OxfordAQA International A-level Psychology (9685): 3.3.2 Schizophrenia – Study Guide

This guide covers section 3.3.2 Schizophrenia in the OxfordAQA International AS and A-level Psychology (9685) specification, Version 3.1 (International A-level exams May/June 2020 onwards). The section sits in Unit 3: Advanced topics and research methods 2. The specification says Unit 3 is a 1 hour 30 minute written exam worth 90 marks and 30% of the International A-level, and that Section B, Schizophrenia, carries 30 marks of compulsory questions.

Use it with the schizophrenia revision notes and the schizophrenia practice questions. The 9685 course hub and 9685 checklist show the rest of the course. Neurotransmitters and the synapse come from the Unit 2 biopsychology guide, and the cognitive approach to depression from the Unit 1 introductory topics guide.

Coverage table

Syllabus reference	What you must know or be able to do (from the document)	Where assessed
3.3.2 bullet 1	Symptoms: positive symptoms, including hallucinations and delusions; negative symptoms, including speech poverty and avolition	Unit 3, Section B
3.3.2 bullet 2	Reliability and validity in the diagnosis of schizophrenia, including reference to culture and gender bias, co-morbidity and symptom overlap	Unit 3, Section B
3.3.2 bullet 3	Biological explanations: genetics and neural correlates, including the dopamine hypothesis	Unit 3, Section B
3.3.2 bullet 4	Cognitive explanations: dysfunctional thought processing	Unit 3, Section B
3.3.2 bullet 5	Therapies: typical and atypical anti-psychotic drugs; cognitive therapy	Unit 3, Section B
3.3 (all Unit 3)	Demonstrate knowledge (AO1), apply it in a range of contexts (AO2), analyse, interpret and evaluate theories, studies and research methods (AO3), and evaluate therapies and treatments	Unit 3

The specification also assesses research methods and mathematical skills in Unit 3, so expect data and study-design questions. Your teacher will confirm question styles and mark tariffs.

Write “a person with schizophrenia”, not “a schizophrenic”: a diagnosis describes a condition, not a whole person.

Symptoms

Schizophrenia is a serious mental disorder in which contact with reality is disrupted. There is no single test; diagnosis rests on observed and reported symptoms.

Key terms

• Positive symptoms: experiences added to normal experience.
• Hallucinations: perceptions with no external stimulus. Hearing voices is the most common type, but they can affect any sense.
• Delusions: firmly held false beliefs that do not change when evidence contradicts them. Examples are delusions of persecution (others are plotting against me), grandeur (I have special powers) and control (my thoughts are being inserted by someone else).
• Negative symptoms: normal abilities that are reduced or lost.
• Speech poverty (alogia): less speech, or speech with little content; brief, empty replies.
• Avolition: a severe loss of motivation to start and keep up goal-directed activity, such as work, study or personal hygiene.

Classification. Clinicians use manuals such as the DSM and the ICD. The specification does not name one; your teacher will confirm which to refer to.

Reliability and validity in diagnosis

Key terms

• Reliability: consistency. Inter-rater reliability means two clinicians give the same diagnosis to the same person. Test-retest reliability means the same clinician gives the same diagnosis on two occasions.
• Validity: accuracy. Is the diagnosis measuring a real, distinct condition? Predictive validity asks whether the diagnosis predicts outcome and response to treatment.
• Co-morbidity: two or more disorders occurring in the same person at the same time.
• Symptom overlap: symptoms shared by different disorders, so the boundary between them is blurred.
• Culture bias: diagnosis distorted by the clinician’s own cultural norms.
• Gender bias: diagnosis distorted by the person’s (or clinician’s) gender rather than their symptoms.

Reliability and validity are taught in depth in Research methods 2.

Evidence

• Rosenhan (1973), published in Science, sent healthy volunteers (“pseudopatients”) to 12 US hospitals claiming to hear voices. Almost all were admitted with a diagnosis of schizophrenia, and stays ranged from 7 to 52 days, averaging 19. In a follow-up, staff at one hospital were told impostors would arrive. Of 193 patients, staff judged 41 to be impostors, although none had been sent. Rosenhan argued diagnosis could not tell the sane from the insane. But the manuals have since been revised, and records uncovered by the journalist Susannah Cahalan cast serious doubt on how the study was run; Scull (2023) called it scientific fraud.
• Cheniaux et al. (2009): two trained psychiatrists independently assessed 100 inpatients using both DSM-IV and ICD-10. Schizophrenia was diagnosed more often under ICD-10 than DSM-IV. The authors linked this to ICD-10 lacking an item that excludes an affective (mood) syndrome. So the manual used changes who gets the diagnosis, which questions validity. Agreement between the manuals was lowest for schizoaffective disorder.
• Luhrmann et al. (2015) interviewed 20 people meeting criteria for schizophrenia in each of the USA, India and Ghana about their voices. US participants more often reported violent commands and used diagnostic labels. Participants in India and Ghana more often reported rich relationships with their voices. Culture shapes how symptoms are experienced and reported, so a clinician from another culture may misjudge them.
• Loring and Powell (1988): 290 psychiatrists rated two case studies in which only the client’s sex and race varied (some were given no sex or race). Diagnoses changed with the sex and race of both client and psychiatrist, even with clear DSM-III criteria.
• Cotton et al. (2009) audited records of 661 patients with first-episode psychosis in Melbourne. Males had more severe symptoms and lower functioning. If women function better, their schizophrenia may be missed or diagnosed as a mood disorder.
• Buckley et al. (2009) estimated that comorbid depression occurs in about 50% of patients with schizophrenia, and that about 47% have a lifetime diagnosis of substance abuse.

