Schizophrenia — AQA A-Level Psychology
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Schizophrenia explained
Schizophrenia is a psychosis affecting about 1% of people, and there is no blood test: a clinician matches the patient against a list of symptoms.
Read the full explanation
Positive symptoms are additions to ordinary experience, chiefly hallucinations (usually voices) and delusions of persecution, grandeur or control. Negative symptoms are losses, chiefly speech poverty and avolition, which Andreasen pinned down as neglected hygiene, low energy and abandoned goals. The manuals disagree: DSM needs one positive symptom, ICD accepts two negative ones. Cheniaux had two psychiatrists diagnose the same 100 patients; one found 26 cases by DSM against 44 by ICD, the other 13 and 24. Validity suffers too, from co-morbidity, symptom overlap with bipolar disorder and cultural bias.
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 Bateson's double bind traps a child in contradictory messages punished by withdrawn love, so the world comes to seem dangerous.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. Token economies as used in the management of schizophrenia.
None of these cures schizophrenia; each makes living with it easier, normally alongside medication. CBT for psychosis runs for roughly five to twenty sessions in which the patient traces where a belief came from and tests it against reality: explaining voices as the patient's own inner speech does not remove them, but it strips out the terror. Jauhar reviewed 34 trials and found a clear if small effect on positive and negative symptoms. Family therapy works on the household instead, lowering expressed emotion and sharing the care burden; Pharaoh's meta-analysis found better medication compliance and fewer relapses. Token economies come from operant conditioning: tokens are secondary reinforcers, earned for washing or dressing and swapped for privileges, which manages institutional behaviour rather than treating illness.
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
- Describe hallucinations, delusions, speech poverty and avolition, and state which are additions and which are losses.
- Explain how Cheniaux's study shows low inter-rater reliability and disagreement between DSM and ICD on the same patients.
- Apply symptom overlap and co-morbidity to explain why one patient may be called schizophrenic by ICD and bipolar by DSM.
Show all 26 objectives
- Evaluate the validity of diagnosis using African-Caribbean diagnosis rates and Loring and Powell's gender bias figures.
- 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.
- Explain how CBT for psychosis changes what a patient makes of their voices rather than removing them.
- Describe what family therapy targets in the home and what Pharaoh's meta-analysis found it improved.
- Explain how a token economy uses secondary reinforcers to change behaviour that institutionalisation produced.
- Apply the distinction between treating and managing to place CBT, family therapy and token economies correctly.
- Evaluate token economy evidence using Glowacki's handful of quality studies and the file-drawer problem.
- 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
- Classification is the grouping of symptoms into a syndrome, and diagnosis is deciding a particular patient shows it; both rest on DSM-5 or ICD-10 rather than on any biological test.
- Positive symptoms are experiences added to normal functioning: hallucinations, which are perceptions with no basis in reality and are most often auditory, and delusions, which are irrational beliefs such as persecution, grandeur or bodily control.
- Negative symptoms are functions lost: speech poverty means reduced fluency and quality of speech, and avolition means a sharp reduction in goal-directed activity, marked by poor hygiene, low persistence in work or education and lack of energy.
- Reliability means consistency of diagnosis, tested as inter-rater agreement: Cheniaux et al. had two psychiatrists assess 100 patients and their totals were 26 and 13 under DSM and 44 and 24 under ICD.
- Criterion validity is undermined by the same patients being far more likely to receive the diagnosis under ICD than under DSM, so the two systems cannot both be measuring one condition.
- Co-morbidity: Buckley et al. found around half of patients also had depression and nearly half a substance-abuse problem, which raises the question of whether schizophrenia is a single distinct condition.
- Symptom overlap: delusions occur in bipolar disorder and avolition in depression, so under ICD a patient may be schizophrenic and under DSM bipolar.
- Culture bias: African-Caribbean people in Britain are diagnosed at several times the rate of white British people, partly because experiences such as hearing the voice of an ancestor are acceptable in some cultures and are reported to a white clinician as a symptom.
