a level psychology schizophrenia essays

Schizophrenia A-level Revisions Notes

Bruce Johnson

A-level Psychology Teacher

B.A., Educational Psychology, University of Exeter

Bruce Johnson is an A-level psychology teacher, and head of the sixth form at Caterham High School.

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Saul Mcleod, PhD

Editor-in-Chief for Simply Psychology

BSc (Hons) Psychology, MRes, PhD, University of Manchester

Saul Mcleod, PhD., is a qualified psychology teacher with over 18 years of experience in further and higher education. He has been published in peer-reviewed journals, including the Journal of Clinical Psychology.

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What do the examiners look for?

• Accurate and detailed knowledge
• Clear, coherent, and focused answers
• Effective use of terminology (use the “technical terms”)

In application questions, examiners look for “effective application to the scenario” which means that you need to describe the theory and explain the scenario using the theory making the links between the two very clear. If there is more than one individual in the scenario you must mention all of the characters to get to the top band.

Difference between AS and A level answers

The descriptions follow the same criteria; however you have to use the issues and debates effectively in your answers. “Effectively” means that it needs to be clearly linked and explained in the context of the answer.

Read the model answers to get a clearer idea of what is needed.

Exam Advice

You MUST revise everything – because the exam board could choose any question, however, it does make sense to spend more time on those topics which have not appeared for a while.

With these particular questions there is a sizeable risk that people don’t understand the difference between the questions, and then write about the wrong thing.

Make sure you know which is which, for example do you understand the difference between “genetic explanation” and “neural correlates explanation”, and do you have a model essay for each?

Schizophrenia is a severe mental illness where contact with reality and insight are impaired, an example of psychosis.

Section 1: Diagnosis and Classification of Schizophrenia

Classification is the process of organising symptoms into categories based on which symptoms cluster together in sufferers. Psychologists use the DSM and ICD to diagnose a patient with schizophrenia.

Diagnosis refers to the assigning of a label of a disorder to a patient. The ICD-10 (only negative symptoms need to be present) is used worldwide and the DSM-5 (only positive symptoms need to be present) is used in America.

In order to diagnose Schizophrenia the Mental Health Profession developed the DSM (Diagnostic and Statistical Manual) still used today as a method of classifying mental disorders (particularly in the USA).

It is also used as a basis for the ICD (International Classification of Diseases) used by the World Health Organisation in classifying all disorders (mental and physical).

Note: you may come across the terms DSM-IV and ICD-10. These refer to the latest editions of the two classification systems.

Positive Symptoms

an excess or distortion of normal functions: including hallucinations and delusions.

Positive symptoms are an excess or distortion of normal functions, for example hallucinations, delusions and thought disturbances such as thought insertion.

• Hallucinations are usually auditory or visual perceptions of things that are not present. Imagined stimuli could involve any of the senses. Voices are usually heard coming from outside the person’s head giving instructions on how to behave. • Delusions are false beliefs. Usually the person has convinced him/herself that he/she is someone powerful or important, such as Jesus Christ, the Queen (e.g. Delusions of Grandeur). There are also delusions of being paranoid, worrying that people are out to get them. • Psychomotor Disturbances: Stereotypyical – Rocking backwards and forwards, twitches, & repetitive behaviors. Catatonia- staying in position for hours/days on end, cut off from the world.

Negative Symptoms

where normal functions are limited: including speech poverty and avolition.

Negative symptoms are a diminution or loss of normal functions such as psychomotor disturbances, avolition (the reduction of goal-directed behavior), disturbances of mood and thought disorders.

• Thought disorder in which there are breaks in the train of thought and the person appears to make illogical jumps from one topic to another (loose association). Words may become confused and sentences incoherent (so called ‘word salad). Broadcasting is a thought disorder whereby a person believes their thoughts are being broadcast to others, for example over the radio or through TV. Alogia – aka speech poverty – is a thought disorder were correct words are used but with little meaning. • Avolition: Lack of volition (i.e. desire): in which a person becomes totally apathetic and sits around waiting for things to happen. They engage in no self motivated behavior. Their get up and go has got up and gone!

Classification

Slater & Roth (1969) say that hallucinations are the least important of all the symptoms, as they are not exclusive to schizophrenic people.

Classification and diagnosis does have advantages as it allows doctors to communicate more effectively about a patient and use similar terminology when discussing them. In addition, they can then predict the outcome of the disorder and suggest related treatment to help the patient.

Scheff (1966) points out that diagnosis classification labels the individual, and this can have many adverse effects, such as a self-fulfilling prophecy (patients may begin to act how they are expected to act), and lower self-esteem.

Ethics – do the benefits of classification (care, treatment, safety) outweigh the costs (possible misdiagnosis, mistreatment, loss of rights and responsibility, prejudice due to labelling).

Reliability and Validity in Diagnosis and Classification of Schizophrenia

with reference to co-morbidity, culture and gender bias and symptom overlap.

Reliability

For the classification system to be reliable, differfent clinicians using the same system (e.g. DSM) should arrive at the same diagnosis for the same individual.

Reliability is the level of agreement on the diagnosis by different psychiatrists across time and cultures; stability of diagnosis over time given no change in symptoms.

Diagnosis of schizophrenia is difficult as the practitioner has no physical signs but only symptoms (what the patient reports) to make a decision on.

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.

Comorbidity describes people who suffer from two or more mental disorders. For example, schizophrenia and depression are often found together. This makes it more difficult to confidently diagnose schizophrenia. Comorbidity occurs because the symptoms of different disorders overlap. For example, major depression and schizophrenia both involve very low levels of motivation. This creates problems of reliability. Does the low motivation reflect depression or schizophrenia, or both?

Gender bias: Loring and Powell (1988) found that some behavior which was regarded as psychotic in males was not regarded as psychotic in females.

Validity – the extent to which schizophrenia is a unique syndrome with characteristics, signs and symptoms.

For the classification system to be valid it should be meaningful and classify a real pattern of symptoms, which result from a real underlying cause.

The validity of schizophrenia as a single disorder is questioned by many. This is a useful point to emphasise in any essay on the disorder. There is no such thing as a ‘normal’ schizophrenic exhibiting the usual symptoms.

Since their are problems with the validity of diagnois classification, unsuitable treatment may be administered, sometimes on an involuntary basis. This raises practical and ethical issues when selecting different types of tretment.

Problems of validity: Are we really testing what we think we are testing? In the USA only 20% of psychiatric patients were classed as having schizophrenia in the 1930s but this rose to 80% in the 1950s . In London the rate remained at 20%, suggesting neither group had a valid definition of schizophrenia.

Neuropsychologist Michael Foster Green suggests that neurocognitive deficits in basic functions such as memory, attention, central executive and problem solving skills may combine to have an outcome which we are labelling “Schizophrenia” as if it was the cause when in fact it is simply an umbrella term for a set of effects.

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.

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.

David Rosenhan (1973) famous experiment involving Pseudopatients led to 8 normal people being kept in hospital despite behaving normally. This suggests the doctors had no valid method for detecting schizophrenia. They assumed the bogus patients were schizophrenic with no real evidence. In a follow up study they rejected genuine patients whom they assumed were part of the deception.

Culture – One of the biggest controversies in relation to classification and diagnosis is to do with cultural relativism and variations in diagnosis. For example in some Asian countries people are not expected to show emotional expression, whereas in certain Arabic cultures public emotion is encouraged and understood. Without this knowledge a person displaying overt emotional behavior in a Western culture might be regarded as abnormal. Cochrane (1977) reported that the incidence of schizophrenia in the West Indies and the UK is 1 %, but that people of Afro-Caribbean origin are seven times more likely to be diagnosed as schizophrenic when living in the UK.

Cultural bias – African Americans and those of Afro-carribean descent are more likely to be diagnosed than their white counterparts but diagnostic rates in Africa and the West Indies is low – Western over diagnosis is a result of cultural norms and the diagnosis lacks validity.

Section 2: Biological Explanations for Schizophrenia

Family studies find individuals who have schizophrenia and determine whether their biological relatives are similarly affected more often than non-biological relatives.

There are two types of twins – identical (monozygotic) and fraternal (dizygotic). To form identical twins, one fertilised egg (ovum) splits and develops two babies with exactly the same genetic information.

• Gottesman (1991) found that MZ twins have a 48% risk of getting schizophrenia whereas DZ twins have a 17% risk rate. This is evidence that the higher the degree of genetic relativeness, the higher the risk of getting schizophrenia. • Benzel et al. (2007) three genes: COMT, DRD4, AKT1 – have all been associated with excess dopamine in specific D2 receptors, leading to acute episodes, positive symptoms which include delusions, hallucinations, strange attitudes. • Research by Miyakawa et al. (2003) studied DNA from human families affected by schizophrenia and found that those with the disease were more likely to have a defective version of a gene, called PPP3CC which is associated with the production of calcineurin which regulates the immune system. Also, research by Sherrington et al. (1988) has found a gene located on chromosome 5 which has been linked in a small number of extended families where they have the disorder. • Evidence suggests that the closer the biological relationship, the greater the risk of developing schizophrenia. Kendler (1985) has shown that first-degree relatives of those with schizophrenia are 18 times more at risk than the general population. Gottesman (1991) has found that schizophrenia is more common in the biological relatives of a schizophrenic, and that the closer the degree of genetic relatedness, the greater the risk.

Very important to note genetics are only partly responsible, otherwise identical twins would have 100% concordance rates.

One weakness of the genetic explanation of schizophrenia is that there are methodological problems. Family, twin and adoption studies must be considered cautiously because they are retrospective, and diagnosis may be biased by knowledge that other family members who may have been diagnosed. This suggests that there may be problems of demand characteristics.

A second weakness is the problem of nature-v-Nurture. It is very difficult to separate out the influence of nature-v-nurture. The fact that the concordance rates are not 100% means that schizophrenia cannot wholly be explained by genes and it could be that the individual has a pre-disposition to schizophrenia and simply makes the individual more at risk of developing the disorder. This suggests that the biological account cannot give a full explanation of the disorder.

A final weakness of the genetic explanation of schizophrenia is that it is biologically reductionist. The Genome Project has increased understanding of the complexity of the gene. Given that a much lower number of genes exist than anticipated, it is now recognised that genes have multiple functions and that many genes behavior.

Schizophrenia is a multi-factorial trait as it is the result of multiple genes and environmental factors. This suggests that the research into gene mapping is oversimplistic as schizophrenia is not due to a single gene.

The Dopamine Hypothesis

• Dopamine is a neurotransmitter. It is one of the chemicals in the brain which causes neurons to fire. The original dopamine hypothesis stated that schizophrenia suffered from an excessive amount of dopamine. This causes the neurons that use dopamine to fire too often and transmit too many messages. • High dopamine activity leads to acute episodes, and positive symptoms which include: delusions, hallucinations, confused thinking. • Evidence for this comes from that fact that amphetamines increase the amounts of dopamine . Large doses of amphetamine given to people with no history of psychological disorders produce behavior which is very similar to paranoid schizophrenia. Small doses given to people already suffering from schizophrenia tend to worsen their symptoms. • A second explanation developed, which suggests that it is not excessive dopamine but that fact that there are more dopamine receptors. More receptors lead to more firing and an over production of messages. Autopsies have found that there are generally a large number of dopamine receptors (Owen et al., 1987) and there was an increase in the amount of dopamine in the left amygdale (falkai et al. 1988) and increased dopamine in the caudate nucleus and putamen (Owen et al, 1978).

One criticism of the dopamine hypothesis is there is a problem with the chicken and egg. Is the raised dopamine levels the cause of the schizophrenia, or is it the raised dopamine level the result of schizophrenia?

It is not clear which comes first. This suggests that one needs to be careful when establishing cause and effect relationships in schizophrenic patients.

One of the biggest criticisms of the dopamine hypothesis came when Farde et al found no difference between schizophrenics’ levels of dopamine compared with ‘healthy’ individuals in 1990.

Noll (2009) also argues around one third of patients do not respond to drugs which block dopamine so other neurotransmitters may be involved.

A final weakness of the dopamine hypothesis is that it is biologically deterministic. The reason for this is because if the individual does have excessive amounts of dopamine then does it really mean that thy ey will develop schizophrenia? This suggests that the dopamine hypothesis does not account for freewill.

Neural Correlates

• Neural correlates are patterns of structure or activity in the brain that occur in conjunction with schizophrenia • People with schizophrenia have abnormally large ventricles in the brain . Ventricles are fluid filled cavities (i.e. holes) in the brain that supply nutrients and remove waste. This means that the brains of schizophrenics are lighter than normal. The ventricles of a person with schizophrenia are on average about 15% bigger than normal (Torrey, 2002).

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, which specialist, high tech equipment such as MRI and PET scans.

These machines take accurate readings of brain regions such as the frontal and pre-frontal cortex, the basil ganglia, the hippocampus and the amygdale. 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 second 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 the dopamine hypothesis does not account for freewill.

Section 3: Psychological Explanations for Schizophrenia

Family dysfunction.

Family Dysfunction refers to any forms of abnormal processes within a family such as conflict, communication problems, cold parenting, criticism, control and high levels of expressed emotions. These may be risk factors for the development and maintenance of schizophrenia.