Co-morbidity and symptom overlap

If half of patients also have depression, is schizophrenia one disorder or several? Co-morbidity makes it hard to say which symptoms belong to which condition. Symptom overlap matters too. Hallucinations and delusions can occur in bipolar disorder, and avolition looks like the low motivation of depression. Schizoaffective disorder sits on the boundary, and Cheniaux et al. found the two manuals agreed least on that diagnosis.

Evaluation

• Modern manuals use operational criteria and structured interviews, which improve inter-rater reliability. Reliability alone does not prove validity: two clinicians can agree and both be wrong.
• Most evidence for bias is correlational or uses vignettes. Vignette studies lack mundane realism, because real diagnosis involves meeting the person over time.

Worked example paragraph

Question focus: explain how culture bias may reduce the validity of diagnosis.

Hearing voices is a key positive symptom, but its meaning differs across cultures (knowledge). A clinician trained in one culture may treat a person who hears an ancestor’s guidance as having a hallucination, when in their community this may be an accepted experience (application). Luhrmann et al. (2015) found that people in India and Ghana were more likely than people in the USA to report rich relationships with their voices, so the same symptom label may cover different experiences (analysis). This suggests diagnosis can reflect the clinician’s norms rather than a real disorder, which lowers validity. However, the study used small samples of 20 per country, so the findings may not generalise (evaluation).

Biological explanations: genetics

Risk rises with closeness of relationship, but families share environments too, so twin and adoption studies are needed.

• Hilker et al. (2018) used Danish national registers covering 31,524 twin pairs. Concordance was 33% for identical (MZ) twins and 7% for non-identical (DZ) twins. Heritability was estimated at 79%.
• Tienari et al. (2004) followed children of mothers with schizophrenia-spectrum disorders who were adopted away, and compared them with low-risk adoptees. In high-risk adoptees, poor adoptive-family functioning predicted schizophrenia-spectrum disorder; in low-risk adoptees it did not. This supports a diathesis-stress view: genes set the vulnerability; environment triggers it.
• The Psychiatric Genomics Consortium (Ripke et al., 2014) compared up to 36,989 cases with 113,075 controls and found 108 genetic loci linked to schizophrenia. These included the dopamine D2 receptor gene (DRD2) and genes involved in glutamate signalling. Schizophrenia is polygenic: many genes, each with a small effect.

Evaluation. If schizophrenia were purely genetic, MZ concordance would approach 100%. At 33%, environment must matter. MZ twins may also be treated more alike, inflating MZ concordance.

Biological explanations: neural correlates and the dopamine hypothesis

Neural correlates are brain structures or activity patterns linked with a symptom.

• Juckel et al. (2006) used fMRI on 10 unmedicated men with schizophrenia and 10 matched controls. Patients showed less activity in the ventral striatum when cues predicted a reward. The lower the activity, the more severe their negative symptoms. Low reward anticipation fits avolition.
• Allen et al. (2007) scanned 20 people with schizophrenia (10 with auditory verbal hallucinations, 10 without) and 11 controls as they heard recordings of their own and others’ voices. Those with hallucinations more often judged their own speech to be someone else’s, and showed altered activity in the superior temporal gyrus and anterior cingulate. This links hallucinations to faulty self-monitoring of speech.

The dopamine hypothesis. The original version says positive symptoms come from hyperdopaminergia: too much dopamine activity in subcortical areas, linked to too many or too sensitive D2 receptors. Evidence: drugs that raise dopamine, such as amphetamines, can produce psychotic symptoms; drugs that block D2 receptors reduce them.

Davis et al. (1991) revised the hypothesis. They proposed low dopamine activity in the prefrontal cortex (causing negative symptoms) alongside high activity in mesolimbic pathways (causing positive symptoms). This explains why one disorder can include both kinds of symptom.

Evaluation

• Strengths: drug evidence and genetic findings (DRD2 among the 108 loci) support a role for dopamine.
• Limitations: dopamine changes may follow the illness, or result from long-term medication. Juckel et al. used very small samples. Some patients do not respond to D2-blocking drugs, and drugs that block glutamate receptors (such as ketamine) can also produce symptoms, so glutamate is involved too. The explanation is reductionist: it says little about why stress or family life matter, as Tienari et al. showed.

