Schizophrenia — AQA A-Level Psychology
Test yourself on Schizophrenia with AQA A-Level practice questions.
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Schizophrenia explained
Schizophrenia diagnosis relies on identifying specific symptoms.
Read the full explanation
Positive symptoms add abnormal experiences, including hallucinations (sensory perceptions without external stimuli, like hearing voices) and delusions (irrational beliefs, such as paranoia). Negative symptoms involve the loss of normal functioning, including speech poverty (reduced quality and quantity of speech) and avolition (severe lack of motivation). Diagnosis faces significant reliability and validity issues. Co-morbidity occurs when schizophrenia exists alongside another condition, like depression. Symptom overlap with disorders like bipolar complicates accurate diagnosis. Furthermore, culture bias and gender bias can lead to misdiagnosis based on demographic factors.
Biological explanations for schizophrenia: genetics and neural correlates, including the dopamine hypothesis.
Schizophrenia runs in families. Gottesman pooled twin and family data and found concordance of 48% for identical twins, 17% for fraternal twins and 9% for siblings, against roughly 1% in the population: strong heritability, but short of the 100% a purely genetic condition would give. It is polygenic; Ripke's genome study found over a hundred variations, several coding for glutamate rather than dopamine. Neural correlates are brain measures that travel with symptoms: Juckel found low ventral striatum activity tracking negative-symptom severity, Allen reduced activation in the superior temporal gyrus in patients who hallucinated. The dopamine hypothesis blames excess subcortical dopamine for positive symptoms; Davis added low prefrontal dopamine for negative ones.
Psychological explanations for schizophrenia: family dysfunction and cognitive explanations, including dysfunctional thought processing.
These explanations put the cause in relationships and in thinking rather than in the brain. Fromm-Reichmann described the schizophrenogenic mother, cold and controlling, creating a family climate of tension and secrecy that breeds distrust and then paranoid delusion. Bateson's double bind traps a child in contradictory messages punished by withdrawn love, so the world comes to seem dangerous. Expressed emotion, meaning criticism, hostility and emotional over-involvement in relatives, is a stressor that predicts relapse rather than onset, roughly doubling relapse rates. Frith names two faults in thought: metarepresentation, our ability to recognise thoughts as our own, whose failure gives voices and thought insertion, and central control, whose failure derails speech. Stirling found patients took twice as long on the Stroop task.
Drug therapy: typical and atypical antipsychotics.
Antipsychotics dampen the dopamine system; they manage symptoms and do not cure. Typical drugs such as chlorpromazine, in use since the 1950s, are dopamine antagonists that block dopamine receptors in the synapse, and within days that reduces hallucinations and delusions. Chlorpromazine is also a powerful sedative acting on histamine receptors, which is why it calms a newly admitted patient. Atypicals act more widely: clozapine works on serotonin and glutamate too, so it lifts mood and is prescribed where a patient is suicidal, while risperidone binds more tightly and so works at lower doses with fewer side effects. Thornley's review found chlorpromazine beat placebo on symptom severity. The costs are real, from tardive dyskinesia to fatal neuroleptic malignant syndrome.
Cognitive behaviour therapy and family therapy as used in the treatment of schizophrenia.
Cognitive behaviour therapy (CBT) for schizophrenia involves 5 to 20 sessions aiming to identify and alter irrational thoughts, such as delusions, by evaluating evidence for these beliefs. For example, a patient might test the reality of auditory hallucinations through collaborative empiricism and normalisation. Family therapy focuses on reducing stress within the home environment, specifically targeting high expressed emotion (EE) like hostility, criticism, and emotional over-involvement. By improving family communication and problem-solving skills, it lowers relapse rates. Neither therapy cures schizophrenia, but both equip patients and families with coping mechanisms to manage symptoms, reduce distress, and improve daily functioning.
The importance of an interactionist approach in explaining and treating schizophrenia; the diathesis-stress model.