• Laing and others rejected the medical / biological explanation of mental disorders. They did not believe that schizophrenia was a disease. They believed that schizophrenia was a result of social pressures from life. Laing believed that schizophrenia was a result of the interactions between people, especially in families. • Bateson et al. (1956) suggested the double bind theory, which suggests that children who frequently receive contradictory messages from their parents are more likely to develop schizophrenia. For example parents who say they care whilst appearing critical or who express love whilst appearing angry. They did not believe that schizophrenia was a disease. They believed that schizophrenia was a result of social pressures from life. • Prolonged exposure to such interactions prevents the development of an internally coherent construction of reality; in the long run, this manifests itself as typically schizophrenic symptoms such as flattening affect, delusions and hallucinations, incoherent thinking and speaking, and in some cases paranoia. • Another family variable associated with schizophrenia is a negative emotional climate, or more generally a high degree of expressed emotion (EE). EE is a family communication style that involves criticism, hostility and emotional over-involvement. The researchers concluded that this is more important in maintaining schizophrenia than in causing it in the first place, (Brown et al 1958). Schizophrenics returning to such a family were more likely to relapse into the disorder than those returning to a family low in EE. The rate of relapse was particularly high if returning to a high EE family was coupled with no medication.

One strength of the double bind explanation comes from further empirical support provided by Berger (1965). They found that schizophrenics reported a higher recall of double bind statements by their mothers than non-schizophrenics.

However, evidence may not be reliable as patient’s recall may be affected by their schizophrenia. This suggests that there is wider academic credibility for the idea of contradictory messages causing schizophrenia.

A second strength of the research into expressed emotion (EE) is that it has practical applications. For example Hogarty (1991) produced a type of therapy session, which reduced social conflicts between parents and their children which reduced EE and thus relapse rates.

This suggests that gaining an insight into family relationships allows psychiatric professionals to help improve the quality of patient’s lives.

Individual differences – EE is associated with relapse but not all patients who live in high EE families relapse and not all patients in low EE families avoid relapse – Family dysfunction is an incomplete explanation for schizophrenia.

A weakness of the family relationsships appraoch is that there is a problem of cause and effect. Mischler & Waxler (1968) found significant differences in the way mothers spoke to their schizophrenic daughters compared to their normal daughters, which suggests that dysfunctional communication may be a result of living with the schizophrenic rather than the cause of the disorder.

This suggests that there is a problem of the chicken and egg scenario in relation to expressed emotion causing schizophrenia.

A second weakness of the double bind theory is that there are ethical issues. There are serious ethical concerns in blaming the family, particularly as there is little evidence upon which to base this.

Gender bias is also an issue as the mother tends to be blamed the most, which means such research is highly socially sensitive. This suggests that the research therefore does not protect individuals from harm.

Cause and effect – It remains unclear whether cognitive factors cause schizophrenia or if schizophrenia causes these cognitions – Family dysfunction may not be a valid explanation for schizophrenia.

Cognitive explanations

including dysfunctional thought processing.

Cognitive approaches examine how people think, how they process information. Researchers have focused on two factors which appear to be related to some of the experiences and behaviors of people diagnosed with schizophrenia.

First, cognitive deficits which are impairments in thought processes such as perception, memory and attention. Second, cognitive biases are present when people notice, pay attention to, or remember certain types of information better than other.

Cognitive Deficits

• There is evidence that people diagnosed as schizophrenic have difficulties in processing various types of information, for example visual and auditory information. Research indicates their attention skills may be deficient – they often appear easily distracted. • A number of researchers have suggested that difficulties in understanding other people’s behavior might explain some of the experiences of those diagnosed as schizophrenic. Social behavior depends, in part, on using other people’s actions as clues for understanding what they might be thinking. Some people who have been diagnosed as schizophrenic appear to have difficulties with this skill. • Cognitive deficits have been suggested as possible explanations for a range of behaviors associated with schizophrenia. These include reduced levels of emotional expression, disorganised speech and delusions.

Cognitive Biases

• Cognitive biases refer to selective attention. The idea of cognitive biases has been used to explain some of the behaviors which have been traditionally regarded as ‘symptoms’ of ‘schizophrenia’. • Delusions: The most common delusion that people diagnosed with schizophrenia report is that others are trying to harm or kill them – delusions of persecution. Research suggests that these delusions are associated with specific biases in reasoning about and explaining social situations. Many people who experience feelings of persecution have a general tendency to assume that other people cause the things that go wrong with their lives.

A strength of the cognitive explanation is that it has practical applications. Yellowless et al. (2002) developed a machine that produced virtual hallucinations, such as hearing the television telling you to kill yourself or one person’s face morphing into another’s.

The intention is to show schizophrenics that their hallucinations are not real. This suggests that understanding the effects of cognitive deficits allows psychologists to create new initiatives for schizophrenics and improve the quality of their lives.

A final strength is that it takes on board the nurture approach to the development of schizophrenia. For example, it suggests that schizophrenic behavior is the cause of environmental factors such as cognitive factors.

One weakness of the cognitive explanation is that there are problems with cause and effect. Cognitive approaches do not explain the causes of cognitive deficits – where they come from in the first place.

Is it the cognitive deficits which causes the schizophrenic behavior or is the schizophrenia that causes the cognitive deficits? This suggests that there are problems with the chicken and egg problem.

A second weakness of the cognitive model is that it is reductionist. The reason for this is because the approach does not consider other factors such as genes.

It could be that the problems caused by low neurotransmitters creates the cognitive deficits. This suggests that the cognitive approach is oversimplistic when consider the explanation of schizophrenia.

Section 4: Drug Therapy: typical and atypical antipsychotics

Drug therapy is a biological treatment for schizophrenia. Antipsychotic drugs are used to reduce the intensity of symptoms (particularly positive symptoms).

Typical Antipsychotics

• First generation Antipsychotics are called “Typical Antipsychotics” Eg. Chlorpromazine and Haloperidol. • Typical antipsychotic drugs are used to reduce the intensity of positive symptoms, blocking dopamine receptors in the synapses of the brain and thus reducing the action of dopamine. • They arrest dopamine production by blocking the D2 receptors in synapses that absorb dopamine, in the mesolimbic pathway thus reducing positive symptoms, such as auditory hallucinations. • But they tended to block ALL types of dopamine activity, (in other parts of the brain as well) and this caused side effects and may have been harmful.

Atypical Antipsychotics

• Newer drugs, called “atypical antipsychotics” attempt to target D2 dopamine activity in the limbic system but not D3 receptors in other parts of the brain. • Atypical antipsychotics such as Clozapine bind to dopamine, serotonin and glutamate receptors. • Atypical antipsychotic drugs work on negative symptoms, improving mood, cognitive functions and reducing depression and anxiety. • They also have some effect on other neurotransmitters such as serotonin . They generally have fewer side effects eg. less effect on movement Eg. Clozapine, Olazapine and Risperidone.

Since the mid-1950s antipsychotic medications have greatly improved treatment. Medications reduce positive symptoms particularly hallucinations and delusions; and usually allow the patient to function more effectively and appropriately.

Antipsychotic drugs are highly effective as they are relatively cheap to produce, easy to administer and have a positive effect on many sufferers. However they do not “cure” schizophrenia, rather they dampen symptoms down so that patients can live fairly normal lives in the community.

Kahn et al. (2008) found that antipsychotics are generally effective for at least one year, but second- generation drugs were no more effective than first-generation ones.

Some sufferers only take a course of antipsychotics once, while others have to take a regular dose in order to prevent symptoms from reappearing.

There is a sizeable minority who do not respond to drug treatment. Pills are not as helpful with other symptoms, especially emotional problems.

Older antipsychotics like haloperidol or chlorpromazine may produce side effects Sometimes when people with schizophrenia become depressed, so it is common to prescribe anti-depressants at the same time as the anti-psychotics.

All patients are in danger of relapsing but without medication the relapses are more common and more severe which suggests the drugs are effective.

Clozapine targets multiple neurotransmitters, not just dopamine, and has been shown to be more effective than other antipsychotics, although the possibility of severe side effects – in particular, loss of the white blood cells that fight infection.

Even newer antipsychotic drugs, such as risperidone and olanzapine are safer, and they also may be better tolerated. They may or may not treat the illness as well as clozapine, however.

Meta–analysis by Crossley Et Al (2010) suggested that Atypical antipsychotics are no more effective, but do have less side effects.

Recovery may be due to psychological factors – The placebo effect is when patients’ symptoms are reduced because they believe that it should.

However, Thornley et al carried out a meta-analysis comparing the effects of Chlorpromazine to placebo conditions and found Chlorpromazine to be associated with better overall functioning – Drug therapy is an effective treatment for SZ.

RWA – Offering drugs can lead to an enhanced quality of life as patients are given independence – Positive impact on the economy as patients can return to work and no longer need to be provided with institutional care.

Ethical issues – Antipsychotics have been used in hospitals to calm patients and make them easier for staff to work with rather than for the patients’ benefit – Can lead to the abuse of the Human Rights Act (no one should be subject to degrading treatment).

Severe side effects – Long term use can result in tardive dyskinesia which manifests as involuntary facial movements such as blinking and lip smacking – While they may be effective, the severity of the side effects mean the costs outweigh the benefits therefore they are not an appropriate treatment.

In most cases the original “typical antipsychotics” have more side effects, so if the exam paper asks for two biological therapies you can write about typical anti-psychotics and emphasise the side effects, then you can write about the atypical antipsychotics and give them credit for having less side effects.

Section 5: Psychological Therapies for Schizophrenia

Family therapy.

Family therapy is a form of therapy carried out with members of the family with the aim of improving their communication and reducing the stress of living as a family.

Family Therapy aims to reduce levels of expressed emotion, and reduced the likelihood of relapse.

Aims of Family Therapy

• To educate relatives about schizophrenia. • To stabilize the social authority of the doctor and the family. • To improve how the family communicated and handled the situation. • To teach patients and carers more effective stress management techniques.

Methods used in Family Therapy

• Pharoah identified examples of how family therapy works: It helps family members achieve a balance between caring for the individual and maintaining their own lives, it reduces anger and guilt, it improves their ability to anticipate and solve problems and forms a therapeutic alliance. • Families taught to have weekly family meetings solving problems on family and individual goals, resolve conflict between members, and pinpoint stressors. • Preliminary analysis: Through interviews and observation the therapist identifies strengths and weaknesses of family members and identifies problem behaviors. • Information transfer – teaching the patient and the family the actual facts about the illness, it’s causes, the influence of drug abuse, and the effect of stress and guilt. • Communication skills training – teach family to listen, to express emotions and to discuss things. Additional communication skills are taught, such as “compromise and negotiation,” and “requesting a time out” . This is mainly aimed at lowering expressed emotion.

A study by Anderson et al. (1991) found a relapse rate of almost 40% when patients had drugs only, compared to only 20 % when Family Therapy or Social Skills training were used and the relapse rate was less than 5% when both were used together with the medication.

Pharaoh et al. (2003) meta – analysis found family interventions help the patient to understand their illness and to live with it, developing emotional strength and coping skills, thus reducing rates of relapse.

Pharoah identified examples of how family therapy works: It helps family members achieve a balance between caring for the individual and maintaining their own lives, it reduces anger and guilt, it improves their ability to anticipate and solve problems and forms a therapeutic alliance.

Economic Benefits: Family therapy is highly cost effective because it reduces relapse rates, so the patients are less likely to take up hospital beds and resources. The NICE review of family therapy studies demonstrated that it was associated with significant cost savings when offered to patients alongside the standard care – Relapse rates are also lower which suggests the savings could be even higher.

Lobban (2013) reports that other family members felt they were able to cope better thanks to family therapy. In more extreme cases the patient might be unable to cope with the pressures of having to discuss their ideas and feelings and could become stressed by the therapy, or over-fixated with the details of their illness.

Token Economy

• Token economies aim to manage schizophrenia rather than treat it. • They are a form of behavioral therapy where desirable behaviors are encouraged by the use of selective reinforcement and is based on operant conditioning. • When desired behavior is displayed eg. Getting dressed, tokens (in the form of coloured discs) are given immediately as secondary reinforcers which can be exchanged for rewards eg. Sweets and cigarettes. • This manages schizophrenia because it maintains desirable behavior and no longer reinforces undesirable behavior. • The focus of a token economy is on shaping and positively reinforcing desired behaviors and NOT on punishing undesirable behaviors. The technique alleviates negative symptoms such as poor motivation, and nurses subsequently view patients more positively, which raises staff morale and has beneficial outcomes for patients. • It can also reduce positive symptoms by not rewarding them, but rewarding desirable behavior instead. Desirable behavior includes self-care, taking medication, work skills, and treatment participation.

Paul and Lentz (1977) Token economy led to better overall patient functioning and less behavioral disturbance, More cost-effective (lower hospital costs)

Upper and Newton (1971) found that the weight gain associated with taking antipsychotics was addressed with token economy regimes. Chronic schizophrenics achieved 3lbs of weight loss a week.

McMonagle and Sultana (2000) reviewed token economy regimes over a 15-year period, finding that they did reduce negative symptoms, though it was unclear if behavioral changes were maintained beyond the treatment programme.

It is difficult to keep this treatment going once the patients are back at home in the community. Kazdin et al. Found that changes in behavior achieved through token economies do not remain when tokens are with¬drawn, suggesting that such treatments address effects of schizophrenia rather than causes. It is not a cure.

There have also been ethical concerns as such a process is seen to be dehumanising, subjecting the patient to a regime which takes away their right to make choices.