- Gender bias: Loring and Powell gave psychiatrists identical case descriptions and 56% gave a diagnosis of schizophrenia when the patient was called male against 20% when called female; women also show better interpersonal functioning, which can mask symptoms.
- 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 a patient identify irrational thoughts and test them against reality; it does not cure the illness but changes how the patient interprets and copes with symptoms, and NICE recommends it.
- A worked CBT mechanism: a patient who hears voices is offered a normalising explanation, that the voices are their own inner speech misattributed, which reduces the anxiety and distress the belief was causing.
- Jauhar et al.'s review of 34 studies found clear evidence of a small effect of CBT on both positive and negative symptoms.
- Family therapy aims to reduce stress in the home, cutting expressed emotion, reducing anger and guilt, improving beliefs about the illness and building a therapeutic alliance with relatives so that care is shared.
- Pharaoh et al.'s meta-analysis found family therapy improved compliance with medication and reduced relapse and readmission, though evidence on quality of life and social functioning was weaker.
- Token economies rest on operant conditioning: tokens are secondary reinforcers given immediately for a target behaviour and later exchanged for primary reinforcers or privileges such as sweets, a walk or a film.
- Targets are the behaviours that develop with institutionalisation, such as personal care, getting dressed and social interaction, so a token economy manages the condition rather than treating it.
- Glowacki et al. found only a handful of high-quality studies of token economies, all showing reduced negative behaviours, which raises the file-drawer problem of unpublished failures.
- 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
- 💡When asked to outline positive symptoms, give each term, a precise definition and a brief example; evaluate classification only when the command word requires it.
- 💡In a discussion, treat co-morbidity, symptom overlap, culture bias, gender bias and inter-rater reliability as distinct issues, explaining what each means for diagnosis or patients.
- 💡Where a scenario names a patient (hearing a dead relative speak, or staying in bed all day), label the symptom as positive or negative before you explain it; the application mark is for the labelling.
- 💡Say which manual you are using. Answers that state "DSM requires one positive symptom, ICD allows two negative symptoms" pick up the classification mark automatically.
- 💡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.
- 💡Structure an extended answer by therapy: explain how each works, then evaluate effectiveness evidence, appropriateness and ethical implications.
- 💡Quote the mechanism, not only the name. "Tokens are secondary reinforcers exchanged for privileges" earns the operant-conditioning mark; "rewards for good behaviour" does not.
- 💡Use the fact that benefits of token economies do not generalise beyond the ward as a specific, not generic, evaluation point.
- 💡If the stem describes a hostile or critical relative, family therapy is the therapy to recommend, and expressed emotion is the term to justify it with.
- 💡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
- Calling positive symptoms "good" and negative symptoms "bad". Positive means added to normal experience and negative means taken away from it, and an answer that treats the words as value judgements loses the definition mark.
- Describing speech poverty as saying strange things. Speech poverty is a reduction in the amount and quality of speech; disorganised or incoherent speech (speech disorganisation) is classified as a positive symptom in DSM.
- Writing "schizophrenia means split personality". It is a split from reality, not dissociative identity disorder, and examiners treat the confusion as a knowledge error.
- Treating reliability and validity as one evaluation point. Reliability is consistency between diagnosticians or across time, validity is whether the diagnosis identifies a real and distinct condition, and co-morbidity and symptom overlap are validity issues, not reliability ones.
- Quoting studies without figures. "Cheniaux showed diagnosis is unreliable" earns far less than the same study with the two psychiatrists and their differing totals.
- 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.
- Claiming CBT removes hallucinations. It changes the meaning a patient puts on the symptom and the distress it causes, and examiners penalise the stronger claim.
- Describing family therapy as therapy for the family's benefit only. It treats the household as the context for the patient's relapse, principally by lowering expressed emotion.
- Calling a token economy a treatment. The specification wording is management, and a token economy improves ward behaviour without touching the underlying condition.
- Forgetting that these therapies are almost always used with antipsychotics, so improvement cannot be attributed to the psychological therapy alone.
- Missing the ethics of token economies: privileges legitimately available to all patients are made conditional, which disadvantages those most severely ill, who can earn fewest tokens.
- 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.