handle there is an automatic urge to open the door. The schizophrenic patient would have difficulty resisting this urge and have difficulty explaining the reason why, the explanation that they can come up with might therefore be a delusion. Speech derailment (where a schizophrenic patient is having a conversation and randomly says something totally inappropriate to the message they are trying to convey) can also be explained by the inability to resist expressing automatic thoughts.

• Firth also talks about Meta-representation. Meta-representation is the ability to identify your own thoughts and actions as your own by paying attention to them. Faults in the system result in delusions of control, feeling that your own actions are being created by an outside force.

• Hemsley (1993) gives an alternative cognitive explanation, that there is a breakdown in new information coming in from the senses and information stored in the memory. This means that schemas are not activated and this produces an overload of information such that the sufferer is unsure of what to attend to or how to respond. Also old memories can be seen as new information resulting in auditory hallucinations.

Evidence for cognitive explanations of schizophrenia

• Firth (1992) supported these ideas with biological/cognitive neuroscience studies. 30 schizophrenic patients with various symptoms had PET scans. The scans indicated a reduction in the blood flow in the frontal cortex of patients with negative symptoms like Avolition and inability to suppress automatic thoughts. Part of the role of the frontal cortex is to make decisions based on behaviours coming from other parts of the brain. Scans also showed increased activity in an area of the temporal lobe responsible for the retrieval of memories (parahippocampal) with patients with reality distortion, supporting Hemsley’s proposal. This demonstrates that there are differences in brain regions associated with the theorised cognitive processes, supporting the idea that cognitive processes are involved in schizophrenia.

• Stirling et al (2006) conducted the stroop test on 30 patients with schizophrenia and 18 control patients. The task involved naming the ink colours without saying the word. This is difficult as there is desire to say the words that needs to be controlled. Stirling found that patients with schizophrenia took twice as long to name the colours as controls. This shows that patients with schizophrenia show deficits in Central control tasks, supporting Firth’s ideas.

• Cognitive behavioural therapy (see below) can be an effective treatment for schizophrenia, indicating that cognitive factors are involved in the disorder.

Drug therapy: typical and atypical antipsychotics

• Antipsychotic drugs are also known as neuroleptics. They work on the dopamine system. There are two types of antipsychotics used to treat schizophrenia, typical antipsychotics (first generation), and atypical antipsychotics.

• Typical antipsychotics were first used to treat schizophrenia in the 1950s but are less popular now due to their severe side effects and only treating the positive symptoms. An example of a typical antipsychotic is Chlorpromazine. Chlorpromazine increases the levels of dopamine before reducing them. The reduction of dopamine normalises neurotransmission in key areas of the brain and so the severity of the symptoms are reduced. Chlorpromazine also works on histamine receptors and so can have a sedative effect. This has led it to be used on anxious patients on their initial admission to hospital.Typical antipsychotics are dopamine antagonists. They reduce dopamine activity by blocking dopamine receptors in the synapse. This results in a reduction in the activity of the dopamine system in the brain, reducing positive symptoms such as hallucinations and delusions. They also have a general sedative effect. As these drugs affect all dopamine receptors in the brain equally, they produce side effects such as dry mouth, constipation, lethargy, confusion, involuntary muscle movements (e.g: tardive dyskinesia- jerky, uncontrollable movements like those in Parkinson’s).

• Atypical antipsychotics started to be used in the 1970s to provide effective treatment for schizophrenia without the side effects of typical antipsychotics such as clozapine and risperidone. Atypical antipsychotics block dopamine receptors but also act on other neurotransmitters such as acetylcholine and serotonin. Atypical antipsychotics also address the negative symptoms such as avolition. Side effects of atypical antipsychotics are weight gain, cardiovascular problems, and agranulocytosis (an autoimmune disorder affecting white blood cells). However they are less likely to cause involuntary movements as a side-effect.

Evaluation

• Leucht (2013) reviewed 212 studies in a meta-analysis on the effectiveness of biological antipsychotic drug treatments that work via normalising levels of dopamine. Treatment of symptoms with drugs was found to be much more effective than a placebo. This suggests that the effectiveness of these treatments is due to dopamine being involved in the underlying mechanisms/causes of schizophrenia, and also generally shows that these drugs are able to treat schizophrenia.

• Bagnall (2003) meta-analysed 232 studies to compare the effectiveness of a range of atypical drugs to each other and to typical antipsychotic drugs. Bagnall found that atypical drugs were more effective than typical in treating overall symptoms, had fewer movement disorder side effects, and fewer people left the drug treatment early, suggesting that its side effects were more tolerable. However clozapine was found to be the most effective in reducing negative symptoms and treating people who were resistant to other drugs. This suggests that atypical antipsychotics have improved treatment of people with schizophrenia.