Neither biology nor environment on its own predicts who becomes ill, so the interactionist view says a vulnerability has to meet a trigger. Meehl's original model made the diathesis a single gene: without it, no amount of stress could produce schizophrenia, while a carrier under chronic stress might. Modern versions widen both halves. Ripke's work replaces the single gene with many, and Read argues early trauma is itself a diathesis because it leaves the stress-response system permanently over-reactive. Stress is now anything that risks triggering onset, including cannabis, which disturbs dopamine and raises risk several times over. Treatment follows the same logic: Tarrier allocated patients to medication with CBT, medication with counselling, or medication alone, and the combined groups showed lower symptom levels.
Your focus
- Differentiate between the positive and negative symptoms of schizophrenia.
- Explain how co-morbidity and symptom overlap affect the validity of diagnosis.
- Analyse the impact of culture and gender bias on the reliability of diagnosing schizophrenia.
Show all 23 objectives
- Describe Gottesman's concordance figures for identical twins, fraternal twins and siblings against population risk.
- Explain the original and revised dopamine hypothesis, stating where dopamine is too high and where too low.
- Apply the difference between a correlate and a cause to Juckel's ventral striatum finding on negative symptoms.
- Evaluate the genetic explanation given concordance of 48% rather than 100% in twins who also share an environment.
- Describe the schizophrenogenic mother and the double bind as two family accounts of disordered thinking.
- Explain why expressed emotion predicts relapse rather than onset, and what counts as high expressed emotion.
- Explain Frith's metarepresentation and central control faults and which symptom each of them produces.
- Apply central control dysfunction to explain why patients took twice as long as controls on Stirling's Stroop task.
- Evaluate family dysfunction explanations as socially sensitive accounts that blame parents on retrospective evidence.
- Explain how typical antipsychotics act as dopamine antagonists and why that reduces positive symptoms.
- Describe how clozapine and risperidone differ from typical drugs in the receptors acted on and the dose needed.
- Apply the side effect profile to justify prescribing clozapine to a suicidal patient despite the blood tests needed.
- Evaluate drug therapy using Thornley's placebo comparison against tardive dyskinesia and neuroleptic malignant syndrome.
- Describe the aims and techniques of cognitive behaviour therapy in treating schizophrenia.
- Explain how family therapy reduces expressed emotion to prevent relapse in patients with schizophrenia.
- Evaluate the effectiveness and appropriateness of psychological therapies for schizophrenia.
- Explain the diathesis-stress model as a vulnerability needing a trigger, using Meehl's original single-gene version.
- Describe how the modern model widens the diathesis to polygenic and traumatic and stress to include cannabis.
- Apply the model to explain why a highly vulnerable person who meets no trigger does not become ill.
- Evaluate combined treatment using Tarrier's three-group trial and the treatment-causation fallacy.
Schizophrenia exam tips
Marking Points
- Distinguish between positive symptoms (atypical additions to normal experience) and negative symptoms (atypical losses of normal functioning).
- Define hallucinations as sensory perceptions without external stimuli and delusions as fixed false beliefs.
- Define speech poverty (alogia) as a reduction in speech output and avolition as a lack of goal-directed behaviour.
- Explain how co-morbidity and symptom overlap challenge the validity of schizophrenia as a distinct psychiatric disorder.
- Discuss how culture bias (e.g., hearing voices being culturally acceptable in some societies) and gender bias affect diagnostic reliability.
- Family studies show risk rising with genetic similarity: Gottesman reports about 48% concordance for monozygotic twins, 17% for dizygotic twins and 9% for siblings against about 1% population risk.
- Schizophrenia is polygenic and aetiologically heterogeneous: Ripke et al. pooled genome-wide data and identified over a hundred candidate variations, so different combinations of genes can produce the same diagnosis.
- Adoption studies such as Tienari separate genes from upbringing, and the raised risk in adopted-away children of affected mothers supports a genetic diathesis.
- Neural correlates are measurements of brain structure or activity that correlate with symptoms: enlarged ventricles and reduced grey matter are structural, and activity levels in the ventral striatum and temporal lobe are functional.
- Juckel et al. found low activity in the ventral striatum, part of the reward system, correlating with the severity of negative symptoms such as avolition.
