AQA A-level Psychology (7182): Paper 3 – Schizophrenia – Revision Notes

For full explanations and worked paragraphs, start with the Schizophrenia study guide.

These notes cover Schizophrenia for AQA A-level Psychology (7182), from the AQA AS and A-level Psychology (7181, 7182) specification, Version 1.4 (1 September 2025), for teaching from September 2025. The content is section 4.3.5 of that document. It is an Option 2 topic, assessed in Section C of Paper 3: Issues and Options in Psychology, which the specification describes as “one topic from option 2, 12–14 above, multiple choice, short answer and extended writing, 24 marks”.

Test yourself afterwards with the Schizophrenia practice questions. The 7182 course hub and the 7182 checklist track the rest of the course.

Paper 3 in one box

• Written exam, 2 hours, 96 marks, 33.3% of A-level.
• What’s assessed: “Compulsory content 8 above” (Issues and debates) and “Optional content, one from option 1, 9–11, one from option 2, 12–14, one from option 3, 15–17”.
• Option 2 topics: 12 Schizophrenia, 13 Eating behaviour, 14 Stress.
• Approximate A-level weightings for Paper 3: AO1 9–12%, AO2 5–8%, AO3 15–17%. Evaluation (AO3) carries the most weight.
• Section 4.3 also expects you to “evaluate therapies and treatments including in terms of their appropriateness and effectiveness”. Research methods and maths skills are assessed in Paper 3 too.

Key terms

Term	Definition
Positive symptom	An experience added to normal functioning, such as hallucinations or delusions.
Negative symptom	A loss or reduction of normal functioning, such as speech poverty or avolition.
Hallucination	A sensory experience with no external stimulus, such as hearing a voice nobody else hears.
Delusion	A firmly held belief not supported by evidence and kept despite contrary evidence.
Speech poverty	Reduced amount and quality of speech; brief, empty replies.
Avolition	Reduced ability to start and keep up goal-directed activity.
Co-morbidity	Two or more conditions occurring in the same person at the same time.
Symptom overlap	Different conditions sharing the same symptoms, making them hard to tell apart.
Culture bias	Diagnosis distorted by the clinician’s own cultural norms.
Gender bias	Diagnosis distorted by the person’s gender.
Polygenic	Risk comes from many genes, each with a small effect.
Neural correlate	A brain structure or activity pattern linked to a symptom (correlation, not cause).
Hyperdopaminergia	Excess dopamine activity, in subcortical areas in the original hypothesis.
Hypodopaminergia	Too little dopamine activity, in the prefrontal cortex in the revised hypothesis.
Expressed emotion (EE)	A family’s level of criticism, hostility and emotional over-involvement.
Double bind	Contradictory messages from a carer, with the child unable to respond safely to either.
Metarepresentation	The ability to reflect on your own thoughts and recognise them as yours.
Central control	The ability to suppress automatic responses during deliberate actions.
Typical antipsychotic	An older drug, such as chlorpromazine, that blocks dopamine D2 receptors.
Atypical antipsychotic	A later drug, such as clozapine, that acts on dopamine and other systems, such as serotonin.
Diathesis-stress model	Disorder develops when a vulnerability (diathesis) meets a trigger (stress).

Theories and studies at a glance

Who	What	Finding	One evaluation point
Buckley et al. (2009)	Review of co-morbidity	About half of people with schizophrenia also had depression; nearly half a substance use disorder	Raises doubt that schizophrenia is one distinct condition
Luhrmann et al. (2015)	Interviews with voice-hearers in the USA, India and Ghana	US voices more often violent; India and Ghana voices more often familiar or positive	Culture shapes symptoms, so one set of criteria may not fit all
Fearon et al. (2006), AESOP	Rates of diagnosis by ethnic group in England	Higher rates among Black Caribbean and Black African groups	Contested: diagnostic bias or social adversity and stress
Gottesman (1991)	Summary of family and twin studies	Risk about 48% identical twin, 17% non-identical twin, 9% sibling, 1% general population	Identical twin concordance below 100%, so not purely genetic
Ripke et al. (2014)	Genome-wide comparison	108 genetic locations linked to schizophrenia	Supports polygenic risk, but each gene adds only a little
Tienari et al. (2004)	Finnish adoption study	Genetic risk mattered mainly when the adoptive family was dysfunctional	Direct support for diathesis-stress
Davis et al. (1991)	Revised dopamine hypothesis	Hypodopaminergia in prefrontal cortex linked to negative symptoms	Explains negative symptoms the original hypothesis missed
Juckel et al. (2006)	Brain scanning during reward anticipation	Lower ventral striatum activity, linked to negative symptoms	Correlational: cannot show cause
Bateson et al. (1956)	Double-bind theory	Contradictory communication may lead to confused thinking	Based on clinical observation, little controlled evidence
Brown, Birley and Wing (1972)	Expressed emotion	More relapse in people returning to high-EE homes	Explains relapse better than onset
Frith (1992)	Dysfunctional thought processing	Faulty metarepresentation and central control	Describes how, not why
Stirling et al. (2006)	Stroop task	People with schizophrenia much slower than controls	Supports weak central control
Leucht et al. (2013)	Comparison of 15 antipsychotics	All beat placebo; clozapine ranked most effective	Side effect profiles differ widely
Jauhar et al. (2014)	Review of CBT trials	Small effect, smaller still in well-masked trials	Questions how effective CBT really is
Pharoah et al. (2010)	Cochrane review of family intervention	May reduce relapse and hospital admission and help people keep taking medication	Usually given with drugs, so effect is hard to isolate
Meehl (1962)	Early diathesis-stress model	Single “schizogene” as the diathesis	Now replaced by polygenic and trauma-based ideas

