AQA A-level Psychology (7182): Paper 3 – Schizophrenia – Study Guide

This guide covers Schizophrenia for AQA A-level Psychology (7182), following the AQA AS and A-level Psychology (7181, 7182) specification, Version 1.4 (1 September 2025), for teaching from September 2025. Schizophrenia is section 4.3.5 of that document, inside section 4.3 Issues and options in Psychology. It is one of the three topics in Option 2, and it is assessed in Section C of Paper 3: Issues and Options in Psychology.

Use the Schizophrenia revision notes to condense this guide, and the Schizophrenia practice questions to test it. The 7182 course hub and the 7182 checklist show the whole course.

Coverage table

Syllabus reference	What you must know or be able to do (from the document)	Where assessed
4.3.5	Positive symptoms, including hallucinations and delusions. Negative symptoms, including speech poverty and avolition.	Paper 3, Section C
4.3.5	Issues in diagnosis: co-morbidity, culture and gender bias and symptom overlap.	Paper 3, Section C
4.3.5	Biological explanations: genetics and neural correlates, including the dopamine hypothesis.	Paper 3, Section C
4.3.5	Psychological explanations: family dysfunction and cognitive explanations, including dysfunctional thought processing.	Paper 3, Section C
4.3.5	Drug therapy: typical and atypical antipsychotics.	Paper 3, Section C
4.3.5	Cognitive behaviour therapy and family therapy as used in the treatment of schizophrenia.	Paper 3, Section C
4.3.5	The importance of an interactionist approach in explaining and treating schizophrenia; the diathesis-stress model.	Paper 3, Section C
4.3	Evaluate therapies and treatments, including in terms of their appropriateness and effectiveness. Research methods and maths skills are also assessed in Paper 3.	Paper 3

How Paper 3 is set out

The specification prints Paper 3 as follows. What’s assessed: “Compulsory content 8 above” (Issues and debates in Psychology) and “Optional content, one from option 1, 9–11, one from option 2, 12–14, one from option 3, 15–17”. Option 2 is 12 Schizophrenia, 13 Eating behaviour and 14 Stress.

It is a written exam of 2 hours, 96 marks in total, 33.3% of A-level. Section A is “multiple choice, short answer and extended writing, 24 marks”. Section C is “one topic from option 2, 12–14 above, multiple choice, short answer and extended writing, 24 marks”. Sections B and D work the same way for options 1 and 3. Which option topics your school teaches is for your teacher to confirm.

The specification says sections B, C and D of Paper 3 contain extended response questions. For Paper 3 it gives approximate weightings of AO1 9–12%, AO2 5–8% and AO3 15–17% of the A-level. So evaluation carries the most weight here.

Symptoms of schizophrenia

Positive symptoms are experiences added to normal functioning. Negative symptoms are the loss or reduction of normal functioning.

• Hallucinations: sensory experiences with no external stimulus. Hearing voices is the best-known example, but any sense can be involved.
• Delusions: firmly held beliefs that are not supported by evidence and that the person keeps despite contrary evidence. Examples include delusions of persecution (being plotted against) and of grandeur (having special powers or importance).
• Speech poverty (alogia): a reduction in the amount and quality of speech, such as brief, empty replies and long delays before answering.
• Avolition: a reduced ability to start and keep up goal-directed activity, such as work, study or self-care.

Worked paragraph. A person with schizophrenia might believe a neighbour is reading their thoughts through the wall (a persecutory delusion). This is a positive symptom because the belief is added to normal experience and is held despite no evidence. If the same person also stops washing and leaves their course, that shows avolition, a negative symptom. Negative symptoms are often harder to spot, because they look like an absence of behaviour rather than an unusual behaviour.

Issues in diagnosis

The specification names four issues.

Co-morbidity is when two or more conditions occur together. Buckley et al. (2009) reviewed research and estimated that around half of people with schizophrenia also have depression and nearly half a substance use disorder, with obsessive-compulsive disorder and post-traumatic stress disorder also common. High co-morbidity raises the question of whether schizophrenia is one condition, and it can complicate treatment.

Symptom overlap is when different conditions share symptoms. Delusions and hallucinations can also occur in bipolar disorder. Avolition and reduced speech can look like depression. If symptoms overlap, two clinicians may reach different diagnoses for the same person.

Culture bias is when diagnosis reflects the clinician’s cultural norms. Luhrmann et al. (2015) interviewed voice-hearers with psychosis in the USA, India and Ghana. US participants more often described voices as violent and hostile. Participants in India and Ghana more often described voices as familiar or even positive. In England, the AESOP study (Fearon et al., 2006) found higher rates of diagnosis among Black Caribbean and Black African groups. Some researchers see this as diagnostic bias. Others point to social adversity and stress. Present both views.