In the 1950s and 60s nurses often “rewarded” patients with cigarettes. Due to the pivotal role of dopamine in schizophrenia this led to a culture of heavy smoking an nicotine addiction in psychiatric hospitals of the era.

Ethical issues – Severely ill patients can’t get privileges because they are less able to comply with desirable behaviors than moderately ill patients – They may suffer from discrimination

Cognitive Behavioral Therapy

In CBT, patients may be taught to recognise examples of dysfunctional or delusional thinking, then may receive help on how to avoid acting on these thoughts. This will not get rid of the symptoms of schizophrenia but it can make patients better able to cope with them.

Central idea: Patients problems are based on incorrect beliefs and expectations. CBT aims to identify and alter irrational thinking including regarding:

• General beliefs.
• Self image.
• Beliefs about what others think.
• Expectations of how others will act.
• Methods of coping with problems.

In theory, when the misunderstandings have been swept away, emotional attitudes will also improve.

Assessment : The therapist encourages the patient to explain their concerns.

• describing delusions • reflecting on relationships • laying out what they hope to achieve through the therapy.

Engagement :

The therapist wins the trust of the patient, so they can work together. This requires honesty, patience and unconditional acceptance. The therapist needs to accept that the illusions may seem real to the patient at the time and should be dealt with accordingly.

ABC : Get the patients to understand what is really happening in their life:

A: Antecedent – what is triggering your problem ? B: behavior – how do you react in these situations ? C: Consequences – what impact does that have on your relationships with others?

Normalisation :

Help the patient realise it is normal to have negative thoughts in certain situations. Therefore there is no need to feel stressed or ashamed about them.

Critical Collaborative Analysis :

Carrying on a logical discussion till the patient begins to see where their ideas are going wrong and why they developed. Work out ways to recognise negative thoughts and test faulty beliefs when they arise, and then challenge and re-think them.

Developing Alternative Explanations :

Helping the patient to find logical reasons for the things which trouble them Let the patient develop their own alternatives to their previous maladaptive behavior by looking at coping strategies and alternative explanations.

Another form of CBT: Coping Strategy Enhancement (CSE)

• Tarrier (1987) used detailed interview techniques, and found that people with schizophrenia can often identify triggers to the onset of their psychotic symptoms, and then develop their own methods of coping with the distress caused. These might include things as simple as turning up the TV to drown out the voices they were hearing! • At least 73% of his sample reported that these strategies were successful in managing their symptoms. • CSE aims to teach individuals to develop and apply effective coping strategies which will reduce the frequency, intensity and duration of psychotic symptoms and alleviate the accompanying distress. There are two components: 1. Education and rapport training: therapist and client work together to improve the effectiveness of the client’s own coping strategies and develop new ones. 2. Symptom targeting: a specific symptom is selected for which a particular coping strategy can be devised Strategies are practised within a session and the client is helped through any problems in applying it. They are then given homework tasks to practice, and keep a record of how it worked.

CBT does seem to reduce relapses and readmissions to hospital (NICE 2014). However, the fact that these people were on medication and having regular meetings with doctors would be expected to have that effect anyway.

Turkington et al. (2006) CBT is highly effective and should be used as a mainstream treatment for schizophrenia wherever possible.

Tarrier (2005) reviewed trials of CBT, finding evidence of reduced symptoms, especially positive ones, and lower relapse rates.

Requires self-awareness and willingness to engage – Held back by the symptoms schizophrenics encounter – It is an ineffective treatment likely to lead to disengagement.

Lengthy – It takes months compared to drug therapy that takes weeks which leads to disengaged treatment as they don’t see immediate effects – A patient who is very distressed and perhaps suicidal may benefit better in the short term from antipsychotics.

Addington and Addington (2005) claim that CBT is of little use in the early stages of an acute schizophrenic episode, but perhaps more useful when the patient is more calm and beginning to worry about how life will be after they recover. In other words, it doesn’t cure schizophrenia, it just helps people get over it.

Research in Hampshire, by Kingdon and Kirschen (2006) found that CBT is not suitable for all patients, especially those who are too thought disorientated or agitated, who refuse medication, or who are too paranoid to form trusting alliances with practitioners.

As there is strong evidence that relapse is related to stress and expressed emotion within the family, it seems likely that CBT should be employed alongside family therapy in order to reduce the pressures on the individual patient.

Section 6: Interactionist Approach

The Interactionist approach acknowledges that there are a range of factors (including biological and psychological) which are involved in the development of schizophrenia.

The Diathesis-stress Model

• The diathesis-stress model states that both a vulnerability to SZ and a stress trigger are necessary to develop the condition. • Zubin and Spring suggest that a person may be born with a predisposition towards schizophrenia which is then triggered by stress in everyday life. But if they have a supportive environment and/or good coping skills the illness may not develop. • Concordance rates are never 100% which suggests that environmental factors must also play a role in the development of SZ. MZ twins may have the same genetic vulnerability but can be triggered by different stressors. • Tienari Et. A. (2004): Adopted children from families with schizophrenia had more chance of developing the illness than children from normal families. This supports a genetic link. However, those children from families schizophrenia were less likely to develop the illness if placed in a “good” family with kind relationships, empathy, security, etc. So environment does play a part in triggering the illness.

Holistic – Identifies that patients have different triggers, genes etc. – Patients can receive different treatments for their SZ which will be more effective.

Falloon et al (1996) stress – such as divorce or bereavement, causes the brain to be flooded with neurotransmitters which brings on the acute episode.

Brown and Birley (1968) 50% people who had an acute schizophrenic episode had experienced a major life event in 3 weeks prior.

Substance abuse: Amphetamine and Cannabis and other drugs have also been identified as triggers as they affect serotonin and glutamate levels.

Vasos (2012) Found the risk of schizophrenia was 2.37 times greater in cities than it was in the countryside, probably due to stress levels. Hickling (1999) the stress of urban living made African-Carribean immigrants in Britain 8 to 10 times more likely to experience schizophrenia.

Faris and Dunham (1939) found clear pattern of correlation between inner city environments and levels of psychosis. Pederson and Mortensen (Denmark 2001) found Scandanavian villages have very LOW levels of psychosis, but 15 years of living in a city increased risk.

Fox (1990): It is more likely that factors associated with living in poorer conditions (e.g. stress) may trigger the onset of schizophrenia, rather than individuals with schizophrenia moving down in social status.

Bentall’s meta-analysis (2012) shows that stress arising from abuse in childhood increases the risk of developing schizophrenia.

Toyokawa, Et. Al (2011) suggest many aspects of urban living – ranging from life stressors to the use of drugs, can have an effect on human epigenetics. So the stressors of modern living could cause increased schizophrenia in future generations.

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AQA A-LEVEL PSYCHOLOGY REVISION NOTES: SCHIZOPHRENIA

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PSYCHOLOGY AQA  A-LEVEL UNIT 3 (7182/3)

The syllabus.

CLASSIFICATION OF SCHIZOPHRENIA

• Positive symptoms of schizophrenia, including hallucinations and delusions
• Negative symptoms of schizophrenia, including speech poverty and avolition
• Reliability and validity in diagnosis and classification of schizophrenia, including reference to co-morbidity, culture and gender bias and symptom overlap

BIOLOGICAL EXPLANATIONS FOR SCHIZOPHRENIA

• The dopamine hypothesis
• Neural correlates
• Evaluation of biological approaches

PSYCHOLOGICAL EXPLANATIONS FOR SCHIZOPHRENIA

• Family dysfunction
• Cognitive explanations, including dysfunctional thought processing

DRUG THERAPY

• Typical and atypical antipsychotics

  PSYCHOLOGICAL THERAPIES

• Cognitive behaviour therapy
• Family therapy
• Token economies

  INTERACTIONIST APPROACHES

• The Diathesis-Stress Model

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INTRODUCTION

Schizophrenia is a severe psychotic disorder which affects about 0.3-0.7% of the population at some point in their lives. Although there are a variety of types of schizophrenia , symptoms commonly involve a loss of contact with reality, delusions and hallucinations.

Traditional, pre-scientific explanations of schizophrenia generally viewed the symptoms as a sign of demonic possession and sufferers would be treated with exorcism. From the 18 th C. onwards, a more compassionate , medical model evolved which viewed the disorder as a biological illness .

During the 20 th C. evidence emerged linking schizophrenia to genetic predisposition, biochemical imbalances and neurological abnormalities , and treatment was largely based around drugs therapies.

Alternative viewpoints have argued that schizophrenia is a fragmented psychological state which individuals are driven to as a result of stress or trauma and that psychiatry is incorrect in its assumptions regarding biological causation. Indeed, some critics have argued that psychiatric explanations are a pseudo-scientific justification for punishing social deviants and/or removing individuals who cannot adjust to or function ‘normally’ in society.

Psychiatrists (doctors specialising in mental health) employ classificatory systems to diagnose schizophrenia – in America, DSM-5-TR (Diagnostic and Statistical Manual of Mental Disorders, 5 th edition).

CLASSIFICATION OF SCHIZOPHRENIA. POSITIVE SYMPTOMS OF SCHIZOPHRENIA, INCLUDING HALLUCINATIONS AND DELUSIONS. NEGATIVE SYMPTOMS OF SCHIZOPHRENIA, INCLUDING SPEECH POVERTY AND AVOLITION. RELIABILITY AND VALIDITY IN DIAGNOSIS AND CLASSIFICATION OF SCHIZOPHRENIA, INCLUDING REFERENCE TO CO-MORBIDITY, CULTURE AND GENDER BIAS AND SYMPTOM OVERLAP ( Psychology A-level revision)

Classification of schizophrenia. positive symptoms of schizophrenia, including hallucinations and delusions. negative symptoms of schizophrenia, including speech poverty and avolition.

Schizophrenia is a severe psychotic disorder which affects about 0.3-0.7% of the population at some point in their lives.

Males are diagnosed at +40% more than females.

Approximately 1/3 rd of sufferers have a single, fairly brief episode ; 1/3 rd follow repetitive episodes throughout their life; 1/3rd experience a constant schizophrenic state .

DSM-5 lists various types of schizophrenia. 3 of the better known are Paranoid , Disorganised and Catatonic .

• Positive symptoms refer to an excess or distortion of a normal function (e.g. a normal behaviour is exaggerated) or to a new function (e.g. a behaviour which has never been shown before occurs).
• Negative symptoms refer to a lessening or loss of normal functions.

POSITIVE SYMPTOMS

• Delusions of grandeur – a belief that one possesses a special personal identity or special powers/abilities.
• Paranoid delusions – a belief that one is being followed, monitored or conspired against by a group who mean to do harm.
• Religious delusions – a belief that one is in communication with or is a supernatural being: e.g. god, a demon, a superhero, etc.
• Hallucinations.  Usually aural – ‘hearing voices’ providing a negative critical commentary on the person or commanding them to do or not do certain things. Can also be visual (seeing things) or tactile (feeling things).
• Experiences of control.  A belief they one is under the control of an outside force which has invaded one’s mind and body: e.g. through implanted transmitters, etc.
• Disordered thinking.  Incoherent or random speech. Feeling that thoughts have been inserted or withdrawn from the mind.

  NEGATIVE SYMPTOMS

• Speech poverty – difficulty with speaking – reduced speech output and verbal fluency.
• Avolition – loss of motivation and the will or desire to participate in activities or do things.
• Affective flattening – a reduction in the range and intensity of emotional expression. Immobile and unresponsive facial expressions often accompanied by poor eye contact and little body language or movement.
• Catatonia – assuming a rigid posture and remaining immobile in a trance-like state.

RELIABILITY AND VALIDITY IN DIAGNOSIS AND CLASSIFICATION OF SCHIZOPHRENIA, INCLUDING REFERENCE TO CO-MORBIDITY, CULTURE AND GENDER BIAS AND SYMPTOM OVERLAP

RELIABILITY

• Reliability refers to the consistency of the diagnosis: i.e. different psychiatrists diagnosing the individual should all agree that schizophrenia is the correct diagnosis (inter-rater reliability) and the same diagnosis should be given over time (test-retest reliability). Schizophrenia is diagnosed after a lengthy clinical interview, however, there is no objective test (e.g. a blood test) for the disorder.
• Evidence shows that there were problems with the reliability of diagnosis some years ago. Copeland (‘71) gave a description of a patient to 134 US and 194 British psychiatrists . 69% of the US psychiatrists diagnosed schizophrenia whereas only 2% of the British psychiatrists gave the same diagnosis. This indicates very poor reliability .
• To address lack of reliability, DSM has been revised through several additions. However, some research suggests that poor reliability is still a problem. Whaley (‘01) found inter-rater reliability correlations in the diagnosis of schizophrenia as low as 0.11 .
• Validity refers to how accurate and true the diagnosis is: i.e. a diagnosis is valid if a schizophrenic is diagnosed with schizophrenia and not another disorder.
• Rosenhan’s (’73) sent ‘normal’ people to a number of psychiatric hospitals claiming that they were hearing unfamiliar voices in their heads. They were all admitted into the hospitals and diagnosed with schizophrenia or manic-depression. On entry they all stopped faking their symptoms and acted normally, yet were still treated as being mentally ill by staff. Thus, psychiatrists and staff were, apparently, unable to make a valid diagnosis of schizophrenia.
• Predictive validity refers to the extent to which the diagnosis of schizophrenia can predict the likely outcome of the illness (the prognosis ). It is usually the case that there should be a predictable course that a disorder will take. However, this is not the case with schizophrenia. Thus diagnosis has low predictive validity .