- Allen et al. found lower activation in the superior temporal gyrus and anterior cingulate in patients who experienced auditory hallucinations, linking hallucination to the speech-processing areas.
- The original dopamine hypothesis: hyperdopaminergia in subcortical mesolimbic pathways is used to explain positive symptoms such as hallucinations and delusions.
- The revised hypothesis (Davis): hypodopaminergia in the prefrontal cortex accounts for negative and cognitive symptoms, so both too much and too little dopamine matter, in different places.
- Supporting evidence is drug-based: amphetamines raise dopamine and produce psychosis-like symptoms, antipsychotics lower dopamine activity and reduce symptoms, and L-dopa given for Parkinson's can produce similar effects.
- Family dysfunction explanations claim abnormal communication and relationships within the family cause or maintain the disorder.
- The schizophrenogenic mother (Fromm-Reichmann) is cold, rejecting and controlling, and creates a family climate of tension and secrecy that leads to distrust and paranoid delusions.
- The double bind (Bateson) is a child receiving contradictory messages with no way to comment on them and punishment by withdrawal of love; the child comes to see the world as confusing, which shows in disorganised thinking and paranoid delusions. Bateson called it a risk factor, not the cause.
- Expressed emotion is verbal criticism, hostility and emotional over-involvement in a relative; it is a source of stress that raises the chance of relapse in a recovering patient, with high-EE homes roughly doubling relapse compared with low-EE homes.
- Cognitive explanations locate the problem in dysfunctional thought processing rather than in the family.
- Metarepresentation dysfunction (Frith): metarepresentation is the ability to reflect on thoughts and behaviour as one's own, so its disruption means a patient hears their own inner speech as an external voice, and experiences thought insertion.
- Central control dysfunction (Frith): central control is the ability to suppress automatic responses while performing deliberate ones, so its disruption means each word triggers unsuppressed associations and speech derails.
- Stirling et al. supported central control dysfunction: patients took about twice as long as controls on the Stroop test, where an automatic response must be suppressed.
- Antipsychotics are the main treatment, taken in the short term to calm an acute episode or in the long term to prevent relapse, and they reduce symptoms rather than cure the condition.
- Typical antipsychotics such as chlorpromazine are dopamine antagonists: they block dopamine receptors in the synapse, reducing dopamine action, which fits the original dopamine hypothesis and reduces positive symptoms.
- Chlorpromazine has a strong sedative effect through histamine receptors, so it is used to calm patients on admission, and dosage has fallen over time from the very high levels used in the past.
- Atypical antipsychotics such as clozapine also act on serotonin and glutamate receptors, which improves mood and reduces anxiety and depression, and clozapine is prescribed where a patient is at risk of suicide.
- Risperidone is a more recent atypical that binds more strongly to dopamine receptors, so it is effective in smaller doses and produces fewer side effects than typical drugs.
- Typical drugs carry serious side effects: weight gain, dizziness, sleepiness, and tardive dyskinesia, the involuntary facial movements caused by dopamine supersensitivity.
- Neuroleptic malignant syndrome is a rare but potentially fatal reaction causing high temperature, delirium and coma; clozapine can cause agranulocytosis, so patients need regular blood tests.
- Thornley et al.'s review of chlorpromazine trials found better overall functioning and reduced symptom severity compared with placebo, and Meltzer concluded clozapine is more effective than typical drugs and helps a substantial minority of treatment-resistant patients.
- CBT helps patients identify irrational thoughts and reality-test their hallucinations or delusions.
- CBT uses techniques like normalisation to reduce anxiety associated with psychotic symptoms.
- Family therapy aims to reduce levels of expressed emotion (EE), specifically criticism, hostility, and emotional over-involvement.
- Family therapy improves communication and problem-solving skills within the family unit to prevent relapse.
- Evaluation points often focus on the appropriateness of psychological therapies, noting they require active engagement which may be difficult for severely ill patients.
- The interactionist approach acknowledges biological, psychological and societal factors together, rather than treating schizophrenia as purely genetic or purely environmental.
- Diathesis means vulnerability and stress means a negative experience that triggers it: both are needed, so a vulnerable person who meets no trigger does not develop the disorder.