Gender bias is when diagnosis is distorted by the person’s gender. Research often reports more men than women diagnosed. One suggested reason is that women may keep up relationships and daily functioning better, so their symptoms may be noticed less. This is debated, so treat it as an argument to evaluate, not a settled fact.

Evaluation. Diagnosis guides treatment, so a wrong diagnosis may mean unsuitable treatment. But overlap and co-morbidity are partly real features of mental health, not only clinicians’ errors.

Worked paragraph. Symptom overlap is a problem for diagnosing schizophrenia. A clinician who sees a person with a persecutory delusion and low motivation might diagnose schizophrenia, while another might focus on low mood and diagnose depression with psychotic features. This matters because the two diagnoses lead to different treatment plans. However, overlap may show that our categories are too rigid rather than that clinicians are careless.

Biological explanations: genetics

Schizophrenia runs in families. Gottesman (1991) summarised family and twin studies. The risk was about 48% for an identical twin of a person with schizophrenia, about 17% for a non-identical twin, about 9% for a sibling and about 1% in the general population. Risk rises with genetic similarity.

Schizophrenia is polygenic: many genes each add a small amount of risk. Ripke et al. (2014) compared the genomes of tens of thousands of people with and without schizophrenia and identified 108 separate genetic locations linked to it.

Evaluation.

• Strength: family and twin evidence is consistent across many studies.
• Limitation: concordance for identical twins is well below 100%, so genes cannot be the whole cause.
• Limitation: families share environments as well as genes. Twin studies cannot fully separate the two.
• Counter-evidence and nuance: Tienari et al. (2004) studied adopted children in Finland. Children whose biological mothers had a schizophrenia-spectrum diagnosis were more likely to develop schizophrenia-spectrum disorders mainly when their adoptive family was rated as dysfunctional. This supports genes as a vulnerability, not destiny.

Biological explanations: neural correlates and dopamine

A neural correlate is a pattern of brain structure or activity linked to a symptom. It is a correlation, so it does not show cause.

The original dopamine hypothesis proposed hyperdopaminergia: too much dopamine activity in subcortical areas (such as pathways to the striatum). This was linked to positive symptoms. Evidence came from amphetamines, which raise dopamine activity and can produce psychotic symptoms, and from antipsychotics, which block dopamine D2 receptors and reduce positive symptoms.

The revised dopamine hypothesis (Davis et al., 1991) added hypodopaminergia: too little dopamine activity in the prefrontal cortex. This was linked to negative symptoms such as avolition. Howes and Kapur (2009) later argued that dysregulated dopamine is a “final common pathway” that many other risk factors lead to.

Other neural correlates include enlarged ventricles in some people with schizophrenia. Juckel et al. (2006) found lower activity in the ventral striatum when people with schizophrenia anticipated a reward, and this was linked to negative symptoms. Mechelli et al. (2007) found differences in connections between the left superior temporal cortex and anterior cingulate cortex in people with auditory hallucinations when they judged whether recorded speech was their own.

Evaluation.

• Strength: the hypothesis explains why antipsychotics that block dopamine reduce positive symptoms.
• Limitation: this is treatment-aetiology reasoning. A drug working does not prove the cause.
• Limitation: other neurotransmitters, especially glutamate, are also implicated.
• Limitation: some people do not respond to dopamine-blocking drugs, which suggests dopamine is not the full story for everyone.

Worked paragraph. The dopamine hypothesis is supported by the effects of drugs. Amphetamines increase dopamine activity and can produce hallucinations and delusions in people without schizophrenia. Antipsychotics block D2 receptors and reduce positive symptoms. However, this evidence is indirect. It shows that dopamine can change symptoms, not that dopamine started the disorder. The fact that glutamate is also involved suggests a reductionist single-neurotransmitter account is incomplete.

Psychological explanations: family dysfunction

Family dysfunction means patterns of family interaction that may raise risk or relapse.

• Schizophrenogenic mother (Fromm-Reichmann, 1948): a cold, rejecting and controlling mother was said to create tension and distrust. This idea is now heavily criticised and has little support.
• Double-bind theory (Bateson et al., 1956): a child receives contradictory messages, such as words of love with a rejecting manner, and is punished for any response. Bateson suggested this could lead to confused thinking.
• Expressed emotion (EE): a family’s level of criticism, hostility and emotional over-involvement. Brown, Birley and Wing (1972) found higher relapse rates in people who returned to high-EE homes. EE is strongest as an explanation of relapse, not onset.

Evaluation.

• Strength: EE research led to family therapy, which has evidence of reducing relapse.
• Limitation: the early theories relied on clinical impressions, not controlled data.
• Ethical and social sensitivity: blaming parents can add guilt and distress to families who are often the main carers.
• Direction of causality: living with a person with severe symptoms may raise family stress, rather than family stress causing the symptoms.

Psychological explanations: cognitive

Cognitive explanations focus on dysfunctional thought processing. Frith (1992) proposed two faulty processes.