  CULTURE BIAS

• Fernando claims that British psychiatrists hold conscious or unconscious stereotypes about race which affect diagnosis. Loring (’88) gave 290 psychiatrists a transcript of a patient interview and told half of them that the patient was black and the other half white . Black males were more likely to be diagnosed with paranoid schizophrenia . This indicates that certain people are more likely to be diagnosed based on criteria other than the presented symptoms: in this case, race . It may also explain why there are disproportionately large numbers of ethnic minorities in the UK and USA forcibly placed in institutions.

  GENDER BIAS

• Males may be more likely to be involuntarily committed to a mental institution as psychiatrists label them as being more likely to be violent/criminal .
• Women are more likely to commit themselves to a mental institution as it is more socially acceptable for women to seek help for emotional/psychological problems.
• Broverman (’70) found that psychiatrists in the USA tended to think of mentally healthy behaviour in terms of stereotypically male traits , therefore, females were more likely to be judged as mentally ‘unhealthy’ .

CO-MORBIDITY

The reliability of diagnosis is complicated by the fact that schizophrenia is often co-morbid with depression, anxiety and substance abuse (co-morbidity = 2 illnesses occurring at the same time). For example, co-morbid depression occurs in 50% of schizophrenics , and co-morbid substance abuse occurs in 47% . Thus, it is very difficult to draw a line between schizophrenia and other disorders, and questions whether a single, simple classification of ‘schizophrenia’ is valid and useful.

SYMPTOM OVERLAP

It can also be difficult to define the boundaries between schizophrenia and other disorders such as bi-polar disorder . For example, both disorders may experience delusions of grandeur. Psychiatric classificatory systems have tried to address the problem of symptom overlap by proposing mixed disorder categories such as schizoaffective disorder (schizophrenia + depression), but the validity of such categories has also been questioned.

BIOLOGICAL EXPLANATIONS FOR SCHIZOPHRENIA: GENETICS, THE DOPAMINE HYPOTHESIS AND NEURAL CORRELATES ( A-level Psychology revision)

Biological explanations view schizophrenia as an inheritable disorder (genetics) associated with abnormal neurotransmitter function (dopamine) and brain structure .

The likelihood of a person with unaffected relatives developing schizophrenia is 0.2-2%, however with affected relatives the likelihood increases: one parent (approx. 25%), two parents (approx. 50%).

Using a sample of 57 twins, Gottesman (’66) reported a concordance rate (the average % probability of an individual developing the disorder if they have an affected relative) of 42% for monozygotic twins (MZ) and 9% for dizygotics (DZ) . All major twin studies consistently report higher concordance rates for MZ’s than DZ’s although the highest concordance rates for MZs are rarely above 50% implying that social , psychological and environmental factors must play a role. However, Heston found that if an MZ had a schizophrenic disorder there was a 90% chance the other twin had some sort of mental disorder .

CONCORDANCE RATES FOR SCHIZOPHRENIA

Family history and twin studies fail to separate the influence of nature (genetics) and nurture (environment) and twins and family members tend to share similar parenting styles, learning experiences and social environments .

Adoption studies , on the other hand, involve studying the concordance rates of adopted-away offspring of schizophrenic mothers thus untangling the influence of biology and environment . Heston found a concordance rate of 10% between adopted away children and their schizophrenic mothers, and children of schizophrenic mothers were more likely to be sociopathic, neurotic and criminal .

NEUROTRANSMITTERS – THE DOPAMINE HYPOTHESIS

Excessive levels of the neurotransmitter dopamine are associated with schizophrenia. Phenothiazines (drugs used to treat schizophrenia) inhibit dopamine activity and reduce symptoms, and L-Dopa (used to treat Parkinson’s disease) stimulates dopamine production and produces schizophrenic symptoms in unaffected individuals .

Amphetamines (a street drug) increase the release of dopamine at synapses, and the symptoms of amphetamine psychosis (caused by taking too much of the drug) resembles paranoid schizophrenia.

THE RELATIONSHIP BETWEEN DOPAMINE, PHENOTHIAZINES & L-DOPA

It is impossible to establish, however, whether increased dopamine activity causes schizophrenia or whether schizophrenia has social/psychological causes which interfere with dopamine: i.e. we cannot determine the direction of the cause-effect relationship.

NEUROLOGICAL FACTORS – NEURAL CORRELATES

Post-mortems reveal increased dopamine in the left amygdala and increased dopamine receptor density in the caudate nucleus putamen . This finding was confirmed using PET scans by Wong .

Ianoco argued that dopamine deficiency may be the cause of ventricular enlargement – one of schizophrenia’s most noticeable neurological effects.

As with abnormal neurotransmitter levels, it is impossible to establish cause and effect relationships between abnormal neurological structure and schizophrenia.

FURTHER EVALUATION & COMMENTARY

• Although the above theories are supported by scientific evidence based on observation of physical, biological processes often using advanced technological equipment , critics argue that medical psychiatry is biologically determinist and reduces the schizophrenic’s experience to a simple ‘illness’ which can only be managed by drug therapy .
• Alternative psychological explanations tend to focus on the role of stress as a trigger, often in the context of family and interpersonal conflict . Anti-psychiatrists such as Laing argued that families characterised by high emotional tension where children received conflicting messages of care and criticism can cause a withdrawal into a schizophrenic state, and research with discharged schizophrenics has found that high levels of family expressed emotion (hostility, criticism, over-involvement and over-concern) are associated with high relapse rates .
• The fact that schizophrenia is more common among immigrant and socio-economically deprived groups indicates that stress and life events are likely to act as a trigger .
• The diathesis-stress model combines evidence from different approaches to suggest that individuals inherit a biological predisposition to develop schizophrenia which is then triggered by social and/or psychological stressors .

PSYCHOLOGICAL EXPLANATIONS FOR SCHIZOPHRENIA: FAMILY DYSFUNCTION AND COGNITIVE EXPLANATIONS, INCLUDING DYSFUNCTIONAL THOUGHT PROCESSING ( AQA A-level Psychology revision)

Family dysfunction.

 In the 50s and 60s, it was thought that people suffering from schizophrenia were from dysfunctional families . The term ‘schizophrenogenic family’ was used to describe families with high emotional tension , many secrets , close alliances and conspiracies .

Expressed emotion (EE) is a family communication style that involves criticism , hostility and over-concern. It is predicted that high levels of EE are likely to influence relapse rates (be readmitted to a psychiatric institution). The negative emotional climate in these families seems to arouse the patient and leads to stress beyond his or her already impaired coping mechanisms . EE is assessed by taping an interview with a relative of someone with schizophrenia and rating the frequency of critical comments , the frequency of expressions of dislike towards the patient, and the frequency of expression of over-protectiveness towards the patient

Research has generally been supportive. Linszen found that a patient returning to a family with high EE is about x4 more likely to relapse than a patient whose family is low EE .

A research study into schizophrenia and EE

• Subotnik (’02) gave 100 schizophrenics’ parents a Thematic Apperception Test . This test asks people to view a picture of a scene and describe their thoughts and feelings about the people pictured. The researcher then measures how critical and hostile their communication style Subotnik found that mothers of schizophrenics were particularly likely to be critical/hostile even though these mothers showed no sign of schizophrenia themselves. He concluded that mothers can pass on schizophrenic genes to offspring despite showing no sign of the disorder themselves.

However, studies of EE are correlational and may reflect the consequences of living with a severely disturbed individual, rather than having any causal significance: i.e. it may be the patient’s mental health problem which causes the family/parent to become high EE.

High EE patterns have also been found in the families of patients with other disorders such as depression and eating disorders , so high EE may not only be a cause of schizophrenia, rather of mental health breakdown in general.

COGNITIVE EXPLANATIONS, INCLUDING DYSFUNCTIONAL THOUGHT PROCESSING

Schizophrenics exhibit dysfunctional thought processing : i.e. they process information differently to non-schizophrenics.

Cognitive explanations have focussed on how schizophrenics’ cognitions may form the basis for their delusions and hallucinations .

• Delusions such as paranoia involve distorted patterns of thinking which exaggerate how important/central the individual is to irrelevant/meaningless events . For example, if someone looks at a schizophrenic accidentally the schizophrenic may interpret it as having meaning: e.g. ‘I am being watched’. This is referred to as ‘ egocentric bias’ . Schizophrenics also fail to ‘ reality test’ their beliefs: i.e. they fail to assess whether a belief they hold is rational/irrational and fail to recognise their cognitions as illogical and distorted .

HALLUCINATIONS

• It has been argued that the schizophrenic experience of hearing voices is simply an excessive focus on auditory stimuli (hypervigilance) and a high expectation that they will hear voices. Thus, their exaggerated expectancy of hearing voices and their interpretation of random auditory stimuli as possessing meaning produce auditory hallucinations.

A RESEARCH STUDY INTO SCHIZOPHRENICS’ PERCEPTION

• Shin (’08) investigated schizophrenics information processing abilities by testing their facial recognition abilities . 20 schizophrenics were matched against 20 non-schizophrenic controls and asked to perform a variety of perceptual tasks to do with spotting similarities and differences between images of faces . Schizophrenics performed poorly compared to non-schizophrenics on all facial-perceptual tasks. Shin interpreted this as evidence in favour of the idea that schizophrenics are likely to misinterpret other peoples’ facial expression and thus misinterpret their intentions : e.g. they may believe others are planning to harm them.

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DRUG THERAPY: TYPICAL AND ATYPICAL ANTIPSYCHOTICS ( AQA A-level Psychology revision guide)

ANTIPSYCHOTIC DRUGS

• Drugs that are effective in treating the most disturbing forms of psychotic illness, such as schizophrenia are called antipsychotics.
• Typical antipsychotic drugs (e.g. chlorpromazine ) are used primarily to combat the positive symptoms of schizophrenia, such as hallucinations and thought disturbances , products of an overactive dopamine system.
• Atypical antipsychotic drugs (e.g. clozapine ) combat positive symptoms but may also have some beneficial effects on negative symptoms.

TYPICAL ANTIPSYCHOTICS

The basic mechanism of typical antipsychotic drugs is to reduce the effects of dopamine and thus reduce symptoms of schizophrenia. Conventional antipsychotics are dopamine antagonists in that they bind to but do not stimulate dopamine receptors (particularly D2 receptors ), thus blocking their action and reducing delusions and aural hallucinations.

ATYPICAL ANTIPSYCHOTICS

Atypical antipsychotic drugs also act on the dopamine system but additionally act on serotonin systems in the brain that might be involved in schizophrenia.

These drugs temporarily occupy D2 dopamine receptors and then rapidly dissociate to allow normal dopamine transmission. It is this characteristic of atypical antipsychotics that is thought to be responsible for the lower levels of side-effects (such as tardive dyskinesia – involuntary movements of the mouth and tongue) compared to typical antipsychotics.

• The World Health Organization (‘01) reported that relapse rates in schizophrenics after 1 year were
• 55% with placebos
• 25% with chlorpromazine alone
• 2-23% when chlorpromazine was combined with family intervention

This suggests that whilst placebos can have a significant effect, typical antipsychotics have a far superior impact, particularly when combined with psychotherapy of some sort.

• Adams conducted a meta-analysis of 50 randomised controlled trials of the use of chlorpromazine for schizophrenia. In total, they included 5,276 individuals (in treatment or placebo groups). Overall, they found that chlorpromazine failed to produce global improvement in 76% of patients, and commonly produced adverse side-effects such as sedation, a risk of movement disorders and dizziness.
• One of the main reasons that drug therapies fail is because side-effects cause patients to stop taking their medication. Relatively minor side effects include drowsiness, visual disturbance, dryness of the mouth, changes in weight and depression. More seriously, they can induce a disorder called tardive dyskinesia which is irreversible and involves uncontrollable lip and tongue movements and facial tics. Around 24% develop this after taking typical antipsychotics for 7 years. Clearly there are ethical issues to consider when prescribing these drugs.
• Clozapine is associated with potentially fatal lowering of the white blood count and its use requires regular blood monitoring. Other side effects include sedation, hyper-salivation and weight gain.
• Some have criticised the medicalisation of mental disorders, saying that it is inappropriate to treat people like machines that have broken and need to be fixed. It has been argued that schizophrenics should be offered more enabling therapies which will allow them to manage their own conditions . Biological therapies are considered to be reductionist , assuming that the disorder is simply biologically causes and ignoring the social and emotional factors surrounding the individual’s condition and how they make sense of their disorder.
• There may also be publication bias . Non-significant results are less likely to be published so meta-analyses may over-exaggerate positive findings form research studies. Drug companies often fund research – they might suppress negative results to protect their profits . The result will be that drug therapy appears more successful than it actually is.

COGNITIVE BEHAVIOUR THERAPY AND FAMILY THERAPY AS USED IN THE TREATMENT OF SCHIZOPHRENIA. TOKEN ECONOMIES AS USED IN THE MANAGEMENT OF SCHIZOPHRENIA ( A-level Psychology resources)

Cognitive behaviour therapy and family therapy.

COGNITIVE BEHAVIOUR THERAPY ( CBTP)

Cognitive-behavioural therapy for psychosis (CBTp) is used with schizophrenics whose symptoms have been partially stabilised with drug therapies but who still experience some milder strength positive and negative symptoms: e.g. paranoid delusions.