• Drug therapies are often cheaper to prescribe than providing hospital treatment or psychological therapies such as CBT and family therapy. This means that more people can be treated with the same amount of money.

• Drug therapies may only be suppressing symptoms and not treating the underlying problem, as symptoms quickly return when the drugs stop. There is a lack of evidence showing the long-term benefits of medication as most studies look at the short term effects.

• The use of drug treatments has resulted in the end of long-term institutionalisation in mental hospitals for those with schizophrenia. Now people can be treated at home and perhaps have enhanced quality of life as they have additional independence.

• Drugs are often prescribed and forcefully given to those experiencing severe schizophrenia symptoms. There are ethical issues with this as the patients cannot give informed consent. This is particularly problematic given the severe side effects.

• Both types of drugs have side effects, and due to the severity of the side effects two thirds of people stop taking them, resulting in symptoms returning and a ’revolving door’ effect of people leaving treatment and returning when their symptoms get too bad to handle.

Cognitive behaviour therapy and family therapy as used in the treatment of schizophrenia 

• Cognitive behavioral therapy (CBT) works by identifying and changing faulty cognitions such as delusions. The therapist’s role is to challenge the irrational beliefs of the patient. This could be by logically disputing the reality of the delusions and helping the patient to develop alternative belief systems. Therapists often use the ABC model by Ellis to understand the source of the faulty cognition and to provide a process by which to change it. In the ABC model Ellis says that our faulty cognitions start with an activating event (A). This activating event will lead to a belief (B) that can be rational or irrational. As a result of this belief the person will behave in a certain way (C- consequences). If this is an irrational belief then the consequences will be negative, and vice versa. The therapist can then help the patient dispute (D) the belief if it is irrational using logical or empirical evidence, and thus have the effect (E) helping the patient to of restructure their belief into a rational one. For example the activating event could be drug treatments causing side effects in the patient. The patient then believes based on these side effects that the drugs are being used by the hospital to poison and so kill them. The negative consequence of this is that they refuse to take the drugs. So the therapist dispute the irrational belief by pointing out that the staff at the hospital have no reason to kill them and explain to them why the drugs are necessary, leading them to hold the restructured belief that it is necessary for them to take the drugs in order to not have symptoms, so whilst the side effects are unpleasant they are necessary.

• Reality testing is a process in which the patient can demonstrate for themselves that their irrational thoughts (hallucinations and delusions) are not real (symptom targeting). The clinician does this by testing an irrational belief (i.e: if the patient believes that they can see the future, ask them to predict the cards the clinician will randomly draw from the deck. After enough wrong guesses the patient may correct their initial delusion).

Evaluation

• Sensky (2000) showed that patients who had resisted drug treatments had a reduction in positive and negative symptoms when treated with CBT. They also continued to improve even 9 months after treatment had ended. This suggests that psychological therapy can be effective even in cases when drugs are not, but are also an improvement on drug therapies as drugs only reduce the symptoms in the short term.

• The success of CBT as a treatment provides support for the theory that cognitive factors are involved in the disorder.

• Patients often end treatment early. This is because the treatment is long (can be up to a year), so symptoms may get worse during treatment before they get better.

• CBT requires engagement from the patient, but negative symptoms like avolition may lead the patient to be unwilling to take part, or positive symptoms lead to distrust of the therapist, meaning that it may not be a practical treatment for severely schizophrenic individuals.

• Some patients due to the severity of their symptoms or personality may not be able to cope with the therapist repeatedly challenging their beliefs as CBT requires.
  
  

Family therapy

• Family dysfunction can increase the risk of relapse of schizophrenic patients, so family therapies attempt to improve the home situation of the person with schizophrenia to reduce this risk. This is a family-centred therapy, intended to change the behaviour of the whole family, not just the person with schizophrenia. One of the main aims of family therapy is to educate the family on the symptoms of schizophrenia (psychoeducation) in order to help them to be more understanding of the patient’s behaviour. The other aims of family therapy are to reduce the conflict in the family by addressing anger within the family, to reduce the stress caused by caring for the schizophrenic person, to reduce the self-sacrifice by getting carers to consider and find ways to make time for their own needs, to improve communication by considering how to limit expressed emotion, and by improving problem solving skills within the family by predicting problems and having solutions ready.

Evaluation

• Leff (1985) looked at the aftercare of patients who had been hospitalised with schizophrenia. Of those provided with standard outpatient care, 50% had relapsed within 9 months, compared to only 8% of those who received family therapy. After two years this had risen to 50% of those who received the therapy and 75% of those with standard outpatient care. This suggests that family therapy is helpful in reducing readmission in the short term, however families may not maintain positive behaviour patterns in the longer term.