- Meehl's original model: the diathesis was entirely genetic, a single "schizogene" producing a schizotypic personality, and chronic stress, including a schizophrenogenic mother, could trigger it in a carrier only.
- The modern diathesis is polygenic, following Ripke, and psychological as well as genetic: Read's neurodevelopmental model treats early childhood trauma as a diathesis that leaves the HPA axis over-active.
- The modern definition of stress is anything that raises the chance of triggering the disorder, which need not be psychological: cannabis use is a stressor because it interferes with the dopamine system, and risk rises with dose.
- Treatment under an interactionist model combines antipsychotic medication with psychological therapy, most often CBT, rather than choosing between them.
- Tarrier et al. randomly allocated patients to medication plus CBT, medication plus supportive counselling, or medication alone; both combination groups showed lower symptom levels, though there was no difference in hospital readmission.
- The treatment-causation fallacy: because a drug helps does not prove a biological cause, so combining therapies does not require a decision about which explanation is right.
Examiner Tips
- 💡Provide specific examples of delusions (e.g., delusions of grandeur) and hallucinations (e.g., auditory) to demonstrate clear understanding.
- 💡Use the concepts of reliability (consistency of diagnosis) and validity (accuracy of diagnosis) to structure evaluation paragraphs on diagnostic issues.
- 💡When discussing culture bias, reference specific cultural variations in symptom presentation, such as the interpretation of auditory hallucinations in different societies.
- 💡For "explain what is meant by neural correlates" give the definition first (a measurement of brain structure or function that correlates with an experience), then one named example, then the symptom it tracks.
- 💡Balance accurate explanation of genetics, neural correlates and dopamine with evaluation of correlation and causation, polygenic complexity and alternative neurochemical accounts; apply each point to any supplied scenario.
- 💡Use the drug evidence both ways. Antipsychotics working supports dopamine, but they do not work for every patient and improvement can be slow, which weakens it.
- 💡Avoid generic "biologically determinist" evaluation; tie it to a consequence, such as a patient being told nothing but medication will help.
- 💡Where a scenario shows a parent contradicting themselves or criticising constantly, name the concept (double bind, expressed emotion) and quote the line from the stem that shows it; application marks are for the link, not the theory.
- 💡Use the success of CBT for psychosis as evidence for the cognitive explanation, but note that a treatment working does not prove the cause (the treatment-causation fallacy).
- 💡In a "discuss psychological explanations" answer, cover family and cognitive explanations rather than one at length, then evaluate each; the question names both.
- 💡Contrast with the biological explanation for extra AO3: neither family nor cognitive accounts explain the twin concordance data, which points to an interactionist model.
- 💡Always link the drug back to the dopamine hypothesis; the mechanism mark is for explaining that blocking dopamine receptors reduces dopamine action, not for naming the drug.
- 💡For evaluation, weigh effectiveness evidence against side effects and against the point that reducing dopamine only makes sense if the dopamine hypothesis is correct.
- 💡In an application question, use the detail in the stem. A suicidal patient points to clozapine; a patient troubled by side effects points to risperidone or a lower dose.
- 💡Name at least one specific typical and one specific atypical drug. An answer written entirely about "antipsychotics" cannot reach the top band.
- 💡Use specific terminology like 'expressed emotion' and 'normalisation' when describing how these therapies work.
- 💡When evaluating, contrast the active patient engagement required for CBT with the passive nature of taking antipsychotic medication.
- 💡Reference specific evidence to support your evaluation of their effectiveness, ensuring you distinguish between symptom reduction and relapse prevention.
- 💡Use the diathesis-stress model to integrate biological and psychological explanations and explain why identical-twin concordance remains below 100%.
- 💡In application questions, split the stem in two, naming what is the diathesis (family history, early trauma) and what is the stressor (cannabis, a bereavement, moving away from home).
- 💡Give the original and the modern version of the model. Contrasting Meehl with polygenic diathesis and trauma diathesis is a ready-made evaluation point.
- 💡When evaluating combined treatment, note that improved symptom scores without lower readmission rates is a partial success, not a straightforward one.