  STAGES OF CBTP

• Assessment and Engagement – the patient expresses how they perceive their disorder, the therapist shows empathy and goals are set.
• ABC Model – therapist and patient explore Activating Events (A) which underlie emotional and behavioural (B) consequences (C). Maladaptive cognitions are identified, challenged and corrected to make them more logical, rational and adaptive.
• Alternative explanations – the therapist and patient develop healthier, adaptive ways of explaining the symptoms the patient experiences. For example, they will be encouraged to recognise that their disorder can cause irrational ways of thinking , but these thoughts are not accurate interpretations of reality . By finding alternative explanations of their cognitions they will be less likely to experience the maladaptive emotions and behaviours schizophrenics show. This will improve general functioning in social situations and reduce distress .

  EVALUATION

• Morrison (’14) randomly divided 74 schizophrenic patients who were not taking any medication into 2 groups – 1 of whom received CBTp over 26 sessions for a 9-month period . Although treatment was tailored to each individual the focus was on maladaptive cognitions and trying to alter these cognitions to improve cognitive and behavioural responses to situations . After 9 months , positive outcomes were twice as high in the CBTp group and these positive outcomes were still present at an 18-month follow-up . CBTp had improved the patients’ psychological, social and emotional functioning. Therefore, CBTp seems to be a successful add-on or alternative to drug therapies and avoid drugs unpleasant side-effects.
• A National Institute for Health and Care Excellence study (’14) found that when compared against a group receiving only anti-psychotic medication, those receiving medication and CBTp showed lower rates of hospitalisation, lowered symptom severity and improvement in social functioning .
• During the initial stages of schizophrenia cognitive therapy is often not appropriate as the patient lacks insight into their condition. Therefore, it is important that CBTp is delivered at the right stage in the disorder.
• Cuts to government funded mental health services mean that few schizophrenics are offered CBTp (estimate of 7% in 2013). Furthermore, schizophrenics may refuse or fail to attend scheduled CBTp sessions.

FAMILY THERAPY

Research into the role of expressed emotion (EE) in families affecting schizophrenics’ recovery and relapse rates indicates that families can do a lot to aid and support (or at least not worsen) a schizophrenic relative’s symptoms.

Family therapy involves:

• Psychoeducation . Family members are taught about the symptoms of schizophrenia and why their relative is behaving in the way that they are. This can lessen emotions such as anger, guilt and shame .
• Social Support . The therapist will encourage the family to seek social support from other relatives and government funded groups and try to create a home environment which is as calm and stress-free as possible. A supportive, understanding family will make it much easier for the schizophrenic to engage in therapy such as CBTp and stick to drug therapies .
• Behavioural Family Therapy . Family members are trained in appropriate problem-solving skills and communication skills relevant to aiding the affected relative: for example, anticipating what kind of situations might worsen a schizophrenic’s symptoms and how to avoid these situations occurring.
• Pharoah (’10) conducted a meta-analysis of 53 studies conducted in Europe, Asia and America. Studies compared family therapy to drug therapies . Overall conclusions were that family therapy caused (i) an overall improvement in patients’ mental health; (ii) better compliance to recommended medication; (iii) improvements in general functioning but not ability to live independently; (iv) a reduction in relapse rates.

It has been suggested that the key factor that family therapy improves is compliance with medication . Therefore, it is not family therapy itself that helps – simply that patients are better at taking prescribed medication .

• Family therapy is regarded as economically beneficial as it is associated with decreased relapse rates and (expensive) re-hospitalisation of schizophrenics, and thus saves government expenditure .
• Living with a schizophrenic can have negative effects on family members’ mental health (e.g. depression, anxiety). Family therapy can have a positive impact on family members’ mental health by introducing coping strategies and problem-solving skills . Thus, family members become better carers which, again, can decrease government expenditure .

TOKEN ECONOMIES

Negative symptoms of schizophrenia such as social withdrawal , lack of motivation and loss of interest in normal activities can lead to poor self-care such as washing, clothing, eating, sleeping normally, etc.

Token economies are a behaviour modification system based on the principles of operant conditioning whereby desirable behaviours are positively reinforced , and thus are more likely to be repeated in the future .

• Participants are given tokens for socially constructive behaviour such as getting up on time, washing, engaging in therapy, helping others, etc.
• Tokens are withheld when unwanted behaviours are exhibited.
• Tokens can then be exchanged for desirable items and activities such as sweets or time away from the ward.
• Tokens are given immediately after the desired behaviour so that the reinforcement is associated with the behaviour just displayed.
• Building up socially constructive behaviours may allow the patient to be discharged from the institution.
• Socially constructive behaviours acquired in the institution will be naturally reinforced by members of the public in the outside world (i.e. helping a member of the public would result in positive reinforcement of praise, attention, respect, etc.)
• Token economy programmes were widespread in the 60’s-70’s in institutions where long-stay patients were being prepared for transfer into the community .
• Patients with negative symptoms : e.g. catatonia, are difficult to reward as they show very few positive behaviours worth rewarding.
• However, Paul (’77) found that after 4 years of treatment, 98% of patients under a token economy system had been released from their institution compared with 71% who had not received this programme. This shows that token economies can have long-term beneficial outcomes for patients.
• Li (‘94) randomised 52 negative-symptom schizophrenic patients to a token economy programme or to a treatment-as-usual condition in which they did not receive training or reinforcement but were individually asked to perform the same daily tasks and activity programme as the experimental subjects. After 3 months , the severity of negative symptoms had declined in both groups , but the effect was much greater in the experimental group.

Despite evidence to suggest that token economies worked, they have declined in popularity .

Criticisms include:

• The success of token economies could be due to the close interaction between therapist and patient, rather than the therapy itself.
• It is not a ‘cure’ for schizophrenia, simply encouraging patients to mask their symptoms through ‘normal’ outward behaviour.
• It ignores the cognitive distress of those affected and simply encouraging them to ‘act’ as if they were well doesn’t rid them of their symptoms.
• It is patronising and demeaning to ‘bribe’ adults with rewards to behave in certain ways.
• Although the socially constructive behaviours acquired in the institution through the token economy programme are supposed to maintained outside of the institution through naturally occurring reinforcement , this may not be the case. In the token economy programme reinforcement always follows a desired behaviour, whereas in the real world people are often not reinforced for engaging in socially constructive behaviour.

THE INTERACTIONIST APPROACH IN EXPLAINING AND TREATING SCHIZOPHRENIA; THE DIATHESIS-STRESS MODEL ( AQA A-level Psychology resources)

It is clear that both biological and social/environmental factors have a part to play in the onset of schizophrenia – i.e. there is an interaction between nature and nurture .

The diathesis-stress model suggests that certain individuals have a genetic predisposition (diathesis) to the disorder, but they will only go onto develop it if they are exposed to a certain degree of stress .

As different individuals have different degrees of predisposition , different levels of stress will be required to trigger the disorder .

Even with identical twins (who share 100% genetic similarity) concordance rates are < 50% which indicates that social/environmental stressors must play a role and influence whether individuals with a predisposition actually do develop the disorder .

Stressful life events could vary from an abusive childhood to divorce to financial troubles to racism .

• Varese (’12) found that children who experienced extreme trauma before the age of 16 were x 3 as likely to develop schizophrenia in later life compared to the general population, and there was a positive correlation between intensity of trauma and chances of developing schizophrenia .
• Vassos (’12) found that the stresses of living in crowded urban environments increased risk for schizophrenia by x 2.37 . This could be due to stressors such as over-crowding, noise, poverty, crime, etc.

EVALUATION & COMMENTARY

A study into diathesis-stress

• Tienari (’04) compared 145 children adopted away from schizophrenic mothers (high risk group) to 158 children adopted from non-schizophrenic mothers (low risk group). Both groups were assessed aged 12 and 21 and all families were assessed for how well-functioning they were (e.g. degree of conflict, empathy, insecurity, etc.).
• Overall 14 children went on to develop schizophrenia – 11 from the high risk group , 3 from the low risk group . Being adopted into a well-functioning family appeared to have a protective effect on those from the high risk group – they were significantly less likely to develop schizophrenia than high risk children adopted into poorly functioning families.

  Other factors apart from genetic predisposition have been shown to influence chances of developing schizophrenia. Verdoux (’98) found that birth complications which cause oxygen starvation cause a x 4 increase in vulnerability to schizophrenia.

Early research suggested that stressors increased levels of dopamine which could trigger schizophrenic breakdown. More recently, attention has focused on cortisol . Cortisol is released in times of stress to increase levels of glucose which provides energy to cope with stressors. However, long-term stressors leading to long-term high levels of cortisol have been shown to have an adverse effect on mental health . Therefore, maintaining high levels of cortisol could trigger schizophrenia is a genetically predisposed individual .

The diathesis-stress model often assumes that stressors directly lead to schizophrenic breakdown . However, stressors and experiences in early life could affect individuals’ ability to cope with stress . Therefore, individuals with poor stress coping mechanisms who are genetically predisposed to schizophrenia could be more at risk of being unable to cope with stress and thus have schizophrenia triggered . Therefore, we should add ‘individuals’ stress-coping ability’ into the equation of the diathesis-stress model.

Overview – Schizophrenia

Schizophrenia is a psychological disorder characterised by loss of contact with reality. This A Level psychology topic looks at the symptoms of schizophrenia and how it is diagnosed , as well as various approaches to explaining and treating schizophrenia:

• The biological approach to schizophrenia (including genetic explanations, neural explanations , and the dopamine hypothesis , as well as drug therapy as treatment for schizophrenia)
• Psychological approaches to schizophrenia (including family dysfunction and cognitive explanations of schizophrenia, as well as treatments including CBT , family therapy , and token economies )
• Interactionist approaches to schizophrenia (including the diathesis-stress model )

Classification of schizophrenia

Schizophrenia is a psychological condition characterised by a loss of contact with reality. It affects around 0.7% of the population. There is no single defining symptom of schizophrenia but a cluster of (often seemingly unrelated) symptoms. These symptoms may be positive (experiences in addition to ordinary experience, such as hallucinations ) or negative (a lack of abilities associated with normal experience, such as reductions in speech ).

Positive symptoms of schizophrenia

Hallucinations

Hallucinations are perceptions that are not based in reality, or distorted perceptions of reality.

For example, a schizophrenic person may hallucinate hearing voices that aren’t really there, or seeing someone who isn’t really there.

Delusions are beliefs that are not based in reality.

For example, a schizophrenic person may have a delusion that they are the victim of a grand conspiracy, or that they are an important person with a unique mission (e.g. Jesus Christ reborn).

Negative symptoms of schizophrenia

Negative symptoms are a lack of abilities associated with normal psychological functioning. Negative symptoms associated with schizophrenia include speech poverty and avolition .

Speech poverty

Speech poverty is a reduction in the quality and amount of speech.

For example, a schizophrenic person may give one-word answers to questions without elaborating any further detail.

Avolition is a lack of desire and motivation for anything.

For example, a schizophrenic person may sit around without engaging in everyday tasks such as work, socialising, or maintaining personal hygiene.

Diagnosis of schizophrenia

There are two main classification systems for diagnosing schizophrenia: The American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and the World Health Organisation’s International Statistical Classification of Diseases and Related Health Problems (ICD-10) . These manuals enable doctors to label a patient’s symptoms as those of schizophrenia (rather than some other disorder).

The criteria for DSM-5 and ICD-10 differ slightly: DSM-5 requires at least one positive symptom to be present, whereas diagnosis of schizophrenia using ICD-10 can be based on negative symptoms alone.

Reliability of schizophrenia diagnosis

Reliability refers to how consistently schizophrenia is diagnosed. For example, if multiple different doctors diagnose the same person as schizophrenic based on the same symptoms, then their diagnosis is reliable .

Various studies have attempted to quantify the reliability of schizophrenia diagnosis. For example:

• Beck et al (1962) found a concordance rate of 54% among psychiatrists in their diagnosis of schizophrenia.
• Söderberg et al (2005) found a concordance rate of 81% among psychiatrists using the DSM classification to diagnose schizophrenia.
• Jakobsen et al (2005) found a concordance rate of 98% among psychiatrists using the ICD-10 classification to diagnose schizophrenia.
• In Cheniaux et al (2009) , two psychiatrists evaluated 100 patients using both the DSM-4 and ICD-10 criteria. Psychiatrist 1 found 26 patients had schizophrenia according to DSM-4 and 44 according to ICD-10. Psychiatrist 2 found 13 patients had schizophrenia according to DSM-5 and 24 according to ICD-10. This suggests both low inter-observer reliability and low reliability between the two classification systems.
• Improvements in inter-observer reliability : Although research is conflicting (see studies above), more recent studies of schizophrenia diagnosis generally find higher concordance rates among psychiatrists compared to older studies. This suggests that diagnosis of schizophrenia has become more reliable over time.
• Low reliability between DSM and ICD: Cheniaux et al (2009) demonstrates different incidence of schizophrenia diagnosis by the same observer depending on which manual they use. In general, the DSM classification is considered more reliable as the descriptions of symptoms are more specific.
• Co-morbidity: People with schizophrenia often suffer from psychological disorders in addition to schizophrenia, which confuses diagnosis. For example, people with schizophrenia often suffer from depression as well. This can reduce the reliability of diagnosis as one evaluator may pick up on the depressive symptoms and diagnose the patient with depression, whereas another evaluator may pick up on the schizophrenic symptoms and diagnose the patient with schizophrenia.