Worked example paragraph

Question focus: evaluate the dopamine hypothesis.

A strength is that drugs which block D2 receptors reduce positive symptoms, which fits the claim that excess dopamine causes hallucinations and delusions (knowledge and analysis). However, the original hypothesis cannot explain avolition or speech poverty. Davis et al. (1991) addressed this by proposing low prefrontal dopamine alongside high mesolimbic dopamine, so the revised theory covers both symptom types (evaluation). Even so, the fact that drugs work does not show dopamine is the cause (analysis).

Cognitive explanations: dysfunctional thought processing

Frith (1992) argued that symptoms come from faulty information processing. He related many symptoms to a problem of metarepresentation: the ability to reflect on mental states, your own and other people’s.

• Faulty self-monitoring. If you cannot recognise your own inner speech or actions as self-generated, inner speech can be experienced as an external voice (auditory hallucination), and your own thoughts or actions can feel controlled by someone else (delusions of control). Frith (1995) linked positive symptoms such as hallucinations to defects of self-monitoring.
• Faulty willed action. Willed action is starting and controlling deliberate, self-generated behaviour, such as deciding what to say. Frith (1995) linked negative signs such as poverty of speech to defects of willed action.

Evidence

• Frith and Done (1989) gave 23 drug-free acute psychotic patients a motor task designed to cause errors. Patients who reported experiences of alien control were less likely to correct errors without visual feedback. The ability to correct depends on knowing what response you have just made, so this fits faulty central monitoring of action.
• Stirling et al. (2006) tested 30 people with schizophrenia and 18 controls. Patients with more thought disorder did worse on tests of executive function and semantic processing.

Evaluation. The explanation fits specific symptoms and has led to cognitive therapy. But it describes how symptoms happen (proximal causes) rather than why the processing is faulty in the first place (distal causes). Deficits may be a consequence of the disorder or medication. The accounts can combine: faulty self-monitoring may have a neural basis, as Allen et al. (2007) suggest.

Therapies: anti-psychotic drugs

Typical anti-psychotics (first generation), such as chlorpromazine (developed in the 1950s) and haloperidol, are dopamine antagonists: they block D2 receptors, reducing dopamine transmission and positive symptoms.

Atypical anti-psychotics (second generation), such as clozapine, risperidone and olanzapine, act on dopamine and other neurotransmitters such as serotonin. They are generally less likely than potent typical drugs such as haloperidol to cause movement side effects. Whether they help negative symptoms more is debated.

Evidence

• A Cochrane review (Adams et al., 2014) found chlorpromazine reduced relapse compared with placebo over six months to two years, but rated the quality of evidence as very low.
• Kane et al. (1988) studied 268 patients who had not responded to at least three previous drugs. On a pre-set criterion, 30% of those given clozapine improved, against 4% given chlorpromazine. Clozapine improved negative as well as positive symptoms.

Evaluation. Typical drugs can cause movement problems, including tardive dyskinesia (involuntary movements). Clozapine carries a risk of agranulocytosis, a dangerous fall in white blood cells, so patients need regular blood tests. Atypicals can cause weight gain. Side effects reduce adherence, and drugs manage symptoms rather than cure.

Therapies: cognitive therapy

Cognitive therapy (often called CBT for psychosis) is usually given alongside medication. It aims to reduce distress, not necessarily remove symptoms.

• Normalisation: explaining that hearing voices is more common than people think, which reduces fear.
• Reality testing: the therapist and client examine the evidence for a delusional belief and test it.
• Re-attribution: reframing a voice as the person’s own inner speech, which links directly to Frith’s model.
• Coping strategies: for example, distraction or humming when voices are present.

Evidence. Jauhar et al. (2014) pooled randomised trials. The effect on overall symptoms was small (34 studies), smaller on positive symptoms (33 studies) and very small on negative symptoms (34 studies). Effects shrank further in trials where assessors did not know which treatment patients had received.

Evaluation. Cognitive therapy has no physical side effects and gives the person an active role. But it needs insight and motivation, which avolition and some delusions reduce. Combining drugs and cognitive therapy fits the diathesis-stress evidence.

Common errors

• Defining negative symptoms as “bad” symptoms. Negative means a loss of normal function.
• Calling a hallucination a false belief. Hallucinations are perceptions; delusions are beliefs.
• Treating reliability and validity as the same.
• Confusing co-morbidity (two disorders in one person) with symptom overlap (shared symptoms across disorders).
• Using twin concordance as proof that schizophrenia is genetic, without noting the gap from 100%.
• Saying drug evidence proves the cause (the “treatment aetiology fallacy”).

Continue with the revision notes, test yourself with the practice questions, and see the 9685 exam preparation guide.

Official syllabus

OxfordAQA International AS and A-level Psychology (9685) specification, Version 3.1 (International A-level exams May/June 2020 onwards), section 3.3.2 Schizophrenia; Unit 3 details in section 2.3.