Common Mistakes
- Confusing positive and negative symptoms; correct this by remembering positive means 'added' experiences (hallucinations) and negative means 'subtracted' functions (avolition).
- Using co-morbidity and symptom overlap interchangeably; correct this by defining co-morbidity as having two distinct conditions simultaneously, whereas symptom overlap refers to two conditions sharing the same symptoms.
- Assuming gender bias only means women are underdiagnosed; correct this by explaining that men are often diagnosed earlier and more frequently, potentially due to women having better interpersonal functioning that masks symptoms.
- Treating concordance rates as proof of genetics. If identical twins share all their genes and concordance is only about 48%, the figure itself proves the environment contributes, and the best answers say so.
- Writing "schizophrenia is caused by too much dopamine" without location. The claim is excess dopamine in subcortical areas for positive symptoms and too little in the prefrontal cortex for negative symptoms; the undifferentiated version is the outdated original.
- Describing a correlate as a cause. Enlarged ventricles co-occur with schizophrenia, but the illness or its medication may be causing the change, so nothing about direction of causation follows.
- Forgetting glutamate. Candidate genes and drugs such as ketamine implicate glutamate, so an answer that treats dopamine as the whole biochemistry misses an obvious AO3 point.
- Saying twins share the same environment as a throwaway line. Name the confound: identical twins are treated more alike than fraternal twins, so concordance inflates heritability.
- Confusing the double bind with expressed emotion. The double bind is contradictory communication proposed as a cause of onset; expressed emotion is negative emotional tone that predicts relapse in someone already diagnosed.
- Presenting the schizophrenogenic mother and double bind as established fact. Both rest on retrospective clinical impressions of the parents of unwell adults, and the evidence base is weak, which is the evaluation the marks are for.
- Ignoring the ethical implications of parent-blaming. Socially sensitive research that blames mothers adds guilt to families already carrying the care burden, and this is a strong AO3 point.
- Treating cognitive explanations as explaining the origin. They describe the proximal cause, what is happening in the mind now, and say nothing about the distal cause, what started it.
- Describing Frith with no named study. The Stroop finding is what turns a description of central control into credited evidence.
- Saying antipsychotics cure schizophrenia. They suppress symptoms while taken, and relapse is common when medication stops, which is why compliance is a central issue.
- Muddling the two types. Typical drugs are dopamine antagonists with strong side effects; atypical drugs act on a wider range of receptors, with a better side-effect profile, and both block dopamine.
- Naming tardive dyskinesia without saying what it is. Marks come from describing involuntary movements of the face and tongue caused by dopamine supersensitivity, not from the term alone.
- Assuming effectiveness evidence is clean. Healy pointed out that some trial data were published more than once, exaggerating the apparent evidence, and that the calming effect can be mistaken for a reduction in psychosis.
- Leaving out the ethical argument. Antipsychotics used to make patients easier for staff to manage, the chemical-cosh criticism, raise a human-rights issue that is worth a full AO3 paragraph.
- Error: Claiming that CBT cures schizophrenia. Correction: State that CBT helps manage symptoms and reduces distress, but does not cure the underlying condition.
- Error: Confusing family therapy with general counselling. Correction: Specify that family therapy actively targets expressed emotion (EE) and provides psychoeducation to relatives.
- Error: Stating that psychological therapies work immediately while contrasting them with medication. Correction: Explain that both CBT and family therapy require time, commitment, and multiple sessions to show efficacy.
- Describing the model as "nature and nurture both matter" and stopping. The marks are for the specific claim that vulnerability alone and stress alone are each insufficient.
- Using Meehl's single schizogene as the current model. Modern genetics finds many genes of small effect, which is a development of the model and a good AO3 point.
- Assuming the diathesis must be genetic. Read's work makes childhood trauma a diathesis in its own right, so the vulnerability half is not automatically biological.
- Forgetting that stress in this model is not only life events; cannabis is the example the specification content is usually examined on.
- Writing about the interactionist approach only as an explanation. The specification asks about explaining and treating, so combined treatment and its evidence must appear.