Validity of schizophrenia diagnosis

Validity refers to how accurately schizophrenia is diagnosed. For example, if doctors frequently diagnose patients with autism as suffering from schizophrenia, then their diagnosis is not valid .

Rosenhan (1973) questions the validity of schizophrenia diagnosis. In this study, eight healthy volunteers (i.e. subjects who did not have schizophrenia) presented themselves to various psychiatric hospitals claiming to hear voices. All eight volunteers were successfully admitted to the hospitals and diagnosed with schizophrenia. Depending on the ‘patient’, doctors took between 7-52 days to release them. In a later experiment, doctors were falsely told that healthy patients would attempt to admit themselves, which led doctors to turn genuine schizophrenic patients away because they thought they were actors. The results of these experiments suggest the doctors did not have valid methods for diagnosing schizophrenia.

• Improvements in validity : Although Rosenhan (1973) casts doubt on the validity of schizophrenia diagnosis, more recent studies suggest schizophrenia diagnosis has become more accurate. For example, Mason et al (1997) found that improvements to diagnostic manuals (DSM and ICD) over time led to more accurate diagnosis of schizophrenia.
• Symptom overlap: Schizophrenia shares symptoms with other psychological disorders, such as depression and autism. For example, both people with schizophrenia and people with autism often suffer with speech poverty . This overlap of symptoms may reduce the validity of schizophrenia diagnosis because an evaluator may incorrectly attribute these symptoms to a different disorder.
• Gender differences: Several studies suggest differences between men and women in the rates of schizophrenia, average age of onset, and severity of symptoms. For example, a meta-analysis from Aleman et al (2003) found men were 42% more likely to suffer from schizophrenia than women. This is supported by Castle et al (1993) , who found that when diagnostic criteria were strictly defined, the rate of schizophrenia in men was more than twice that of women. Is this disparity a result of gender bias in diagnosis, or do these findings reflect a valid difference in the incidence of schizophrenia between men and women? Cotton et al (2009) suggest that the better interpersonal functioning of women may cause doctors to miss schizophrenia diagnosis in women, supporting the existence of gender bias. However, Kulkarni et al (2001) found that administration of estrogen (the female hormone) reduces schizophrenia symptoms, which suggests biological differences may partly explain gender differences in schizophrenia.
• Invalid diagnosis: Afro-Caribbean people in Britain are being over diagnosed with schizophrenia due to cultural bias (or Afro-Caribbean people in the Caribbean are being under diagnosed).
• Valid diagnosis: The diagnosis reflects a valid difference in schizophrenia rates and so environmental stressors in Britain (e.g. racism, increased risk of flu) are causing increased rates of schizophrenia among people of Afro-Caribbean descent.

Biological approach to schizophrenia

Biological explanations of schizophrenia.

Biological explanations of schizophrenia look at biological factors linked to schizophrenia. These include genetics , neural (brain) abnormalities , and abnormalities in dopamine .

The genetic explanation of schizophrenia looks at hereditary factors – i.e. genes – that contribute to the development of schizophrenia.

As always, twin studies are a useful way to determine whether or not a condition is inherited through genetics. If it is more common for both identical twins to suffer from schizophrenia than it is for both non-identical twins, this would suggest a genetic component to schizophrenia. The reason for this is that identical twins have 100% identical genetics whereas non-identical twins only share 50% of their genes and so any genetic condition would be equally common to both identical twins.

Several studies have attempted to determine the genetic heritability of schizophrenia. Perhaps the most widely-cited source is Gottesman (1991) , who looked at how different familial relationships to someone with schizophrenia are linked with risk of developing schizophrenia:

Gottesman found that the closer the genetic relationship to the person with schizophrenia, the greater the risk of developing schizophrenia. For example, the concordance rate for schizophrenia among identical twins is 48%, whereas for non-identical twins it is 17%. This supports the idea that genetics play a role in developing schizophrenia.

Other familial and twin studies into schizophrenia include:

• Cardno et al (1999) found identical twins had a concordance rate for schizophrenia of 40.8%, whereas non-identical twins had a concordance rate of 5.3%.
• Tienari et al (1985) conducted a longitudinal study comparing adopted children whose biological mothers had schizophrenia with a control group of adoptees whose biological mothers did not have schizophrenia. The researchers found that the children of schizophrenic mothers were more likely to develop schizophrenia compared to controls, supporting the role of genetics in the development of schizophrenia.
• Kety and Ingraham (1992) is another adoption study. Adoption studies like this are useful because they separate (and thus control for ) environmental factors: If schizophrenia was passed on from parents to children through environmental factors only, you would expect adoptees whose biological parents had schizophrenia to have the same rates of schizophrenia as the control group. However, the researchers found that adoptees whose biological parents had schizophrenia were 10 times more likely to develop schizophrenia than a control group of adoptees whose biological parents did not have schizophrenia, supporting a genetic basis of the disorder.

Strengths of genetic explanations of schizophrenia:

• Supporting evidence: The familial and twin studies of schizophrenia above support the genetic explanation of schizophrenia because they show that being closely related (and thus having similar genes) to someone with schizophrenia increases the likelihood of suffering from schizophrenia.
• Multiple genes: It is unlikely that there is a single gene responsible for schizophrenia. Instead, multiple genes likely combine to increase a person’s risk of developing schizophrenia. In a study of more than 36,000 schizophrenic patients, Ripke et al (2014) found 108 different genetic variations that were correlated with schizophrenia, supporting the existence of a genetic component to the disorder. Further, many of these genetic variations were related to dopamine transmission, so genetic explanations can be combined with the dopamine hypothesis to provide a holistic explanation of schizophrenia.

Weaknesses of genetic explanations of schizophrenia:

• Other factors: Although most studies suggest genetics play a part in the development of schizophrenia, it is clear that other factors are important too. If schizophrenia was 100% genetic, you would expect concordance rates between identical twins to be 100%. However, most studies find concordance rates among identical twins to be less than 50%, which suggests there is more to schizophrenia than just genetics. This suggests an interactionist approach is best for explaining schizophrenia.
• Methodological issues surrounding twin studies: Twin studies typically assume that twins have identical upbringings and so any differences in concordance rates between identical and non-identical twins must be explained by genetics. However, environmental factors likely play a role too. For example, looking identical probably makes parents treat identical twins more similarly than they would non-identical twins. As such, greater similarities in environment could contribute to higher concordance rates for schizophrenia among identical twins, with the influence of genetics being exaggerated.

Neural correlates

The neural explanation of schizophrenia looks at correlations among the brain structures of people with schizophrenia.

There are several ways to examine the brain, such as post-mortem and fMRI scanning . By using these methods, researchers can compare the brains of schizophrenic people with non-schizophrenic people to identify differences in brain structures that may cause schizophrenia.

For example, the images above from Kim et al (2010) show fMRI scans of a schizophrenic patient and a non-schizophrenic control during a working memory task.

Other studies looking at the neural basis of schizophrenia include:

• Enlarged ventricles: Several studies have found correlations between enlarged ventricles in the brain and schizophrenia. For example, Johnstone et al (1976) and Suddath et al (1990) . Enlarged ventricles are particularly linked with the negative symptoms of schizophrenia, as shown in studies such as Andreasen et al (1982) .
• Reduced grey matter and cortical thinning: Boos et al (2012) compared MRI scans of 155 schizophrenic patients, 186 non-schizophrenic family members, and 122 non-schizophrenic controls. The researchers found that the schizophrenic patients had reduced grey matter and cortical thinning compared to their non-schizophrenic family members and the non-schizophrenic controls. This further supports the existence of a neural basis for schizophrenia.
• Facial emotion processing: A common symptom of schizophrenia is difficulty perceiving emotions. A meta-analysis by Li et al (2010) looked at fMRI scans of schizophrenic patients and non-schizophrenic controls during facial expression processing tasks. The researchers found that people with schizophrenia have reduced activity in the bilateral amygdala and right fusiform gyri compared to controls, suggesting a neural basis for this symptom.
• Supporting evidence: The studies above support several neural explanations of schizophrenia because they demonstrate correlations between neural structures and schizophrenia.

Weaknesses of neural explanations of schizophrenia:

• Conflicting evidence: Although several studies have found correlations between enlarged ventricles and schizophrenia, there are many exceptions. There are many people with enlarged ventricles who do not have schizophrenia, and there are many people with schizophrenia who do not have enlarged ventricles.
• Correlation vs. causation: Although there are correlations between schizophrenia and certain neural patterns, it can be difficult to determine whether abnormal brain functioning causes schizophrenia symptoms or whether it is an effect of schizophrenia. For example, does reduced activity in the bilateral amygdala of schizophrenic patients cause difficulties in emotional processing, or do schizophrenics’ reduced emotional processing (caused by some other factor) result in reduced blood flow and activity in the bilateral amygdala?

The dopamine hypothesis

The dopamine hypothesis became popular in the 1970s when studies (e.g. Seeman et al (1976) , Creese et al (1976) , and Snyder (1976) ) reported that several drugs that reduce schizophrenia symptoms are dopamine receptor antagonists: They reduce dopamine activity. The implication is that schizophrenia is caused by increased dopamine activity and that these drugs work by reducing dopamine activity.

Further evidence supporting the dopamine hypothesis includes:

• Dopamine agonists: Several studies have demonstrated that drugs that increase dopamine activity – dopamine agonists, such as amphetamines – can induce schizophrenic symptoms in non-schizophrenic people. For example, a systematic review by Curran et al (2004) found that amphetamine use makes schizophrenia symptoms worse in schizophrenic patients. Further, McKetin et al (2013) found that non-schizophrenic methamphetamine addicts demonstrated a 5-fold increase in schizophrenia-like symptoms during periods when they were using methamphetamine. This link is further supported by animal studies, such as Randrup and Munkvad (1966) , who were able to induce schizophrenic behaviour in rats with amphetamines and then reverse these symptoms with dopamine-reducing drugs ( ant agonists).
• Post-mortem evidence: Bird et al (1979) used post-mortems to compare dopamine levels in the brains of 50 schizophrenic patients with 50 non-schizophrenic controls. The schizophrenic patients had increased dopamine concentrations in some areas of the brain compared to controls.
• Brain scans: Some studies using brain-scanning techniques have found increased dopamine activity in schizophrenic patients. For example, Lindström et al (1999) compared PET scans of 12 schizophrenic patients with 10 controls and found the schizophrenic patients had increased dopamine activity in the striatum and parts of medial prefrontal cortex. Further, a review of MRI scans by Alves et al (2008) found support for the (revised) dopamine hypothesis.

Over the years, the dopamine hypothesis of schizophrenia has been refined. It’s not as simple as high dopamine = schizophrenia. Instead, research suggests that schizophrenia is linked with high dopamine activity in some areas of the brain (e.g. the subcortex) but low dopamine activity in other areas (e.g. prefrontal cortex).

The dopamine hypothesis of schizophrenia remains somewhat controversial. The AO3 evaluation points below provide examples of evidence against the dopamine hypothesis.

Strengths of the dopamine hypothesis of schizophrenia:

• Supporting evidence: The studies above support the dopamine hypothesis of schizophrenia in several different ways. For example, drugs that lower dopamine have been shown to reduce schizophrenia symptoms, and brain scans have shown higher dopamine activity in schizophrenic patients.

Weaknesses of the dopamine hypothesis of schizophrenia:

• Conflicting evidence: Farde et al (1990) compared brain scans of 18 schizophrenia patients with 20 non-schizophrenic controls. They found no difference in dopamine activity between the two groups. Similarly, in a review of post-mortem studies, Haracz (1982) found little evidence to support the dopamine hypothesis.
• Other neurotransmitters: Evidence suggests that other neurotransmitters besides dopamine are involved in the development of schizophrenia, such as glutamate and serotonin. For example, a meta-analysis of brain scans by Marsman et al (2013) found decreased glutamate activity in schizophrenic patients compared to controls. Further, like with the dopamine hypothesis, there is some evidence that drugs that alter glutamate activity can successfully treat schizophrenia. It’s important to note that the glutamate hypothesis does not contradict the dopamine hypothesis: Both neurotransmitters may be involved in schizophrenia. Serotonin may also be implicated in schizophrenia, as suggested by the efficacy of atypical antipsychotic drugs .
• Allegations of bias: Psychiatrist David Healy (2002) argues that pharmaceutical companies exaggerated the dopamine hypothesis of schizophrenia to sell more drugs. The overly-simplified hypothesis that schizophrenia is caused by high dopamine makes it easy to market antipsychotic drugs as ‘cures’ for schizophrenia.

Biological treatment of schizophrenia: Drug therapy

Antipsychotic drugs are the primary biological treatment for schizophrenia. These drugs are divided into two categories: Typical antipsychotics and atypical antipsychotics .

Typical antipsychotics

Typical antipsychotic drugs for schizophrenia work by reducing dopamine activity – they are dopamine antagonists – and are thus strongly associated with the dopamine hypothesis of schizophrenia . They have been used since the 1950’s and are sometimes referred to as first-generation antipsychotics.

Chlorpromazine was the first antipsychotic drug developed. It is a dopamine antagonist, which means it works by blocking dopamine receptors in the brain. Chlorpromazine also has sedative effects.

Typical antipsychotic drugs, such as chlorpromazine and haloperidol, can cause several side effects. Among the most serious of these side effects are extrapyramidal symptoms , which are problems with movement similar to Parkinson’s disease.