Must-know distinctions

• Positive vs negative symptoms. Positive means added (hallucinations, delusions). Negative means lost (speech poverty, avolition). Neither word means good or bad.
• Hallucination vs delusion. A hallucination is a perception. A delusion is a belief.
• Co-morbidity vs symptom overlap. Co-morbidity is two conditions present together. Symptom overlap is two different conditions sharing symptoms. Both can lead to misdiagnosis, but for different reasons.
• Original vs revised dopamine hypothesis. Original: too much subcortical dopamine, positive symptoms. Revised: also too little prefrontal dopamine, negative symptoms.
• Typical vs atypical antipsychotics. Typical: older, mainly block D2, more movement side effects. Atypical: later, act on dopamine and other systems, different side effects such as weight gain.
• Onset vs relapse. EE research mainly predicts relapse. Do not use it as proof of cause.
• Explaining vs treating. The interactionist approach applies to both: combined causes and combined treatment.

Mini essay plan

Question style: “Discuss the dopamine hypothesis as an explanation of schizophrenia.” (extended response)

1. AO1, about a third of the answer. Original hypothesis: hyperdopaminergia in subcortical areas, linked to positive symptoms. Revised hypothesis: hypodopaminergia in prefrontal cortex, linked to negative symptoms. Howes and Kapur’s “final common pathway” idea.
2. AO3 point 1. Drug evidence: amphetamines can produce psychotic symptoms; antipsychotics that block D2 reduce positive symptoms. Then the counterpoint: treatment-aetiology reasoning.
3. AO3 point 2. Juckel et al. (2006) on ventral striatum and negative symptoms. Correlation, not cause.
4. AO3 point 3. Glutamate and non-responders: dopamine is not the full story.
5. AO3 point 4, issues and debates. Biological reductionism; the diathesis-stress model offers a fuller account by adding stressors such as family environment.
6. Judgement. Dopamine is a strong part of the explanation, especially for positive symptoms, but best seen as one level within an interactionist account.

Quick self-test

1. Name two positive and two negative symptoms in the specification.
2. What is avolition?
3. Define co-morbidity.
4. Give one example of symptom overlap involving schizophrenia.
5. What did Luhrmann et al. (2015) find?
6. Why does a concordance rate below 100% for identical twins matter?
7. State the difference between the original and revised dopamine hypotheses.
8. What is expressed emotion, and what does it best predict?
9. What does a failure of metarepresentation produce, according to Frith?
10. Why do people taking clozapine need regular blood tests?
11. What did Jauhar et al. (2014) conclude about CBT?
12. What is the diathesis in Meehl’s (1962) model?

Answers

1. Positive: hallucinations, delusions. Negative: speech poverty, avolition.
2. A reduced ability to start and keep up goal-directed activity, such as work or self-care.
3. Two or more conditions occurring together in the same person.
4. Avolition and reduced speech also occur in depression; delusions and hallucinations also occur in bipolar disorder.
5. Voice-hearers in the USA more often described violent, hostile voices; those in India and Ghana more often described familiar or positive voices.
6. Identical twins share all their genes, so if genes were the whole cause, concordance would be 100%. Environment must also play a part.
7. Original: excess subcortical dopamine linked to positive symptoms. Revised: adds too little prefrontal dopamine linked to negative symptoms.
8. A family’s level of criticism, hostility and emotional over-involvement. It best predicts relapse.
9. The person may not recognise their own thoughts or inner speech as their own, so they may experience hallucinations or delusions such as thought insertion.
10. Clozapine can cause a serious fall in white blood cells.
11. CBT has a small effect on symptoms, which shrinks further in trials where assessors are masked.
12. A single gene (the “schizogene”).

Where marks are usually lost

• Defining positive symptoms as “good” rather than added to normal experience.
• Naming a diagnosis issue without explaining how it reduces the accuracy of diagnosis.
• Quoting Gottesman’s figures without saying what they show and what they do not show.
• Writing that antipsychotics “cure” schizophrenia. They reduce symptoms and relapse risk.
• Using EE as evidence for the cause of schizophrenia, when it mainly predicts relapse.
• Describing CBT in general terms (as for depression) with no mention of voices, delusions or reality testing.
• Giving evaluation as one-word labels (“reductionist”) with no explanation of why it matters here.
• In application questions, ignoring the details of the scenario.
• Using stigmatising language such as “schizophrenics” or “split personality”.

For the same therapies applied to other disorders, see the Paper 1 Introductory revision notes. For the biological and cognitive approaches behind these explanations, see the Approaches revision notes. For the debates used in evaluation, see the Issues and debates revision notes. The other Option 2 topics are Eating behaviour and Stress.

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.