• Therapy is long (often taking up to a year), meaning that patients and family may drop out part way through therapy at times of severe episodes as symptoms may get worse before they get better.

• Also some families may not be willing to engage in family therapy, seeing it as needlessly interfering, or some family members may engage whilst others withdraw.

• This is not a cure for schizophrenia, but simply controls symptoms to reduce relapse and thus readmission.

How token economies as used in the management of schizophrenia

• Token economies are a behavioural therapy technique based on Skinner’s operant conditioning. This is learning through reinforcement of desired behaviours. The tokens themselves are used as a kind of positive reinforcement. They are given as an immediate reward for patients showing a predefined target behaviour (such as washing). The tokens are then exchanged for something the patient wants such as activities or chocolate. This may involve behaviour shaping, where behaviours are progressively changed, with tokens first given for small changes in behaviour leading up to the ideal behaviour.

• The treatment is designed to produce easier to manage behaviour within the mental hospital, or to prepare long stay patients for transfer into the community.

Evaluation

• Treatment is not effective with severely unresponsive patients such as those with strong negative symptoms, so not allowing them to take part but letting the more mildly affected patients take part in token therapy could be seen as punishing them for the severity of their illness.

• Dickinson found in a review of 13 studies that 11 showed that token economies can be effective at improving behaviour when used in psychiatric therapies.

• Token economies do not directly treat symptoms of schizophrenia, they only attempt to manage negative symptoms such as poor attention, poor motivation, and withdrawal.

• Token economies may make the patient’s schizophrenia worse if target behaviours are unsuitable or unattainable for the patient (i.e: if the schizophrenic patient is rewarded whenever they behave like they aren’t hallucinating, they may continue hallucinating but just get better at suppressing the outward symptoms of such (i.e: talking back out loud to the voice in their head), making it harder for staff to protect them (i.e: the voice tells them to jump out of a window and they do, and because the patient looked fine externally staff were attending to another patient instead at the time and did not notice).

• Some more mildly affected patients may refuse to engage in this therapy as they may find it infantilising/degrading as it is very similar in procedure to the sticker charts that small children have to encourage good behaviour, with valueless tokens used to indicate a small treat when behaviour is good, and to the clicker training that is used on dogs and other animals.

The importance of an interactionist approach in explaining and treating schizophrenia; the diathesis stress model

• The interactionist approach to schizophrenia is the idea that the interaction of multiple factors cause schizophrenia.

• An interactionist model for schizophrenia is the diathesis stress model. The diathesis-stress model is the psychological concept that a disorder is due to the interaction between predisposed vulnerability (this is the diathesis) and an environmental trigger later in life such as stress. 

• In schizophrenia the primary diathesis is typically a genetic vulnerability that results in a dopamine imbalance. However flu in pregnant mothers in the second trimester, birth complications, and very early psychological trauma such as child abuse have also been linked to the later development of schizophrenia in the children produced, so each of these factors could act as the primary (if there is no genetic disposition) or secondary (if there is genetic disposition) diathesis. 

• One or more diatheses need to be combined with a trigger to result is schizophrenia. Stressors that act as triggers for schizophrenia include family dysfunction, drug abuse, or a major negative life event such as death of a loved on or divorce. The excessive use of cannabis in particular has been linked to schizophrenia as it interferes with the dopamine system.

• Combinations of CBT and drug therapies are seen as a particularly effective interactionist treatment for schizophrenia as they address both the diathesis and the trigger for the condition. Biological therapies such as drugs allow patients to reduce their symptoms so that they can engage in psychological therapies that give them skills to change their underlying faulty cognitions.

Evaluation

• The interactionist approach is supported by Tienari (2004). The diathesis in this case is the genetic predisposition and the trigger/stressor is the family dysfunction.

• Gottesman (1991) also acts as evidence as dizygotic twins are more likely to both have schizophrenia than normal siblings despite sharing the same amount of DNA. This may be because twins are the same age so more likely to share an environment and thus more likely to share environmental triggers/stressors.Similarly, concordance rate for identical twins is not 100% despite the fact that they share 100% of their DNA, so there must be an environmental trigger/stressor affecting one twin but not the other to cause schizophrenia to develop.

• The interactionist approach is holistic as it considers a range of factors in the development and explanation of schizophrenia (biological, cognitive, social ..etc). Also provides balance to the nature/nurture debate.

• However the mechanism by which the diathesis stress response works in triggering the onset of schizophrenia is unknown.