Atypical antipsychotics

Atypical antipsychotic drugs have been around since the 1970’s and are sometimes referred to as second-generation antipsychotics. The aim of these drugs is to improve upon the efficacy of typical antipsychotics while reducing side effects.

Atypical antipsychotics target several neurotransmitters , not just dopamine. For example, clozapine is an atypical antipsychotic that acts on the neurotransmitters dopamine, serotonin, and glutamate. Risperidone , another atypical antipsychotic, targets dopamine and serotonin.

Some evidence suggests atypical antipsychotics are superior to typical antipsychotics (see AO3 evaluation points below). However, atypical antipsychotics also carry a risk of side effects including weight gain, increased risk of heart attack, increased risk of diabetes, and extrapyramidal symptoms.

In general, there is no one-size-fits-all drug therapy for schizophrenia. The different mechanisms of action and side effect profiles of the various drugs (both typical and atypical) mean the best treatment option will vary from patient to patient. Further, drug therapy can be combined with psychological treatments such as CBT .

Strengths of drug therapy:

• Evidence supporting drug therapy: Several studies have found both typical and atypical antipsychotics to be more effective than placebo in reducing schizophrenia symptoms.
• Atypical antipsychotics more effective than typical antipsychotics: A systematic review by Bagnall et al (2003) looked at data from over 200 trials of antipsychotic drugs. In general, atypical antipsychotics were more effective than typical antipsychotics. However, data supporting the most recent atypical antipsychotics was of poor quality.

Weaknesses of drug therapy:

• Criticism of the distinction between typical and atypical: While atypical antipsychotics were designed to be more effective with less side effects than typical antipsychotics, some studies question whether this is actually the case. Further, while typical antipsychotic drugs were thought to target the dopamine neurotransmitter only, more recent evidence suggests both generations of antipsychotics target other neurotransmitters such as serotonin. For these reasons, some commentators (e.g. Leucht et al (2013) and Tyrer and Kendall (2008) ) have questioned whether the distinction between typical and atypical antipsychotics is a meaningful one.
• Side effects: All antipsychotics carry a risk of side effects to varying degrees. These side effects can range from mild (e.g. weight gain, dizziness) to potentially fatal (e.g. heart attack, stroke, neuroleptic malignant syndrome). Lieberman et al (2005) found that 74% of 1,342 schizophrenic patients discontinued antipsychotic drug treatment within 18 months due to side effects.

Psychological approach to schizophrenia

Psychological explanations of schizophrenia.

Psychological explanations of schizophrenia include family dysfunction and cognitive explanations (e.g. dysfunctional thought processing) .

Family dysfunction

Several psychologists have proposed that family dysfunction (e.g. high levels of conflict or difficulties communicating) can influence the development of schizophrenia.

One example of this is Bateson et al (1956) , who proposed the double bind explanation of schizophrenia. According to this explanation, children who often get conflicting messages from their parents are more likely to develop schizophrenia. For example, a mother who loves her child but has trouble expressing it may exhibit contradictory behaviours (e.g. hugging the child but being critical with her words). Another example is a parent who tells their child to be more spontaneous: Whatever the child does, they can’t fulfil this request because if they do act more spontaneous because their parent tells them then they aren’t acting spontaneously! Constant exposure to these mixed messages and impossible demands mean the child is unable to form a coherent picture of reality. This leads to disorganised thinking which in extreme cases can manifest as symptoms of schizophrenia such as delusions and hallucinations .

Another familial explanation of schizophrenia is expressed emotion . An environment with a high degree of expressed emotion – particularly negative, such as criticism and hostility – causes stress, which increases the risk of schizophrenia. Expressed emotion is primarily associated with relapse in schizophrenic patients.

Strengths of the family dysfunction explanation:

• Evidence supporting the family dysfunction explanation: Adoption studies suggest that dysfunctional family environments increase the risk of schizophrenia. For example, in a follow-up to their longitudinal study described above , Tienari et al (2004) rated familial dysfunctionality among the adoptive environments of adoptees whose biological mothers had schizophrenia. They found that adoptees raised in families rated as dysfunctional had much higher rates of schizophrenia (36.8%) compared to adoptees raised in families rated as healthy (5.8%).
• Evidence supporting the role of expressed emotion: A meta-analysis of 26 studies by Butzlaff and Hooley (1998) found relapse rates are higher among schizophrenic patients who return to live with families with a high degree of expressed emotion. The role of expressed emotion in schizophrenia is further supported by the success of family therapies that aim to reduce expressed emotion. However, this research doesn’t support expressed emotion as a cause of schizophrenia, but it does suggest it contributes to maintaining schizophrenia.

Weaknesses of the family dysfunction explanation:

• Exceptions: Not everyone raised in a dysfunctional family goes on to develop schizophrenia, and not everyone with schizophrenia was raised in a dysfunctional family. This suggests that other factors are important in explaining schizophrenia, such as biology .
• Correlation vs. causation: Even if schizophrenia is correlated with family dysfunction, this doesn’t prove that family dysfunction causes schizophrenia – it could be the other way round. For example, it seems possible that having a schizophrenic family member could itself cause stress and dysfunction within the family, rather than that family dysfunction causes schizophrenia. It’s a chicken or egg scenario: Which comes first?
• Methodological concerns: Bateson et al’s double bind explanation of schizophrenia is based on a handful of case studies and interviews . Some critics have suggested researchers focus on examples that support the explanation while ignoring examples that conflict with it (selection bias).

Cognitive explanations

Cognitive explanations of schizophrenia look at how schizophrenic patients think and process information. Schizophrenic cognition may differ from non-schizophrenic cognition in several ways:

• Dysfunctional thought processing: Metacognition is the ability to think about and reflect on one’s own thoughts, emotions, and behaviours. Schizophrenic patients are seen as suffering from metacognitive dysfunction, which may explain some symptoms of schizophrenia such as hallucinations . For example, an inability of schizophrenic patients to recognise their thoughts as their own may explain hearing voices: The patient attributes their own thoughts to some external source outside their mind.
• Cognitive biases: Positive symptoms of schizophrenia, such as delusions , can be explained as a result of cognitive biases . For example, bias may mean a schizophrenic person interprets the ordinary actions of other people as sinister, supporting their delusion that they are a victim of a conspiracy or that people are trying to harm them.
• Attention deficits: Schizophrenic patients often have difficulty concentrating and paying attention.
• Speech deficits: Schizophrenic patients often have low verbal fluency and difficulty finding words. This may explain the symptom of speech poverty .
• Memory deficits: Schizophrenic patients often have impaired working memory , particularly verbal working memory.

Strengths of cognitive explanations:

• Evidence supporting cognitive explanations: Several studies have found evidence of cognitive impairment in schizophrenic patients. Bowie and Harvey’s (2006) review above cites many examples. Cognitive impairments are often present before the patient’s first schizophrenic episode and persist throughout the disorder, but therapies that reduce cognitive impairment (e.g. CBT ) often improve schizophrenia symptoms. This all supports a role for cognitive explanations of schizophrenia.
• Practical applications: Cognitive explanations have been used to develop effective therapies for treating schizophrenia, such as CBT .
• Complements other explanations: Cognitive explanations can be combined with other explanations (e.g. biological ) to give a more holistic account of schizophrenia.

Weaknesses of cognitive explanations:

• Evidence against cognitive explanations: Many people have the cognitive biases and cognitive deficits associated with schizophrenia (for example, as a result of brain damage) and yet do not develop schizophrenia. This suggests that cognitive explanations alone are too reductionist : There is more to explaining schizophrenia than just cognitive explanations.
• Does not explain the cause of schizophrenia: Cognitive theories simply describe the thought processes of schizophrenia but do not explain why people with schizophrenia have these thought processes in the first place.

Psychological treatment of schizophrenia

In addition to antipsychotic drugs , various psychological treatments for schizophrenia exist such as cognitive behavioural therapy (CBT) , family therapy , and the use of token economies .

Cognitive behavioural therapy (CBT)

Cognitive behavioural therapy (CBT) is the main psychological treatment for schizophrenia. There are many different forms of CBT, but the main aim is to help patients identify and challenge the irrational and maladaptive thoughts underlying schizophrenia.

CBT involves talking through irrational thoughts like this. The patient is encouraged to describe their thoughts to the therapist. The therapist then helps the patient identify and challenge the reality of these thoughts. For example, the therapist may ask the patient to consider how likely these thoughts are to be true and consider alternative explanations. The therapist may also help the patient tackle their symptoms from the behavioural angle (e.g. by teaching behavioural coping skills) and the emotional angle (e.g. by teaching relaxation techniques).

CBT is primarily used to treat positive symptoms of schizophrenia and is commonly used in combination with antipsychotic drug therapy . A typical course of CBT for schizophrenia might consist of 12 sessions spaced 10 days apart.

Strengths of CBT for schizophrenia:

• Evidence supporting efficacy of CBT: Several studies have shown that CBT effectively reduces schizophrenia symptoms. For example, a meta-analysis of 14 studies involving 1,484 schizophrenia patients by Zimmermann et al (2005) found CBT significantly reduced positive symptoms of the disorder.
• Complements other treatments: CBT can be used in conjunction with other treatments, such as antipsychotic drugs . Some evidence suggests this combined therapy is more effective than antipsychotic drugs or CBT alone.
• Less side effects than antipsychotic drugs: CBT has very few side effects. By comparison, antipsychotic drugs carry a risk of serious and potentially fatal side effects such as pyramidal symptoms, increased risk of heart attack, and weight gain.

Weaknesses of CBT for schizophrenia:

• Conflicting evidence: Contrary to Zimmerman et al (2005) , a meta-analysis by Jauhar et al (2014) found CBT only had minor effects on schizophrenia symptoms. Further, when the researchers looked at blinded studies only (i.e. studies where the researchers were not aware which patients received CBT and which didn’t), even this small effect size disappeared. This calls into question the efficacy of CBT and suggests that research supporting the efficacy of CBT for schizophrenia may simply be the result of researcher bias .
• Not suitable for all patients: An important aspect of CBT is developing a trusting alliance between patient and therapist. However, some schizophrenic patients may be too paranoid or anxious to develop such a trusting alliance and so are not suitable candidates for CBT.

Family therapy

Family therapy is a treatment for schizophrenia based on the family dysfunction explanation of schizophrenia . According to this explanation, schizophrenia is caused (at least in part) by familial dysfunction and so family therapy aims to address this dysfunction rather than focusing on the schizophrenic patient in isolation. This involves talking openly about the patient’s illness and how it affects them with an aim to:

• Improve communication patterns: Increase positive communication and decrease negative communication among the family (i.e. reduce levels of expressed emotion )
• Increase tolerance and understanding: Educate family members about schizophrenia and how to deal with it (e.g. how to support each other)
• Reduce feelings of guilt and anger: Family members may feel guilty (e.g. that they are responsible for causing schizophrenia) or angry towards the schizophrenic patient

A typical course of family therapy may consist of weekly sessions for a year, after which the family members will have developed skills that they can use after therapy has ended.

Strengths of family therapy for schizophrenia:

• Evidence supporting efficacy of family therapy: Several studies have demonstrated lower rates of schizophrenia relapse among patients receiving family therapy. For example, a meta-analysis by Pilling et al (2002) looked at 18 studies of family therapy for schizophrenia and found that it had a clear effect on reducing relapse rates.
• Complements other treatments: Evidence suggests that family therapy plus antipsychotic drug therapy is more effective at reducing relapse than antipsychotic drug therapy alone. For example, Xiong et al (1994) randomly allocated 63 subjects to either a drug therapy group or a drug therapy plus family therapy group. After one year, relapse rates were lower in the drug therapy plus family therapy group (33%) compared to the drug therapy only group (61%).
• Less side effects: Family therapy has very few (if any) side effects relative to antipsychotic drugs .
• Cost effective: The Schizophrenia Commission (2012) estimate that family therapy results in cost savings of around £1000 per patient over a 3 year period.

Weaknesses of family therapy for schizophrenia:

• Could be counterproductive: Family therapy for schizophrenia emphasises being open and honest. However, in some families, open communication may reveal difficult truths or reignite old arguments. This could increase, rather than decrease, negative communication and potentially make the problem worse.
• Not suitable for all patients: Some schizophrenic patients do not have dysfunctional families and so family therapy is unlikely to be an effective treatment for them.

Token economies

Token economies are mainly used to treat negative symptoms of schizophrenia, such as avolition . For example, avolition may mean the patient has little motivation to undertake tasks such as getting out of bed, washing, and socialising. Token economies provide an incentive for the patient to undertake these tasks, changing their behaviour.

Token economies are primarily used for schizophrenic patients who are in institutions for long time periods. As well as schizophrenia, token economies are also used to deal with criminal behaviour ( see the forensic psychology page for more details ).

Strengths of token economies:

• Evidence supporting efficacy of token economies: Several studies suggest token economies can improve symptoms of schizophrenia. For example, a review of studies by McMonagle and Sultana (2000) found token economies reduced the negative symptoms of schizophrenia. However, the researchers note that the evidence is not conclusive, with questions about the replicability of the findings and uncertainty about whether behavioural changes can be maintained after the treatment ends.
• Complements other treatments: Token economies can be used in conjunction with other treatments, such as antipsychotic drugs .