• Metarepresentation: the ability to reflect on your own thoughts and recognise them as your own. If this fails, a person may experience their own inner speech as an external voice (hallucination), or their own thoughts as inserted (a delusion).
• Central control: the ability to suppress automatic responses while carrying out a deliberate action. If this fails, word associations may break into speech, giving derailed or disorganised speech.

Stirling et al. (2006) found people with schizophrenia were much slower than a control group on the Stroop task, where you name the ink colour of a colour word. This fits weak central control.

Evaluation.

• Strength: lab tasks give objective evidence of differences in processing.
• Limitation: it describes how symptoms work more than where the faulty processing comes from. It sits well alongside biological explanations.
• Strength: it led directly to CBT for psychosis.

Drug therapy

Typical antipsychotics, such as chlorpromazine and haloperidol, were introduced from the 1950s. They are dopamine antagonists: they block D2 receptors and reduce dopamine activity, which reduces positive symptoms.

Atypical antipsychotics, such as clozapine and risperidone, came into wide use later. They also act on dopamine but often affect other systems too, such as serotonin. Clozapine is used when other drugs have not worked, but it can cause a serious fall in white blood cells, so people taking it need regular blood tests.

Evaluation.

• Effectiveness: Leucht et al. (2013) compared 15 antipsychotics across 212 trials. Every drug did better than placebo, and clozapine ranked most effective for overall symptoms.
• Side effects: typical drugs are linked with movement problems such as tardive dyskinesia. Some atypicals, such as clozapine and olanzapine, are linked with weight gain.
• Appropriateness: drugs act quickly and can allow people to engage in therapy. Critics argue drugs may sometimes be used to manage behaviour rather than help the person. Present both views.

CBT and family therapy

CBT for psychosis usually runs over several sessions. The therapist helps the person trace where their beliefs and voices come from, then tests beliefs against evidence (reality testing) and builds coping strategies. The aim is often to reduce distress, not to remove every symptom.

Jauhar et al. (2014) reviewed 34 trials and found CBT had a small effect on symptoms. The effect shrank further in trials where assessors did not know which treatment people had received.

Family therapy works with the person and their family. It aims to reduce expressed emotion, improve communication, build problem-solving skills and help families understand the condition. Pharoah et al. (2010), a Cochrane review of 53 trials, found family intervention may reduce relapse and hospital admission and help people keep taking medication, though poor trial quality may overstate this.

Evaluation. Both therapies are usually given alongside medication, so isolating their effect is hard. They need trained staff and time, and a person with severe symptoms may need medication before they can take part. NICE guidance in England recommends offering both CBT and family intervention to people with psychosis or schizophrenia.

The interactionist approach and the diathesis-stress model

An interactionist approach explains schizophrenia through the combined effect of biological, psychological and social factors. The diathesis-stress model says a person develops schizophrenia when a vulnerability (diathesis) meets a trigger (stress).

• Meehl (1962) proposed the diathesis was a single gene (“schizogene”). Modern research suggests many genes, and possibly early trauma, can create vulnerability.
• Stressors can include stressful life events, a high-EE home and heavy cannabis use.

In treatment, the interactionist approach means combining drugs with CBT and family therapy.

Evaluation.

• Strength: Tienari et al. (2004) support it directly: genetic risk mattered mainly in dysfunctional adoptive families.
• Strength: it fits the evidence that no single factor explains all cases.
• Limitation: it is harder to test than a single-cause model. It is not clear how diathesis and stress combine.

Worked paragraph. The diathesis-stress model explains why only some people with high genetic risk develop schizophrenia. In Tienari et al.’s adoption study, children with a biological mother who had a schizophrenia-spectrum diagnosis were at higher risk mainly when the adoptive family was dysfunctional. This suggests the family environment acted as the stressor that triggered a genetic vulnerability. This links to the nature-nurture debate, as it supports an interactionist position rather than either extreme.

Common errors

• Saying positive symptoms are “good” symptoms. Positive means added to experience.
• Calling avolition “laziness”. It is reduced ability to start and persist with goal-directed activity.
• Saying the dopamine hypothesis is “proven” because drugs work. That is treatment-aetiology reasoning.
• Describing EE as the cause of schizophrenia. The strongest evidence links it to relapse.
• Listing diagnosis issues without explaining why each makes diagnosis less accurate.
• Writing “schizophrenics”. Use “people with schizophrenia”.

Read the Paper 1 Introductory topics guide for CBT and drug therapy in other disorders, the Approaches in Psychology guide for the biological and cognitive approaches, and the Issues and debates guide for reductionism and nature-nurture.

Official syllabus

AQA AS and A-level Psychology (7181, 7182) specification, Version 1.4 (1 September 2025), for teaching from September 2025. Schizophrenia is section 4.3.5; the Paper 3 structure appears in the specification at a glance.