Weaknesses of token economies:

• Ethical concerns: Use of token economies could be seen as unethical for several reasons. Firstly, some argue that token economies are dehumanising as they take away the patient’s rights to make their own choices. Secondly, some argue that token economies are discriminatory: Severely ill patients will have greater difficulty complying with behavioural demands and thus get fewer privileges than patients who are less severely ill. Token economies may thus discriminate against the most severely ill patients.
• Relapse: If improvements in behaviour are dependent on receiving tokens, the schizophrenic patient may relapse once token economy therapy is withdrawn.

Interactionist approach to schizophrenia

Rather than trying to reduce schizophrenia to either a psychological or biological phenomena, interactionist approaches to schizophrenia explain the disorder as a combination of various factors. One example of this is the diathesis-stress model .

Diathesis-stress model

The diathesis-stress model of schizophrenia explains the disorder as a combination of genetic and environmental factors. According to this model, biology determines a person’s vulnerability to schizophrenia (biological diathesis), but schizophrenia is only triggered in response to environmental stressors (stress).

So, a person with a high genetic predisposition towards schizophrenia may never develop the disorder (e.g. if they live in a supportive low-stress environment) but a person with a lower genetic disposition may develop schizophrenia if exposed to enough environmental stress (e.g. dysfunctional family upbringing , drug abuse, etc.). In other words, genetic disposition is necessary to developing schizophrenia, but not sufficient by itself.

The diathesis-stress model originated with Meehl (1962) , who proposed the existence of a single ‘schizogene’ – the effects of which are activated in response to stress. However, more recent research (e.g. Ripke et al (2014) ) suggests multiple genes contribute to genetic risk for schizophrenia. Also, ‘stress’ in the diathesis-stress model is not just the emotion – it includes anything that increases the risk of triggering schizophrenia (e.g. drug use, illness, physical trauma, sexual abuse).

Strengths of diathesis-stress model:

• Evidence supporting diathesis-stress model: There is strong evidence for both the genetic and environmental components of schizophrenia. For example, Gottesman’s family studies described above support a role for genetics but schizophrenia concordance rates among identical twins are much less than 100%, demonstrating environmental plays a role too. With regards to the diathesis-stress model specifically, several studies suggest that stress is a key environmental component. For example, a review by Walker et al (2008) found schizophrenia is associated with elevated baseline stress hormones (e.g. cortisol) and that drugs that increase stress hormones worsen schizophrenia symptoms. Further, a meta-analysis by Varese et al (2012) found that stressful events in childhood increase the risk of schizophrenia, further supporting the hypothesis that stress is a key trigger of schizophrenia in those genetically prone.
• Holistic: Rather than reducing schizophrenia to one single cause, the diathesis-stress model accounts for the multitude of factors that contribute to the disorder. This can be seen as a more complete picture of schizophrenia.

Weaknesses of diathesis-stress model:

• Incomplete: Although there is strong evidence supporting the role of both biological diathesis and stress in the development of schizophrenia, the mechanisms through which they cause schizophrenia are not clear.

Interactionist treatment of schizophrenia

Interactionist treatment approaches to schizophrenia tackle the disorder from multiple angles.

For example, a patient may be given antipsychotic drug therapy (a biological approach to treatment) in combination with cognitive behavioural therapy (a psychological approach to treatment). In general, research suggests such interactionist approaches are more effective than either treatment in isolation.

Although interactionist treatment approaches seem to be most effective, there is no one-size-fits-all solution. For example, family therapy will be more beneficial to a schizophrenic patient who was raised in a dysfunctional family environment , and the most suitable antipsychotic drug therapy for each patient will vary depending on efficacy and side effects. Costs are another factor to consider: It might not be economically viable to provide all schizophrenic patients with every possible treatment option.

Strengths of interactionist treatment approaches:

• Evidence supporting interactionist treatment approaches: Several studies suggest combination therapy is more effective than monotherapy. For example, Xiong et al (1994) randomly allocated 63 schizophrenic patients to either a drug therapy group or a drug therapy plus family therapy group. After one year, relapse rates were lower in the drug therapy plus family therapy group (33%) compared to the drug therapy only group (61%). These findings are supported by a study of 103 schizophrenic patients conducted by Hogarty et al (1986) , who reported relapse rates of 19% among patients treated with drug therapy plus family therapy compared to 41% for patients treated with drug therapy alone. Further, Sudak (2011) describes how cognitive behavioural therapy makes patients more likely to adhere to drug therapy because it helps the patient rationally understand the benefits of doing so. This suggests antipsychotic drug therapy plus cognitive behavioural therapy will be more effective than drug therapy alone.
• Holistic: There are both biological and psychological components to schizophrenia, but interactionist approaches treat both. This is a more complete approach to treatment, which might explain why interactionist approaches are more effective. For example, antipsychotic drugs may address the chemical imbalances of schizophrenia while cognitive behavioural therapy addresses the irrational thought processes.

Weaknesses of interactionist treatment approaches:

• Increased costs: Interactionist treatment approaches will be more expensive than monotherapy because you have to pay for multiple treatments (e.g. CBT , family therapy , and antipsychotic drugs ) rather than just one. However, if interactionist treatment approaches lead to lower relapse rates than monotherapy, this may save money in the long run because it prevents further costs to the health service down the line.
• Conflicting evidence: Some studies raise questions as to whether some interactionist approaches to therapy really are more effective than monotherapy. For example, Jauhur’s meta analysis described in the AO3 points for CBT above questions whether CBT really is an effective treatment for schizophrenia. If CBT is not an effective treatment for schizophrenia, then CBT+antipsychotic drug therapy is unlikely to be any more effective than antipsychotic drug therapy alone.

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Example Answers for Schizophrenia: A Level Psychology, Paper 3, June 2019 (AQA)

Last updated 23 Dec 2019

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Here are some example answers to the two Paper 3 questions on Schizophrenia in the 2019 AQA exams.

Question 13

One reason is that a volunteer sample has been used and it is possible that the members of the self-help group with schizophrenia who volunteered had better language ability then most people with schizophrenia. This means it would not be appropriate to generalise the findings to all people with schizophrenia. This study could be modified by using a random sample of people diagnosed with schizophrenia, as this should produce a less biased and more representative sample, meaning that the findings could be generalised more widely.

Question 14

The interactionist approach considers the combined effects of biological, psychological and social factors on the development of schizophrenia. The most well-known is the diathesis-stress model which was first proposed by Meehl (1962) who suggested that the diathesis (vulnerability) was entirely genetic and the result of a single ‘schizogene’. He said that if a person did not have the gene, they would not be able to develop schizophrenia, regardless of much stress they were exposed to. However, if someone did have the gene, then chronic stress through childhood and adolescence, maybe as a result of having a ‘schizophrenogenic mother’, would trigger the gene and result in schizophrenia.

However, Meehl’s original model has been criticised for being too simplistic and has now been revised to account for the discovery that schizophrenia is a polygenetic condition and there is no single ‘schizogene’. It is also accepted that a range of factors can cause the predisposition or diathesis, and these include physical and psychological trauma that effect the developing brain. In addition, the range of stressors that can trigger schizophrenia has been widened to include cannabis use, as it appears to increase the risk of developing schizophrenia by up to 7 times. Evidence to support this comes from research by Brzustowicz et al. which found early trauma, defined as a threat to physical, emotional or sexual integrity at or younger than 19 years, was significantly associated with the expression of schizophrenia in families demonstrating genetic predisposition to schizophrenia.

Further evidence to support the interactionist approach to explaining schizophrenia comes from Tienari et al. who investigated the combination of genetic vulnerability and parenting style in children adopted from Finnish mothers with schizophrenia. The adoptive parents were assessed for child-rearing style and the rates of schizophrenia were compared to those in a control group of adoptees without any genetic risk. They found that a child rearing style with high levels of criticism and conflict and low levels of empathy appeared to be associated with developing schizophrenia but only for the children with high genetic risk. This supports the interactionist explanation that both genetic vulnerability and family-related stress are important in the development of schizophrenia.

The interactionist approach to treatment involves combining anti-psychotic medication (either typical or atypical) with a psychological therapy, most commonly CBT. The antipsychotic medication will reduce the activity of dopamine, while the CBT will help those with schizophrenia to identify negative thoughts and try to change them. This is standard practice in the UK, however in the USA it has been slower to be accepted. This is despite there being evidence to show that combining treatments is more effective than using them alone. For example, Tarrier et al. randomly allocated patients to either a medication plus CBT group, a medication plus supportive counselling group and a control group who just took medication. They found that patients in the two combination groups showed lower levels of symptoms than those in the control group, although there was no difference in hospital readmissions. This could be due to patients stopping their medication because of the side effects. This evidence suggests that taking an interactionist approach to treatment is beneficial and reduces suffering. However, the fact that combining treatment works does not necessarily mean that the interactionist approach is correct. Suggesting that it does could actually be an error known as the treatment causation fallacy.

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Schizophrenia: negative symptoms of schizophrenia, schizophrenia: comorbidity, schizophrenia: culture, schizophrenia: gender bias, schizophrenia: what is schizophrenia, schizophrenia: reliability and validity, our subjects.

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A-Level AQA Psychology - Psychology in Context

Schizophrenia, classification of schizophrenia.

Schizophrenia is a severe mental disorder which occurs in around 1% of the population. It is more commonly found in men, more common in urban environments, and more common in working-class populations. Schizophrenia is classified (the grouping of symptoms into categories) according to symptoms listed in diagnostic manuals- the two main ones used are the ICD-10 (International Classification of Disease, edition 10) and the DSM-5 (Diagnostic and Statistical manual of Mental Disorders, edition 5). According to the DSM, one ‘positive symptom’ needs to be present. According to the ICD, two ‘negative symptoms’ are sufficient. Therefore, there are slight differences with how it is classified.

Positive symptoms: Refer to an excess of usual functioning; an ‘added’ behaviour or experience. For example, hallucinations are additional sensory experiences such as hearing voices, seeing things that aren’t there, or seeing images in a distorted way. Delusions are irrational beliefs, for example delusions of persecution are thoughts that the sufferer is being watched, monitored or controlled by outside forces. Delusions of grandeur involve the belief that the sufferer is an important historical figure. Some delusions can lead to aggressive acts, but it is far more common for sufferers to be victims of violence.

Negative symptoms: Refer to a loss of usual functioning. For example, avolition is the reduction of goal-directed activity, manifested as a lack of motivation and drive, making it difficult to go to work, maintain personal hygiene, or get out of bed. Speech poverty (‘alogia’) refers to changes in speech patterns, usually a reduction in the amount and quality of speech. Speech disorganisation involves incoherence and suddenly changing topic mid-sentence (disorganisation is classified in the DSM-5 as a positive symptom).

Reliability & Validity

Reliability: This refers to consistency of diagnosis. Inter-rater reliability is the extent to which different assessors will arrive at the same conclusion when diagnosing the same patient. If schizophrenia is diagnosed inconsistently, this could be problematic, as it may be over or under-diagnosed by psychiatrists, meaning patients will be incorrectly labelled as ‘schizophrenic’, or not diagnosed, meaning they won’t receive the treatment they need.

Validity: The extent to which the classification of ‘schizophrenia’ is a true reflection of the illness the patient is suffering from (does it measure what it intends to measure?). Criterion validity is the extent to which using different classification systems produces the same diagnosis in the same patient. If there are differences here, then it suggests there is a lack of agreement over what schizophrenia actually is. This issue is also made problematic by:

• Co-morbidity: The presence of two different disorders at the same time. If this is common, it may be that the two disorders are actually one disorder, and perhaps should be seen as one condition (for example, schizophrenia and depression).
• Symptom overlap: When two or more disorder share some of the symptoms needed for classification. Schizophrenia and bipolar disorder share many symptoms (such as delusions and avolition), meaning that the same patient could receive two different diagnoses. As with co-morbidity, if disorders share many symptoms it may be more helpful to see them as one disorder.

Evaluation:

• Cheniaux et al (2009) found that inter-rater reliability amongst two psychiatrists was low. One diagnosed 26 out of 100 patients with schizophrenia using the DSM, and 44 out of 100 using the ICD. The other diagnosed 13 using the DSM and 24 using the ICD. This supports that the classification and diagnosis of the disorder is lacking in reliability and validity.
• Buckley et al (2009) found that 50% of schizophrenia patients also had a diagnosis of depression, 29% had a post-traumatic stress diagnosis, and 23% had an OCD diagnosis. This supports that there are problems with validity, namely the issue of co-morbidity.
• There is gender and cultural bias present in the diagnosis of schizophrenia. Men are far more likely to be diagnosed, potentially because women are able to cope better with the symptoms, and people of African origin are also more likely to be diagnosed. Perhaps this is due to the cultural significance of ‘hearing voices’, which may be seen by white Western psychiatrists as unusual or bizarre. These factors support that the classification of schizophrenia lacks validity and reliability.

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• Created on: 25-01-19 17:27
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AQA A Level Psychology Schizophrenia essay plans

Subject: Psychology

Age range: 16+

Resource type: Assessment and revision

Last updated

10 April 2021

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These are all A Level Psychology essay plans for Schizophrenia. This includes AO1 and AO3. This is from the most recent specification (2015)

Topics include: classification and diagnosis, biological explanation and treatment, psychological explanation and treatment, cognitive explanation and the interactionist approach.

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AQA Psychology A Level paper 3 essay plan

These are essay plans for AQA A Level Psychology essay plans paper 3. The topics are: Schizophrenia, Forensic Psychology and Relationships.

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